5-Minute Pediatric Emergency Medicine Consult

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LWBK822-FM LWBK822-Hoffman April 19, 2011 8:53
Fleisher & Ludwigs

5-Minute
Pediatric
Emergency
Medicine
Consult
i
EDITORS ASSOCIATE EDITORS

Robert J. Hoffman, MD, MS Sandip A. Godambe, MD, PhD, MBA
Associate Professor of Emergency Medicine Associate Professor of Pediatrics
Albert Einstein College of Medicine University of Tennessee Health Science Center
Bronx, New York Medical Director, Medical Staff Quality and
Research Director Quality Education
Department of Emergency Medicine Associate Medical Director-EDT, Emergency Services
Beth Israel Medical Center LeBonheur Childrens Hospital
New York, New York Memphis, Tennessee
Director, Medical Toxicology
Emergency Services Institute Raymond Pitetti, MD, MPH
Sheikh Khalifa Medical City Associate Professor of Pediatrics
Abu Dhabi, United Arab Emirates University of Pittsburgh School of Medicine
Medical Director, Sedation Services
Vincent J. Wang, MD, MHA Associate Medical Director, Emergency Department
Associate Professor of Pediatrics Childrens Hospital of Pittsburgh of UPMC
Keck School of Medicine of the University of Pittsburgh, Pennsylvania
Southern California
Associate Division Head
Division of Emergency Medicine
Childrens Hospital Los Angeles
Los Angeles, California
Richard J. Scarfone, MD
Associate Professor of Pediatrics
University of Pennsylvania School of Medicine
Medical Director, Emergency Preparedness
The Childrens Hospital of Philadelphia
Philadelphia, Pennsylvania
ii
Fleisher & Ludwigs

5-Minute
Pediatric
Emergency
Medicine
Consult Editors
Robert J. Hoffman, MD, MS
Vincent J. Wang, MD, MHA
Richard J. Scarfone, MD
Associate Editors
Sandip A. Godambe, MD, PhD, MBA
Raymond Pitetti, MD, MPH
iii
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1605477497
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iv
PREFACE
W
e have produced this first edition of The 5-Minute Pedi- ough but very concise, succinct manner so that all key points about
atric Emergency Medicine Consult with the specific goal clinical presentations, differential diagnoses, diagnostic investiga-
of providing a concise, formatted resource for the clinical tions, therapeutic interventions including medications and doses,
management of pediatric emergencies and common pediatric com- and admission or discharge criteria are presented. This text has
plaints encountered in emergency departments and other settings. been authored by selected pediatric emergency physicians from
As academic pediatric emergency physicians, our goal is to apply both emergency and pediatric medicine backgrounds to provide
the best evidence, published clinical practice guidelines, and other true subspecialty expertise.
information to optimize patient care. Numerous constraints may in- The 5-Minute Pediatric Emergency Medicine Consult will be use-
terfere with ones ability to stay appraised of the most current evi- ful to trainees as well as to clinicians far beyond training. Though the
dence and guidelines applicable to pediatric emergency medicine. editors and authors practice pediatric emergency medicine within
We recognize this and present this book as a resource for those the confines of emergency departments in academic medical cen-
who also wish to practice evidence-based medicine but require the ters, we recognize that most pediatric emergencies are not treated
information distilled in a single, easily accessible reference. This in such settings, and many pediatric emergencies are treated out-
5-Minute Pediatric Emergency Medicine Consult is exactly such a side of an emergency department altogether. Thus, we have taken
reference book. Honorifically named for the Fleisher and Ludwig great strides to produce a reference that represents optimal man-
Textbook of Pediatric Emergency Medicine, which is the seminal agement of emergent and urgent pediatric conditions as well as
comprehensive textbook of pediatric emergency medicine, our text common pediatric complaints in all such locations. Clinicians prac-
seeks to provide a rapid reference for use in the clinical workplace ticing in a tertiary care academic medical center with extensive
rather than thorough, extensive coverage of the subject matter. The subspecialty support or those in the community setting in which
5-Minute Pediatric Emergency Medicine Consult is intended to be little or no subspecialty support will find this text to be an invaluable
accurate, pointed, and readily integrated into practice rather than resource.
definitive. We hope this book will serve as a useful and frequently used
Clinicians at all levels of training and all stages of career de- resource to assist in our common goal of providing the best possible
velopment need references to facilitate the provision of optimal pediatric emergency care to our patients.
patient management. Each chapter presents information in a thor-
v
FOREWORD
F
ive Minutes What can you do in 5 minutes? Working in the portant overview. At other points, it will be used for a familiar or
pediatric emergency department for more than 35 years has common clinical situation but a 5-minute refresher will provide a re-
often been a humbling experience. Along the way, we have assuring double check to make sure nothing has been overlooked
learned many lessons. One of the most important has been the or forgotten. In either case, that initial orientation and preparation
value of orientation and preparation. We have all provided care for will prove most valuable.
children when they suddenly burst through the doors in the arms We are honored to have our names as part of the title of this
of a police officer or paramedic with major multisystem trauma or book. We view it as a perfect companion to the Textbook of Pediatric
cardiac arrest. We have been in the same critical situation when we Emergency Medicine, 6th Edition where more in-depth information
had just 5 minutes to prepare for the event. As many of the readers can be learned. We thank the editors and authors for allowing us
of this book know, that extra 5 minutes makes a world of difference to share in this work. We see it as yet another important step in
to the outcome and perceived quality of care provided. Even when improving the emergency care to ill and injured children, which has
residents are assigned to the emergency department for a rotation been the foundation of our lifes work.
it is our perception that those who get a brief orientation to the site Five minutes can mean a lot, and 5 minutes of reading one of
perform much better than those who do not. And those who take a the topics that follow will set you on a pathway toward rewarding
minute to prepare before going into a treatment room also evolve clinical care.
to be better physicians.
That brings us to this book, The 5-Minute Pediatric Emergency STEPHEN LUDWIG, MD
Medicine Consult. We know that using this book will provide physi- Philadelphia, Pennsylvania
cians with the orientation and preparation needed to address a wide GARY R. FLEISHER, MD
range of clinical problems. Sometimes it will be a new condition that Boston, Massachusetts
the physician has not faced before, and the topic will give an im- February 2011
vi
LWBK822-FM LWBK822-Hoffman May 4, 2011 21:59
ACKNOWLEDGMENTS
I
thank my wife Miya for her understanding, support, and sacrifice I would like to thank my patients, colleagues, and mentors who have
during the production of this text. taught me so much in my career. Your collective inquisitiveness,
I sincerely thank Lewis Goldfrank and Steve Davidson for giving selflessness, and support have inspired me to become a clinician
me the most formative academic opportunities of my career, and worthy of your trust. I am grateful to the many authors of this book
Lewis Nelson and Bob Hoffman for serving as ideal models of aca- who have worked so hard to create an outstanding resource for
demic emergency physicians and clinician educators. To the many patient care. Thank you to my wife, Karen, for your love and support,
emergency medicine residency classes and notably the chief res- and thank you to my wonderful children Steven and JuliaI love you
idents of Beth Israel Medical Center, I extend thanks for years of and Im proud of the young people that you have become.
rewarding interaction and inspiration to remain in academics. R.J.S.
I acknowledge friends across the globe past and present who
have assisted my endeavors by helping me balance productive work This book is the result of the hard work of countless dedicated
with enjoyable recreation. Lastly, I thank the families and patients authors. It has been a pleasure to work with them and the editorial
to whom Ive provided emergency care for the privilege of treating and publishing team of this book. I want to extend a special thanks to
them. the many residents and fellows past and present whose questions
R.J.H. and pursuit of knowledge have made me a better clinicianeducator.
I would also like to thank my many mentors throughout my training.
With any significant work, there are inevitably numerous individuals Finally, many thanks to my loving family, especially my wife, Libby,
who have contributed to bring this project to fruition. I would like to and three children, Maya, Samir, and Riya, who have made sacrifices,
thank the authors and editors, who have spent enormous amounts yet have been there to support, entertain, and inspire me.
of their own personal time to produce this book. Thanks to the
patients and my colleagues: my co-attendings, the residents and S.A.G.
fellows, and the nurses, who have inspired me to be a better clinician
and teacher. I also want to acknowledge Gary Fleisher and the late I would first like to thank my wife, Leslie, my sons Noah, Ben and
Michael Shannon for their mentorship and guidance. Finally, I deeply Logan, and my daughter Lia, for all of their support and love. Ev-
appreciate my wife Esther, and my parents Jaw and Jean, for their erything I am, I owe to them. I would also like to thank the au-
continual support, patience, and sacrifice. thors that I have worked with, the editorial staff for their support,
V.J.W. and my co-editors who had to put up with me. It has truly been a
pleasure to work on this project, and I have learned a great deal
from all.
R.P.
vii
viii
CONTRIBUTORS
Tzvi Aaron, MD Carla Maria P. Alcid, MD Bhawana Arora, MD

Fellow Assistant Professor Pediatric Emergency Medicine Fellow
Department of Pediatric Emergency Department of Pediatrics Department of Emergency Medicine
Medicine Tulane University School of Medicine Childrens Hospital of Michigan
New York-Presbyterian Hospital Medical Director Detroit, Michigan
Weill Cornell Medical Center Department of Pediatric Emergency
Dana Aronson Schinasi, MD
New York, New York Tulane University Hospital and Clinics
Fellow
Jacobo Abadi, MD New Orleans, Louisiana
Department of Emergency Medicine
Associate Professor Michelle J. Alletag, MD The Childrens Hospital of Philadelphia
Department of Pediatrics Fellow Philadelphia, Pennsylvania
Albert Einstein College of Medicine Pediatric Emergency Medicine
Jacobi Medical Center Magdy W. Attia, MD
Yale University
Bronx, New York Professor
New Haven, Connecticut
Department of Pediatrics
Alyssa Abo, MD
Nahar D. Alruwaili, MD Jefferson Medical College
Assistant Clinical Professor, Pediatrics
Toronto, Ontario, Canada Philadelphia, Pennsylvania
UC Davis School of Medicine
Fellowship Director
Sacramento, California Caroline Altergott, MD
Associate Director
Jennifer Adu-Frimpong, MD Attending Physician
Cooper University Hospital Division of Emergency Medicine
Alfred I. duPont Hospital for Children
Camden, New Jersey Childrens Hospital Los Angeles
Wilmington, Delaware
Dewesh Agrawal, MD
Mark A. Auerbach, MD
Associate Professor Robin L. Altman, MD
Assistant Professor of Pediatrics
Department of Pediatrics and Emergency Associate Professor
Yale University School of Medicine
Medicine Department of Pediatrics
Attending Physician
George Washington University School New York Medical College
Section of Pediatric Emergency Medicine
of Medicine Chief
Yale New Haven Childrens Hospital
Director Section of General Pediatrics
New Haven, Connecticut
Pediatric Residency Program Maria Fareri Childrens Hospital at
Childrens National Medical Center Westchester Jeffrey R. Avner, MD
Washington, DC Valhalla, New York Professor
Faiz Ahmad, MD Department of Pediatrics
Christopher S. Amato, MD
Assistant Clinical Professor Albert Einstein College of Medicine
Department of Pediatrics Chief, Childrens Emergency Service
Morristown Hospital
Columbia University College of Physicians Department of Pediatrics
Morristown, New Jersey
and Surgeons Bronx, New York
Attending Physician Yasmeen Ansari, MD
Michael R. Baker, MBBS
Division of Pediatric Emergency Medicine Department of Emergency Medicine
Morgan Stanley Children Hospital of North Shore University Hospital
New York Presbyterian Manhasset, New York
New York, New York Alexandre Arkader, MD
Sara Ahmed, MD Assistant Professor
Assistant Professor Department of Orthopaedic Surgery
Department of Pediatric Emergency Keck School of Medicine of the University
Medicine of Southern California
The Childrens Hospital of Michigan Director, Bone and Soft Tissue Tumor
Detroit, Michigan Program
Khalid Alansari, MD Childrens Orthopaedic Center
Department of Pediatrics Childrens Hospital Los Angeles
Pediatric Emergency Center Al-Sadd Los Angeles, California
Hamad Medical Corporation
Doha, Qatar
ix
x r r r Contributors
Michael D. Baldovsky, DO, MBA Robert A. Belfer, MD Stuart A. Bradin, DO

Fellow Attending Physician Assistant Professor of Pediatrics and
Division of Emergency Services Department of Pediatrics Emergency Medicine
LeBonheur Childrens Medical Center Childrens Hospital of Philadelphia The University of Michigan
Memphis, Tennessee Philadelphia, Pennsylvania Attending Physician
Director, Pediatric Emergency Medicine Childrens Emergency Services
Nelson H. Bansil, DO
Department of Pediatrics Department of Emergency Medicine,
Fellow
Virtua Hospital Division of Pediatric EMergency
Department of Pediatric Emergency
Voorhees, New Jersey Medicine
Medicine
The University of Michigan Helath System
Loma Linda University Medical Center Brenda J. Bender, MD Ann Arbor, Michigan
Loma Linda, California Attending Physician
Department of Emergency Medicine Kristen Breslin, MD
Besh Barcega, MD
Alfred I. duPont Hospital for Children Fellow
Assistant Professor
Wilmington, Delaware Division of Emergency Medicine
Department of Emergency Medicine and
Childrens National Medical Center
Pediatrics
Eyal Ben-Isaac, MD Washington, DC
Loma Linda University School of Medicine
and Childrens Hospital Assistant Professor Seth L. Brindis, MD
Medical Director, Pediatric Keck School of Medicine of the University Clinical Instructor
Department of Emergency Medicine of Southern California Department of Pediatrics
Loma Linda University Medical Center Director, Pediatric Residency Program David Geffen School of Medicine at
Loma Linda, California Department of Pediatrics University of California, Los Angeles
Childrens Hospital Los Angeles Attending Physician
Peter L.J. Barnett MBBS, MSc, MSpMed Los Angeles, California Department of Emergency Medicine
Associate Clinical Professor
Childrens Hospital of Orange County
Department of Paediatrics Seema Bhatt, MD Orange, California
University of Melbourne Attending Physician, Emergency Medicine
Deputy Director Cincinnati Childrens Hospital Medical Kevin D. Buckley, MD
Department of Emergency Medicine Center Director, Medical Services
Royal Childrens Hospital Cincinnati, Ohio Emergency Department
Parkville, Victoria, Australia Naval Hospital Sigonella
Mercedes M. Blackstone, MD Sicily, Italy
Sylvia Baszak, MD
Assistant Professor of Clinical Pediatrics
Assistant Professor Casey W. Buitenhuys, MD
University of Pennsylvania School of
Department of Pediatrics, Division of Clinical Instructor
Medicine
Emergency Medicine Department of Emergency Medicine
Attending Physician
Robert Wood Johnson Medical School, Harbor University of California Medical
University of Medicine and Dentistry of Center
New Jersey Torrance, California
Medical Staff
Kristy Bunagan, MD
Department of Pediatrics, Division of Keith Blum, MD
Emergency Care University of Nevada, Las Vegas
Robert Wood Johnson University Hospital Sunrise Hospital Medical Center Sean E. Button, MD
New Brunswick, New Jersey Las Vegas, Nevada Fellow
Jeff Beecher, DO Department of Pediatric Emergency
Division of Neurosurgery Richard G. Boles, MD Medicine
State University of New York, Stony Brook Associate Professor of Pediatrics Childrens Hospital of Pittsburgh of UPMC
Stony Brook, New York Keck School of Medicine of the University Pittsburgh, Pennsylvania
of Southern California
Solomon Behar, MD Division of Medical Genetics James M. Callahan, MD
Assistant Professor Childrens Hospital Los Angeles Associate Professor of Clinical Pediatrics
Keck School of Medicine of the University Los Angeles, California Division of Emergency Medicine,
of Southern California Department of Pediatrics
Attending Physician Cara Bornstein, DO University of Pennsylvania School of
Department of Emergency Medicine Attending Physician Medicine
Los Angeles County Medical Center Department of Pediatric Emergency Attending Physician
Division of Emergency Medicine Medicine Emergency Department
Childrens Hospital Los Angeles Long Island Jewish Medical Center The Childrens Hospital of Philadelphia
Los Angeles, California New Hyde Park, New York Philadelphia, Pennsylvania
Contributors r r r xi
Kerry Caperell, MD Lauren S. Chernick, MD Ilene A. Claudius, MD

Fellow Assistant Professor of Clinical Pediatrics Assistant Professor
Department of Pediatrics Attending Physician Department of Emergency Medicine
University of Pittsburgh Division of Pediatric Emergency Medicine LAC + USC and Childrens Hospital
Childrens Hospital of Pittsburgh Columbia University Los Angeles, California
Pittsburgh, Pennsylvania New York, New York Stephanie G. Cohen, MD
Chung Chiang, DO Fellow
Brandon C. Carr, MD Attending Physician Department Pediatric Emergency
Department of Emergency Medicine Department of Pediatrics Medicine
Childrens Hospital of Alabama Childrens Hospital of Philadelphia Newark Beth Israel Medical Center
Birmingham, Alabama Philadelphia, Pennsylvania Newark, New Jersey
Virtua Hospital Keri Cohn, MD, DTMH
Voorhees, New Jersey Fellow
Christopher S. Cavagnaro, MD
Kevin Ching, MD Division of Pediatric Emergency Medicine
Attending Physician
Assistant Professor Division of Pediatric Infectious Diseases
Montefiore Childrens Hospital
Department of Emergency Medicine Childrens Hospital Boston
Bronx, New York
New York University School of Medicine Boston, Massachusetts
Assistant Professor M. Sitki Copur, MD
Andy Y. Chang, MD Department of Emergency Medicine Associate Professor
Assistant Professor of Urology Bellevue Hospital Department of Internal Medicine
Keck School of Medicine of the University New York, New York University of Nebraska
of Southern California Medical Director
Division of Urology Corrie E. Chumpitazi, MD
Department of Oncology
Childrens Hospital Los Angeles Assistant Professor
Saint Francis Cancer Center
Los Angeles, California Department of Pediatrics, Section of
Grand Island, Nebraska
Emergency Medicine
Baylor College of Medicine Adiana Yock Corrales, MD
Attending Physician Fellow in Paediatric Emergency Medicine
Todd P. Chang, MD
Emergency Center Department of Emergency Medicine
Assistant Professor
Texas Childrens Hospital Royal Childrens Hospital
Houston, Texas Parkville, Victoria, Australia
George Washington University
Attending Physician M. Colleen Costello, MD
Catherine H. Chung, MD, MPH
Division of Emergency Medicine Fellow
Childrens National Medical Center Division of Emergency Medicine
Washington, DC Sarita Chung, MD Miami Childrens Hospital
Assistant Professor Miami, Florida
Department of Pediatrics Kelly J. Cramm, MD, MPH
David Chao, MD Harvard Medical School Clinical Assistant Professor
Fellow Assistant in Medicine Department of Emergency Medicine
Department of Pediatric Emergency Childrens Hospital Boston Florida State University
Medicine Boston, Massachusetts Assistant Fellowship Director
The Childrens Hospital of Philadelphia Mark X. Cicero, MD Department of Pediatric Emergency
Philadelphia, Pennsylvania Assistant Professor Medicine
Department of Pediatrics Arnold Palmer Hospital for Children
Yale University School of Medicine Orlando, Florida
Jennifer H. Chao, MD
Attending Physician Kate Cronan, MD
Clinical Assistant Professor
Department of Pediatrics Associate Professor
Associate Fellowship Director
Yale-New Haven Childrens Hospital Jefferson Medical College
Division of Pediatric Emergency Medicine
New Haven, Connecticut Philadelphia, Pennsylvania
SUNY Downstate Medical Center
Brooklyn, New York Lynn Babcock Cimpello, MD Attending Physician
Associate Professor Division of Emergency Medicine
Department of Pediatrics Department of Pediatrics
Yu-Tsun Cheng, MD University of Cincinnati Nemours/Alfred I. duPont Hospital for
Fellow Division of Emergency Medicine Children
Division of Emergency Medicine Cincinnati Childrens Hospital Medical Wilmington, Delaware
Childrens Hospital of Los Angeles Center
Los Angeles, California Cincinnati, Ohio
xii r r r Contributors
Barbara Csanyi, MD Naomi Dreisinger, MD Ara Festekjian, MD, MS

Department of Pediatrics Assistant Professor Assistant Professor of Pediatrics
Fundacion Hospital Asil Granollers Albert Einstein College of Medicine Keck School of Medicine of the University
Granollers, Spain Bronx, New York of Southern California
Co-Director of Pediatric Education at Division of Emergency Medicine
Lauren Daly, MD
Beth Israel Medical Center Childrens Hospital Los Angeles
Emergency Department Los Angeles, California
Beth Israel Medical Center
Nemours/Alfred I. DuPont Hospital for
New York, New York Alan T. Flanigan, MD
Children
Yamini Durani, MD Clinical Instructor
Assistant Professor Department of Emergency Medicine
Valerie Davis, MD, PhD Department of Pediatrics University of Cincinnati
Assistant Professor Thomas Jefferson University/Jefferson Cincinnati, Ohio
Department of Pediatrics Medical College
University of Alabama at Birmingham Philadelphia, Pennsylvania Stephen G. Flynn, MD
Attending Physician Attending Physician Fellow
Department of Pediatric Emergency Division of Emergency Medicine Department of Anesthesia and
Medicine Alfred I. DuPont Hospital for Children Critical Care
Childrens Hospital of Alabama Wilmington, Delaware The Hospital of the University of
Birmingham, Alabama Pennsylvania
Marsha Ayzen Elkhunovich, MD
Julia K. Deanehan, MD Fellow
Fellow Division of Emergency Medicine
Division of Emergency Medicine Childrens Hospital Los Angeles
Karen Franco, MD
Childrens Hopital Boston Los Angeles, California
Attending Physician
Boston, Massachusetts Donald Thomas Ellis, II, MD Department of Emergency Medicine
Nathalie Degaiffier Assistant Professor Miami Childrens Hospital
Philadelphia, Pennsylvania Department of Pediatrics, Hospital and Miami, Florida
Emergency Medicine
Atima Chumpa Delaney, MD Duke University Medical Center Broderik J. Franklin, MD
Instructor Durham, North Carolina Senior Consultant, Emergency Medicine
Department of Pediatrics Sheik Khalifa Medical City Abu Dhabi,
Angela M. Ellison, MD
Harvard Medical School United Arab Emirates
Attending Physician
Attending Physician
Division of Emergency Medicine Lana Friedman, MD
Childrens Hospital Boston Fellow
Boston, Massachusetts Division of Pediatric Emergency Medicine
Jennifer Eng Lunt, DO, MHSA
Poonam Desai, MD Mount Sinai Medical Center
Pediatric Emergency Medicine Fellow
Weill Cornell Medical College New York, New York
Cohen Childrens Medical Center of
New York, New York New York
Department of Emergency Medicine Rachel Gallagher, MD
North Shore-Long Island Jewish Health
New York Hospital Queens Fellow
System
Flushing, New York Division of Emergency Medicine
New Hyde Park, New York
Childrens Hospital Boston
Maria Carmen G. Diaz, MD Michael P. Epter, DO Boston, Massachusetts
Department of Pediatrics, Division of Assistant Professor
Pediatric Emergency Medicine University of Nevada School of Medicine Fidel Garcia, MD
Nemours/Alfred I. duPont Hospital University Medical Center Baptist Health
Wilmington, Delaware Program Director, Emergency Medicine Jacksonville, Florida
Faye E. Doerhoff, MD Residency
Associate Professor Las Vegas, Nevada Gregory P. Garra, DO
Department of Pediatrics Kumarie Etwaru, MD Clinical Assistant Professor
St. Louis University School of Medicine Assistant Professor Department of Emergency Medicine
Attending Physician Albert Einstein College of Medicine Stony Brook University School of
Division of Pediatric Emergency Medicine Bronx, New York Medicine
Cardinal Glennon Childrens Medical Attending Physician Residency Program Director
Center Co-director of Pediatric Emergency Medicine Department of Emergency Medicine
St. Louis, Missouri Beth Israel Medical Center Stony Brook University Medical Center
New York, New York Stoney Brook, New York
Contributors r r r xiii
Marianne Gausche-Hill, MD Sandip A. Godambe, MD, PhD, MBA Ewa Grochowalska, MD

Professor Associate Professor of Pediatrics Clinical Instructor of Pediatrics
Department of Medicine University of Tennessee Health Sciences Department of Pediatrics, Division of
David Geffen School of Medicine Center Pediatric Emergency Medicine
Position Director of EMS and Pediatric Medical Director, Medical Staff Quality and Robert Wood Johnson Medical
Emergency Medicine Fellowships Quality Education School - UMDNJ
Department of Emergency Medicine Associate Medical Director-EDT, Medical Staff
Harbor-UCLA Medical Center Emergency Services Division of Pediatric Emergency Medicine
Torrance, California Staff Physician, Emergency Services Rober Wood Johnson University Hospital
LeBonheur Childrens Medical Center New Brunswick, New Jersey
Barry G. Gilmore, MD, MBA Memphis, Tennessee
Toni K. Gross, MD, MPH
Associate Professor
Nina Gold, MD Attending Physician
University of Medicine and Dentistry of Emergency Department
University of Tennessee Health Sciences
New Jersey Phoenix Childrens Hospital
Center - Memphis
Newark, New Jersey Phoenix, Arizona
Director of Emergency Services
Pediatric Emergency Medicine Attending
LeBonheur Childrens Hospital Sandra L. Grossman, MD
Memphis, Tennessee Assistant Professor
Hackensack University Medical Center
Hackensack, New Jersey
Beth Y. Ginsburg, MD UMDNJ-Robert Wood Johnson Medical
Assistant Professor Karen Goodman, MD School
Department of Emergency Medicine Assistant Professor Attending Physician
Mount Sinai School of Medicine Department of Emergency Medicine and Department of Emergency Medicine,
New York, New York Pediatrics Division of Pediatric Emergency
Attending Physician New York University Medical Center Medicine
Department of Emergency Medicine Bellvue Hospital Center Cooper University Hospital
Elmhurst Hospital Center New York, New York Camden, New Jersey
Elmhurst, New York Marc Gorelick, MD, MSCE Amit K. Gupta, MD
Professor Department of Emergency Medicine
Kimberly A. Giusto, MD Department of Pediatrics Staten Island University Hospital
Attending Physician Medical College of Wisconsin Staten Island, New York
Cohen Childrens Medical Center of New Jon E. Vice Chair
York Chiraag Gupta, MD
North Shore-LIJ Health System Childrens Hospital of Wisconsin Maya Haasz, MDCM
New Hyde Park, New York Milwaukee, Wisconsin Fellow
Miguel Glatstein, MD Monika Goyal, MD
Medicine
Staff Physician University of Pennsylvania School of
Hospital for Sick Children
Division of Pediatric Emergency Medicine Medicine
Toronto, Ontario, Canada
Dana Childrens Hospital Attending Physician
Tel Aviv, Israel Division of Emergency Medicine Claire M. Hack, MD
Childrens Hospital of Philadelphia Newark Beth Israel Medical Center
Robert F. Gochman, MD Philadelphia, Pennsylvania Newark, New Jersey
Assistant Professor Daniel A. Green, MD Christopher J. Haines, DO
Department of Pediatrics Clinical Assistant Professor Assistant Professor
Albert Einstein College of Medicine Department of Pediatrics Department of Emergency Medicine and
Bronx, New York Florida International University/Herbert Pediatrics
Program Director - Pediatric Emergency Wertheim College of Medicine Dexel University College of Medicine
Medicine Attending Physician Director
Long Island Jewish Medical Center/ Department of Emergency Medicine Department of Emergency Medicine
Schneider Childrens Hospital Miami Childrens Hospital St. Christophers Hospital for Children
New Hyde Park, New York Miami, Florida Philadelphia, Pennsylvania
xiv r r r Contributors
Matthew Lee Hansen, MD Jeffrey Hom, MD, MPH Nazreen Jamal, MD

Fellow Departments of Emergency Medicine and Fellow
Department of Emergency Medicine Pediatrics/Emergency Services Division of Emergency Medicine
Oregon Health & Science University New York University Childrens National Medical Center
Portland, Oregon Clinical Assistant Professor Washington, DC
New York University Langone Medical
Andrew Heggland, MD
Center David H. Jang
Fellow
New York, New York Medical Toxicology Fellow
Senior Fellow
Miami Childrens Hospital Travis K.F. Hong, MD
Miami, Florida Fellow
New York University
Division of Emergency Medicine and
Benjamin Heilbrunn, MD New York, New York
Transport
Fellow
Childrens Hospital of Los Angeles
Division of Emergency Medicine Jewel Jones-Morales, MD
Childrens Hospital Los Angeles Weill Cornell Medical College
Los Angeles, California Eric C. Hoppa, MD New York, New York
Attending Physician Department of Emergency Medicine
P. Micky Heinrichs, MD
Department of Pediatric Emergency New York Hospital Queens
Attending Physician
Medicine Flushing, New York
Pediatric Urgent Care
Alexander and Stephen Cohen Childrens
Medical Center of New York/Long Rahul Kaila, MD
Kara E. Hennelly, MD Island Jewish Medical Center Pediatric Emergency Medicine Fellow
Fellow New Hyde Park, New York Department of Pediatrics
Division of Emergency Medicine Childrens Hospital of Michigan
Joseph B. House, MD
Childrens Hospital Boston Detroit, Michigan
Clinical Instructor
Boston, Massachusetts
Department of Emergency Medicine and John T. Kanegaye, MD
Stephanie H. Hernandez, MD Pediatrics Clinical Professor
Metropolitan Hospital Center University of Michigan Department of Pediatrics
New York, New York University of Michigan Health System University of California San Diego School
Ann Arbor, Michigan of Medicine
Robert W. Hickey, MD
Division of Pediatric Emergency Medicine La Jolla, California
Carl K. Hsu, MD Attending Physician
Childrens Hospital Pittsburgh
Brooklyn Hospital Center Emergency Care Center
Pittsburgh, Pennsylvania
Brooklyn, New York Rady Childrens Hospital San Diego
Esther D.P. Ho, MD San Diego, California
Associate Clinical Professor Kristopher Hunt, MD
Department of Family Medicine Department of Emergency Medicine
Nirupama Kannikeswaran, MD
University of California, Irvine, School of Beth Israel Medical Center
Medicine New York, New York
Attending Physician
Wayne State University
Department of Family Medicine, Hospital Katrina E. Iverson, MD
Program Pediatric Emergency Medicine Fellow
Childrens Hospital of Michigan
University of California Irvine Medical Division of Emergency Medicine
Detroit, Michigan
Center Childrens Hospital of Michigan
Orange, California Detroit, Michigan
Carl P. Kaplan, MD
Robert J. Hoffman, MD, MS
Sujit Iyer, MD Assistant Professor
Associate Professor of Emergency
Attending Physician Department of Pediatrics and Emergency
Medicine
Department of Pediatric Emergency Medicine
Albert Einstein College of Medicine
Medicine Stony Brook University School of
Bronx, New York
Director Medicine
Research Director
Medical Education for Pediatric Attending Physician
Emergency Medicine Division of Pediatric Emergency Medicine
Beth Israel Medical Center
Emergency Service Partners, LP Stony Brook Long Island Childrens
New York, New York
Austin, Texas Hospital
Director, Medical Toxicology
Stony Brook, New York
Emergency Services Institute
Sheikh Khalifa Medical City
Abu Dhabi, United Arab Emirates
Contributors r r r xv
Mia L. Karamatsu, MD Abu N.G.A. Khan, MD, MSc Young-Jo Kim, MD, PhD
Clinical Instructor Assistant Clinical Professor Associate Professor of Orthopedic
Department of Emergency Medicine Department of Pediatrics Surgery
Loma Linda University Columbia University College of Physicians Department of Orthopaedic Surgery
Loma Linda University Childrens Hospital and Surgeons Childrens Hospital Boston
Loma Linda, California Attending Physician Boston, Massachusetts
Denise G. Karasic, DO Morgan Stanley Children Hospital of Bruce L. Klein, MD
Attending Physician New York Presbyterian Associate Professor
Nemours/A.I. duPont Hospital for Children New York, New York Department of Pediatrics and Emergency
Wilmington, Delaware Medicine
Kajal Khanna, MD, JD George Washington University School of
Harry C. Karydes, DO Fellow Medicine and Health Sciences
Toxicology Fellow Division of Emergency Medicine Section head, Physician Outreach
Department of Emergency Medicine Childrens Hospital Los Angeles Division of Emergency Medicine
Cook County Hospital Los Angeles, California Childrens National Medical Center
Chicago, Illinois Washington, District of Columbia
Anupam Kharbanda, MD, MS
John Kashani, DO Susanne Kost, MD
Assistant Professor
Department of Pediatrics Associate Professor of Pediatrics
New Jersey Medical School Jefferson Medical College
University of Minnesota
University of Medicine and Dentistry of Philadelphia, Pennsylvania
Research Director
New Jersey Medical Director, Day Medicine and
Newark, New Jersey Sedation Service
Amplatz Childrens Hospital
Nemours/A.I.duPont Hospital for Children
Robert M. Kay, MD Minneapolis, Minnesota
Associate Professor
Department of Orthopaedic Surgery Hnin Khine, MD Steven Krebs, MD
Keck School of Medicine of the University Associate Professor of Clinical Pediatrics Department of Pediatrics
of Southern California Albert Einstein College of Medicine St. Louis University School of Medicine
Vice Chief Attending Physician Division of Pediatric Emergency Medicine
Childrens Orthopaedic Center Department of Pediatrics Cardinal Glennon Childrens Medical
Childrens Hospital Los Angeles Childrens Hospital of Montefiore Center
Los Angeles, California Bronx, New York St. Louis, Missouri
Allison A. Keller, MD In K. Kim, MD, MBA William I. Krief, MD

Assistant Professor Associate Professor Assistant Professor
Department of Pediatrics Department of Pediatrics Department of Pediatrics and Emergency
University of Utah University of Louisville Medicine
Pediatric Emergency Medicine Fellowship Director Albert Einstein College of Medicine
Primary Childrens Medical Center Department of Pediatrics Bronx, New York
Salt Lake City, Utah Kosiar Childrens Hospital Steven and Alexandra Childrens Medical
Louisville, Kentucky Center of New York
David O. Kessler, MD, MSc New Hyde Park, New York
Kristin McAdams Kim, MD, PhD Worapant Kriengsoontornkij, MD
Columbia University College of Physicians
Assistant Professor Instructor
and Surgeons
Department of Pediatrics, Division of Department of Pediatrics
Director of Clinical Operations, Attending
Pediatric Emergency Medicine Mahidol University
Physician
University of Minnesota Medical School Attending Physician
Amplatz Childrens Hospital, Department of Pediatrics
New York Presbyterian Morgan Stanley
UMMC/Fairview Siriraj Hospital
Childrens Hospital of New York
Minneapolis, Minnesota Bangkok, Thailand
New York, New York
Janice Kezirian, MD Tommy Y. Kim, MD Eileen Murtagh Kurowski, MD
Fellow Assistant Professor Fellow
Department of Emergency Medicine Department of Emergency Medicine Division of Emergency Medicine
University of Tennessee Loma Linda University School of Medicine Cincinnati Childrens Hospital Medical
Emergency Department Loma Linda University Medical Center Center
LeBonheur Childrens Medical Center and Childrens Hospital Cincinnati, Ohio
Memphis, Tennessee Loma Linda, California
xvi r r r Contributors
Karen Y. Kwan, MD Kerry Leupold, DO Frank LoVecchio, DO

Assistant Professor Department of Pediatrics Co-Medical Director, Banner
Department of Pediatrics Division of Emergency Medicine Good Samaritan Poison and Drug
Keck School of Medicine of the University Robert Wood Johnson Medical School Information Center
of Southern California New Brunswick, New Jersey Banner Good Samaritan Medical Center
Division of Emergency Medicine Phoenix, Arizona
Childrens Hospital Los Angeles Nina Lightdale, MD
Assistant Professor Raemma Paredes Luck, MD
Department of Orthopaedics Associate Professor
Justin LaCorte, DO Keck School of Medicine of the University Department of Pediatrics and Emergency
Assistant Professor of Southern California Medicine
Department of Emergency Medicine Division of Orthopaedics Temple University
Hofstra North Shore-LIJ School of Childrens Hospital Los Angeles Attending Physician
Medicine Los Angeles, California Department of Pediatrics and Emergency
Pediatric Emergency Attending Medicine
Department of Pediatric Emergency Antoinette W. Lindberg, MD Temple University Hospital
Cohen Childrens Medical Center Fellow Philadelphia, Pennsylvania
New Hyde Park, New York Department of Pediatric Orthopaedics
Jyothi Lagisetty, MD Seattle Childrens Hospital Daniel M. Lugassy, MD
Attending Physician Seattle, Washington Medical Toxicology Consultant
Department of Emergency Medicine/ New York City Poison Control Center
Pediatrics Deborah R. Liu, MD New York University School of Medicine
Memorial Herman SouthWest Hospital Assistant Professor of Pediatrics Assistant Professor
Houston, Texas Keck School of Medicine of the University Department of Emergency Medicine
of Southern California New York University-Bellevue Hospital
V. Matt Laurich, MD Fellowship Director Center
Fellow Division of Emergency Medicine New York, New York
Department of Emergency Medicine Childrens Hospital Los Angeles
Mount Sinai School of Medicine Los Angeles, California Vincenzo Maniaci, MD
Mount Sinai Medical Center
Attending Physician
New York, New York Cynthia Lodding, MD
Oregon Health and Science University
Megan E. Lavoie, MD Miami Childrens Hospital
Portland, Oregon
Fellow, Pediatric Emergency Medicine Miami, Florida
Department of Pediatrics John M. Loiselle, MD
Childrens Hospital of Wisconsin Associate Professor Mioara D. Manole, MD
Milwaukee, Wisconsin Department of Pediatrics Assistant Professor of Pediatrics
Audrey H. Le, MD Jefferson Medical College Department of Pediatrics
Clinical Assistant Professor Philadelphia, Pennsylvania University of Pittsburgh
Department of Pediatrics Chief, Emergency Medicine Attending Physician
Tulane University Medical Center Department of Pediatrics Department of Pediatric Emergency
Staff Physician Alfred I. DuPont Hospital for Children Medicine
Tulane University Medical Center Wilmington, Delaware Childrens Hospital of Pittsburgh
New Orleans, Louisiana Pittsburgh, Pennsylvania
Calvin G. Lowe, MD
Lois K. Lee, MD, MPH Assistant Professor of Pediatrics Jennifer R. Marin, MD
Assistant Professor Keck School of Medicine of the University Assistant Professor of Pediatrics
Department of Pediatrics of Southern California Department of Pediatrics
Harvard Medical School Attending Physician University of Pittsburgh School of
Assistant in Medicine Division of Emergency Medicine and Medicine
Division of Emergency Medicine Transport Attending Physician
Childrens Hospital Boston Childrens Hospital of Los Angeles Division of Emergency Medicine
Boston, Massachusetts Los Angeles, California Childrens Hospital of Pittsburgh
Tina S. Lee, MD David A. Lowe, MD
Fellow Fellow
Division of Emergency Medicine Division of Emergency Medicine
St. Louis Childrens Hospital Childrens Hospital Boston
St. Louis, Missouri Boston, Massachusetts
Contributors r r r xvii
D. Richard Martini, MD Lilit Minasyan, MD Brent W. Morgan, MD

Professor Assistant Professor Associate Professor
Department of Pediatrics and Psychiatry Department of Emergency Medicine Department of Emergency Medicine
University of Utah School of Medicine Loma Linda University Medical Center Emory University School of Medicine
Director and Childrens Hospital Assistant Medical Director
Department of Psychiatry and Behavioral Loma Linda, California Georgia Poison Center
Health Attending Physician Atlanta, Georgia
Primary Childrens Medical Center Department of Emergency Medicine
Colette C. Mull, MD
Salt Lake City, Utah Childrens Hospital of Orange County
Orange, California
Todd A. Mastrovitch, MD Alfred I. duPont Hospital for Children
Clinical Instructor of Pediatrics in Rakesh D. Mistry, MD, MS Wilmington, Delaware
Emergency Medicine Assistant Professor of Pediatrics Warees T. Muhammad, MD, PhD
Department of Emergency Medicine University of Pennsylvania School of Fellow
Weill Cornell Medical College Medicine Division of Emergency Services
New York, New York Physician LeBonheur Childrens Hospital
Pediatric Emergency Medicine Attending Division of Emergency Medicine Memphis, Tennessee
Department of Emergency Medicine The Childrens Hospital of Philadelphia
New York Hospital Queens Philadelphia, Pennsylvania John Munyak, M.D
Flushing, New York Sports Medicine Program Director
Manoj K. Mittal, MD Department of Emergency Medicine
David J. Mathison, MD Clinical Assistant Professor North Shore University Hospital
Emergency Medicine Fellow Department of Pediatrics Manhasset, New York
Department of Pediatrics, Division of University of Pennsylvania School of
Medicine Sage Myers, MD
Emergency Medicine
Attending Physician Clinical Instructor
Division of Emergency Medicine University of Pennsylvania School of
Washington, DC
The Childrens Hospital of Philadelphia Medicine
Craig A. McElderry, MD Philadelphia, Pennsylvania Attending Physician
Assistant Professor of Pediatrics The Childrens Hospital of Philadelphia
Keck School of Medicine of the University Ameer P. Mody, MD, MPH Philadelphia, Pennsylvania
of Southern California Assistant Professor of Pediatrics
Frances M. Nadel, MD, MSCE
Attending Physician Keck School of Medicine of the University
Associate Professor
Division of Emergency Medicine of Southern California
Childrens Hospital Los Angeles Attending Physician
Los Angeles, California Division of Emergency Medicine
Medicine
Attending Physician
Mandisa A. McIver, MD Los Angeles, California
Pediatrics Childrens Hospital of Philadelphia
Cary, North Carolina Cynthia J. Mollen, MD, MSCE
Assistant Professor of Pediatrics Philadelphia, Pennsylvania
Garth Meckler, MD, MSHS University of Pennsylvania School of Alan L. Nager, MD, MHA
Assistant Professor Medicine Associate Professor
Departments of Emergency Medicine and Attending Physician, Emergency Medicine Department of Pediatrics
Pediatrics Co-Scientific Director, PolicyLab Keck School of Medicine of the University
Fellowship Director and Assistant Section The Childrens Hospital of Philadelphia of Southern California
Chief Philadelphia, Pennsylvania Head
Pediatric Emergency Medicine Division of Emergency Medicine
Raquel Mora, MD
Oregon Health and Science University Childrens Hospital Los Angeles
Assistant Professor
Portland, Oregon Los Angeles, California
Sanjay Mehta, MD, Med Medicine
Assistant Professor St. Christophers Hospital for Children
Department of Pediatrics Philadelphia, Pennsylvania
University of Toronto
Academic Clinician Lili Moran, MD
Department of Pediatric Emergency Instructor
Hospital for Sick Children NYU Langone Medical Center
Toronto, Ontario, Canada New York, New York
xviii r r r Contributors
Joshua Nagler, MD Kevin C. Osterhoudt, MD Pinaki N. Patel, DO

Assistant Professor Assistant Professor Department of Emergency Medicine
Department of Pediatrics Department of Pediatrics Morristown Hospital
Harvard Medical School University of Pennsylvania School of Morristown, New Jersey
Fellowship Director Medicine
Shilpa Patel, MD
Division of Emergency Medicine Attending Physician
Pediatric Emergency Medicine Fellow
Childrens Hospital Boston Department of Emergency Medicine
Boston, Massachusetts The Childrens Hospital of Philadelphia
Asha G. Nair, MD Washington, DC
Kyle A. Nelson, MD, MPH Patricia Padlipsky, MD
Amy Patwa, MD
Instructor Assistant Professor of Pediatrics
Department of Pediatrics Department of Pediatrics
North Shore University Hospital
Harvard Medical School David Geffen School of Medicine at UCLA
Manhasset, New York
Attending Physician Clinical Attending
Department of Emergency Medicine Department of Pediatric Emergency
Childrens Hospital Boston Raina Paul, MD
Medicine
Boston, Massachusetts Fellow
Torrance, California
Lewis S. Nelson, MD Childrens Hospital Boston
Associate Professor Pradeep Padmanabhan, MD, MSc Boston, Massachusetts
Department of Emergency Medicine Assistant Professor
NYU Emergency Medicine Associates Department of Pediatrics, Division of Asha S. Payne, MD, MPH
New York, New York Pediatric Emergency Medicine Fellow
University of Louisville Department of Pediatric Emergency
Lily Ning, MD Attending Physician, Associate Medical
Weill Cornell Medical College Medicine
Director Childrens National Medical Center
New York, New York Emergency Department
Department of Emergency Medicine Washington, DC
Kosair Childrens Hospital
New York Hospital Queens Louisville, Kentucky
Flushing, New York Bradley Peckler, MD
Assistant Professor
Jeranil Nunez, MD Dante Pappano, MD, MPH Department of Emergency Medicine
Assistant Professor of Pediatrics Pediatrician University of South Florida
Keck School of Medicine of the University Department of Emergency Medicine Attending Physician
of Southern California East Tennessee Childrens Hospital Department of Emergency Medicine
Attending Physician Knoxville, Tennessee Tampa General Hospital
Division of Emergency Medicine Tampa, Florida
Childrens Hospital Los Angeles Darshan Patel, MD
Los Angeles, California Barbara M. Garcia Pena, MD, MPH
Assistant Professor
Associate Professor
Michele M. Nypaver, MD Departments of Pediatrics and
Clinical Associate Professor Emergency Medicine
Florida International University
Department of Emergency Medicine New York Medical College
Research Director
University of Michigan Health System Chief
Ann Arbor, Michigan Pediatric Emergency Department
Miami Childrens Hospital
Maria Fareri Childrens Hospital at
James A. ODonnell, MD Miami, Florida
Westchester Medical Center
Assistant Professor Valhalla, New York
Department of Pediatrics Joseph F. Perno, MD
University of Tennessee Health Sciences Affiliate Assistant Professor
Parul B. Patel, MD, MPH Department of Pediatrics
Center
Assistant Professor of Pediatrics University of South Florida
Attending Physician
Department of Pediatrics Tampa, Florida
Division of Emergency Services
Feinberg School of Medicine/ Assistant Medical Director
LeBonheur Childrens Hospital
Northwestern University Division of Emergency Medicine
Memphis, Tennessee
Attending Physician All Childrens Hospital
Dean Olsen, DO Department of Pediatric Emergency St. Petersburg, Florida
Emergency Physician, Preventative Medicine
Medicine Childrens Memorial Hospital
Quarry Road Emergency Services PC Chicago, Illinois
Bronx, New York
Contributors r r r xix
Mary Jane Piroutek, MD Juliette Quintero-Solivan, MD Lilia Reyes, MD

Fellow, Pediatric Emergency Medicine Clinical Assistant Professor Fellow
Department of Emergency Medicine Department of Pediatrics Department Pediatric Emergency
Loma Linda University Medical Center University of Medicine and Dentistry of Medicine
and Childrens Hospital New Jersey Yale University
Loma Linda, California Robert Wood Johnson University Hospital New Haven, Connecticut
New Brunswick, New Jersey
Raymond Pitetti, MD, MPH
Associate Professor of Pediatrics Joni E. Rabiner, MD Tracey Rico, MD
University of Pittsburgh School of Pediatric Emergency Medicine Fellow Consultant
Medicine Department of Pediatrics Department of Emergency Medicine
Medical Director, Sedation Services Albert Einstein College of Medicine Sheikh Khalifa Medical City
Associate Medical Director, Emergency Childrens Hospital at Montefiore Abu Dhabi, United Arab Emirates
Department Bronx, New York
Childrens Hospital of Pittsburgh of UPMC
Russell Radtke, MD Antonio Riera, MD
Attending Physician Assistant Professor
Beverly A. Poelstra, MD St. Josephs Childrens Hospital Department of Pediatric Emergency
Attending Physician Tampa, Florida Medicine
Pediatric Emergency Medicine Yale University
Jose Ramirez, MD
Robert Wood Johnson University Hospital Yale New Haven Hospital
New Brunswick, New Jersey New Haven, Connecticut
Nicole D. Porti, MD Florida State University College - Orlando
Fellow Pediatric Emergency Medicine Attending Ruby F. Rivera, MD
Department of Emergency Medicine Physician Assistant Professor of Clinical Pediatrics
Maimonides Medical Center Department of Emergency Medicine Albert Einstein College of Medicine
Brooklyn, New York Aronld Palmer Hospital for Children- Attending Physician
Orlando Health Department of Pediatrics
Kari R. Posner, MD
Orlando, Florida Childrens Hospital at Montefiore
Fellow
Bronx, New York
Division of Emergency Medicine Kimberly A. Randell, MD, MSc
The Childrens Hospital of Philadelphia Assistant Professor
Philadelphia, PA Department of Pediatrics Joshua A. Rocker, MD
University of Missouri-Kansas City Assistant Professor
Amanda Pratt, MD
Department of Pediatrics, Emergency Department of Pediatrics and Emergency
Medicine Medicine
Medicine
Childrens Mercy Hospital Albert Einstein College of Medicine
Robert Wood Johanson Medical School
Kansas City, Missouri Bronx, New York
Robert Wood Johnson University Hospital
Assistant Director of Education for
New Brunswick, New Jersey Stephen M. Reingold, MD
Pediatric Emergency Medicine
Charles W. Pruitt, MD Fellowship
Associate Professor Department of Emergency Medicine
Robert Wood Johnson Medical School
Department of Pediatrics Steven and Alexandra Cohen Childrens
University of Medicine and Dentistry of
University of Utah Medical Center of New York/Long
New Jersey
Medical Advisor for Child Advocacy Island Jewish Medical Center
Active Medical Staff
Department of Pediatric Emergency New Hyde Park, New York
Medicine
Bristol-Myers Squibb Childrens Hospital
Primary Childrens Medical Center
Robert Wood Johnson University Hospital Teresa M. Romano, MD
Salt Lake City, Utah
New Brunswick, New Jersey Fellow
Mohan Punja, MD Department of Emergency Medicine
Katherine Remick, MD
St. Christophers Hospital for Children
Fellow, Pediatric Emergency Medicine
Eileen C. Quintana, MD, MPH Department of Emergency Medicine
Assistant Professor Harbor-UCLA Medical Center
Department of Pediatrics and Emergency Torrance, California Emily Rose, MD
Medicine Internist
St. Christophers Hospital for Children Brigham and Womens Hospital
Drexel University School of Medicine Boston, Massachusetts
xx r r r Contributors
Michael D. Rosen, MD Mary T. Ryan, MD Kalyani Samudra, MD

Clinical Assistant Professor of Emergency Clinical Instructor in Emergency Adjunct Assistant Professor of Psychiatry
Medicine Medicine University of Utah
Department of Emergency Medicine Weill College of Medicine Salt Lake City, Utah
New Jersey Medical School Cornell University Medical Director
University of Medicine and Dentistry of New York, New York Department of Intensive Psychiatric
New Jersey Attending Physician Residential and DBT Day Treatment
Medical and Fellowship Director Department of Emergency Medicine Valley Mental Health
Department of Pediatric Emergency Lincoln Medical and Mental Health Midvale, Utah
Medicine Center
Childrens Hospital of New Jersey at Bronx, New York
Newark Beth Israel Medical Center Marcelo Sandoval, MD
Newark, New Jersey Assistant Professor
Heather R. Saavedra, MD Department of EMergency Medicine
Michael G. Rosenberg, MD Department of Emergency Medicine Albert Einstein College of Medicine
Department of Pediatrics Childrens Hospital of Wisconsin Beth Israel Medical Center
Jacobi Medical Center Milwaukee, Wisconsin New York, New York
Bronx, New York
Cindy Ganis Roskind, MD Sunil Sachdeva, MD Genevieve Santillanes, MD

Assistant Clinical Professor of Pediatrics Clinical Assistant Professor Assistant Professor of Clinical Emergency
Columbia University College of Physicians Department of Emergency Medicine Medicine
and Surgeons State University of New York, Downstate Department of Emergency Medicine
Attending Physician Medical Center Keck School of Medicine of the University
Department of Pediatrics, Division of Assistant Director of Southern California
Pediatric Emergency Medicine Department of Emergency Medicine LAC and USC Medical Center
New York-Presbyterian Morgan Stanley Long Island College Hospital Los Angeles, California
Childrens Hospital Brooklyn, New York
New York, New York
Masafumi Sato, MD
Michael Rosselli, MD Fellow
Nagela Sainte, MD Department of Emergency Medicine
Sports Medicine Fellow Department of Pediatrics
Department of Emergency Medicine St. Christophers Hospital for Children
Robert Wood Johnson Medical School Philadelphia, Pennsylvania
North Shore University Hospital New Brunswick, New Jersey
Manhasset, New York
Rasha Dorothy Sawaya, MD
Sudha A. Russell, MD
Sandy Saintonge, MD Fellow
Department of Emergency Medicine Department of Pediatric Emergency
Keck School of Medicine of the University
Weill Cornell Medical College Medicine
New York, New York Columbia University Medical Center
Attending Physician KidsCare
Pediatric Emergency Medicine New York, New York
Attending
Los Angeles, California Catherine Scarfi, MD
New York Hospital - Queens
Flushing, New York Physician
Christopher J. Russo, MD Department of Pediatric Emergency
Attending Physician Medicine
Division of Emergency Medicine Efren A. Salinero, MD Newark Beth Israel Medical Center
Nemours/A.I. duPont Hospital for Children Newark, New Jersey
Wilmington, Delaware Esther Maria Sampayo, MD, MPH
University of Pennsylvania School of Richard J. Scarfone, MD
Deirdre D. Ryan, MD Medicine Associate Professor of Pediatrics
Assistant Clinical Professor Attending Physician University of Pennsylvania School of
Department of Orthopaedic Surgery Childrens Hospital of Philadelphia Medicine
Keck School of Medicine of the University Philadelphia, Pennsylvania Medical Director, Emergency
of Southern California Preparedness
Childrens Hospital Los Angeles The Childrens Hospital of Philadelphia
Los Angeles, California Philadelphia, Pennsylvania
Contributors r r r xxi
Emily Schapiro, MD Hanan Sedik, MD Adhi Sharma, MD

Professor of Clinical Pediatrics Attending Physician Assistant Professor
Department of Pediatrics Division of Emergency Medicine Department of Emergency Medicine
University of Pennsylvania School of Childrens Hospital Los Angeles Mount Sinai School of Medicine
Medicine Los Angeles, California Chairman
Director, Extended Care Unit Department of Emergency Medicine
Desiree M. Seeyave, MBBS
Attending Physician Good Samaritan Hospital Medical Center
Department of Emergency Medicine New York, New York
University of Michigan
Philadelphia, Pennsylvania Sophia Sheikh, MD
Ann Arbor, Michigan
Instructor
Dana Aronson Schinasi, MD Department of Emergency Medicine
Department of Emergency Medicine Emory University
Medicine
The Childrens Hospital of Philadelphia Atlanta, Georgia
Hurley Medical Center
Flint, Michigan
James M. Shen, MD
Suzanne Schmidt, MD Jeffrey A. Seiden, MD Attending Physician
Instructor Assistant Professor of Clinical Pediatrics Emergency Department
Department of Pediatrics University of Pennsylvania School of Hoag Hospital
Northwestern University Feinberg School Medicine Newport Beach, California
of Medicine Associate Medical Director CHOP at
Childrens Memorial Hospital Virtua Pediatric Emergency Care
Chicago, Illinois Philadelphia, Pennsylvania Cathy E. Shin, MD
Janet Semple-Hess, MD Assistant Professor
Suzanne Schuh, MD Department of Surgery
Professor Keck School of Medicine of the University
Department of Paediatrics of Southern California
Keck School of Medicine of the University
University of Toronto Attending Physician
Staff Emergency Physician Department of Surgery
Department of Paediatrics Childrens Hospital Los Angeles
The Hospital for Sick Children Los Angeles, California
Toronto, Ontario, Canada Usha Sethuraman, MD
Childrens Hospital of Michigan Victoria Shulman, MD
Sandra H. Schwab, MD
Ami P. Shah, MD, MPH Albert Einstein College of Medicine
Attending Physician
Fellow Attending Physician
Department of Pediatric Emergency Childrens Emergency Service
Peyton Manning Childrens Hospital -
St. Vincents
Childrens Hospital of Pittsburgh of UPMC Childrens Hospital of Montefiore
Indianapolis, Indiana
Pittsburgh, Pennsylvania Bronx, New York
Dennis Scolnik, DCH, MSc, MB, ChB Lawrence Siew, MD
Manish I. Shah, MD
Associate Professor Clinical
Department of Pediatrics Department of Pediatric Emergency
Department of Pediatrics, Section of
University of Toronto Medicine
Emergency Medicine
Staff Physician Yale New Haven Childrens Hospital
Baylor College of Medicine
Division of Pediatric Emergency Medicine New Haven, Connecticut
Attending Physician
The Hospital for Sick Children
Emergency Center Adam M. Silverman, MD, FAAP
Texas Childrens Hospital Assistant Professor
Halden F. Scott, MD Houston, Texas Department of Pediatrics
Instructor University of Connecticut School of
Nikhil B. Shah, MD, MS
Department of Pediatrics Medicine
Assistant Professor
University of Pennsylvania School of Farmington, Connecticut
Medicine Attending Physician
Weill Cornell Medical College
Attending Physician Department of Pediatrics, Division of
Attending Physician
Division of Emergency Medicine Critical Care and Emergency Medicine
Department of Pediatrics Connecticut Childrens Medical Center
New York Presbyterian Hospital - Cornell
Childrens Hospital of Philadelphia Hartford, Connecticut
New York, New York
xxii r r r Contributors
Donna M. Simmons, MD Kai M. Sturmann, MD Jennifer Thull-Freedman, MD, MSc

Department of Emergency Medicine Chairman Assistant Professor
Maimonides Medical Center Department of Emergency Medicine Department of Pediatrics
Brooklyn, New York Brookhaven Memorial Hospital University of Toronto
Patchogue, New York Staff Physician
Sari Soghoian, MD
Paediatric Emergency Medicine
Assistant Professor Mark Su, MD
The Hospital for Sick Children
Department of Emergency Medicine Family Practitioner
NYU Langone Medical Center Holistic Family Practice, Inc.
New York, New York Newbury, Massachusetts Helene Tigchelaar, MD
Louis A. Spina, MD Payal Sud, MD Professor
Assistant Professor Department of Emergency Medicine Departments of Pediatrics and
Departments of Emergency Medicine and North Shore University Hospital Emergency Medicine
Pediatrics Manhasset, New York Wayne State University
Mount Sinai Medical Center Attending Physician
Attending Physician Srinivasan Suresh, MD, MBA Department of Pediatrics, Division of
Department of Emergency Medicine Assistant Professor of Pediatrics Emergency Medicine
Mount Sinai Medical Center and Emergency Medicine Childrens Hospital of Michigan
New York, New York Wayne State University Detroit, Michigan
Medical Director, Emergency Department
Curt Stankovic, MD Chief Medical Information Officer Lindsey Tilt, MD
Assistant Professor Childrens Hospital of Michigan Fellow
Department of Pediatric and Emergency Detroit, Michigan Department of Pediatric Emergency
Medicine Medicine
Wayne State University Linda Szema, MD Columbia University
Fellowship Director Department of Emergency Medicine New York Presbyterian Hospital
Department of Pediatrics Albert Einstein College of Medicine New York, New York
Childrens Hospital of Michigan Beth Israel Medical Center
Detroit, Michigan New York, New York Howard Topol, MD
Ee Tein Tay, MD
Danniel J. Stites, MD Childrens Hospital of Philadelphia
Attending Physician
Weill Cornell Medical College Philadelphia, Pennsylvania
New York, New York
Mount Sinai School of Medicine Nicholas Tsarouhas, MD
Mount Sinai Hospital Professor of Clinical Pediatrics
New York Hospital Queens
New York, New York Department of Pediatrics
Flushing, New York
Natasha A. Tejwani, MD
David J. Story Medicine
Fellow Associate Medical Director
St. Barnabas Hospital
New York City Poison Control Center Emergency Department
Bronx, New York
Bellevue Hospital Center Medical Director
New York, New York Ravi Thamburaj, DO Emergency Transport Team
Attending Physician The Childrens Hospital of Philadelphia
Christopher G. Strother, MD Department of Emergency Medicine Philadelphia, Pennsylvania
Assistant Professor Newark Beth Isreal Medical Center
Department of Emergency Medicine Newark, New Jersey Laura Umbrello, MD
Mount Sinai School of Medicine Fellow
Physician Lindsay Thomas, MD Division of Emergency Medicine
Department of Emergency Medicine Department of Emergency Medicine Miami Childrens Hospital
Mount Sinai Hospital North Shore University Hospital Miami, Florida
New York, New York Manhasset, New York
Neil G. Uspal, MD
Amy D. Thompson, MD Fellow
Instructor Department of Emergency Medicine
Kristin S. Stukus, MD Department of Pediatrics Childrens Hospital of Philadelphia
Fellow Jefferson Medical College Philadelphia, Pennsylvania
Department of Pediatric Emergency Philadelphia, Pennsylvania
Attending Physician Diana Valcich, MD
Medicine
Department of Emergency Medicine Sports Medicine Fellow
Childrens Hospital of Pittsburgh of UPMC
Alfred I duPont Hospital for Children North Shore University Hospital
Wilmington, Delaware Manhasset, New York
Contributors r r r xxiii
Michael E. Valente, MD Vincent J. Wang, MD, MHA Derek A. Wong, MD

Fellow Associate Professor of Pediatrics Assistant Professor
Division of Emergency Medicine Keck School of Medicine of the University Department of Pediatrics
Childrens Hospital Los Angeles of Southern California David Geffen School of Medicine at UCLA
Los Angeles, California Associate Division Head Los Angeles, California
Eugenio Vazquez, MD James M. Wu, MD
Department of Pediatrics Fellow
Childrens Hospital of Orange County Department of Emergency Medicine
Orange, California Marie Waterhouse, MD Childrens Mercy Hospital
Fellow Kansas City, Missouri
Adam Vella, MD
Assistant Professor of Pediatrics and Shira Yahalom, MD
Emergency Medicine Attending Physician
Director of Pediatric Emergency Medicine Department of Emergency Medicine
Emergency Department Beth Israel Medical Center
Tara Webb, MD
Mount Sinai Medical Center New York, New York
Fellow
New York, New York
Department of Pediatric Emergency Yuki Yasaka, MD
Rebecca L. Vieira, MD Medicine Fellow
Instructor in Pediatrics Childrens Hospital of Wisconsin Department of Pediatric Critical Care
Harvard Medical School Wauwatosa, Wisconsin Childrens Hospital Los Angeles
Assistant in Medicine, Staff Physician Los Angeles, California
Kristin Welch, MD Sabina Zavolkovskaya, MD
Childrens Hospital Boston
Assistant Professor Attending
Boston, Massachusetts
Department of Pediatrics Department of Emergency Medicine,
Phillip Visser, MBCHB University of Connecticut School of Division of Pediatric Emergency
Fellow in Pediatric Emergency Medicine Medicine Medicine
Department of Emergency Medicine Farmington, Connecticut Maimonides Medical Center
Royal Childrens Hospital Attending Physician Brooklyn, New York
Parkville, Victoria, Australia Department of Pediatric Emergency Arezoo Zomorrodi, MD
David M. Walker, MD Medicine Department of Pediatrics
Assistant Professor Connecticut Childrens Medical Center Jefferson Medical College
Department of Pediatric Emergency Hartford, Connecticut Philadelphia, Pennsylvania
Medicine Attending Physician
Yale University School of Medicine Emily L. Willner, MD Department of Pediatrics
Director of Quality and Safety/ Assistant Professor of Pediatrics Alfred I duPont Hospital for Children
Attending Physician Department of Pediatrics Wilmington, Delaware
Department of Pediatric Emergency Keck School of Medicine of the University Mark R. Zonfrillo, MD, MSCE
Medicine of Southern California Assistant Professor
Yale-New Haven Hospital Associate Fellowship Director Department of Pediatrics
New Haven, Connecticut Division of Emergency Medicine University of Pennsylvania School of
Jaw J. Wang, MD Childrens Hospital of Los Angeles Medicine
Attending Physician Los Angeles, California Attending Physician
Montebello Pediatrics Division of Emergency Medicine
Montebello, California Childrens Hospital of Pennsylvania
xxiv
CONTENTS
Preface v Apparent Life-Threatening Event 70

Foreword vi Appendicitis 72
Acknowledgments vii Arthritis, Rheumatoid 74
Contributors ix Arthritis, Septic 76
Ascaris Lumbricoides 78
Abdominal Distention 2 Ascites 80
Abruptio Placenta 4 Asthma 82
Abscess, Bartholin Gland 6 Asystole 84
Abscess, Dentoalveolar 8 Ataxia 86
Abscess, Gluteal 10 Atlantoaxial Instability 88
Abscess, Intracranial 12 Atopic Dermatitis 90
Abscess, Ludwig Angina 14 Avascular Necrosis of the Femoral Head 92
Abscess, Perianal 16 Bacteremia 94
Abscess, Peritonsillar 18 Balanitis/Balanoposthitis 96
Abscess, Rectal 20 Barotrauma, Sinus 98
Abscess, Retropharyngeal 22 Beta-Blocker Poisoning 100
Acetaminophen Poisoning 24 Biliary Tract Disease 102
Acne 26 Bipolar Disorder/Mania 104
Acute Hemolytic Anemia 28 Bite, Animal 106
Acute Renal Failure 30 Bite, Human 108
Acute Respiratory Failure 32 Blepharitis 110
Adrenal Insufficiency 34 Blindness 112
Agitation 36 Body Packers (Ingested Drug Packages) 114
Altered Level of Consciousness/Coma 38 Botulism 116
Altitude Sickness 40 Brachial Plexus Injury 118
Amenorrhea 42 Bradycardia 120
Anal Fissure 44 Branchial Cleft Cyst 122
Anaphylaxis 46 Breast Lesions 124
Anemia 48 Bronchiolitis 126
Angioedema 50 Burn, Chemical 128
Ankle Sprain 52 Burn, Thermal 130
Anterior Uveitis (Iritis) 54 Caffeine/Theophylline Poisoning 132
Anticholinergic Poisoning 56 Calcium Channel Blocker Poisoning 134
Anticoagulant Poisoning 58 Candidiasis 136
Anticonvulsant Poisoning 62 Carbon Monoxide/Cyanide Poisoning
and Smoke Inhalation 138
Aphthous Stomatitis 64
Cardiogenic Shock 140
Aplastic Anemia 66
Cardiomyopathy 142
Apnea 68
xxv
xxvi r r r Contents
Carpal Tunnel Syndrome 144 Cystic Hygroma 230

Cat Scratch Disease 146 Dacryocystitis/Dacryostenosis 232
Cauda Equina Syndrome 148 Decompression Sickness 234
Caustic Exposure 150 Deep Vein Thrombosis 236
Cavernous Sinus Thrombosis 152 Dehydration 238
Celiac Disease 154 Dengue Fever 240
Cellulitis 156 Depression 242
Cerebral Contusions 158 Dermatomyositis 244
Cervical Lymphadenitis 160 Diabetes Insipidus 246
Chalazion 162 Diabetic Ketoacidosis 248
Chancroid 164 Diaper Rash 250
Chickenpox/Shingles 166 Diarrhea 252
Child Abuse 168 Digoxin Toxicity 254
Cholelithiasis 170 Diphtheria 256
Cholinergic Poisoning 172 Discitis 258
Cocaine Poisoning 174 Dislocation, Knee 260
Colitis 176 Dislocation, Patella 262
Collagen Vascular Disease 178 Dislocation, Temporomandibular Joint 264
Compartment Syndrome 180 Disorders of Energy Metabolism
Concussion 182 (Mitochondrial Disease) 266
Congenital Adrenal Hyperplasia 184 Disseminated Intravascular Coagulation 268
Congenital Heart Disease 186 Dizziness/Vertigo 270
Congestive Heart Failure 188 Drowning 272
Conjunctival Injury 190 Ductal-Dependent Cardiac Emergencies 274
Conjunctivitis 192 Dysrythmia, Atrial 276
Conjunctivitis, Neonatal 194 Dysrythmia, Ventricular 278
Constipation 196 Dystonia 280
Constricting Band/Tourniquet Syndrome 198 Eating Disorders 282
Contact Dermatitis 200 Ectopic Pregnancy 284
Conversion Disorder 202 Eczema Herpeticum 286
Corneal Abrasion 204 Edema 288
Costochondritis 206 Electrical Injury 290
Cough 208 Emergency Contraception 292
Croup 210 Empyema 294
Crying/Colic 212 Encephalitis 296
Cryptorchidism 214 Endometriosis 298
Cushing Syndrome 216 Envenomation, Insect Bites and Stings 300
Cutaneous Larva Migrans 218 Envenomation, Marine 302
Cyanosis 220 Envenomation, Scorpion 304
Cyanotic Heart Disease 222 Envenomation, Snake 306
Cyclic Vomiting 224 Envenomation, Spider 308
Cystic Fibrosis: Exacerbation 226 Epididymitis and Orchitis 310
Cystic Fibrosis: New Diagnosis 228 Epidural Hematoma 312
Contents r r r xxvii
Epiglottitis/Supraglottitis 314 Fracture, Pelvic Avulsion 400

Epistaxis 316 Fracture, Rib 402
Erythema Infectiosum 318 Fracture, Scaphoid 404
Erythema Multiforme 320 Fracture, Scapula 406
Erythema Nodosum 322 Fracture, Skull 408
Erythema Toxicum 324 Fracture, Supracondylar 410
Esophageal Varices 326 Fracture, Tibial Avulsion 412
Esophagitis 328 Fracture, Toddlers 414
Ethanol Poisoning 330 Fracture, Torus (Buckle) 416
Eye, Red 332 Fracture, Zygoma 418
Eye, Strabismus 334 Frostbite 420
Eye, Visual Disturbance 336 Ganglion Cyst 422
Facial Nerve Palsy 338 Gastritis 424
Failure to Thrive 340 Gastroenteritis 426
Fasciitis 342 Gastroesophageal Reflux 428
Febrile Seizure 344 Gastrointestinal Bleeding: Lower 430
Felon 346 Gastrointestinal Bleeding: Upper 432
Fever in Children Older than 3 Months 348 Gastrointestinal Polyps 434
Fever in Infants 03 Months of Age 350 Genital Warts 436
Fever of Unknown Origin 352 Giardiasis 438
Flail Chest 354 Globe Rupture 440
Food Poisoning 356 Glomerulonephritis 442
Foreign Body Aspiration 358 Gonorrhea 444
Foreign Body Ingestion 360 Groin Mass 446
Foreign Body, Cornea 362 Group B Streptococcal Infection 448
Foreign Body, Disc Battery 364 Guillain-Barre Syndrome 450
Foreign Body, Ear 366 Gynecomastia 452
Foreign Body, Esophagus 368 Hair-Thread Tourniquet 454
Foreign Body, Nose 370 Hallucinogen Poisoning 456
Foreign Body, Rectum 372 Hand-Foot-and-Mouth Disease 458
Foreign Body, Soft Tissue 374 Headache 460
Fracture, Cervical Spine 376 Hearing Loss 462
Fracture, Clavicle 378 Heart Block 464
Fracture, Coccyx 380 Heart Murmur 466
Fracture, Femur 382 Heat Illness 468
Fracture, Foot 384 Hemangioma 470
Fracture, Forearm/Wrist 386 Hematuria 472
Fractures, Greenstick/Bowing 388 Hemolytic Disease of the Newborn 474
Fracture, Humerus 390 Hemolytic Uremic Syndrome 476
Fracture, Mandibular 392 Hemophilia 478
Fracture, Nasal 394 Hemoptysis 480
Fracture, Orbital 396 Hemothorax 482
Fracture, Patella 398 Henoch-Schonlein Purpura 484
xxviii r r r Contents
Hepatic Encephalopathy 486 Irritable Bowel Syndrome 572

Hepatitis, Acute 488 Jaundice, Conjugated Hyperbilirubinemia 574
Hepatomegaly 490 Jaundice, Unconjugated Hyperbilirubinemia 576
Hernia 492 Kawasaki Disease 578
Herpes Simplex 494 Labial Adhesions 580
Hirschsprung Disease 496 Laceration Repair 582
HIV/AIDS 498 Laryngitis 584
Hydrocarbon Poisoning 500 Laryngomalacia/Tracheomalacia 586
Hydrocephalus 502 Lead Poisoning 588
Hydronephrosis 504 Leukemia 590
Hypercalcemia 506 Lice (Pediculosis) 592
Hyperemesis Gravidarum 508 Limp 594
Hyperglycemia 510 Lyme Disease 596
Hyperkalemia 512 Lymphadenopathy 598
Hypernatremia 514 Lymphogranuloma Venereum 600
Hypertension 516 Malaria 602
Hyperthermia 518 Mallet Finger 604
Hyperthyroidism 520 Mastitis 606
Hyperventilation 522 Mastoiditis 608
Hyphema 524 Measles 610
Hypocalcemia 526 Meckels Diverticulum 612
Hypoglycemia 528 Mediastinal Mass 614
Hypoglycemic Agents Poisoning 530 Meningitis 616
Hypokalemia 532 Meningococcemia 618
Hyponatremia 534 Menses, Dysmenorrhea 620
Hypoparathyroidism 536 Menses, Oligomenorrhea 622
Hypotension 538 Mesenteric Adenitis 624
Hypothermia 540 Metabolic Acidosis 626
Idiopathic Thrombocytopenic Purpura 542 Methemoglobinemia 628
Immobile Arm 544 Migraine Headaches 630
Imperforate Hymen 546 Molluscum Contagiosum 632
Impetigo 548 Mumps 634
Inborn Errors of Metabolism 550 Munchausen Syndrome by Proxy 636
Infantile Spasm 552 Muscular Dystrophy 638
Infectious Mononucleosis 554 Myasthenia Gravis 640
Infective Endocarditis 556 Myocardial Contusion 642
Inflammatory Bowel Disease 558 Myocardial Infarction 644
Influenza 560 Myocarditis 646
Inhalant Abuse/Poisoning 562 Nail Bed Injuries 648
Intestinal Malrotation 564 Neck Mass 650
Intraosseous Infusions 566 Neck Stiffness 652
Intussusception 568 Necrotizing Enterocolitis 654
Iron Poisoning 570 Needle Stick 656
Contents r r r xxix
Neoplasm, Brain 658 Pertussis 742

Neoplasm, Lymphoma 660 Phimosis 744
Neoplasm, Neuroblastoma 662 Pilonidal Cyst 746
Nephrotic Syndrome 664 Pinworms 748
Neuroleptic Malignant Syndrome 666 Pityriasis Rosea 750
Nonsteroidal Anti-Inflammatory Drug (NSAID) Pleural Effusion 752
Poisoning 668 Pneumonia, Aspiration 754
Nursemaids Elbow 670 Pneumonia, Bacterial 756
Obstructive Sleep Apnea Syndrome 672 Pneumothorax/Pneumomediastinum 758
Omphalitis 674 Poison Ivy/Oak/Sumac 760
Opioid Poisoning 676 Polycystic Kidney Disease 762
Oral Lesions 678 Polycystic Ovarian Syndrome 764
Orbital Cellulitis 680 Polycythemia 766
Orchitis 682 Polyuria 768
Osgood-Schlatter Disease 684 Pregnancy 770
Osteogenesis Imperfecta 686 Priapism 772
Osteomyelitis 688 Procedural Sedation and Analgesia 774
Osteosarcoma 690 Prolonged QT Interval 776
Otitis Externa 692 Pseudotumor Cerebri 778
Otitis Media 694 Psoriasis 780
Ovarian Cyst 696 Psychosis 782
Ovarian Torsion 698 Pulmonary Contusion 784
Pain, Abdomen 700 Pulmonary Edema 786
Pain, Back 702 Pulmonary Embolism 788
Pain, Chest 704 Pyloric Stenosis 790
Pain, Extremity 706 Pyogenic Granuloma 792
Pain, Eye 708 Rash, Maculopapular 794
Pain, Throat 710 Rash, Neonatal 796
Palpitations 712 Rash, Petechiae 798
Pancreatitis 714 Rash, Purpura 800
Panic Attack 716 Rash, Urticaria 802
Panniculitis 718 Rash, Vesiculobullous 804
Paraphimosis 720 Rectal Bleeding 806
Paronychia 722 Rectal Prolapse 808
Parotitis 724 Renal Vein Thrombosis 810
Patent Ductus Arteriosus 726 Respiratory Distress 812
Patent Urachus 728 Reye Syndrome 814
Pelvic Inflammatory Disease 730 Rhabdomyolysis 816
Pericardial Effusion/Tamponade 732 Rheumatic Fever 818
Pericarditis 734 Rickettsial Disease 820
Perichondritis, Ear 736 Roseola Infantum 822
Periorbital Cellulitis 738 Rubella 824
Peritonitis 740 Salmonella 826
xxx r r r Contents
Salicylate Poisoning 828 Testicular Torsion 912

Scabies 830 Tetanus 914
Scarlet Fever 832 Tetanus Prophylaxis 916
Scrotal Mass 834 Tetralogy of Fallot 918
Scrotal Pain 836 Thrush 920
Scrotal Swelling 838 Thyroglossal Duct Cyst 922
Seborrheic Dermatitis 840 Tick Bite 924
Seizure 842 Tinea Capitis 926
Sepsis 844 Tinea Corporis 928
Serum Sickness 846 Tinea Versicolor 930
Sexual Assault 848 Tinnitus 932
Sexually Transmitted Infections 850 Toxic Alcohols Poisoning 934
Shock, Cardiogenic 852 Toxic Shock Syndrome 936
Shock, Hypovolemic 854 Tracheitis 938
Shock, Neurogenic 856 Tracheoesophageal Fistula 940
Sickle Cell Disease 858 Transfusion Reaction 942
Sinusitis 860 Transient Synovitis 944
Slipped Capital Femoral Epiphysis (SCFE) 862 Transverse Myelitis 946
Spinal Cord Compression 864 Trauma, Abdominal 948
Splenomegaly 866 Trauma, Ankle 950
Staphylococcal Scalded Skin Syndrome 868 Trauma, Chest 952
Status Epilepticus 870 Trauma, Dental 954
Stevens-Johnson Syndrome/TEN Spectrum 872 Trauma, Elbow 956
Stomatitis 874 Trauma, Facial 958
Strabismus, Chronic (Primary) 876 Trauma, Foot/Toe 960
Strangulation 878 Trauma, Hand/Finger 962
Stridor 880 Trauma, Head 964
Stroke 882 Trauma, Knee 966
Subarachnoid Hemorrhage 884 Trauma, Neck 968
Subdural Hematoma 886 Trauma, Penetrating 970
Sudden Infant Death Syndrome (SIDS) 888 Trauma, Perineal 972
Suicide 890 Trauma, Scrotal and Penile 974
Sympathomimetic Poisoning 892 Trauma, Shoulder 976
Syncope 894 Trauma, Spinal Cord 978
Syndrome of Inappropriate Antidiuretic Hormone Trauma, Vaginal 980
Secretion (SIADH) 896 Traumatic Brain Injury 982
Syphilis 898 Tricyclic Antidepressant Poisoning 984
Systemic Lupus Erythematosus 900 Tuberculosis 986
Tachycardia 902 Tympanic Membrane Perforation 988
Tapeworm and Cestode Infestations 904 Umbilical Granuloma 990
Teething 906 Upper Respiratory Infection 992
Tendon Laceration 908 Urethral Prolapse 994
Tendonitis 910 Urethritis 996
Contents r r r xxxi
Urinary Retention 998 Ventriculoperitoneal Shunt Malfunction 1020

Urinary Tract Infection 1000 Volvulus 1022
Urolithiasis 1002 Vomiting 1024
Vaginal Bleeding During Early Pregnancy Warts 1026
(<20 Weeks) 1004 Weakness 1028
Vaginal Bleeding During Pregnancy Wheezing 1030
(>20 Week Gestation) 1006
Wilms Tumor 1032
Vaginal Bleeding, Prepubertal 1008
Withdrawal Syndromes 1034
Vaginal Bleeding, Pubertal/DUB 1010
Vaginal Discharge, Prepubertal 1012 Appendix A Cardiac Emergencies 1037
Vaginal Discharge, Pubertal 1014 Appendix B Respiratory Emergencies 1039
Vaginitis 1016 Appendix C Other Emergencies 1041
Ventriculoperitoneal Shunt Infection 1018 Index 1045
xxxii
TOPICAL TABLE OF CONTENTS
Cardiovascular Emergencies Abscess, Rectal 20

Bradycardia 120 Acne 26
Cardiogenic Shock 140 Atopic Dermatitis 90
Cardiomyopathy 142 Avascular Necrosis of the Femoral Head 92
Congenital Heart Disease 186 Branchial Cleft Cyst 122
Congestive Heart Failure 188 Breast Lesions 124
Cyanosis 220 Burn, Chemical 128
Cyanotic Heart Disease 222 Burn, Thermal 130
Ductal-Dependent Cardiac Emergencies 274 Candidiasis 136
Dysrythmia, Atrial 276 Cellulitis 156
Dysrythmia, Ventricular 278 Cervical Lymphadenitis 160
Heart Block 464 Constricting Band/Tourniquet Syndrome 198
Heart Murmur 466 Contact Dermatitis 200
Hypertension 516 Cutaneous Larva Migrans 218
Hypotension 538 Cystic Hygroma 230
Infective Endocarditis 556 Diaper Rash 250
Myocardial Contusion 642 Eczema Herpeticum 286
Myocardial Infarction 644 Erythema Infectiosum 318
Myocarditis 646 Erythema Multiforme 320
Palpitations 712 Erythema Nodosum 322
Patent Ductus Arteriosus 726 Erythema Toxicum 324
Pericardial Effusion/Tamponade 732 Fasciitis 342
Pericarditis 734 Felon 346
Prolonged QT Interval 776 Foreign Body, Soft Tissue 374
Pulmonary Edema 786 Ganglion Cyst 422
Pulmonary Embolism 788 Gynecomastia 452
Rheumatic Fever 818 Hair-Thread Tourniquet 454
Shock, Cardiogenic 852 Hemangioma 470
Sudden Infant Death Syndrome (SIDS) 888 Impetigo 548
Syncope 894 Lymphadenopathy 598
Tachycardia 902 Mastitis 606
Tetralogy of Fallot 918 Molluscum Contagiosum 632
Neck Mass 650
Dermatology/Soft Tissue Emergencies Omphalitis 674
Abscess, Bartholin Gland 6 Panniculitis 718
Abscess, Gluteal 10 Paronychia 722
Abscess, Ludwig Angina 14 Pilonidal Cyst 746
Abscess, Perianal 16 Pityriasis Rosea 750
xxxiii
xxxiv r r r TOPICAL TABLE OF CONTENTS
Poison Ivy/Oak/Sumac 760 Drowning 272

Psoriasis 780 Electrical Injury 290
Pyogenic Granuloma 792 Envenomation, Insect Bites and Stings 300
Rash, Maculopapular 794 Envenomation, Marine 302
Rash, Neonatal 796 Envenomation, Scorpion 304
Rash, Petechiae 798 Envenomation, Snake 306
Rash, Purpura 800 Envenomation, Spider 308
Rash, Urticaria 802 Foreign Body, Soft Tissue 374
Rash, Vesiculobullous 804 Frostbite 420
Scabies 830 Hair-Thread Tourniquet 454
Seborrheic Dermatitis 840 Heat Illness 468
Staphylococcal Scalded Skin Syndrome 868 Hyperthermia 518
Stevens-Johnson Syndrome/TEN Spectrum 872 Hypothermia 540
Tendon Laceration 908 Poison Ivy/Oak/Sumac 760
Thyroglossal Duct Cyst 922 Tick Bite 924
Tinea Capitis 926
Tinea Corporis 928 Gastrointestinal Emergencies
Tinea Versicolor 930 Abdominal Distention 2
Umbilical Granuloma 990 Abscess, Perianal 16
Warts 1026 Abscess, Peritonsillar 18
Abscess, Rectal 20
Endocrine Emergencies
Abscess, Retropharyngeal 22
Adrenal Insufficiency 34
Anal Fissure 44
Congenital Adrenal Hyperplasia 184
Appendicitis 72
Cushing Syndrome 216
Ascaris Lumbricoides 78
Diabetic Insipidus 246
Ascites 80
Diabetic Ketoacidosis 248
Biliary Tract Disease 102
Gynecomastia 452
Botulism 116
Hyperthyroidism 520
Celiac Disease 154
Hypoparathyroidism 536
Cholelithiasis 170
Inborn Errors of Metabolism 550
Colitis 176
Menses, Oligomenorrhea 622
Constipation 196
Polycystic Ovarian Syndrome 764
Cyclic Vomiting 224
Syndrome of Inappropriate Antidiuretic Hormone
Dehydration 238
Secretion (SIADH) 896
Diarrhea 252
Environmental Emergencies Esophageal Varices 326
Altitude Sickness 40 Esophagitis 328
Barotrauma, Sinus 98 Food Poisoning 356
Bite, Animal 106 Foreign Body Ingestion 360
Bite, Human 108 Foreign Body, Disc Battery 364
Burn, Thermal 130 Foreign Body, Esophagus 368
Contact Dermatitis 200 Foreign Body, Rectum 372
Decompression Sickness 234 Gastritis 424
TOPICAL TABLE OF CONTENTS r r r xxxv
Gastroenteritis 426 Groin Mass 446

Gastroesophageal Reflux 428 Herpes Simplex 494
Gastrointestinal Bleeding: Lower 430 Lymphogranuloma Venereum 600
Gastrointestinal Bleeding: Upper 432 Orchitis 682
Gastrointestinal Polyps 434 Paraphimosis 720
Giardiasis 438 Patent Urachus 728
Hepatic Encephalopathy 486 Phimosis 744
Hepatitis, Acute 488 Priapism 772
Hepatomegaly 490 Scrotal Mass 834
Hernia 492 Scrotal Pain 836
Hirschsprung Disease 496 Scrotal Swelling 838
Inflammatory Bowel Disease 558 Sexually Transmitted Infections 850
Intestinal Malrotation 564 Syphilis 898
Intussusception 568 Testicular Torsion 912
Irritable Bowel Syndrome 572 Trauma, Perineal 972
Jaundice, Conjugated 574 Trauma, Scrotal and Penile 974
Jaundice, Unconjugated 576 Urethral Prolapse 994
Meckels Diverticulum 612 Urethritis 996
Mesenteric Adenitis 624 Urinary Retention 998
Necrotizing Enterocolitis 654 Urinary Tract Infection 1000
Pain, Abdomen 700 Gynecologic/Obstetric Emergencies
Pancreatitis 714
Abruptio Placenta 4
Peritonitis 740
Abscess, Bartholin Gland 6
Pinworms 748
Amenorrhea 42
Pyloric Stenosis 790
Chancroid 164
Rectal Bleeding 806
Ectopic Pregnancy 284
Rectal Prolapse 808
Emergency Contraception 292
Reye Syndrome 814
Endometriosis 298
Salmonella 826
Genital Warts 436
Splenomegaly 866
Gonorrhea 444
Tapeworm and Cestode Infestations 904
Herpes Simplex 494
Thrush 920
Hyperemesis Gravidarum 508
Tracheoesophageal Fistula 940
Imperforate Hymen 546
Trauma, Abdominal 948
Labial Adhesions 580
Volvulus 1022
Menses, Dysmenorrhea 620
Vomiting 1024
Menses, Oligomenorrhea 622
Genitourinary Emergencies Ovarian Cyst 696
Balanitis/Balanoposthitis 96 Ovarian Torsion 698
Chancroid 164 Pelvic Inflammatory Disease 730
Cryptorchidism 214 Pregnancy 770
Epididymitis and Orchitis 310 Sexually Transmitted Infections 850
Genital Warts 436 Syphilis 898
Gonorrhea 444 Trauma, Perineal 972
xxxvi r r r TOPICAL TABLE OF CONTENTS
Trauma, Vaginal 980 Stomatitis 874

Urethritis 996 Strangulation 878
Vaginal Bleeding During Early Pregnancy Stridor 880
(<20 Weeks) 1004 Teething 906
Vaginal Bleeding During Pregnancy Thyroglossal Duct Cyst 922
(>20 Week Gestation) 1006
Tracheitis 938
Vaginal Bleeding, Prepubertal 1008
Trauma, Dental 954
Vaginal Bleeding, Pubertal/DUB 1010
Trauma, Facial 958
Vaginal Discharge, Prepubertal 1012
Trauma, Head 964
Vaginal Discharge, Pubertal 1014
Trauma, Neck 968
Vaginitis 1016
Upper Respiratory Infection 992
Head/Neck Emergencies
Hematologic/Oncologic Emergencies
Abscess, Dentoalveolar 8
Acute Hemolytic Anemia 28
Abscess, Intracranial 12
Anemia 48
Abscess, Ludwig Angina 14
Aplastic Anemia 66
Abscess, Peritonsillar 18
Cavernous Sinus Thrombosis 152
Disseminated Intravascular Coagulation 268
Aphthous Stomatitis 64
Epistaxis 316
Branchial Cleft Cyst 122
Fever of Unknown Origin 352
Hemolytic Disease of the Newborn 474
Cerebral Contusions 158
Hemolytic Uremic Syndrome 476
Cervical Lymphadenitis 160
Hemophilia 478
Cystic Hygroma 230
Idiopathic Thrombocytopenic Purpura 542
Dislocation, Temporomandibular Joint 264
Leukemia 590
Dizziness/Vertigo 270
Mediastinal Mass 614
Epistaxis 316
Methemoglobinemia 628
Facial Nerve Palsy 338
Neoplasm, Brain 658
Foreign Body, Ear 366
Neoplasm, Lymphoma 660
Foreign Body, Nose 370
Neoplasm, Neuroblastoma 662
Fracture, Mandibular 392
Osteosarcoma 690
Fracture, Nasal 394
Polycythemia 766
Fracture, Orbital 396
Renal Vein Thrombosis 810
Fracture, Skull 408
Sickle Cell Disease 858
Fracture, Zygoma 418
Spinal Cord Compression 864
Hand-Foot-and-Mouth Disease 458
Splenomegaly 866
Laryngitis 584
Transfusion Reaction 942
Mastoiditis 608
Wilms Tumor 1032
Oral Lesions 678
Otitis Externa 692 Immunologic Emergencies
Otitis Media 694 Anaphylaxis 46
Parotitis 724 Angioedema 50
Perichondritis, Ear 736 Arthritis, Rheumatoid 74
Sinusitis 860 Collagen Vascular Disease 178
TOPICAL TABLE OF CONTENTS r r r xxxvii
Dermatomyositis 244 Epiglottitis/Supraglottitis 314

Erythema Multiforme 320 Erythema Infectiosum 318
Erythema Nodosum 322 Eye, Red 332
Hemolytic Disease of the Newborn 474 Fasciitis 342
Kawasaki Disease 578 Febrile Seizure 344
Lymphadenopathy 598 Felon 346
Serum Sickness 846 Fever in Children Older than 3 Months 348
Stevens-Johnson Syndrome/TEN Spectrum 872 Fever in Infants 03 Months of Age 350
Systemic Lupus Erythematosus 900 Fever of Unknown Origin 352
Transfusion Reaction 942 Food Poisoning 356
Gastroenteritis 426
Infectious Disease Genital Warts 436
Abscess, Bartholin Gland 6 Giardiasis 438
Abscess, Dentoalveolar 8 Gonorrhea 444
Abscess, Gluteal 10 Group B Streptococcal Infection 448
Abscess, Intracranial 12 Hand-Foot-and-Mouth Disease 458
Abscess, Ludwig Angina 14 Hematuria 472
Abscess, Perianal 16 Hepatitis, Acute 488
Abscess, Peritonsillar 18 Herpes Simplex 494
Abscess, Rectal 20 HIV/AIDS 498
Abscess, Retropharyngeal 22 Impetigo 548
Arthritis, Septic 76 Infectious Mononucleosis 554
Ascaris Lumbricoides 78 Infective Endocarditis 556
Bacteremia 94 Influenza 560
Biliary Tract Disease 102 Laryngitis 584
Botulism 116 Lice (Pediculosis) 592
Bronchiolitis 126 Lyme Disease 596
Candidiasis 136 Lymphogranuloma Venereum 600
Cat Scratch Disease 146 Malaria 602
Cellulitis 156 Mastitis 606
Cervical Lymphadenitis 160 Mastoiditis 608
Chancroid 164 Measles 610
Chickenpox/Shingles 166 Meningitis 616
Conjunctivitis, Neonatal 194 Meningococcemia 618
Croup 210 Mesenteric Adenitis 624
Cutaneous Larva Migrans 218 Molluscum Contagiosum 632
Dengue Fever 240 Mumps 634
Diphtheria 256 Myocarditis 646
Discitis 258 Neck Stiffness 652
Eczema Herpeticum 286 Needle Stick 656
Empyema 294 Omphalitis 674
Encephalitis 296 Orbital Cellulitis 680
Epididymitis and Orchitis 310 Orchitis 682
xxxviii r r r TOPICAL TABLE OF CONTENTS
Osteomyelitis 688 Upper Respiratory Infection 992

Otitis Externa 692 Urethritis 996
Otitis Media 694 Urinary Retention 998
Paronychia 722 Urinary Tract Infection 1000
Parotitis 724 Vaginal Discharge, Prepubertal 1012
Pelvic Inflammatory Disease 730 Vaginal Discharge, Pubertal 1014
Pericarditis 734 Vaginitis 1016
Perichondritis, Ear 736 Ventriculoperitoneal Shunt Infection 1018
Periorbital Cellulitis 738 Ventriculoperitoneal Shunt Malfunction 1020
Peritonitis 740 Vomiting 1024
Pertussis 742 Warts 1026
Pilonidal Cyst 746
Pinworms 748 Metabolic Emergencies
Pneumonia, Aspiration 754 Acute Renal Failure 30
Pneumonia, Bacterial 756 Adrenal Insufficiency 34
Rash, Petechiae 798 Congenital Adrenal Hyperplasia 184
Rash, Purpura 800 Diabetic Ketoacidosis 248
Rash, Vesiculobullous 804 Disorders of Energy Metabolism 266
Reye Syndrome 814 Hepatic Encephalopathy 486
Rheumatic Fever 818 Hypercalcemia 506
Rickettsial Disease 820 Hyperglycemia 510
Roseola Infantum 822 Hyperkalemia 512
Rubella 824 Hypernatremia 514
Salmonella 826 Hypocalcemia 526
Scabies 830 Hypoglycemia 528
Scarlet Fever 832 Hypokalemia 532
Sepsis 844 Hyponatremia 534
Sexually Transmitted Infections 850 Hypoparathyroidism 536
Sinusitis 860 Rhabdomyolysis 816
Staphylococcal Scalded Skin Syndrome 868
Stridor 880 Nephrology
Syphilis 898 Acute Renal Failure 30
Tapeworm and Cestode Infestations 904 Diabetes Insipidus 246
Tetanus 914 Glomerulonephritis 442
Tetanus Prophylaxis 916 Hematuria 472
Thrush 920 Henoch-Schonlein Purpura 484
Tick Bite 924 Hydronephrosis 504
Tinea Capitis 926 Metabolic Acidosis 626
Tinea Corporis 928 Nephrotic Syndrome 664
Tinea Versicolor 930 Polycystic Kidney Disease 762
Toxic Shock Syndrome 936 Renal Vein Thrombosis 810
Tracheitis 938 Urinary Tract Infection 1000
Tuberculosis 986 Urolithiasis 1002
TOPICAL TABLE OF CONTENTS r r r xxxix
Neurologic Emergencies Subdural Hematoma 886

Abscess, Intracranial 12 Syncope 894
Altered Level of Consciousness/Coma 38 Syndrome of Inappropriate Antidiuretic Hormone
Secretion (SIADH) 896
Altitude Sickness 40
Tinnitus 932
Apnea 68
Transverse Myelitis 946
Ataxia 86
Trauma, Head 964
Atlantoaxial Instability 88
Trauma, Spinal Cord 978
Blindness 112
Traumatic Brain Injury 982
Botulism 116
Ventriculoperitoneal Shunt Infection 1018
Brachial Plexus Injury 118
Ventriculoperitoneal Shunt Malfunction 1020
Carpal Tunnel Syndrome 144
Weakness 1028
Cauda Equina Syndrome 148
Withdrawal Syndromes 1034
Cerebral Contusions 158 Nontraumatic Musculoskeletal Emergencies
Concussion 182 Arthritis, Rheumatoid 74
Dizziness/Vertigo 270 Arthritis, Septic 76
Dystonia 280 Brachial Plexus Injury 118
Encephalitis 296 Carpal Tunnel Syndrome 144
Epidural Hematoma 312 Costochondritis 206
Eye, Strabismus 334 Deep Vein Thrombosis 236
Eye, Visual Disturbance 336 Discitis 258
Facial Nerve Palsy 338 Dystonia 280
Febrile Seizure 344 Fasciitis 342
Fracture, Cervical Spine 376 Immobile Arm 544
Fracture, Skull 408 Limp 594
Guillain-Barre Syndrome 450 Lyme Disease 596
Headache 460 Osteomyelitis 688
Hearing Loss 462 Osteosarcoma 690
Hepatic Encephalopathy 486 Rheumatic Fever 818
Hydrocephalus 502 Slipped Capital Femoral Epiphysis (SCFE) 862
Infantile Spasm 552 Spinal Cord Compression 864
Meningococcemia 618 Transient Synovitis 944
Migraine Headaches 630
Muscular Dystrophy 638 Ophthalmologic Emergencies
Myasthenia Gravis 640 Anterior Uveitis (Iritis) 54
Neuroleptic Malignant Syndrome 666 Blepharitis 110
Pseudotumor Cerebri 778 Blindness 112
Seizure 842 Chalazion 162
Shock, Neurogenic 856 Conjunctival Injury 190
Status Epilepticus 870 Conjunctivitis 192
Strabismus, Chronic (Primary) 876 Conjunctivitis, Neonatal 194
Stroke 882 Corneal Abrasion 204
Subarachnoid Hemorrhage 884 Dacryocystitis/Dacryostenosis 232
xl r r r TOPICAL TABLE OF CONTENTS
Eye, Red 332 Trauma, Knee 966

Eye, Strabismus 334 Trauma, Neck 968
Eye, Visual Disturbance 336 Trauma, Shoulder 976
Foreign Body, Cornea 362 Trauma, Spinal Cord 978
Fracture, Orbital 396 Presenting Signs and Symptoms
Globe Rupture 440
Abdominal Distention 2
Hyphema 524
Acute Respiratory Failure 32
Orbital Cellulitis 680
Altered Level of Consciousness/Coma 38
Periorbital Cellulitis 738
Apnea 68
Strabismus, Chronic (Primary) 876
Apparent Life-Threatening Event 70
Orthopedic Injuries Atlantoaxial Instability 88
Ankle Sprain 52 Blindness 112
Carpal Tunnel Syndrome 144 Breast Lesions 124
Compartment Syndrome 180 Constipation 196
Dislocation, Knee 260 Cough 208
Dislocation, Patella 262 Croup 210
Dislocation, Temporomandibular Joint 264 Crying/Colic 212
Fracture, Cervical Spine 376 Cryptorchidism 214
Fracture, Clavicle 378 Cyanosis 220
Fracture, Coccyx 380 Cyclic Vomiting 224
Fracture, Femur 382 Dehydration 238
Fracture, Foot 384 Diaper Rash 250
Fracture, Forearm/Wrist 386 Diarrhea 252
Fractures, Greenstick/Bowing 388 Dizziness/Vertigo 270
Fracture, Humerus 390 Dystonia 280
Fracture, Patella 398 Edema 288
Fracture, Pelvic Avulsion 400 Epistaxis 316
Fracture, Scaphoid 404 Esophagitis 328
Fracture, Scapula 406 Eye, Red 332
Fracture, Supracondylar 410 Eye, Strabismus 334
Fracture, Tibial Avulsion 412 Eye, Visual Disturbance 336
Fracture, Toddlers 414 Facial Nerve Palsy 338
Fracture, Torus 416 Failure to Thrive 340
Immobile Arm 544 Fever in Children Older than 3 Months 348
Mallet Finger 604 Fever in Infants 03 Months of Age 350
Nursemaids Elbow 670 Fever of Unknown Origin 352
Osgood-Schlatter Disease 684 Gastritis 424
Osteogenesis Imperfecta 686 Groin Mass 446
Slipped Capital Femoral Epiphysis (SCFE) 862 Gynecomastia 452
Trauma, Ankle 950 Headache 460
Trauma, Elbow 956 Hearing Loss 462
Trauma, Foot/Toe 960 Heart Murmur 466
Trauma, Hand/Finger 962 Hematuria 472
TOPICAL TABLE OF CONTENTS r r r xli
Hemoptysis 480 Panic Attack 716

Hepatomegaly 490 Psychosis 782
Hypertension 516 Suicide 890
Hyperthermia 518 Respiratory Emergencies
Hyperventilation 522
Hypotension 538
Acute Respiratory Failure 32
Hypothermia 540
Altitude Sickness 40
Immobile Arm 544
Apnea 68
Laryngitis 584
Apparent Life-Threatening Event 70
Limp 594
Asthma 82
Lymphadenopathy 598
Bronchiolitis 126
Neck Mass 650
Cough 208
Neck Stiffness 652
Croup 210
Oral Lesions 678
Cyanosis 220
Pain, Abdomen 700
Cystic Fibrosis: Exacerbation 226
Pain, Back 702
Cystic Fibrosis: New Diagnosis 228
Pain, Chest 704
Diphtheria 256
Pain, Extremity 706
Drowning 272
Pain, Eye 708
Empyema 294
Pain, Throat 710
Epiglottitis/Supraglottitis 314
Palpitations 712
Flail Chest 354
Polyuria 768
Fracture, Rib 402
Procedural Sedation and Analgesia 774
Hemoptysis 480
Rectal Bleeding 806
Hemothorax 482
Rectal Prolapse 808
Hyperventilation 522
Respiratory Distress 812
Influenza 560
Scrotal Pain 836
Laryngomalacia/Tracheomalacia 586
Scrotal Swelling 838
Obstructive Sleep Apnea Syndrome 672
Strabismus, Chronic (Primary) 876
Pertussis 742
Syncope 894
Pleural Effusion 752
Tachycardia 902
Pneumonia, Aspiration 754
Teething 906
Pneumonia, Bacterial 756
Vomiting 1024
Pneumothorax/Pneumomediastinum 758
Weakness 1028
Pulmonary Contusion 784
Wheezing 1030
Pulmonary Edema 786
Psychiatric Emergencies Pulmonary Embolism 788
Agitation 36 Respiratory Distress 812
Bipolar Disorder/Mania 104 Strangulation 878
Child Abuse 168 Stridor 880
Conversion Disorder 202 Sudden Infant Death Syndrome (SIDS) 888
Depression 242 Tracheoesophageal Fistula 940
Eating Disorders 282 Tuberculosis 986
Munchausen Syndrome by Proxy 636 Wheezing 1030
xlii r r r TOPICAL TABLE OF CONTENTS
Surgical Emergencies Calcium Channel Blocker Poisoning 134

Abdominal Distention 2 Carbon Monoxide/Cyanide Poisoning and
Smoke Inhalation 138
Abscess, Ludwig Angina 14
Caustic Exposure 150
Appendicitis 72
Cholinergic Poisoning 172
Arthritis, Septic 76
Cocaine Poisoning 174
Cholelithiasis 170
Digoxin Toxicity 254
Colitis 176
Envenomation, Insect Bites and Stings 300
Compartment Syndrome 180
Envenomation, Marine 302
Ectopic Pregnancy 284
Envenomation, Scorpion 304
Epidural Hematoma 312
Envenomation, Snake 306
Foreign Body Aspiration 358
Envenomation, Spider 308
Gastrointestinal Bleeding: Lower 430
Ethanol Poisoning 330
Gastrointestinal Bleeding: Upper 432
Food Poisoning 356
Hirschsprung Disease 496
Foreign Body, Disc Battery 364
Intestinal Malrotation 564
Hallucinogen Poisoning 456
Intussusception 568
Hydrocarbon Poisoning 500
Meckels Diverticulum 612
Hypoglycemic Agents Poisoning 530
Necrotizing Enterocolitis 654
Inhalant Abuse 562
Orbital Cellulitis 680
Iron Poisoning 570
Ovarian Torsion 698
Lead Poisoning 588
Pain, Abdomen 700
Methemoglobinemia 628
Pericardial Effusion/Tamponade 732
Nonsteroidal Anti-Inflammatory Drug (NSAID)
Pericarditis 734 Poisoning 668
Pneumothorax/Pneumomediastinum 758 Opioid Poisoning 676
Pyloric Stenosis 790 Salicylate Poisoning 828
Rectal Bleeding 806 Sympathomimetic Poisoning 892
Scrotal Mass 834 Toxic Alcohols Poisoning 934
Spinal Cord Compression 864 Tricyclic Antidepressant Poisoning 984
Testicular Torsion 912 Withdrawal Syndromes 1034
Trauma, Abdominal 948
Trauma
Ventriculoperitoneal Shunt Malfunction 1020
Volvulus 1022 Ankle Sprain 52
Barotrauma, Sinus 98
Toxicology/Poisoning Bite, Animal 106
Acetaminophen Poisoning 24 Bite, Human 108
Anticholinergic Poisoning 56 Brachial Plexus Injury 118
Anticoagulant Poisoning 58 Cerebral Contusions 158
Anticonvulsant Poisoning 62 Child Abuse 168
Beta-Blocker Poisoning 100 Compartment Syndrome 180
Body Packers (Ingested Drug Packages) 114 Concussion 182
Botulism 116 Conjunctival Injury 190
Burn, Chemical 128 Corneal Abrasion 204
Caffeine/Theophylline Poisoning 132 Decompression Sickness 234
TOPICAL TABLE OF CONTENTS r r r xliii
Dislocation, Knee 260 Pericardial Effusion/Tamponade 732

Dislocation, Patella 262 Pulmonary Contusion 784
Electrical Injury 290 Sexual Assault 848
Fracture, Clavicle 378 Shock, Neurogenic 856
Fracture, Coccyx 380 Strangulation 878
Fracture, Femur 382 Subdural Hematoma 886
Fracture, Foot 384 Tendon Laceration 908
Fracture, Forearm/Wrist 386 Tendonitis 910
Fractures, Greenstick/Bowing 388 Tetanus Prophylaxis 916
Fracture, Humerus 390 Trauma, Abdominal 948
Fracture, Mandibular 392 Trauma, Ankle 950
Fracture, Nasal 394 Trauma, Chest 952
Fracture, Orbital 396 Trauma, Dental 954
Fracture, Patella 398 Trauma, Elbow 956
Fracture, Pelvic Avulsion 400 Trauma, Facial 958
Fracture, Scaphoid 404 Trauma, Foot/Toe 960
Fracture, Scapula 406 Trauma, Hand/Finger 962
Fracture, Skull 408 Trauma, Head 964
Fracture, Supracondylar 410 Trauma, Knee 966
Fracture, Tibial Avulsion 412 Trauma, Neck 968
Fracture, Toddlers 414 Trauma, Penetrating 970
Fracture, Torus (Buckle) 416 Trauma, Perineal 972
Fracture, Zygoma 418 Trauma, Scrotal and Penile 974
Globe Rupture 440 Trauma, Shoulder 976
Hemothorax 482 Trauma, Spinal Cord 978
Intraosseous Infusions 566 Trauma, Vaginal 980
Laceration Repair 582 Traumatic Brain Injury 982
Mallet Finger 604 Tympanic Membrane Perforation 988
Myocardial Contusion 642
Nail Bed Injuries 648 Vascular Emergencies
Needle Stick 656 Collagen Vascular Disease 178
Nursemaids Elbow 670 Esophageal Varices 326
xliv
Fleisher & Ludwigs

5-Minute
Pediatric
Emergency
Medicine
Consult
1
LWBK822-driver-A LWBK822-Hoffman ch001.xml April 15, 2011 13:20
ABDOMINAL DISTENTION
Besh Barcega
Eugenio Vazquez
ETIOLOGY r Chronic isolated abdominal distention in otherwise

BASICS r Neonates: healthy children is suspicious for neoplasm,
Bowel obstruction: organomegaly, or ascites.
DESCRIPTION Malrotation with volvulus r A history of weight gain and edema can be seen in
r Abdominal distention is an increase in the volume of Necrotizing enterocolitis nephrotic syndrome.
the abdominal cavity as the anterior abdominal wall Hirschsprung disease with toxic megacolon r Gross hematuria may suggest kidney disease such
is forced outwardly by rising internal pressure from Inguinal hernia with incarceration as polycystic kidney disease or Wilms tumor.
either gas, fluid, stool, an enlarged organ, or a mass. Intra-abdominal masses. Up to 2/3 originate from r Inquire about sexual history and menstruation in
r Abdominal distention may be difficult to discern in the kidneys or the urinary tract, with most being adolescent females.
infants and children, as they normally have multicystic kidneys or hydronephrosis in this age r Inquire about direct trauma to the abdominal region.
protuberant bellies secondary to their immature group.
abdominal musculature, relatively large internal These neonatal abdominal masses usually do PHYSICAL EXAM
organs, and physiologic lordosis. not present as medical emergencies but require r Look for signs of toxicity including pallor,
urgent attention. diaphoresis, hypotension, rapid pulse, shallow
RISK FACTORS r Infants and children: breathing, poor capillary refill, and lethargy.
r Prematurity is a risk factor for several abdominal
Bowel obstruction: r Conduct a detailed visual exam looking for
emergencies that may present as abdominal
Intussusception is the most common etiology in generalized edema, bruises, pallor, jaundice, or
distention.
r Previous abdominal surgeries may cause the children <2 yr old. surgical scars.
Adhesive bands from prior surgery (1) r Detailed abdominal exam:
formation of adhesions leading to bowel
Intra-abdominal masses: Hydronephrosis, Wilms Auscultate:
obstruction (1). Hyperactive bowel sounds are heard with acute
r Children with neuromuscular disease are more tumor, neuroblastoma, lymphoma
Trauma intestinal obstruction, malabsorption
prone to abdominal distention from an ileus. Peritonitis: Ruptured appendicitis is a common syndromes, or gastroenteritis.
PATHOPHYSIOLOGY etiology in children <2 yr old. Hypoactive bowel sounds suggest ileus.
r Abdominal distention is a nonspecific sign that can Ileus from infection or electrolyte abnormalities Percuss:
be caused by a large number of pathologic and Constipation Tympanitic abdomen suggests gaseous
physiologic processes, most all of them falling into Nephrotic syndrome distention.
one of the following categories: r Adolescent females: Localized tympany may result from a proximal
Increased intraluminal volume of the GI tract Hematocolpos obstruction, while a generalized tympanic note
caused by oral intake of food, swallowed air, Ovarian cyst(s) suggests either a distal obstruction or free
trapped air from obstruction, or production of gas peritoneal air.
from malabsorption or bacterial overgrowth Generalized shifting dullness when the patient
Increased extraluminal accumulation of gas or DIAGNOSIS is placed on the lateral decubitus position is
fluid: indicative of free peritoneal fluid.
Free peritoneal air after a perforation of the GI HISTORY Palpate:
r The history should be comprehensive due to the
tract, pneumomediastinum infiltrating the Masses may consist of stool, enlarged organs,
large number of processes that can cause abdominal
abdominal cavity, or air introduced from surgery cysts, or tumors. Location, mobility, and contour
distention but can be focused by age, risk factors,
or trauma of the mass should be noted.
Extraluminal fluid can originate from an and duration of symptoms. Rebound tenderness and involuntary guarding
r In the neonate:
effusion, an exudate (pus), a hemorrhagic suggest peritonitis.
process (blood), the disruption of the Bilious emesis suggests intestinal obstruction r A pelvic exam on sexually active females and genital
gallbladder (bile), the genitourinary tract (urine), beyond the ampulla of Vater and can be seen with
exam on males may be indicated.
or the lymphatic vessels (chyle). malrotation, intestinal atresias, or ileus. r Rectal examination is recommended if a lower
Severe organomegaly: Delayed passage of meconium can be seen in
cystic fibrosis and Hirschsprung disease. quadrant abdominal mass is found on exam.
Hepatomegaly and splenomegaly can develop
from inflammation, venous congestion, an Fever may be from an infectious process such as DIAGNOSTIC TESTS & INTERPRETATION
infiltrative processes, or trauma. sepsis causing ileus, a GI infection, or peritonitis Lab
Enlarged kidneys can be seen from obstructive due to perforation. Initial Lab Tests
uropathies causing hydronephrosis or from A weak urinary stream may be secondary to Obstructive bowel process is common cause, and
polycystic kidney disease. posterior urethral valves causing hydronephrosis. laboratory testing is of limited value for diagnosis but
r Masses such as cysts, tumors, and even pregnancy r In the infant and older child:
can be used as an adjunct for patient management:
r Abdominal wall hypotonia from either weak Inquire about previous abdominal surgeries. r CBC with peripheral smear is recommended to
Inquire about the stooling pattern. evaluate for inflammatory or infectious process or
musculature or fascia
Pain should be thoroughly evaluated and malignancy.
differentiated, as it may render important clues to r Assess electrolytes if an ileus is suspected
the etiology of the disease: r Order BUN/creatinine if concerned for renal disease.
Acute onset of inconsolability or increased
r LFTs if hepatomegaly is found
irritability should alert toward abdominal
r Urinalysis if concerned for renal etiology or if
emergencies such as intussusception,
obstruction, or infection. generalized edema is found on exam
Chronic irritability may point to infant colic,
formula intolerance, malabsorption, or
constipation.
2
ABDOMINAL DISTENTION
A
Imaging
r A 2- or 3-view abdominal radiograph is the most
DISPOSITION ADDITIONAL READING
Admission Criteria r Long FR, Kramer SS, Markowitz RI, et al.
helpful initial diagnostic study to perform for a r Newborns with fever or infants and children who
patient presenting with abdominal distention. The are ill appearing Radiographic patterns of intestinal malrotation on
findings on the radiograph will aid to determine r Peritoneal signs and those who may also require children. Radiographics. 1996;16:547556.
what additional lab and/or imaging studies will be r Louie JP. Essential diagnosis of abdominal
urgent surgical intervention
needed (2,3). Look at the intraluminal gas pattern, r Poorly controlled pain and/or intractable vomiting emergencies in the first year of life. Emerg Med Clin
presence of free air, calcifications, constipation, and without a specific diagnosis North Am. 2007;25:10091040.
some soft tissue masses: r Intra-abdominal organ trauma r McCollough M, Sharieff G. Abdominal surgical
An intestinal obstruction or a paralytic ileus can r Nephrotic syndrome with hypoalbuminemia emergencies in infants and young children. Emerg
cause distended loops of bowel and air-fluid levels. Med Clin North Am. 2003;21:909935.
Double bubble sign is appearance of a gas-filled refractory to oral corticosteroids r Rao P. Neonatal gastrointestinal imaging. Eur J
stomach and duodenum separated by the pylorus Discharge Criteria Radiol. 2006;60:171186.
and is seen in neonates and infants with duodenal r Patients who are well appearing and have a
atresia or malrotation with volvulus. definitive nonemergent etiology of the abdominal See Also (Topic, Algorithm, Electronic
r Abdominal US is useful for initial evaluation of an distention Media Element)
r Patients who are well appearing and do not have a r Hirschsprung Disease
abdominal mass and can also be used to diagnose
r Nephrotic Syndrome
intussusception. definitive etiology of the abdominal distention but
r Abdominal CT is the most sensitive imaging do have reliable follow-up r Pain, Abdomen
modality for detailed evaluation of intra-abdominal r Patients with abdominal pain and/or vomiting r Peritonitis
solid organ pathology, especially if US findings are whose symptoms are relieved or improved
inconclusive, but it does run the risk of radiation
exposure (3). CODES
r Upper GI series is indicated if malrotation or upper FOLLOW-UP
GI obstruction is suspected. Obtain only if the FOLLOW-UP RECOMMENDATIONS ICD9
patient is clinically stable. r 24-hr follow-up with either the primary care 787.3 Flatulence, eructation, and gas pain
r Air or barium enema is indicated if intussusception
provider or ED if etiology of abdominal distention
is highly suspected. The pediatric surgeon should be has not been determined and symptoms persist
involved due to the risk of bowel perforation. r 2448-hr follow-up with primary care provider if PEARLS AND PITFALLS
etiology has been determined and additional r Necrotizing enterocolitis may occur in term infants
DIFFERENTIAL DIAGNOSIS
r Extra-abdominal pathology such as pulmonary evaluation is needed and should be in the differential diagnosis of any
hyperinflation from bronchiolitis or an asthma r Discharge instructions and medications: newborn with feeding intolerance and abdominal
exacerbation Return if patient develops vomiting, severe distention.
r Unrecognized pregnancy abdominal pain, or fever. r An obstructive bowel process is the most common
If pain is mild, provide an analgesic: cause of acute onset of abdominal distention with
Acetaminophen 1015 mg/kg/dose PO or abdominal pain.
TREATMENT PR q46h r Abdominal masses are usually an incidental finding
PROGNOSIS on abdominal exam. Patients usually present with
INITIAL STABILIZATION/THERAPY abdominal pain only when the mass is causing an
Assess and stabilize airway, breathing, and Dependent on the underlying etiology
obstruction.
circulation. COMPLICATIONS r It is critical to rule out neoplasm in children with
r Bowel obstruction
MEDICATION abdominal swelling.
r Broad-spectrum IV antibiotics if suspicious for r Bowel perforation
peritonitis or sepsis: r Gut necrosis
Gentamicin 2.5 mg/kg/dose PLUS ampicillin/ r Sepsis
sulbactam 50 mg/kg/dose of ampicillin r Death
component OR
Piperacillin/tazobactam 100 mg/kg/dose of
piperacillin component OR REFERENCES
Ampicillin 50 mg/kg/dose PLUS gentamicin
2.5 mg/kg/dose PLUS metronidazole 7.5 mg/kg/ 1. Grant HW, Parker MC, Menzies D, et al. Adhesions
dose after abdominal surgery in children. J Pediatr Surg.
r Analgesic if patient is in pain: 2008;43:152156.
Morphine 0.1 mg/kg IV/IM/SC q2h PRN: 2. Hughes U, Thomas K, Shuckett T, et al. The
Initial morphine dose 0.1 mg/kg IV/SC may be abdominal radiographic series in children with
repeated q1520min until pain is controlled suspected bowel obstructionshould the second
then q2h PRN view be abandoned? Pediatr Radiol. 2002;32:
r Antiemetic if patient has persistent nausea and/or 556560.
vomiting: Ondansetron 0.15 mg/kg/dose IV/PO q6h 3. Lameris W, van Randen A, van Es HW, et al.
PRN Imaging strategies for detection of urgent
r Maintenance IV fluids if patient is found to be conditions in patients with acute abdominal pain:
Diagnostic accuracy study. BMJ. 2009;339:b2431.
dehydrated
SURGERY/OTHER PROCEDURES
r Immediate surgical consultation is required for any
ill-appearing patient with suspected peritonitis from
bowel perforation or malrotation with mid-gut
volvulus.
r Nasogastric tube placement if intractable vomiting
or if a bowel obstruction is suspected
3
ABRUPTIO PLACENTA
Shira Yahalom
Imaging
BASICS DIAGNOSIS r US demonstrates abruptio placenta in only 50% of
cases:
DESCRIPTION HISTORY US use to demonstrate hematoma is of limited
r Abruptio placenta refers to separation of the r Triad of severe abdominal/back pain, vaginal
value since most abruptions will not be detected.
placenta from the uterus after 20 wk gestation and bleeding, and fetal distress should alert the clinician US should be used to locate the placenta.
prior to delivery. for the presence of abruptio placenta. r MRI is sensitive in detecting small or posterior
r The severity of separation can range from mild to r Since the bleeding may be concealed, the absence
abruptions.
fatal for both mother and fetus. of vaginal bleeding does not rule out the diagnosis
of abruptio placenta. DIFFERENTIAL DIAGNOSIS
EPIDEMIOLOGY r Abdominal/Back pain may persist between r Placenta previa is associated with painless vaginal
r Abruptio placenta complicates 1% of pregnancies. bleeding.
r 1/3 of all antepartum bleeding is attributed to contractions.
r Decrease in fetal activity as sensed by the mother r Uterine rupture causes severe abdominal pain,
abruptio placenta. r Obtain history regarding cocaine use or recent bleeding, and fetal distress/demise.
r Vasa previa will result in massive fetal blood loss.
RISK FACTORS trauma.
r Maternal HTN r Vaginal or cervical laceration
r Multiple gestation PHYSICAL EXAM r Preterm labor
r Since blood loss may be severe, maternal
r Uterine malformations
tachycardia and hypotension can occur.
r Tobacco or cocaine use r Fundal tenderness may be palpated, and fundal
r Polyhydramnios with sudden uterine decompression
TREATMENT
height may increase due to an expanding
r Previous abruption hematoma. INITIAL STABILIZATION/THERAPY
r Thrombophilias r The amount of vaginal bleeding does not correlate r Obtain large-bore IV access, and start fluid
r Trauma with the degree of abruption: resuscitation with 20 mL/kg crystalloid; repeat as
Avoid pelvic examination until location of the needed.
PATHOPHYSIOLOGY r Supplemental oxygen
r Rupture of blood vessels in the placenta leads to placenta is verified given the differential diagnosis
of placenta previa. r Continuous fetal heart rate and contractions
hematoma formation and placental separation. monitoring
r Placental separation releases prostaglandins, and DIAGNOSTIC TESTS & INTERPRETATION r Close monitoring of the mother for signs of
contractions occur worsening separation and Lab hemodynamic instability
bleeding. r CBC
r Fetal age should be assessed and complications of
r Dissection of blood into the decidua basalis may r Serum electrolytes, LFTs, BUN, and creatinine
prematurity anticipated.
progressively increase the shearing force on r PT/PTT/INR, fibrinogen
placenta. r Blood type and Rh status
ETIOLOGY
Bleeding may result from trauma, defective placental
blood vessels, thrombophilias, drug abuse, or uterine
malformations.
4
ABRUPTIO PLACENTA
A
MEDICATION Discharge Criteria See Also (Topic, Algorithm, Electronic
r All patients presenting to the ED with suspected Media Element)
First Line
RhoGAM IM 300 g: abruptio placenta require admission for monitoring. Vaginal Bleeding in Pregnancy
r Given as soon as possible within 72 hr of event for r Transfer to a facility with a neonatal ICU should be
Rh-negative mothers >12 wk gestation considered for stable patients. Transfer should be
Second Line
done after delivery if delivery is required to stabilize CODES
r Typed and crossed-matched packed RBCs or the mother.
r Patients with no evidence of abruption or other
platelets may be indicated. ICD9
significant injury may be discharged after 46 hr of r 641.20 Premature separation of placenta,
r Fresh frozen plasma if disseminated intravascular
normal maternal and fetal monitoring. unspecified as to episode of care
coagulation (DIC) occurs r 641.21 Premature separation of placenta, with
r Tocolytics may be considered with obstetric
FOLLOW-UP delivery
consultation. r 641.23 Premature separation of placenta,
SURGERY/OTHER PROCEDURES FOLLOW-UP RECOMMENDATIONS antepartum
r Obtain immediate obstetric consultation.
Discharge instructions include pelvic rest, no
r Anticipate prematurity of fetus and consult neonatal intercourse, no heavy lifting, and no prolonged
ICU if precipitous delivery of an infant >20 wk standing. PEARLS AND PITFALLS
gestation may occur.
COMPLICATIONS r Patients may not present with the classic triad.
DISPOSITION r Maternal: Hemorrhagic shock, transfusion-related
Consider the diagnosis in all patients presenting
Admission Criteria complications, DIC with preterm labor.
r All patients should be admitted. r Fetal: Complications of prematurity, perfusion r The presenting complaint may only be a decrease in
r Decision to deliver should be made with obstetric compromise, anoxic insult fetal activity per the patient.
consultation and consideration of prematurity risks r Lack of vaginal bleeding does not exclude abruptio
versus fetal and maternal morbidity and mortality. placenta.
r Critical care admission criteria: ADDITIONAL READING r US should not be used to exclude the diagnosis
All hemodynamically unstable patients, either r Abbrescia K, Sheridan B. Complications of second given the low sensitivity of the test. Diagnosis of
before or after delivery, should receive ICU care. and third trimester pregnancies. Emerg Med Clin abruptio placenta remains clinical.
North Am. 2003;21:695710. r Anticipate shock and DIC.
r Ferentz KS, Nesbitt LS. Common problems and r Consult an obstetrician early in the course of
emergencies in the obstetric patient. Prim Care. suspected abruptio placenta.
2006;33(3):727750.
r Francois KE, Foley MR. Antepartum and postpartum
hemorrhage. In Gabbe SG, Niebyl JR, Simpson JL,
et al., eds. Obstetrics: Normal and Problem
Pregnancies. 5th ed. Philadelphia, PA: Churchill
Livingstone Elsevier; 2007.
r Sakornbut E, Leeman L, Fontaine P. Late pregnancy
bleeding. Am Fam Physician. 2007;75(8):
11991206.
5
ABSCESS, BARTHOLIN GLAND

Carl P. Kaplan
BASICS DIAGNOSIS TREATMENT

DESCRIPTION HISTORY INITIAL STABILIZATION/THERAPY
r The Bartholin glands are the major mucus-secreting r Acute labial swelling, redness, and pain
r Dyspareunia Analgesics:
sites of the vulva, with ducts located at 5 and r NSAIDs
7 oclock on the mucosal aspect of introitus r Dysuria
r Opioids
adjacent to the labia minora. r Pain with movement or sitting
r Topical viscous lidocaine
r Trauma or local inflammation leads to duct r Spontaneous discharge of pus
r Locally injected or regional anesthesia
obstruction, cyst formation, and bacterial
colonization leading to localized abscess sometimes PHYSICAL EXAM
r Unilateral labia swelling, redness, and tenderness MEDICATION
with accompanying cellulitis. r Antibiotics for empiric coverage of STIs:
r Diagnosis is clinical. r 25-cm tender unilateral fluctuant mass
r Surrounding cellulitis Ceftriaxone 125 mg IM or cefixime 400 mg PO
r Therapy focuses on surgical incision and drainage plus azithromycin 1 g PO or doxycycline 100 mg
r Rarely fever
with fistulization as well as antimicrobial therapy PO b.i.d. for 714 days (or azithromycin 2 g PO)
r Spontaneous purulent discharge Or alternately, a single dose of azithromycin 2 g
aimed at common flora.
DIAGNOSTIC TESTS & INTERPRETATION PO as sole therapy
EPIDEMIOLOGY r Antibiotics for common flora:
Incidence Lab
r Lab testing is not necessary for diagnosis. Given if abscess is complicated by cellulitis
2% of postmenarchal females Amoxicillin/clavulanate 875 mg PO b.i.d. for
r Cultures may be sent to assess for specific diagnosis,
RISK FACTORS 710 days OR
r Vulvovaginitis including gonorrhea. Trimethoprim/sulfamethoxazole 160 mg PO b.i.d.
r Sexual activity/Trauma Imaging for 710 days if suspected of MRSA
r Sexually transmitted infections (STIs) Soft tissue US may be employed to aid in diagnosis or For sepsis, consider combined therapy with all of
r Black and non-Hispanic white females to guide drainage. the following:
Vancomycin 500100 mg IV q12h PLUS
DIFFERENTIAL DIAGNOSIS Doxycycline 100 mg IV q12h PLUS
PATHOPHYSIOLOGY r Labial abscess
Inflammation at the site of the duct leads to r Enterocutaneous fistula (inflammatory bowel Metronidazole 500 mg IV q8h
obstruction, mucocele formation, and suppurative r NSAIDs:
infection by local flora. disease)
r Hematoma Consider NSAIDs in anticipation of prolonged pain
ETIOLOGY r Mucocele and inflammation:
r Anaerobic vaginal species: Ibuprofen 10 mg/kg/dose PO/IV q6h PRN
r Genital ulcers Ketorolac 0.5 mg/kg IV/IM q6h PRN
Bacteroides r Chancroid Naproxen 5 mg/kg PO q8h PRN
Peptostreptococcus r Vulvovaginitis r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN
Prevotella
r Endometriosis
Escherichia coli
r Gonorrhea r Malignancy
r Staphylococcus species (MSSA/MRSA)
r Streptococcal species
6
ABSCESS, BARTHOLIN GLAND

A
r Local anesthetics: DISPOSITION ADDITIONAL READING
Infiltration with a local anesthetic may achieve Admission Criteria r Aghajanian A, Bernstein L, Grimes DA. Bartholins
significant analgesia. Patients typically are discharged, but consider
r Opioids: admission for severe associated cellulitis, pelvic duct abscess and cyst: A case-control study. South
Morphine 0.1 mg/kg IV/IM/SC q2h PRN: inflammatory disease, intractable pain requiring Med J. 1994;87:2629.
Initial morphine dose of 0.1 mg/kg IV/SC may r Roberts JR, Hedges JR. Clinical Procedures in
parenteral opioids, or immunocompromise.
be repeated q1520min until pain is controlled, Emergency Medicine. 4th ed. Philadelphia, PA:
Discharge Criteria Saunders; 2004:731733.
then q2h PRN. r Pain controlled
Fentanyl 12 g/kg IV q2h PRN: r Tanaka K, Mikamao H, Ninomiya M, et al.
r Spontaneous urination
Initial dose of 1 g/kg IV may be repeated Microbiology of Bartholins gland abscess in Japan.
r Ability to obtain and tolerate antibiotics if prescribed
q1520min until pain is controlled, then q2h J Clin Microbiol. 2005;43(8):42584261.
r Ability to follow up in 4872 hr r Wechter ME, Wu JM, Marzano D, et al. Management
PRN.
Codeine or codeine/acetaminophen dosed as of Bartholin duct cysts and abscesses: A systematic
0.51 mg/kg of codeine component PO q4h PRN review. Obstet Gynecol Surv. 2009;64(6):395404.
Hydrocodone or hydrocodone/acetaminophen
FOLLOW-UP
dosed as 0.1 mg/kg of hydrocodone component
See Also (Topic, Algorithm, Electronic
FOLLOW-UP RECOMMENDATIONS Media Element)
PO q46h PRN r Discharge instructions and medications: r Pelvic Inflammatory Disease
Issues for Referral Analgesics as needed. See Medication section. r Sexually Transmitted Infections
Recurrence It is unclear if antibiotics are necessary after
successful incision and drainage.
COMPLEMENTARY & ALTERNATIVE If cellulitis is present, antibiotics are necessary.
THERAPIES Warm compresses or sitz baths t.i.d.q.i.d. for CODES
r Warm compresses
4872 hr
r Sitz baths ICD9
Maintain placement of Word catheter port in
vagina (if applicable). 616.3 Abscess of Bartholins gland
r Incision and drainage is the mainstay of therapy. r Activity:
r Analgesia should be administered prior to the Avoid vaginal intercourse for 24 wk.
Wear loose-fitting undergarments.
PEARLS AND PITFALLS
procedure. This may be local infiltration or regional
anesthesia. Avoid running during placement while devices are r Incision and drainage alone is inferior to the
r Various drainage approaches include: in place. addition of a fistulization procedure.
Simple incision and drainage Patient Monitoring r Topical viscous lidocaine and systemic opioids prior
Fistulization procedures (Word catheter, Jacobi Follow up in 4872 hr in ED or with primary care to incision and drainage will facilitate some
ring, etc.) provider. procedures, but consider procedural sedation.
Marsupialization r During any procedure, wear appropriate personal
PROGNOSIS
r Average healing time is 4.8 days to 2.2 wk. protective equipment since abscess contents are
r Recurrence after fistulization procedure is 417% at under pressure.
r Gonorrhea cultures from abscess contents must be
6 mo compared to 038% recurrence after simple
needle aspiration. ordered and collected with appropriate media, as
routine wound culture will not detect Gonococcus.
COMPLICATIONS
r Recurrence
r Cyst formation
r Cellulitis
r Sepsis
r Scarring
7
ABSCESS, DENTOALVEOLAR
Kristin S. Stukus
Raymond Pitetti
PATHOPHYSIOLOGY DIAGNOSTIC TESTS & INTERPRETATION

BASICS r Oral bacteria adhere to the tooth enamel.
Lab
r Remaining food particles ferment to form organic Initial Lab Tests
DESCRIPTION acids. r In uncomplicated dentoalveolar abscess, lab testing
r Untreated bacterial caries, gingivitis, and r Lower pH from organic acids and bacterial is not warranted.
periodontitis may result in infection in the adjacent production causes tooth demineralization. r Strongly consider CBC, C-reactive protein, and blood
space surrounding the teeth. r If untreated, tooth demineralization may progress to culture in toxic-appearing children.
r A dentoalveolar abscess is typically characterized by r If needle aspiration of the abscess is performed,
form pits and fissures.
localization of pus in the structures that surround r Oral bacteria colonize the demineralized area and send aspirate for Gram stain and aerobic and
the teeth as well as infection of adjacent soft tissues. may invade the tooth. anaerobic cultures:
r May progress to life-threatening infections of the r Deeper infections may involve the dental pulp or Aspirate may be sent in blood culture bottles.
deep spaces of the neck. alveolar bone. Imaging
EPIDEMIOLOGY r If left untreated, localized dental infections may
The diagnosis is primarily clinical. However, the
Incidence progress to cause facial swelling and tenderness. following imaging modalities may help with the
r Decreasing over the last 30 years due to fluoridation diagnosis if indeterminate:
ETIOLOGY
of the water supply r Polymicrobial, with an average of 46 different r Plain radiographs may be useful in diagnosing early
r More common in lower socioeconomic groups infection.
causative bacteria
r Exact incidence is unknown, as most cases are not r Most commonly: r Maxillofacial CT scan with contrast:
reported. Oral Streptococcus (viridans) May help rule out other problems such as sinusitis,
Prevalence Oral anaerobes (Bacteroides) lymphadenitis, and peritonsillar or retropharyngeal
r Dental caries occur in 3050% of at-risk children, Prevotella species abscess
including those from low-income homes and Fusobacterium species May also determine the location, size, extent, and
developing countries. relationship of the inflammatory process to the
r Dental abscess accounts for 47% of all COMMONLY ASSOCIATED CONDITIONS surrounding vital structures
Dental caries Particularly important if there is concern for deep
dental-related visits to pediatric emergency
departments (1). space neck abscess, such as Ludwig angina, or
DIAGNOSIS retropharyngeal, parapharyngeal, or lateral
RISK FACTORS pharyngeal abscesses
r Tooth morphology: HISTORY r Parotitis may be seen on CT.
Abnormal crown anatomy r Pain at the tooth that is the nidus for the infection is
Abnormal structure of the dentin invariably present.
Diagnostic Procedures/Other
r Pre-eruptive intracoronal resorption r Pain may radiate to the jaw or ear on the affected Needle aspiration:
r Mandibular infected buccal cyst r Warranted in complicated cases and is therapeutic
side.
r Factors associated with caries: r Preceding history suggestive of caries may be and provides material for lab analysis
r Not routinely necessary and not used in
Multiple tooth surfaces with caries increase the present: Dentalgia, temperature sensitivity
likelihood of additional teeth developing caries. r Young children may not localize pain as well as uncomplicated cases
High carbohydrate consumption: Sucrose is the older children and adolescents. DIFFERENTIAL DIAGNOSIS
most cariogenic sugar because its by-product r Progressive swelling and tenderness of the gingival r Parotitis
helps bacteria adhere to the tooth surface. surface and of the adjacent buccal tissue is typical. r Sialadenitis
Use of nonfluoridated water r Fever is often present. r Facial cellulitis
Poor oral hygiene r Decreased oral intake as a result of pain r Lymphadenitis
r Poor bone mineralization due to prematurity or r Sinusitis
medications PHYSICAL EXAM r Ludwig angina
r Preceding dental trauma r Frank, severe erosive dental caries of the affected
tooth is typically readily apparent. r Peritonsillar, retropharyngeal, parapharyngeal, or
GENERAL PREVENTION r Localized swelling, warmth, and tenderness of the lateral pharyngeal abscess
r Screening dental exams performed by pediatricians r Osteomyelitis
gingival surface and face:
at well-child visits May see a fluctuant mass that extends toward the
r Early referral for dental exams
buccal side of the gum
r Good general dental hygiene with daily brushing r Tenderness to percussion of the affected tooth,
with fluoridated toothpaste though it is usually unnecessary to perform as the
r Fluorine supplementation for those with infection is readily apparent
unfluoridated water r Bimanual palpation of the adjacent buccal tissues is
r Limiting carbohydrate-containing beverages, performed to detect any large abscess that could be
especially drinking from bottles at bedtime drained for diagnostic and therapeutic purposes.
r Anterior cervical lymphadenopathy is present on the
affected side.
r Trismus is infrequently present.
r Assess for neck or facial swelling.
8
ABSCESS, DENTOALVEOLAR
A
Second Line REFERENCE
TREATMENT Clindamycin for penicillin-allergic patients,
1. Graham DB, Webb MD, Seale NS. Pediatric
10 mg/kg/dose PO/IV q6h:
PRE HOSPITAL r Considered second-line parenteral therapy emergency room visits for nontraumatic dental
Assess and stabilize airway, breathing, and r Treatment of choice for penicillin-allergic patients disease. Pediatr Dent. 2000;22:134140.
circulation.
INITIAL STABILIZATION/THERAPY r Incision and drainage of complicated dentoalveolar ADDITIONAL READING
r Assess and stabilize airway, breathing, and
abscesses r Brook I. Microbiology and management of
circulation. r Following resolution of acute infection, pulpectomy
r Antibiotic therapy endodontic infections in children. J Clin Pediatr
is indicated. Dent. 2003;28:1317.
r Pain control r Nerve block: r Delaney JE, Keels MA. Pediatric oral pathology: Soft
r IV hydration, if warranted Block of individual tooth is contraindicated due to tissue and periodontal conditions. Pediatr Clin North
MEDICATION local infection. Am. 2000;47:11251147.
Regional blockage, such as alveolar or maxillary r Krebs KA, Clem DS III. Guidelines for the
First Line dental block, may be performed:
r Oral or parenteral antibiotics: management of patients with periodontal diseases.
Only perform if trained and comfortable in the
Severe infections require parenteral therapy; mild J Periodontol. 2006;77:16071611.
procedure
infections with only moderate swelling without
high fevers may be treated with oral antibiotics. DISPOSITION
Ampicillin/sulbactam 50 mg/kg/dose IV q6h; Admission Criteria CODES
adolescent/adult 12 g IV q6h r Complicated abscess
Penicillin 50 mg/kg PO divided b.i.d.q.i.d. 10 r Inability to handle secretions ICD9
days; adolescent/adult 500 mg PO t.i.d.q.i.d.: r Airway compromise r 522.5 Periapical abscess without sinus
Traditionally was first-line oral or parenteral r Involvement of facial spaces of the head and neck r 522.7 Periapical abscess with sinus
medication used, but due to pathogen r Systemic involvement
resistance, infections requiring parenteral r Failure of outpatient therapy
antibiotics are not treated with penicillin alone. PEARLS AND PITFALLS
Acceptable for traetment of mild oral infections, r Need for IV hydration
but not indicated for moderate to severe r Critical care admission criteria: r Most patients with uncomplicated dentoalveolar
infections requiring parenteral antibiotics due to Airway compromise: Present or pending abscess can be treated as an outpatient.
increased pathogen resistance. Discharge Criteria r Failure to recognize a complicated abscess
r Opioids: r Failure to adequately assess or recognize airway
Uncomplicated dentoalveolar abscess
Morphine 0.1 mg/kg IV/IM/SC q2h PRN: Issues for Referral compromise
Initial morphine dose of 0.1 mg/kg IV/SC may Refer to a maxillofacial or oral surgeon or dentist.
be repeated q1520min until pain is controlled,
then q2h PRN.
Codeine or codeine/acetaminophen dosed as FOLLOW-UP
0.51 mg/kg of codeine component PO q4h PRN
Hydrocodone or hydrocodone/acetaminophen FOLLOW-UP RECOMMENDATIONS
dosed as 0.1 mg/kg of hydrocodone component Discharge instructions and medications:
PO q46h PRN r Follow-up evaluation by a dentist
r NSAIDs: r Complete antibiotic course
Consider NSAID medication in anticipation of Patient Monitoring
prolonged pain and inflammation: Monitor improvement of infection closely.
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN
Ketorolac 0.5 mg/kg IV/IM q6h PRN DIET
Naproxen 5 mg/kg PO q8h PRN r As tolerated
r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN r Soft diet for comfort
r Local anesthetic:
PROGNOSIS
Lidocaine 1% or 2% with or without epinephrine, Uncomplicated dental abscess typically resolves easily
max 5 mg/kg used to infiltrate with proper treatment.
Ropivacaine 1 mg/kg/dose, max 2 mg/kg:
Is optimal isomer of bupivacaine that lacks COMPLICATIONS
r Dentocutaneous fistulas
deadly cardiotoxicity of bupivacaine
Preferred agent due to duration of action and r Acute suppurative osteomyelitis
lack of cardiotoxicity r Cavernous sinus thrombosis
r Suppurative complications:
ALERT Acute suppurative lymphadentis
r Inadvertent IV administration of bupivacaine may
Peritonsillar or pharyngeal abscess
cause immediate cardiac arrest and death. Ludwig angina
Bupivacaine used for nerve block should be placed Maxillary sinusitis
by clinicians with vast experience performing such r Necrotizing fasciitis
a block. Ropivacaine is strongly recommended for
this procedure due to lack of the severe
cardiotoxicity of bupivacaine.
9
ABSCESS, GLUTEAL
David O. Kessler
ETIOLOGY Imaging
BASICS Subcutaneous abscesses are often polymicrobial, r Bedside US has been used to help distinguish
including common skin flora such as Staphylococcus between cellulitis and abscess when the clinical
DESCRIPTION and Streptococcus (2): exam is inconclusive (3).
r Gluteal abscess is a type of localized infection r Enteric organisms may also be found in abscesses r Bedside US can also be used to help guide a
located beneath the skin: with close proximity to the anus. drainage procedure.
Gluteal describes the location of the abscess r Abscesses are also well visualized with other
being in close proximity to the gluteus muscles. It COMMONLY ASSOCIATED CONDITIONS
r Abscesses are more commonly seen in modalities such as MRI and contrast-enhanced CT
is otherwise similar to simple subcutaneous scans:
abscesses in other locations. immunocompromised patients who are more
However, these imaging tests have been largely
A boil, furuncle, or carbuncle refers to a type of susceptible to infection.
r Comorbid disease should be considered in those replaced by US.
abscess that is associated with a hair follicle and
typically involves the skin. with recurrent or multiple abscesses: Diagnostic Procedures/Other
Folliculitis refers to an infection at a hair follicle HIV, diabetes mellitus, IV drug users Depending on the size, location, and extent of a
that is more superficial with inflammation and pus May also be associated with genetic lesion, needle aspiration or incision and drainage may
localized to the epidermal layer. immunodeficiency syndromes be used.
r A simple gluteal abscess may occur spontaneously DIFFERENTIAL DIAGNOSIS
in a healthy host as a result of localized infection r Hidradenitis suppurativa: Recurrent inflammatory
with common skin flora. DIAGNOSIS disorder affecting the apocrine glands (typically seen
EPIDEMIOLOGY HISTORY in the axilla or buttocks)
r Abscesses or subcutaneous soft tissue infections are r Many abscesses start off as a small pimple or r Pilonidal cyst or abscess
folliculitis that expands over days to weeks. r Necrotizing fasciitis
thought to be common but are poorly reported.
r There is a wide range of presentation and need for r They are usually tender, swollen, red, and warm and r Pyomyositis
intervention; therefore, not all abscesses will present may spontaneously express pus. r Botfly myiasis
for medical care. r Fever may be present. r Osteomyelitis: May also present with drainage to
r Published rates vary between 2.5% and 21.5% in r An abscess may be spontaneous or surface
certain populations and appear to be on the rise (1). chronic/recurrent in nature:
There may be a history of previous abscesses.
RISK FACTORS r History of a cyst at the site of the lesion TREATMENT
r Subcutaneous abscesses may be seen in normal
r History of close contacts with similar lesions
healthy hosts but are more commonly seen in those INITIAL STABILIZATION/THERAPY
r Recent hot tub use r In the initial management of an abscess, warm,
who are immunocompromised, have poor hygiene,
r Comorbidities (Crohn disease, diabetes, etc.) clean compresses (or sitz baths) may be used to help
or have close contact with others who have similar
infections. PHYSICAL EXAM promote spontaneous drainage.
r Outbreaks have occurred in communities that r Abscesses exhibit the signs of an acute infection: r Abscesses are usually extremely painful, so
become colonized with MRSA: Erythema, swelling, warmth, and tenderness. analgesia should be administered early, though full
Athletes (wrestlers) r Induration may be present as a hardened mass of pain relief is often not achieved until pressure is
Military personnel fibrous tissue that is often palpable in an abscess relieved from the wound with a procedure.
IV drug users beneath the skin. MEDICATION
r Simple cysts may be secondarily infected. r Fluctuance may be present as a spongy softness r Recent literature suggests that antibiotics may not
GENERAL PREVENTION indicative of pus or fluid. be necessary in the treatment of gluteal abscess
Good hygiene, antistaphylococcal soap, and proper r There may be overlying cellulitis or central extrusion following successful incision and drainage (4)
care early in the disease course may help prevent of pus. r Incision and drainage is thought to be efficacious
development of larger abscesses. r Regional lymphadenopathy may be associated with regardless of the use of antibiotics
an abscess. r The presence of overlying cellulitis or comorbidities
PATHOPHYSIOLOGY r If an abscess is in close proximity to the anus, a
r Subcutaneous abscesses form when the bodys requires the use of antibiotics, despite the
rectal exam may help to evaluate for rectal performance of incision and drainage
immune system walls off an infection that is often r Debate does exist as to whether incision and
the result of an inoculum of skin flora that enters involvement or communication.
either through a break in the epidermis or a hair drainage alone is enough to treat gluteal abscess.
DIAGNOSTIC TESTS & INTERPRETATION Many practitioners continue to use antibiotics.
follicle.
r A fibrous capsule surrounds a core of liquefied Lab r 1st-generation cephalosporins:
r A simple abscess does not require any lab
necrotic tissue, inflammatory cells, and bacteria in Cefazolin 50100 mg/kg IV divided q8h, max dose
confirmation. Cephalexin 50 mg/kg PO divided t.i.d., max dose
the bodys attempt to expel the foreign material. r Basic labs may be considered with chronic infection
2 g/day
or to evaluate or rule-out comorbid conditions: r MSSA:
Wound cultures, particularly to track rates and Dicloxacillin: <40 kg, 50100 mg/kg/24 hr PO
susceptibilities of MRSA infections or to help guide divided q6h; >40 kg, 250500 mg/dose PO q6h
management in complicated chronic cases (1) (max dose 4 g/24 hr)
Nafcillin: <40 kg, 50200 mg/kg/24 hr PO/IV
divided q6h; >40 kg, 5002,000 mg PO/IV q6h
(max daily dose 12 g).
10
ABSCESS, GLUTEAL
A
r MRSA: DISPOSITION REFERENCES
Clindamycin: <40 kg, PO 1030 mg/kg/24 hr Admission Criteria
divided q68h, IV 2540 mg/kg/24 hr divided r A simple skin abscess does not typically require 1. Korownyk C, Allan G. Evidence-based approach to
q68h; >40 kg, PO 300 mg/dose q68h, IV admission unless there is a comorbid condition, abscess management. Can Fam Physician. 2007;
1,2001,800 mg/24 hr divided q612h (max daily complication, or a social reason for admission. 53:16801684.
dose 4.8 g/24 hr) r Large abscesses (>5 cm) may be more likely to 2. Stevens DL, Bison AL, Chambers HF, et al. Practice
Trimethoprim/sulfamethizole (dosing based on require inpatient management. guidelines for the diagnosis and management of
trimethoprim): <40 kg, 5 mg/kg/dose PO/IV r A rapidly spreading overlying cellulitis may require skin and soft tissue infections. Clin Infect Dis.
q12h; >40 kg, 160 mg/dose PO/IV q12h admission.
2005;41(10):13731406. [Erratum in Clin Infect
Vancomycin: <40 kg, 10 mg/kg/dose IV q8h (max Dis. 2005;41(12):1830, Clin Infect Dis. 2006;42(8):
1 g/dose); >40 kg, 2 g/24 hr IV divided q612h Issues for Referral 1219.]
(max dose 4 g/24 hr) Subspecialist involvement should be strongly 3. Ramirez-Schrempp D, Dorfman D, Baker W, et al.
Drug of choice, first-line parenteral medication considered for abscesses in children <6 mo of age, Ultrasound soft tissue applications in the pediatric
for MRSA recurrent abscesses, or abscesses also involving emergency department. Pediatr Emer Care.
When antibiotics are used (such as in the case of sensitive locations such as the genitals or perianal 2009;25:4448.
secondary cellulitis), consideration should be area, where concern for a fistula may exist: 4. Hankin A, Everett W. Are antibiotics necessary after
made for whether coverage is warranted for r Depending on the institution, specific referrals may
incision and drainage of a cutaneous abscess? Ann
community- or hospital-acquired MRSA. be handled by pediatric surgery, plastic surgery, or Emerg Med. 2007;50:4951.
gynecology.
r The definitive treatment for a gluteal abscess is
ADDITIONAL READING
incision and drainage of the abscess cavity. FOLLOW-UP
Technique varies widely and is only briefly described Chambers H, Moellering R, Kamitsuka P. Management
here: FOLLOW-UP RECOMMENDATIONS of skin and soft tissue infection. N Engl J Med.
Confirm location for incision and drainage. This r After uncomplicated incision and drainage, patients
2008;359:10631067.
may be done with US, if available, to help identify should follow up within 2448 hr with a provider
fluid pockets and avoid vascular structures. experienced in wound care. See Also (Topic, Algorithm, Electronic
Adequate analgesia is often difficult to achieve, r Warm compresses and/or sitz baths can help provide Media Element)
r Abscess, Perianal
but several strategies may be used. A local field comfort and may promote healing.
r Cellulitis
block (1% or 2% lidocaine with or without
epinephrine depending on the location) provides PROGNOSIS r Pilonidal Cyst
r Most abscesses resolve within 12 wk after incision
injections of anesthetic in a ring around the
indurated space. Injecting into the wound itself is and drainage.
r Recurrence is not uncommon and may be seen in up
typically ineffective because of the acidity of the
to 25% of cases.
CODES
abscess space, and increased pressure from an
injection may worsen pain. COMPLICATIONS ICD9
For superficial abscess, topical anaesthetics such r The most common complications include failure of 682.5 Cellulitis and abscess of buttock
as ethyl chloride spray may help numb the skin the wound to heal and recurrence that often
immediately prior to incision. requires re-exploration or a 2nd incision and
Some patients may require sedation in order to drainage procedure. PEARLS AND PITFALLS
obtain adequate pain control prior to the r Bleeding may also occur but is usually controlled
r Distinguishing between cellulitis and deeper
procedure. spontaneously or with local pressure.
A needle aspiration may be attempted 1st to r Rare complications may be seen with the less infection (eg, abscess) can sometimes be difficult on
confirm the location of the fluid pocket. physical exam alone. Bedside US can be helpful in
frequent causes of an abscess: identifying fluid collections.
Fluctuance typically represents fluid immediately Fistulas can occur in patients with inflammatory
beneath the surface of the skin and may also be r Differentiate between gluteal and rectal abscess. If
bowel disease or if the abscess is in
used to guide the initial incision. in doubt, consult a pediatric surgeon for evaluation.
communication with the bowels.
After topical cleansing with povidone-iodine or an Recurrence is more common in a cyst that has
alcohol solution, incision is made using an become secondarily infected, such as a pilonidal
11-blade scalpel inserted 0.51 cm deep through cyst.
the epidermis and dermal layer and in 1 Severe bleeding can occur if a vessel is lacerated
continuous motion incising 75% of the length during the procedure.
of the wound.
The wound is then explored with a surgical clamp,
and any loculations or fibrous strands should be
broken apart to help release any additional fluid
pockets.
If the wound is deep, a small amount of packing
material may be used to help keep skin layer from
healing prior to granulation of the inside of the
wound.
r Needle aspiration is performed using a small syringe
attached to an 18-gauge needle, withdrawing
slightly on the plunger as the needle is inserted into
the area of greatest fluctuance and aspirating fluid.
11
ABSCESS, INTRACRANIAL
Kerry Caperell
Raymond Pitetti
r Other pathogens: DIAGNOSTIC TESTS & INTERPRETATION

BASICS Bacteroides, Prevotella, Propionibacterium, Lab
Fusobacterium, Eubacterium, Veillonella, Initial Lab Tests
DESCRIPTION Actinomyces, Klebsiella pneumoniae, r Laboratory studies such as CBC, ESR, and C-reactive
r An intracranial abscess is a bacterial, suppurative, Pseudomonas, Escherichia coli, Proteus, protein (CRP) are not generally helpful in the acute
life-threatening infection inside the cranial cavity. Haemophilus, Actinobacillus, Salmonella, and setting but may be used to follow clinical response
r Most typically, this is an abscess involving the brain. Enterobacter to therapy.
r Subdural empyemas and epidural abscesses are rare, r Up to 30% of brain abscesses contain mixed flora. r Blood cultures are positive in only 10% of brain
clinically distinct entities that will not be discussed r Gram-negative bacteria are an important cause in abscesses.
here. neonates. r Lumbar puncture is contraindicated until imaging
r Immunocompromised patients have esoteric has excluded increased ICP.
EPIDEMIOLOGY
pathogens: Toxoplasmosis, Listeria, Nocardia, r CSF in 20% of cases is normal.
Incidence
r Rare in developed countries Cryptococcus, Coccidioides, Candida. r Serologic test may assist in diagnosing
r 25% occur in children <15 yr old COMMONLY ASSOCIATED CONDITIONS toxoplasmosis or cysticercosis.
r In children, the incidence is highest between ages r Cyanotic congenital heart disease r If abscess aspirate is obtained, culture and Gram
4 and 7 yr. r Ventriculoperitoneal shunt stain are key in identifying pathogen(s).
r Unusual in neonates except in the setting of r Chronic suppurative otitis media Imaging
gram-negative meningitis r Sinusitis r Contrast-enhanced CT scan of the brain shows a
r Mastoiditis ring-enhancing area:
RISK FACTORS r Dental infection
r Cyanotic congenital heart disease Obtain both axial and coronal views that extend
r Otitis media r Meningitis through the frontal bone and the sellar region.
r Mastoiditis This may be normal in the 1st few days of abscess
formation.
r Meningitis r MRI is the test of choice:
r Penetrating head trauma
DIAGNOSIS
Can detect smaller lesions
r Sinusitus HISTORY Can show greater soft tissue detail
r Cystic fibrosis r The classic triad of fever, headache, and focal
r Ventriculoperitoneal shunt infection neurologic deficit is present in <50% of children. DIFFERENTIAL DIAGNOSIS
r Mean duration of signs and symptoms prior to r Meningitis
r Post neurosurgery r Encephalitis
r Endocarditis diagnosis is 2 wk but can be as long as 4 mo.
r Most common symptoms are headache, fever, and r Space-occupying lesion or mass
r Lung infections r Stroke
r Other infections in the head vomiting.
r A unilateral headache is especially concerning. r Migraine
PATHOPHYSIOLOGY r Mental status changes and seizures are less r Venous sinus thrombosis
r Brain abscesses are almost always caused by common. r Trauma
hematogenous spread of bacteria from distant sites. r Toxic/metabolic effects
r Can occur secondarily to infection from contiguous PHYSICAL EXAM
r Fever may or may not be present.
structures, such as from suppurative infection in the r Headache, seizure, or focal neurologic deficit,
mastoid, in the sinuses, or from dentoalveolar TREATMENT
abscesses including cranial nerve deficit
r Violation of the integrity of the skull and dura may r Papilledema INITIAL STABILIZATION/THERAPY
r Meningeal signs: r Manage airway and resuscitate as needed.
result in abscess. This includes penetrating trauma r Patients with depressed level of consciousness
as well as cranial surgery. These signs are seen in <1/2 of all children with
brain abscess. should be intubated immediately for controlled
ETIOLOGY r Signs of sepsis may be present, such as tachycardia, ventilation.
r Most intracranial abscesses are due to streptococcal r Early neurosurgical consultation; emergent surgery
tachypnea, decreased perfusion, delayed capillary
species, both aerobic and anaerobic. refill, and hypotension. may be needed
r Staphylococcus aureus, particularly after penetrating r Signs of raised intracranial pressure (ICP), such as r IV access should be obtained immediately.
trauma or surgery, is common. Cushing triad: Irregular respirations, bradycardia, r Treatment with broad-spectrum antibiotics and
r Cysticercosis is relatively commonly seen in
and HTN surgical decompression is routine.
immigrants from Mexico and Central America.
12
ABSCESS, INTRACRANIAL
A
MEDICATION SURGERY/OTHER PROCEDURES
r Guided surgical aspiration is indicated to obtain
ADDITIONAL READING
First Line r Frazier J, Ahn E, Jallo GI. Management of brain
r Antimicrobial therapy is the treatment of choice and infected material for cultures to guide definitive
should be broad spectrum until culture results are antimicrobial therapy. abscesses in children. Neurosurg Focus. 2008;
available. r Cultures should be sent for both aerobic and 24(6):E8.
r When the apparent source is otitis media, r Shachor-Meyouhaus Y, Bar-Joseph G, Guilburd JN,
anaerobic pathogens.
mastoiditis, sinusitis, or congenital heart disease, a r Surgical excision is occasionally necessary. et al. Brain abscess in childrenepidemiology,
3rd-generation cephalosporin plus metronidazole is predisposing factors and management in the
DISPOSITION modern medicine era. Acta Paediatr. 2010;99(8):
indicated:
Ceftriaxone or cefuroxime plus metronidazole Admission Criteria 11631167.
r All children with brain abscess should be admitted r Yogev R. Focal suppurative infections of the central
Ceftriaxone 100 mg/kg/dose IV q12h, max single
dose 2 g/24 hr to the hospital. nervous system. In Long S, Pickering L, Prover C,
r Many of these children will warrant admission to a eds. Principles and Practice of Pediatric Infectious
Cefuroxime 50 mg/kg/dose IV q8h, max single
dose 1 g/24 hr pediatric ICU for monitoring, including ICP Disease. 2nd ed. New York, NY: Churchill
Metronidazole 30 mg/kg/day IV q6h, max single monitoring in select cases. Livingstone; 2003:302312.
dose 4 g/24 hr r Yogev R, Maskit B. Management of brain abscesses
Issues for Referral
r When the apparent source includes penetrating r Infectious disease consultation may be useful. in children. Pediatr Infect Dis J. 2004;23:157159.
trauma, ventriculoperitoneal shunt, meningitis, or r Referral to a Critical care specialist is recommended.
endocarditis, a 3rd-generation cephalosporin plus Media Element)
vancomycin is indicated: r Abscess, Dentoalveolar
Vancomycin 10 mg/kg/dose IV q6h, max FOLLOW-UP r Mastoiditis
individual dose 1 g r Meningitis
r In neonates, ampicillin should be added if Listeria is FOLLOW-UP RECOMMENDATIONS
a possibility: Patient Monitoring
Ampicillin 100 mg/kg/dose IV q6h, max single Most patients will initially require monitoring in the
dose 12 g/24 hr pediatric ICU. CODES
r In immunosuppressed children, coverage for fungal DIET
organisms should be strongly considered. Patients should be NPO given the likelihood for ICD9
procedures requiring sedation/anesthesia. 324.0 Intracranial abscess
Second Line
r Ampicillin/Sulbactam 100 mg/kg/dose IV q6h, max
PROGNOSIS
single dose 12 g ampicillin/24 hr r Even with optimal treatment, mortality from brain PEARLS AND PITFALLS
r Meropenem 40 mg/kg/dose IV q8h, max single dose abscess is as high as 15%.
r A more recent case series had a mortality rate of r Routine lab tests, including CSF, are not generally
6 g/24 hr
r Ciprofloxacin 10 mg/kg/dose IV q12h, max single only 4%. helpful in ruling out brain abscess.
r Factors associated with increased morbidity and r Early imaging is warranted if brain abscess is
dose 1 g/24 hr
r Corticosteroids: mortality include age <1 yr, coma at diagnosis, suspected.
r Empiric antibiotic therapy should cover
Dexamethasone 0.5 mg/kg/dose IV q24h rapidly progressive neurologic deterioration, and
Methylprednisolone 30 mg/kg IV loading dose multiple foci of infection. gram-positive, gram-negative, and anaerobic
followed by 5.4 mg/kg/hr for 23 hr organisms.
COMPLICATIONS r Specific populations may be at risk for unique
This is same dose used in spinal trauma; another
Up to 1/3 of surviving patients will have permanent pathogens, such as Mexican and Central American
dosing regimen may be recommended by the
neurologic disabilities. immigrants with a likelihood for cysticercosis or
neurosurgeon.
Glucocorticoids may lead to an improvement in HIV/immunosuppressed patients at risk for
signs and symptoms secondary to mass effect, but toxoplasmosis, Cryptococcus, and Candida.
they should not be used if a well-defined capsule
is not apparent on imaging.
13
ABSCESS, LUDWIG ANGINA

Michelle A. Alletag
Marc A. Auerbach
r Diagnostic criteria: DIAGNOSTIC TESTS & INTERPRETATION

BASICS Occurs bilaterally, in >1 space Lab
Infiltrate is gangrenous or serosanguineous with Initial Lab Tests
DESCRIPTION little or no pus r Aerobic and anaerobic blood cultures should be
r Ludwig angina is a rapidly spreading deep cellulitis Involves connective tissue, fascia, and muscle obtained (although they are positive in only 30% of
of the submandibular, submental, and sublingual (rarely involves glandular structures) cases).
space. Spreads by continuity (not hematogenous or r CBC will show elevated WBC count with left shift;
r Generally originates as an odontogenic infection lymphatic) C-reactive protein will be elevated.
r Poses high risk for airway compromise and loss
r Untreated, has a high risk of mortality ETIOLOGY Imaging
Most common microbes include Staphylococcus r Plain radiographs of the neck will show soft tissue
EPIDEMIOLOGY aureus, Streptococcus viridans, and beta-hemolytic swelling of the submandibular region.
r Incidence is rare, with 1 report citing 5 of 117 total streptococcus, with oral anaerobes (Bacteroides, r Contrast CT scan of the neck is not necessary for
pediatric head and neck infections treated in a 6-yr Fusobacterium, Enterobacter, Peptostreptococcus) diagnosis but may be used to assess for extent of
period. also frequently cultured. retropharyngeal involvement and abscess
r More common in adults: r Majority of infections are polymicrobial, with a mix formation:
Pediatric patients make up 2530% of all cases. of aerobic and anaerobic organisms CT should be deferred until a stable airway is
r Accounts for 13% of all deep neck infections r Candida may also be present in confirmed or established.
immunocompromised patients
RISK FACTORS DIFFERENTIAL DIAGNOSIS
r In adults and older children, poor dental hygiene is COMMONLY ASSOCIATED CONDITIONS r Retropharyngeal or parapharyngeal abscess
the primary risk factor (with spread of infection from Dental caries r Epiglottitis
the 2nd and 3rd molars being the most frequent r Sialadenitis
cause). r Dental abscesses
r In children, oral lacerations, sialadenitis DIAGNOSIS r Infected congenital (eg, branchial cleft or
(submandibular), and mandibular trauma are other HISTORY thyroglossal duct) cyst
frequent causes. Patients often present with complaints of fever, throat
r Piercings of the lingual frenulum or tongue pain, trismus, dysphagia, dysphonia, or
r Patients with systemic diseases, such as diabetes drooling. Poor oral intake and decreased urine output TREATMENT
mellitus, and immunocompromised patients are at are common occurrences among younger patients.
increased risk. r Onset is generally acute, with patients presenting PRE HOSPITAL
r Many pediatric cases of Ludwig angina have no after 23 days of symptoms.
r Often, patients will have been initially managed circulation.
identifiable preceding risk factor. r Allow patients to maintain a position of comfort, as
GENERAL PREVENTION with oral antibiotics.
they may prefer to be upright or even leaning
Good oral and dental hygiene significantly decreases PHYSICAL EXAM forward to keep the airway patent.
the risk of this rare but life-threatening infection. r Induration of the floor of the mouth with bilateral
submandibular swelling and posterior and superior INITIAL STABILIZATION/THERAPY
PATHOPHYSIOLOGY r Assess and stabilize airway, breathing, and
r Caused by infection originating in the oropharynx, displacement of the tongue are considered
pathognomonic signs: circulation.
with contiguous (not lymphatic) spread through the r Airway management is critical, with preparation for
submandibular and neck soft tissue spaces: Classically, the tongue protrudes from the oral
cavity. an emergent or surgical airway should it become
Polymicrobial nature of oropharyngeal infections r Systemic findings may include fever, toxic necessary.
predisposes to gangrenous cellulitis. r Consult ENT or head/neck surgeon:
Anatomy of the submandibular space allows rapid appearance, and evidence of dehydration.
r Impending airway compromise may be heralded by Most pediatric patients can be managed
spread of infection along fascial planes and for conservatively with antibiotics and steroids, but
rapid airway impingement. stridor, drooling, dyspnea, or cyanosis:
Carefully evaluate patency of the airway. the airway should be actively monitored.
14
ABSCESS, LUDWIG ANGINA

A
MEDICATION DISPOSITION ADDITIONAL READING
First Line Admission Criteria r Busch RF, Shah D. Ludwigs angina: Improved
Parenteral antibiotics should provide coverage for r All patients should be admitted to the hospital with
anaerobes and aerobes, with a penicillin and suspected Ludwig angina. treatment. Otolaryngol Head Neck Surg. 1997;117:
metronidazole, or ampicillin/sulbactam may be used r Critical care admission criteria: S172S175.
r Chou Y, Lee C, Chao H. An upper airway obstruction
alone or in combination with metronidazole Any child with concern for potential airway
considered first-line treatment. compromise should be admitted to the critical emergency: Ludwig angina. Pediatr Emerg Care.
r Oral antibiotic therapy is not appropriate. care unit for observation. 2007;23(12):892896.
r Lin H, ONeill A, Cunningham M. Ludwigs angina in
r Ampicillin/Sulbactam 50 mg/kg/dose IV q6h, adult The hospitals airway team (anesthesia, ENT, or
both) should be made aware of any patient being the pediatric population. Clin Pediatr. 2009;48(6):
dose 12 g/dose, max single dose ampicillin
admitted with Ludwig angina. 583587.
8 g/24 hr r Marcus BJ, Kaplan J, Collins KA. A case of Ludwig
r Metronidazole 30 mg/kg/day q6h, max single dose Discharge Criteria
angina. A case report and review of the literature.
4 g/24 hr No patient with suspected Ludwig angina should be
Am J Forensic Med Path. 2008;23(3):255259.
Second Line discharged from the ED given the high risk of airway
r Clindamycin 40 mg/kg/day q6h, adult dose 900 mg compromise and death. See Also (Topic, Algorithm, Electronic
IV q8h, max single dose 4.8 g/24 hr: Media Element)
r Abscess, Dentoalveolar
Used in patients with penicillin allergy FOLLOW-UP
r Dexamethasone 12 mg/kg/24 hr divided q6h: r Abscess, Retropharyngeal
r Cystic Hygroma
Decreases airway swelling and decreases length of PROGNOSIS
illness Mortality remains 10% in both children and adults, r Epiglottitis
primarily due to airway compromise:
SURGERY/OTHER PROCEDURES r Mortality exceeded 50% in the 1800s when Ludwig
r Extraction of necrotic or abscessed teeth is
important to remove the nidus for infection. angina was 1st described but decreased CODES
r Surgical drainage is reserved for patients with substantially with the advent of antibiotics.
abscess formation and is generally deferred for COMPLICATIONS ICD9
12 days after initiation of antibiotics: r Spread of infection to lateral pharyngeal or 528.3 Cellulitis and abscess of oral soft tissues
Patients unresponsive to medical therapy may also retropharyngeal spaces is common and can cause
require surgical exploration and drainage. retropharyngeal abscess, mediastinitis, empyema, or
Unlike adults (most of whom require surgical
PEARLS AND PITFALLS
even pericarditis.
drainage and surgical airways), most pediatric r Bacteremia r Prompt recognition and initiation of antibiotic
patients respond well to medical management r Sepsis therapy is lifesaving and may prevent significant
alone. morbidity by avoiding the need for surgical airway
management.
r The rarity of this disease may lead to delays in
diagnosis, and mortality rates remain high.
15
ABSCESS, PERIANAL
Antonio Riera
David M. Walker
COMMONLY ASSOCIATED CONDITIONS Imaging

BASICS r Fistula-in-ano (anal fistula) present in 1/3 of cases r Endoscopic US:
r Immunodeficiency syndromes 8090% accurate for perianal disease when
DESCRIPTION r Chronic granulomatous disease compared to surgical exam under anesthesia
r A perianal abscess is a localized collection of pus at r Inflammatory bowel disease Accuracy depends on proper technique
or near the anus or perianal skin. r Crohn disease r MRI:
r A perianal abscess often originates from occluded
r Diabetes mellitus 8090% accurate for perianal disease when
and infected anal glands. r Hirschsprung disease compared to surgical exam under anesthesia
r May be associated with underlying pathology
r Local trauma Pathological Findings
EPIDEMIOLOGY r Neoplasm Abscess wall can be examined histologically for
r Overall incidence is unknown. r Enterobius vermicularis (pinworm) infection evidence of Crohn disease.
r Incidence in infants is estimated at 0.54.3%.
r Strong male predominance r Anal fissure
RISK FACTORS
DIAGNOSIS r Skin tags
r Age <1 yr r Hemorrhoids
HISTORY
r Immunodeficiency syndromes r Fever r Pilonidal cyst/abscess
r Local trauma r Mass near anus: r Perianal cellulitis
r In patients >2 yr of age, risk factors include Crohn May be noted by parent or during routine well r Diastasis ani
disease, diabetes mellitus, and immunosuppression child exam
(from disease such as HIV/AIDS or medications r Pain with bowel movements
including steroids and chemotherapy). r Anal discharge TREATMENT
PATHOPHYSIOLOGY PHYSICAL EXAM MEDICATION
r Infection of the perianal skin and anal glands due to r Fever may be present. r Analgesics:
proliferation of local bacteria r Mass has typical inflammatory findings of abscess. Topical anesthetic to abscess prior to incision and
r Congenital predisposition and abnormal hindgut r Warmth drainage
migration may play a role. r Erythema Morphine 0.1 mg/kg IV/IM/SC q2h PRN:
r Other proposed pathogenesis includes: Initial morphine dose of 0.1 mg/kg IV/SC may
r Tender/Painful to touch
Cryptoglandular involvement be repeated q1520min until pain is controlled,
r Fluctuance may be present. then q2h PRN.
Congenital sinus of perianal tissue r It is crucial to examine surrounding gluteal and
Abnormal widening of crypts of Morgagni Codeine or codeine/acetaminophen dosed as
Androgen imbalance buttock area to note extension of abscess. 0.51 mg/kg of codeine component PO q4h PRN
ETIOLOGY DIAGNOSTIC TESTS & INTERPRETATION
dosed as 0.1 mg/kg of codeine component PO
r Bacterial microbiology similar to adults Lab q46h PRN
r Anaerobes outnumber aerobes by 3 to 1 (1). Initial Lab Tests r NSAIDs:
r Local wound culture
r Mixed flora predominate: Consider NSAIDs in anticipation of prolonged pain
r If fever present:
Generally mixed infections caused by enteric flora and inflammation:
such as Escherichia coli and Enterococcus and CBC Ibuprofen 10 mg/kg/dose PO/IV q6h PRN
Bacteroides species C-reactive protein Ketorolac 0.5 mg/kg IV/IM q6h PRN
Other isolated bacteria include group C Blood culture Naproxen 5 mg/kg PO q8h PRN
r Immunodeficiency workup as warranted;
streptococcus and Staphylococcus aureus.
recommended if history of recurrence or other
bacterial infections
16
ABSCESS, PERIANAL
A
r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN DISPOSITION REFERENCES
r Stool-bulking agents and stool softeners to prevent Admission Criteria
constipation (post drainage): r Toxic or ill appearing 1. Brook I, Martin W. Aerobic and anaerobic
Polyethylene glycol 3350: 17 g in 8 oz of water r Suspected or confirmed fistula requiring surgical bacteriology of perirectal abscess in children.
qhs; children >6 mos: 0.51.5 g/kg daily intervention Pediatrics. 1980;66:282284.
r Antibioticsuniversal use is debatable. Anaerobic r Suspected child abuse 2. Christison-Lagay E, Hall JF, Wales PW, et al.
and staphylococcal coverage is recommended if ill r Younger age of child Nonoperative management of perianal abscess in
appearing, febrile, or immunocompromised: r Extensive lesions infants is associated with decreased risk for fistula
Oral first line: r Pain not well controlled formation. Pediatrics. 2007;120:e548e552.
Amoxicillin/Clavulanate 20 mg/kg/dose PO 3. Whiteford M, Kilkenny J 3rd, Hyman N, et al.
q12h OR Discharge Criteria Practice parameters for the treatment of perianal
Clindamycin 810 mg/kg/dose PO q8h r Well appearing abscess and fistula-in-ano (revised). Dis Colon
IV first line: r Small, uncomplicated abscess Rectum. 2005;48:13371342.
Ampicillin/Sulbactam 50 mg/kg/dose IV q6h OR r Pain well controlled 4. Quah HM, Tang CL, Eu KW, et al. Meta-analysis of
Clindamycin 1012 mg/kg/dose IV q8h r Adequate wound care plan arranged randomized control trials comparing drainage alone
Suspected MRSA: r Follow-up for wound check in 24 hr vs primary sphincter-cutting procedures for
Trimethoprim/Sulfamethoxazole (TMP/SMX) anorectal abscess-fistula. Int J Colorectal Dis.
5 mg/kg/dose PO q12h based on TMP Issues for Referral 2006;21:602609.
component OR Consider surgical consultation for initial management
Vancomycin 1015 mg/kg/dose IV; determine and/or follow-up.
interval by trough levels ADDITIONAL READING
Penicillin allergic (PO): r Abercrombie JF, George BD. Perianal abscess in
Clindamycin (for MSSA) FOLLOW-UP
TMP/SMX plus metronidazole 10 mg/kg/dose children. Ann R Coll Surg Engl. 1992;74(6):
FOLLOW-UP RECOMMENDATIONS 385386.
PO q8h (for MRSA) r 24-hr follow-up for wound check and repacking of r Ramanujam PS, Prasad ML, Abcarian H, et al.
Penicillin allergic (IV): abscess cavity
Clindamycin (for MSSA) r Frequent daily sitz baths or warm soaks to promote Perianal abscesses and fistulas. A study of 1023
Vancomycin plus metronidazole 10 mg/kg/dose patients. Dis Colon Rectum. 1984;27(9):593597.
further drainage r Stites T, Lund D. Common anorectal problems.
IV q8h (for MRSA) r Consider home nursing services.
Semin Pediatr Surg. 2007;16(1):7178.
SURGERY/OTHER PROCEDURES PROGNOSIS
r Perianal abscess should be treated in a timely r Simple perianal abscesses have excellent outcomes
fashion by incision and drainage (2): after incision and drainage. CODES
Lack of fluctuance should not delay timely r Perianal abscesses with anal fistula have higher
drainage.
r In infants, medical management may be an rates of complications. ICD9
COMPLICATIONS 566 Abscess of anal and rectal regions
acceptable alternative:
In a retrospective study of 140 children <1 yr of r Fistula-in-ano
age for whom abscess size was not reported, r Recurrence
r Stool incontinence (if sphincter-cutting procedure
PEARLS AND PITFALLS
medical management with local hygiene and
systemic antibiotics had equivalent cure rates performed) r Unlike other skin abscesses, cultures grow a mixed
when compared to traditional surgical drainage population of bacteria with a predominance of gut
(3): anaerobic and aerobic species.
Fistula formation was greater in the surgical r Many cases are associated with underlying
drainage group (60%) vs. the medical conditions.
management group (16%). r Incision and drainage remains the treatment of
r Fistulotomy may be performed: choice.
In a meta-analysis of adult patients, surgical r Conservative medical management may be an
drainage with fistulotomy reduced risk of option for children <1 yr of age.
recurrence by 83% but tended to increase rates of
incontinence to flatus and stool (RR 2.46, 95% CI
0.758.06) when compared to surgical drainage
alone (4).
17
ABSCESS, PERITONSILLAR
Nikhil B. Shah
r CT scan with IV contrast is the preferred imaging

BASICS DIAGNOSIS modality (4) for unclear cases:
Able to distinguish PTA from PTC
DESCRIPTION HISTORY Can demonstrate extension of infection into
r Peritonsillar abscess (PTA), or quinsy, is the most r Fever
contiguous deep neck spaces
common deep neck infection in children, accounting r Severe sore throat, usually unilateral
PTA appears as a hypodense mass with ring
for at least 50% of cases (1). r Hot potato or muffled voice enhancement; PTC findings include soft tissue
r PTA develops when oropharyngeal bacteria invade r Drooling or pooling of saliva may be present. swelling, loss of fat planes, and lack of ring
the peritonsillar space, resulting in a pus collection. r Trismus (in >60% of patients) (1): enhancement.
r Prompt diagnosis and management is essential to Related to irritation and reflex spasm of the CT should be deferred in children with moderate
ensure successful recovery and prevent internal pterygoid muscle to severe distress, especially if sedation is required.
complications. Helps to distinguish PTA from severe pharyngitis r Intraoral US:
or tonsillitis Highly sensitive, cost-effective, nonradiation
EPIDEMIOLOGY r Neck swelling alternative modality (4)
Incidence r Neck pain Distinguishes PTA from PTC
r PTA occurs most frequently in adolescents and
r Ipsilateral ear pain Exam may be limited if trismus is present.
young adults but can occur in younger children. PTA findings include an echofree cavity with an
r Estimated incidence: r Nonspecific symptoms such as fatigue, irritability,
irregular border; PTC appears as a homogeneous
All children (<18 yr): 14 per 100,000 and decreased oral intake
or striated area with no distinct fluid collection.
Adolescents: 40 per 100,000 (2) PHYSICAL EXAM r Lateral neck radiographs:
r Presence of trismus may limit the ability to perform Limited role
RISK FACTORS
r Chronic or recurrent tonsillitis an adequate exam. Useful to rule out other clinically similar conditions
r Smoking may be a risk factor. r If severe airway compromise is present, exam in the such as retropharyngeal abscess
operating room under anesthesia may be Diagnostic Procedures/Other
PATHOPHYSIOLOGY appropriate.
r Peritonsillar infection represents a spectrum ranging r Exam findings consistent with PTA include: See Surgery/Other Procedures for information about
from cellulitis to phlegmon to abscess. abscess incision and drainage.
Unilateral, swollen, fluctuant tonsil seen as a
r Abscess formation occurs in the peritonsillar space, DIFFERENTIAL DIAGNOSIS
convex mass protruding into the posterior pharynx
bound medially by the fibrous peritonsillar capsule and displacing the uvula to the opposite side Includes other causes of upper airway obstruction,
and laterally by the superior pharyngeal constrictor Alternatively, there may be a bulging, fluctuant sore throat, and pharyngeal swelling such as:
muscle. mass or fullness of the posterior soft palate near r Retropharyngeal abscess or cellulitis: Usually seen in
r PTA usually occurs as a well-defined pus collection the tonsil. younger children, neck stiffness more predominant
in the superior pole of the tonsil but may also occur r PTA is usually unilateral; bilateral PTA is uncommon than trismus
in the mid- or inferior pole of the tonsil or be less and can make diagnosis difficult. r Parapharyngeal abscess: Bulging behind tonsillar
well circumscribed with multiple loculations within r Clinical distinction between abscess and pillar rather than superior to tonsil
the peritonsillar space. peritonsillar cellulitis (PTC) can be problematic, r Epiglottitis (now rare in post-Haemophilus influenza
ETIOLOGY although uvular deviation and trismus are often type B vaccine era)
r Most cases are polymicrobial. absent in the latter (3). r Severe tonsillopharyngitis (Epstein-Barr virus,
r PTA frequently includes both aerobic and anaerobic herpangina, diphtheria, gonorrhea)
DIAGNOSTIC TESTS & INTERPRETATION
bacteria: Lab
Streptococcus pyogenes (group A streptococcus
[GAS])
PTA is diagnosed clinically and radiographically. Lab TREATMENT
evidence is not routinely necessary for diagnosis but
Staphylococcus aureus (MRSA) may assist in identifying organism or complications: INITIAL STABILIZATION/THERAPY
Anaerobes such as Fusobacteria, Prevotella, and r Gram stain and culture from abscess aspirate may r Drainage, antibiotic therapy, and supportive care are
Veillonella species
be performed. the mainstays of management.
Occasionally Haemophilus species r Rapid streptococcal antigen test and/or throat r Airway:
COMMONLY ASSOCIATED CONDITIONS culture When severe airway compromise is suspected, all
r PTA is generally preceded by pharyngitis or tonsillitis r Mononucleosis screen interventions should be deferred until the airway
but may occasionally occur without antecedent r CBC with differential is secured.
infection (ie, obstruction of the Weber salivary r C-reactive protein r Supportive care:
glands in the soft palate) r Serum electrolytes Hydration
r Infectious mononucleosis Analgesia
r Kawasaki disease (rarely) Imaging Monitoring for complications
r Imaging studies are generally not required for
diagnosis, but indications may include: MEDICATION
Distinguishing abscess from cellulitis First Line
Determining extent of infection r Early antibiotic therapy may prevent abscess
Exclusion of other deep neck space infections such formation in patients with PTC but must be
as retropharyngeal abscess combined with a drainage procedure once pus has
Inadequate exam secondary to trismus formed.
r Empiric therapy should include coverage for GAS, S.
aureus, and anaerobes and can then be modified
according to culture and sensitivity results if
drainage is performed.
18
ABSCESS, PERITONSILLAR
A
r Potential parenteral regimens include: Admission Criteria REFERENCES
Ampicillin/Sulbactam 200 mg/kg/day divided q6h Critical care admission criteria:
IV OR r Toxicity 1. Ungkanont K, Yellon RF, Weissman JL, et al. Head
Clindamycin 40 mg/kg/day divided q8h IV, which r Potentially life-threatening complications and neck space infections in infants and children.
has the benefit of community-acquired MRSA r Significant airway compromise Otolaryngol Head Neck Surg. 1995;112(3):
coverage 375382.
Vancomycin 4060 mg/kg/day divided q68h IV Discharge Criteria 2. Millar KR, Johnson, DW, Drummond D, et al.
r Patients who are managed as outpatients must be
may be added if no clinical response or in case of Suspected peritonsillar abscess in children. Pediatr
severe infection. observed post-procedure to ensure they can tolerate Emerg Care. 2007;23(7):431438.
r IV antibiotic therapy should be continued until the oral antibiotics, analgesics, and liquids. 3. Szuhay G, Tewfik TL. Peritonsillar abscess or
r Patients who are managed as inpatients may be
patient is afebrile and clinically improved. cellulitis? A clinical comparative paediatric study.
r An oral antibiotic regimen should then be continued discharged home if there is response to treatment as J Otolaryngol. 1998;27(4):206212.
to complete a 14-day course: defined by improvement in pain, fever, and/or 4. Scott PM, Loftus WK, Kew J, et al. Diagnosis of
Amoxicillin/Clavulanate 8090 mg/kg/day divided tonsillar swelling within 24 hr of intervention. peritonsillar infections: A prospective study of
PO b.i.d. OR ultrasound, computerized tomography and clinical
Clindamycin 40 mg/kg/day divided PO q8h diagnosis. J Laryngol Otol. 1999;113(3):229232.
Linezolid may be used when vancomycin has been
FOLLOW-UP
5. Herzon FS, Martin AD. Medical and surgical
added to the parenteral regimen (<12 yr: FOLLOW-UP RECOMMENDATIONS treatment of peritonsillar, retropharyngeal, and
30 mg/kg/day divided PO t.i.d.; 12 yr: r Patients treated as outpatients should have parapharyngeal abscesses. Curr Infect Dis Rep.
20 mg/kg/day divided PO b.i.d). follow-up within 2436 hr, whereas admitted 2006;8(3):196202.
Second Line patients should be seen within several days of
Corticosteroids: discharge.
r Evidence is lacking to support routine use of steroids r Discharge instructions and medications: ADDITIONAL READING
for PTA in children (2). Continue appropriate oral antibiotic regimen. Goldstein NA, Hammerschlag MR. Peritonsillar,
r Some studies demonstrate improvement in pain Analgesics retropharyngeal, and parapharyngeal abscesses. In
scores, symptom severity, and length of stay, while Maintain hydration. Feigin RD, Cherry JD, Demmler-Harrison GJ, et al., eds.
others find no clear difference between treatment Patient Monitoring Textbook of Pediatric Infectious Diseases. 6th ed.
and nontreatment groups. Discharged patients should be instructed that prompt Philadelphia, PA: Saunders; 2009:177.
re-evaluation is necessary for:
SURGERY/OTHER PROCEDURES r Dyspnea
r Drainage in combination with antibiotic therapy and
hydration results in resolution in >90% of cases (5).
r Worsening pain CODES
r Surgical drainage of PTA is performed by one of the r Worsening trismus
following methods: r Enlarging mass ICD9
Needle aspiration r Fever 475 Peritonsillar abscess
Incision and drainage r Neck stiffness
Tonsillectomy r Bleeding (as a complication of drainage procedure)
r Choice of procedure depends upon clinician skill PEARLS AND PITFALLS
level, age and ability of the patient to cooperate, DIET r The diagnosis of PTA is clinical and does not require
cost, and whether the patient has indications for Soft diet and liquids; advance as tolerated lab or imaging tests.
tonsillectomy. PROGNOSIS Classic presentation: Severe sore throat; fever;
r Indications for tonsillectomy include: r PTA usually resolves without sequelae if recognized hot potato voice; drooling; trismus with a
Significant upper airway obstruction either acutely early and treated appropriately. unilaterally enlarged, fluctuant tonsil that pushes
or at baseline (eg, snoring) r Recurrence rate is 1015%. the uvula to the opposite side
Recurrent pharyngitis or PTA r Recurrence rate is higher (40%) in patients with a r Management of PTA includes antibiotic therapy in
Treatment failure with other drainage techniques history of recurrent tonsillitis. combination with a surgical drainage procedure:
r An older, cooperative child or adolescent who is Patients with PTC may be given a trial of
clinically stable without trismus may undergo needle COMPLICATIONS antibiotics alone.
r Airway obstruction
aspiration or incision and drainage with topical r Aspiration pneumonia if the abscess ruptures into
anesthesia or procedural sedation (5).
r If the child is young and unable to cooperate, the the airway
r Sepsis
procedure should be performed in the operating
r Internal jugular vein thrombosis
room.
r Careful attention to maintaining the airway must be r Lemierre syndrome (a potentially fatal condition
given if procedural sedation is undertaken. usually caused by Fusobacterium necrophorum and
r Prompt surgical intervention is indicated in the characterized by thrombophlebitis of head and neck
following circumstances: veins and systemic dissemination of septic emboli)
r Carotid artery rupture
Impending airway compromise (consider exam
under anesthesia) r Carotid artery pseudoaneurysm
Enlarging masses r Mediastinitis
Significant comorbidities (eg, immunodeficiency) r Necrotizing fasciitis
r Sequelae of GAS infection (when GAS is isolated)
DISPOSITION
r Hospitalization may be warranted, particularly in
younger children.
r Older children with uncomplicated PTA who are well
hydrated with adequate pain control may be
managed as outpatients.
19
ABSCESS, RECTAL
Danniel J. Stites
Todd Mastrovitch

BASICS r Generally mixed infections caused by enteric flora
Lab
such as Escherichia coli and Enterococcus and r Culture of abscess contents may be useful for
DESCRIPTION Bacteroides species antibiotic optimization.
r A perirectal (rectal) abscess is a collection of pus in r Other isolated bacteria include group C r CBC and blood culture may be useful adjuncts if
the tissues surrounding the anus or within the wall streptococcus and Staphylococcus aureus. bacteremia is suspected.
of the rectum.
r Perirectal abscesses are classified based on their COMMONLY ASSOCIATED CONDITIONS Imaging
r Inflammatory bowel disease (Crohn disease >> r Imaging is generally not necessary for perianal or
anatomic location.
r The most commonly described locations are perianal ulcerative colitis) ischiorectal abscesses.
r Leukemia r CT or MRI may be required for the diagnosis of
(most common, >50%), ischiorectal, r HIV/AIDS
intersphincteric, and supralevator. intersphincteric or supralevator abscesses.
r Diabetes mellitus r US may aid in the diagnosis of intersphincteric
EPIDEMIOLOGY r Hirschsprung disease or imperforate anus abscess.
r Overall incidence is unknown. r In patients suspected of having Crohn disease or
r Incidence is bimodal: (postoperative sequelae)
with complex abscesses, CT scan or contrast enema
The 1st peak is in children <1 yr of age. may be useful.
The greatest incidence in adults is during the 3rd DIAGNOSIS Diagnostic Procedures/Other
and 4th decades of life. r Biopsy of the abscess wall can aid in determination
r Males are affected more frequently than females, HISTORY
r Perianal abscess: Complaints of dull perianal of etiology if unclear.
with estimated ratios of 2:1 to 3:1 (1). r Needle aspiration may used as an adjunct to incision
r Incidence may be higher in warmer months (spring discomfort and pruritus exacerbated by movement,
sitting, or defecation: and drainage for confirming abscess location and
and summer).
In children, the only historical evidence may be obtaining culture material.
RISK FACTORS increased irritability, refusal to walk, or refusal to r Colonoscopy with biopsy may be needed to confirm
r In children <2 yr of age, there are generally no defecate. Crohn disease.
identifiable risk factors. r Alternatively, perianal disease may be a presenting
r Perirectal abscesses in young children may be a Pathological Findings
symptom of Crohn disease, which often has a Biopsy of the abscess wall may show granulomas that
result of abnormal anal crypt development, which history of abdominal pain, weight loss, diarrhea, may indicate underlying Crohn disease.
may be related to hormonal imbalance of androgen and failure to thrive.
and estrogen during crypt formation. r Ischiorectal abscess: Fevers, chills, and severe DIFFERENTIAL DIAGNOSIS
r In patients >2 yr of age, risk factors include Crohn r Presacral epidermal inclusion cyst
perirectal pain
disease, diabetes mellitus, and immunosuppression r Intersphincteric abscess: Present with rectal pain r Hidradenitis suppurativa
(from disease such as HIV/AIDS or medications r Supralevator abscess: Fevers, chills, severe pelvic or r Pilonidal disease
including steroids and chemotherapy). r Bartholin abscess
anorectal pain, and occasionally urinary retention
r Inflammatory bowel disease
GENERAL PREVENTION PHYSICAL EXAM
r Unknown r Perianal abscess: Small, erythematous, well-defined,
r No direct relationship has been proven between
bowel habits or personal hygiene and the
fluctuant, tender, subcutaneous mass near the anal TREATMENT
orifice (usually lateral to anus)
development of perirectal abscesses. r Ischiorectal abscess: External signs may be minimal INITIAL STABILIZATION/THERAPY
but may include erythema, induration, and r The treatment of all perirectal abscesses is incision
PATHOPHYSIOLOGY
r The vast majority of the perirectal abscesses result fluctuance within the buttocks. On digital rectal and drainage.
from infected anal crypt glands: exam (DRE), a fluctuant, indurated mass may be r Patient comfort and accessibility of the abscess
The infection may then penetrate the surrounding encountered. DRE may require procedural sedation. determine how and where an abscess may be
tissues. r Intersphincteric abscess: Often no external signs. drained.
r Perianal abscesses occur when the infection travels DRE reveals a tender fluctuant mass. r Perianal abscesses may be drained in the office or
through the intersphincteric groove to the perianal r Supralevator abscess: Usually no external signs. DRE ED.
skin. may reveal induration or fluctuance above the r Incision and drainage should always be performed
r Ischiorectal abscesses occur when the infection anorectal ring. with appropriate anesthesia and analgesia, and the
penetrates the external anal sphincter into the abscess should be incised over the area of maximal
ischiorectal space. fluctuance. The cavity should then be probed with a
r Intersphincteric abscesses are a result of spread into finger or hemostat to disrupt any loculations that
the intersphincteric space between the internal and may exist.
external sphincters. r Ischiorectal abscess drainage may be performed in
r Supralevator abscesses are the result of either the office or ED if possible; otherwise, intraoperative
superior spread from the intersphincteric space drainage may be necessary.
through the longitudinal muscles of the rectum or
from primary disease of the pelvis or lower abdomen
(appendicitis, diverticulitis, Crohn disease).
20
ABSCESS, RECTAL
A
r Intersphincteric abscesses must be drained in the Issues for Referral
r Complex abscesses involving the ischiorectal space,
REFERENCE
operating room.
r Supralevator abscesses should be drained according supralevator abscesses, or abscesses that also 1. Serour F, Gorenstein A. Characteristics of perianal
to the site of origin: involve the contralateral side of the anus (horseshoe abscess and fistula-in-ano in healthy children.
If an ischiorectal abscess, drainage should be abscess) require further workup for the possibility of World J Surg. 2006;30:467472.
performed via the skin through the overlying underlying Crohn disease and often require surgical
buttock. consultation for intraoperative drainage.
Abscesses resulting from the extension of an r Nonhealing or recurrent abscesses and/or fistulas ADDITIONAL READING
intersphincteric abscess or from a pelvic process r Chronic drainage or recurrent abscess may be the r Coates WC. Anorectum. In Marx JA, Hockberger RS,
should be drained through the rectal wall to avoid result of an underlying fistula, requiring further Walls RM, et al., eds. Rosens Emergency Medicine:
extrasphincteric fistula formation. exploration and surgical consultation. Concepts and Clinical Practice. 6th ed. Philadelphia,
MEDICATION PA: Mosby Elsevier; 2006.
r Festen C, van Harten H. Perianal abscess and
First Line
r Antibiotics may not be needed in the otherwise
FOLLOW-UP fistula-in-ano in Infants. J Pediatr Surg. 1998;33:
healthy child. FOLLOW-UP RECOMMENDATIONS 711713.
r Possible indications for antibiotics may include r Discharge instructions and medications: r Klein MD, Thomas RP. Surgical conditions of the
immunocompromised states, valvular heart disease, Maintain the area clean and dry. anus, rectum, and colon. In Kleigman RM, Behrman
diabetes mellitus, underlying Crohn disease, Do not remove abscess packing. RE, Jenson HB, Stanton BF, eds. Nelson Textbook of
extensive cellulites, or other significant Keep abscess covered until wound is re-evaluated Pediatrics. 18th ed. Philadelphia, PA: Saunders
comorbidities: by physician 2 days post drainage. Elsevier; 2007.
Clindamycin 1030 mg/kg/day q8h IV/PO If antibiotics are prescribed, take medication as r Marcus RH, Stine RJ, Cohen MA. Perirectal abscess.
Cefazolin 50100 mg/kg/day qh IV directed. Ann Emerg Med. 1995;25(5):597603.
Trimethoprim/Sulfamethoxazole 10 mg/kg/day Wound check with packing removal or dressing
change within 2 days after drainage. See Also (Topic, Algorithm, Electronic
b.i.d. PO
r Tetanus booster if patient has not received one in Sitz baths (23 times/day) and warm compresses Media Element)
r Abscess, Bartholin Gland
after packing removal until complete abscess
the past 510 yr r Abscess, Gluteal
resolution
Second Line Follow up in 23 wk of drainage for wound
r Analgesics:
evaluation and inspection for possible
Morphine 0.1 mg/kg IV/IM/SC q2h PRN: fistula-in-ano. CODES
Initial morphine dose of 0.1 mg/kg IV/SC may r Activity:
be repeated q1520min until pain is controlled, Patients may perform daily activities without ICD9
then q2h PRN. restriction, understanding that good perianal 566 Abscess of anal and rectal regions
Codeine or codeine/acetaminophen dosed as hygiene can minimize postprocedural
0.51 mg/kg of codeine component PO q4h PRN complications such as reinfection.
Hydrocodone or hydrocodone/acetaminophen PEARLS AND PITFALLS
dosed as 0.1 mg/kg of hydrocodone component Patient Monitoring
r No monitoring is generally required for local r Perianal and ischiorectal abscesses may be drained
PO q46h PRN
r NSAIDs: anesthesia and incision and drainage. in the office or ED with appropriate analgesia and
r Patients with complex disease should undergo local anesthesia.
Consider NSAIDs in anticipation of prolonged pain
and inflammation: further evaluation and possibly testing for associated r Intersphincteric, supralevator, and horseshoe
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN underlying medical problems such as Crohn disease. abscesses generally require surgical consultation
Ketorolac 0.5 mg/kg IV/IM q6h PRN DIET and intraoperative drainage.
Naproxen 5 mg/kg PO q8h PRN r Antibiotics are generally not required and do not
High-fiber diet or fiber supplementation
r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN replace incision and drainage as the mainstay of
r Stool-bulking agents and stool softeners to prevent PROGNOSIS treatment.
r Prognosis of perianal abscesses is generally very r Patients should be re-evaluated 23 wk after
constipation (post drainage):
Polyethylene glycol 3350: 17 g in 8 oz of water qhs good when treated appropriately with incision and drainage to ensure abscess resolution and
drainage. evaluation for fistula formation.
DISPOSITION r Incision and drainage in infants works very well but
Admission Criteria in older children may be associated with recurrence
Critical care admission criteria: or fistula formation.
r Signs or symptoms of sepsis
COMPLICATIONS
Discharge Criteria r Patients with rectal abscesses may develop a chronic
r No signs of systemic toxicity fistula, especially if they have a history of Crohn
r Uncomplicated incision and drainage of perianal or disease (1).
ischiorectal abscess r Without appropriate management, up to 85% of
children with perianal abscesses will have recurrent
abscess or fistula formation.
r Fistulas generally do not heal spontaneously and
may require fistulotomy.
21
ABSCESS, RETROPHARYNGEAL
Nikhil B. Shah

BASICS RPA may also be associated with: r Lateral soft tissue neck radiography:
r Accidental trauma Simple screening tool
DESCRIPTION r Foreign body ingestion Prevertebral soft tissue swelling >7 mm at level of
r Retropharyngeal abscess (RPA) is a deep tissue neck C2 vertebra or >14 mm at C6 is concerning for
r Complication of medical procedures
infection: r Immunocompromised states (1,2) RPA but nondiagnostic:
Specifically, it is a suppurative adenitis of the False widening may occur with crying,
paramedial lymph node chain (1). swallowing, expiration, and neck flexion.
RPA develops in the potential space between the DIAGNOSIS Attention to proper technique may yield more
posterior pharyngeal wall and the prevertebral optimal results.
fascia. HISTORY Additional findings include loss or reversal of
r RPA is serious and occasionally life threatening, r Symptoms are often nonspecific, and diagnosis is normal cervical lordosis, radiopaque foreign body,
partly as a result of the anatomic location and the based on clinical suspicion: soft tissue mass, air-fluid level, or gas in the
potential to obstruct the upper airway. Fever prevertebral area.
r RPA has been dubbed the epiglottitis of the new Neck pain, swelling, and/or stiffness Radiography is not useful in distinguishing
millennium. Sore throat cellulitis from abscess unless the presence of gas
r Causes: Odynophagia, dysphagia is noted.
Irritability r Neck CT with IV contrast:
Infectious
Traumatic r Limitation of neck movement associated with Most commonly used diagnostic modality
Idiopathic decreased oral intake or drooling is an important Overcomes many of the limitations associated
diagnostic clue. with radiography
EPIDEMIOLOGY r Symptoms usually progress over several days in Disadvantages:
r RPA due to infectious causes is noted most
contrast to epiglottitis, which progresses more High-dose ionizing radiation
commonly in children <6 yr of age. Potential need for procedural sedation
r Peak incidence occurs at 3 yr of age. quickly.
Very helpful in delineating the location and extent
r Uncommon in older children, as the involved lymph PHYSICAL EXAM
r Neck swelling/mass of infection
node chain atrophies with increasing age Able to differentiate cellulitis from abscess,
r Neck in midline, neutral, or hyperextended
RISK FACTORS though studies correlating CT findings with
position: intraoperative findings demonstrate that CT scan
RPA in children tends to be preceded by infections of Neck stiffness in RPA may be confused with that
the nasopharynx, paranasal sinuses, and middle ear has a false-negative rate of 13% and a
seen in meningitis. false-positive rate of 10%
(2). Refusal to turn neck laterally often distinguishes Area of hypodensity >2 cm2 may be more
PATHOPHYSIOLOGY RPA from meningitis. suggestive of abscess.
r Infection occurs as a result of contiguous spread r Trismus (more commonly seen with peritonsillar Scalloping or irregularity of abscess wall on CT
along a lymphatic chain that originates from the abscess) may represent impending rupture and predict
nasopharynx, adenoids, and paranasal sinuses and r Cervical lymphadenopathy need for surgical intervention (64% sensitivity).
extends to the adjacent pharyngeal tissues. r The classic findings listed below are usually only r Neck US:
r The spectrum may range from cellulitis to frank
seen in more advanced cases: Nonradiation alternative (3)
abscess formation based on the extent of tissue Muffled hot potato voice Useful for evaluation as well as monitoring
involvement, accounting for the diverse clinical Drooling progression
presentation. Torticollis Able to detect infection in early nonsuppurative
ETIOLOGY Respiratory distress stage (when combined with color Doppler),
r The pathogen varies depending on the originating Stridor and/or wheeze thereby allowing for earlier initiation of
source of infection. antimicrobial therapy and a possible reduction in
r Multiple aerobic and anaerobic organisms are the number of surgeries
Lab Able to differentiate between abscess and adenitis
frequently implicated: r CBC (leukocytosis with left shift +/ bands)
May be used to guide intraoperative aspiration
Streptococcus viridans and Streptococcus r Blood cultures, both aerobic and anaerobic (rarely
and drainage
pyogenes positive)
Staphylococcus aureus, including MRSA strains r Throat culture for group A streptococci DIFFERENTIAL DIAGNOSIS
and Staphylococcus epidermidis Other infectious conditions that may mimic RPA
Bacteroides, Peptostreptococcus, Fusobacterium, include:
Haemophilus, and Klebsiella r Epiglottitis (now rare in post Haemophilus
influenzae type b vaccine era)
r Laryngotracheobronchitis (croup)
r Bacterial tracheitis
r Meningitis
r Cervical lymphadenitis
22
ABSCESS, RETROPHARYNGEAL
A
DISPOSITION REFERENCES
TREATMENT Admission Criteria
r Children with suspected or confirmed RPA should be 1. Philpott CM, Selvadurai D, Banerjee AR. Paediatric
INITIAL STABILIZATION/THERAPY hospitalized and managed in consultation with ENT. retropharyngeal abscess. J Laryngol Otol. 2004;
r Initial therapy depends on the severity of respiratory r Critical care admission criteria: 118:919926.
distress and likelihood of drainable fluid (based on Severe airway compromise 2. Ungkanont K, Yellon RF, Weissman JL, et al. Head
CT findings, clinical features, and clinical course) Toxicity and neck space infections in infants and children.
r Airway management: Development of potentially fatal complications Otolaryngol Head Neck Surg. 1995;112:375382.
If the child has significant stridor or respiratory (eg, sepsis, mediastinitis) 3. Glasier CM, Stark JE, Jacobs RF, et al. CT and
distress, a clinician with advanced airway skills ultrasound imaging of retropharyngeal abscesses in
(eg, ENT, anesthesia) should be present for airway children. AJNR Am J Neuroradiol. 1992;13:
stabilization. FOLLOW-UP 11911195.
Diagnostic workup must be deferred until the 4. Gaglani MJ, Edwards MS. Clinical indicators of
FOLLOW-UP RECOMMENDATIONS childhood retropharyngeal abscess. Am J Emerg
airway is stabilized. r Discharge instructions and medications:
In cases of severe airway compromise, a Med. 1995;13:333336.
Children with RPA should be admitted from the
management protocol similar to that previously 5. Page NC, Bauer EM, Lieu JE. Clinical features and
emergency department.
used for epiglottitis should be considered (ie, r When discharged from the hospital after treatment of retropharyngeal abscess in children.
emergent endoscopic airway exam by ENT with no Otolaryngol Head Neck Surg. 2008;138:300306.
interventions initiated until the child is under appropriate therapy:
anesthesia in the operating room). Follow up within few days of discharge.
r IV fluid resuscitation Patients should be advised to return for ADDITIONAL READING
re-evaluation if the following symptoms
MEDICATION develop: Goldstein NA, Hammerschlag MR. Peritonsillar,
First Line Fever retropharyngeal, and parapharyngeal abscesses. In
r The majority of patients may be managed with early Dyspnea Feigin RD, Cherry JD, Kaplan SL, et al., eds. Textbook
administration of IV antibiotics alone (7590% Worsening/Severe pain of Pediatric Infectious Diseases. 6th ed. Philadelphia,
success rate): Trismus PA: Saunders; 2009:177.
Early institution of antibiotics may prevent Enlarging mass
progression to mature abscess (4). Neck stiffness
r Selection of the antibiotic regimen should be based Patient Monitoring CODES
on regional bacterial sensitivity patterns and include Children with retropharyngeal infections should be
coverage against multiple mixed aerobic and monitored closely for persistence or progression of ICD9
anaerobic pathogens: symptoms and development of complications. 478.24 Retropharyngeal abscess
Ampicillin/Sulbactam 200 mg/kg/day divided q6h
IV OR PROGNOSIS
r RPA seldom leads to long-term sequelae when PEARLS AND PITFALLS
Clindamycin 40 mg/kg/day divided q8h IV:
Added benefit of MRSA coverage detected early and appropriately treated.
r Relapse rate of 15%; may be associated with r Consider the diagnosis of RPA in a child with fever,
r Parenteral treatment should be maintained until the
trauma or anatomic abnormality. stiff neck, and dysphagia.
patient is afebrile and clinical improvement is noted. r When a critical airway is suspected, all interventions
r Oral therapy should then be continued to complete COMPLICATIONS
r Infection may spread from the retropharyngeal should be deferred until the airway is secured.
a 14-day course and includes the following r CT with IV contrast provides an optimal image.
regimens: space to other deep neck spaces, contiguous However, if skilled operators are available,
Amoxicillin/Clavulanate 8090 mg/kg/day divided structures, and the bloodstream. sonography may be used to confirm the diagnosis
q12h OR r Complications are rare but potentially fatal and
and assist in drainage.
Clindamycin 40 mg/kg/day divided q8h include: r Hospitalize all children with RPA in consultation
r Analgesia: Airway obstruction with ENT, with careful attention to maintenance of
Acetaminophen 15 mg/kg/dose PO q46h PRN Sepsis the airway.
Ibuprofen 10 mg/kg/dose PO q6h PRN Aspiration pneumonia (if abscess ruptures into the r Initial therapy depends on severity of respiratory
Morphine 0.1 mg/kg IV/IM/SC q2h PRN airway)
Initial morphine dose 0.1 mg/kg IV/SC may be distress and likelihood of drainable fluid.
Internal jugular vein thrombosis r Initiate empiric antibiotic therapy as soon as
repeated q1520min until pain is controlled Lemierre syndrome: A potentially fatal condition
then q2h PRN usually caused by Fusobacterium necrophorum possible in all patients.
Second Line and characterized by thrombophlebitis of head
In patients not responding to parenteral clindamycin and neck veins and systemic dissemination of
or those with severe disease: septic emboli
r Vancomycin 4060 mg/kg/day divided q68h IV Carotid artery rupture
r Linezolid: Mediastinitis (from extension into chest)
Atlantoaxial dislocation
<12 yr: 30 mg/kg/day divided q8h IV Grisels syndrome
12 yr: 20 mg/kg/day divided q12h IV
Max daily dose 1,200 mg
r Indications for surgical drainage (in combination
with empiric antibiotic therapy) include:
Airway compromise or other life-threatening
complications
Large (>2 cm2 ) hypodense area on CT scan
Failure to respond to IV antibiotic therapy
r Factors associated with drainable fluid at surgery
include duration of symptoms >2 days and
hypodense area >2 cm2 on CT scan (5).
r If surgical drainage is performed, aerobic and
anaerobic specimens for culture should be obtained.
23
ACETAMINOPHEN POISONING
Stephanie H. Hernandez
r Toxic acetaminophen ingestions are typically initially r In patients with intentional suicidal gestures, 1 in
BASICS silent, and there is no way by physical exam to 500 will fail to disclose an acetaminophen ingestion
determine which patients will have hepatoxicity. that warrants treatment.
DESCRIPTION r Single ingestions of <200 mg/kg are typically
r Acetaminophen is used as an analgesic and RISK FACTORS
considered nontoxic in children. r Increased NAPQI (N-acetyl-p-benzo-quinone)
antipyretic.
r Acetaminophen toxicity is the leading cause of EPIDEMIOLOGY formation:
r Acetaminophen is among the most commonly CYP2E1 induced
hepatoxicity and toxin-induced hepatic failure.
r Acetaminophen is one of the most commonly ingested drugs reported to poison control centers in Decreased hepatic glutathione (GSH) stores
the U.S., with >90,000 cases of exposure reported Poor nutritional status
ingested toxins in the U.S. r Decreased capacity for nontoxic metabolism
r Acetaminophen ingestion may cause a spectrum of in 2008.
r Acetaminophen combination formulations were r Patients who receive antidote treatment more than
illness from minor symptoms and no hepatoxicity to
among the top 5 ingestions reported to poison after 8 hr after acute ingestion
severe hepatoxicity, liver failure, and death. r Chronic supratherapeutic ingestions
r Use of a nomogram to predict the likelihood of centers associated with death in 2008:
Acetaminophen alone is among the top 10.
toxicity and the antidote N-acetylcysteine (NAC), r Acetaminophen poisoning is the leading cause of GENERAL PREVENTION
used to prevent and treat acetaminophen toxicity, r Appropriate parental weight-based dosing in
fulminant hepatic failure in the U.S. and U.K.
play a key role in management of acetaminophen pediatric patients
ingestions. r Recognition of the difference in concentration
between infant and childrens formulation
PATHOPHYSIOLOGY
r Acetaminophen generates the hepatotoxic
500 metabolite NAPQI, which can be converted to less
450 toxic compounds by endogenous glutathione.
400 r Toxicity occurs when excessive NAPQI is produced
350 and glutathione stores are exhausted.
300
ETIOLOGY
250 r Acetaminophen is commonly referred to as Tylenol in
200 (200, 4 Hrs.) the U.S. However, depending on the manufacturer, it
may be recognized by different names worldwide.
If Concentration Values Fall Above Solid
150 Some of these common names include but are not
Line, Hepatoxicity is Likely To Occur
Plasma or Serum Acetaminophen Concentration (mcg/ml)
limited to Panadol, paracetamol, Crocin, and Dolex.

r There are many over-the-counter and prescriptive
100 products that contain acetaminophen.
90 r Examples include but are not limited to:
80
70 Vicodin (hydrocodone/acetaminophen)
60 Percocet (oxycodone/acetaminophen)
50 (50, 12 Hrs.) Darvocet (propoxyphene/acetaminophen)
Fioricet (butalbital/caffeine/acetaminophen)
40 r Over-the-counter cold and cough medications
30 COMMONLY ASSOCIATED CONDITIONS

r Toddlers with febrile illnesses
r Chronic pain syndromes and tolerance to opiate
20 analgesics
Initiate r Ignorance of the acetaminophen component in
NAC if level
combination medications
is above r Suicidality and psychiatric illness
broken line r Prescriptive drug abuse: Patients taking
10
9 opioid/acetaminophen combinations may take toxic
8 doses of acetaminophen in order to ingest the
7 quantity of opioid they desire.
6
5
DIAGNOSIS
4
HISTORY
3
Continue Mucomyst if Assay Value r Time of ingestion
Falls On or Above Broken Line
r Single acute ingestion or multiple ingestions
r Acetaminophen formulation
2 r Combination products that may delay absorption;
opiates or anticholinergic agents
PHYSICAL EXAM
r Physical exam is usually unremarkable in acute
1
5 10 15 20 25 30 ingestion.
r GI distress may be observed.
Hours Post Ingestion r In massive overdoses, early clinical signs may be
seen (metabolic acidosis accompanied by
Rumack-Matthew nomogram. (Adapted from Rumack BH, Matthew H. Acetaminophen poisoning tachypnea, altered mental status and, renal
and toxicity. Pediatrics. 1975;55:871876.) impairment) in the absence of hepatic impairment.
24
ACETAMINOPHEN POISONING
A
r Hepatotoxicity occurs most commonly within 24 hr r It is ideal to start NAC within 8 hr of ingestion in
post-ingestion if not treated or if treatment is order to prevent significant hepatoxicity and FOLLOW-UP
initiated >8 hr post-ingestion: mortality.
Clinical findings include jaundice, right upper r NAC IV dosing (21-hr NAC protocol): 150 mg/kg FOLLOW-UP RECOMMENDATIONS
quadrant pain, coagulopathy, and over 60 min, then 50 mg/kg over 4 hr, then Patient Monitoring
encephalopathy. 100 mg/kg over 16 hr: r Psychiatric consultation is required for all intentional
It is usually mixed with 5% dextrose. For patients overdoses.
DIAGNOSTIC TESTS & INTERPRETATION r Patients who recover from hepatotoxicity do not
<40 kg, assure appropriate weight-based
Lab calculation and administration of NAC in IV fluid. require repeat liver function evaluations.
Initial Lab Tests
r Serum acetaminophen concentrations should be See http://www.acetadote.net for a dose
PROGNOSIS
calculator. r If NAC is started within 8 hr from the time of
obtained: Status epilepticus and death have been associated
These must be interpreted according to the ingestion in an acute single ingestion, morbidity and
with medication errors with NAC in pediatric
circumstances of ingestion: Time from ingestion, mortality is very low.
patients. r Chronic overdoses and patients who present late for
coingestants, and LFTs. A loading bolus over 15 min is advocated by
In a single acute ingestion, a serum concentration some, but we advise 60 min due to lower treatment with NAC have increased morbidity and
should be obtained ideally no earlier than 4 hr incidence of severe anaphylactoid reaction with mortality.
post-ingestion, and results should be available no r Poor prognosisthe Kings College criteria:
the longer initial infusion.
later than 8 hr post-ingestion in order to initiate r NAC oral dosing: 140 mg/kg PO loading dose pH <7.3 at 2 days after overdose despite volume
treatment if needed.
followed by 70 mg/kg PO q4h for 72 hr. resuscitation and PT >100, serum creatinine
In single acute ingestions, utilize the r Oral dosing often causes vomiting. >3.3 mmol/L, or severe hepatic encephalopathy
Rumack-Matthew nomogram to determine if r Due to vomiting and length of treatment (72 hr vs. Other criteria predictive of poor prognosis:
treatment with NAC is warranted. Serum lactate >3 mmol/L after fluid resuscitation
In chronic multiple ingestions, call your nearest 21 hr), oral administration is not typically the or phosphate >2.65 on day 2
poison center and/or consult a toxicologist to first-line therapy: IV NAC is preferable.
r Consult your poison control center and/or COMPLICATIONS
determine if treatment is warranted. r Encephalopathy
r LFTs should be routinely obtained if the toxicologist in the setting of multiple or chronic
ingestions in order to decide if NAC is indicated. r Coagulopathy
acetaminophen concentration is in the toxic range or
r An oral NAC regimen should be considered for r Renal failure
in cases of late presentation.
LFTs are usually within normal limits until 24 hr patients with severe and/or active asthma or prior r Fulminant hepatic failure
post-ingestion with the exception of massive severe anaphylactoid reaction to NAC. r Acidosis
overdoses. r Death
Second Line
LFTs may be abnormal with relatively low or r Consider activated charcoal if the risk of aspiration
absent acetaminophen concentrations in chronic is low and the airway is intact:
overdoses. 1 g/kg orally if within 1 hr of ingestion ADDITIONAL READING
r Specific lab tests that indicate poor prognosis
With ingestions of acetaminophen and other r Alander SW, Dowd MD, Bratton SL, et al. Pediatric
include PT >100, creatinine 3.3 mmol/L, lactate substances that may diminish GI motility, such as acetaminophen overdose: Risk factors associated
>3 mmol/L, phosphate >2.6 mmol/L on day 2, pH diphenhydramine or opioids, charcoal may be with hepatocellular injury. Arch Pediatr Adolesc
<7.3. administered even after 1 hr of ingestion.
r Fresh frozen plasma if coagulopathic Med. 2000;154:346.
r Dart RC, Erdman AR, Olson KR, et al.
r Vitamin K if coagulopathic
TREATMENT r Renal replacement therapy for persistent acidosis
Acetaminophen poisoning: An evidence-based
consensus guideline for out-of-hospital
PRE HOSPITAL despite supportive care and/or renal failure management. Clin Toxicol (Phila). 2006;44:1.
General supportive care should be provided. r Mohler CR, Nordt SP, Williams SR, et al. Prospective
INITIAL STABILIZATION/THERAPY Liver transplant may be necessary. evaluation of mild to moderate pediatric
r Maintain vital signs within normal limits; IV fluid acetaminophen exposures. Ann Emerg Med.
DISPOSITION 2000;35:239.
administration is usually indicated.
r Assess the serum acetaminophen concentration at Admission Criteria
r All patients who require treatment with NAC must See Also (Topic, Algorithm, Electronic
least 4 hr post-ingestion. Media Element)
r If the patient has a toxic acetaminophen be admitted.
r Critical care admission criteria: IV NAC administration information (including
concentration as indicated by the Rumack-Matthew weight-based infusion): http://www.acetadote.net
Consider admission to a critical care unit if the
nomogram, administer NAC. In the U.S., toxicity is
patient has the following:
any value above the lower (dashed) line. Altered mental status or encephalopathy
r If the patient reaches 8 hr post-ingestion and the CODES
Metabolic acidosis
serum acetaminophen level is not known, Coagulopathy
immediately administer NAC. Renal failure ICD9
r NAC is most effective when given within 8 hr of
Rising LFTs 965.4 Poisoning by aromatic analgesics, not
ingestion. If a nontoxic serum acetaminophen elsewhere classified
concentration is subsequently noted, the NAC Discharge Criteria
therapy may be discontinued. Treatment with NAC may be terminated and the
patient may be discharged after LFTs are assured to be PEARLS AND PITFALLS
MEDICATION within normal limits and acetaminophen concentration
First Line is less than the limits of detection. r Inappropriate utilization of the Rumack-Matthew
r IV NAC is indicated in a single acute ingestion of nomogram and misinterpretation of acetaminophen
Issues for Referral
acetaminophen when the acetaminophen r Patients with poor prognostic criteria should be concentrations
concentration 4 hr post-ingestion is above the referred for liver transplant: PT >100, creatinine r Premature termination of NAC therapy or failure to
treatment line on the Rumack-Matthew nomogram. 3.3 mmol/L, lactate >3 mmol/L, phosphate continue therapy beyond 21 hr when indicated
r NAC should be started in the setting of suspected >2.65 mmol/L on day 2, pH <7.3. r IV NAC administration should be given carefully;
chronic supratherapeutic acetaminophen dosing r All cases should be reported to the local poison center. dosing errors are common due to the 3 different
with low or nondetectable acetaminophen r Unclear cases or cases of chronic supratherapeutic concentrations of infusion required.
concentration and elevated LFTs. ingestion should be discussed with a poison
specialist and/or toxicologist.
25
ACNE
Helene Tigchelaar
ETIOLOGY DIFFERENTIAL DIAGNOSIS

BASICS r Neonatal: Possibly related to sebaceous gland r Neonatal acne may be confused with:
stimulation by maternal androgens. There is Cephalic pustulosis, sometimes used
DESCRIPTION controversy regarding the relationship to cephalic synonymously with acne (lacks comedones and
r Acne is any cutaneous disease that begins with the pustulosis. Neither entity has comedonal lesions. possibly related to Malassezia species overgrowth)
formation of a microcomedo. r Infantile acne: Hyperplasia of sebaceous glands due Miliaria rubra (heat rash): Obstruction of eccrine
r Acne has the potential for scarring and invasive to androgenic stimulation with full spectrum of acne sweat ducts due to keratin (may have papules and
infection and may be associated with psychosocial lesions pustules); caused by excessive warming of young
disorders including depression, social isolation, and r Acne vulgaris: Precipitating events that lead to infant
suicide. formation of the initial hyperkeratotic plug are Milia: Keratin retention in pilaceous follicles;
r Severity ranges from mild comedones to extensive multifactorial but in general are hormonally common areas of distribution include the nose
nodular acne, with usual distribution over the face, mediated: and cheeks; occurs during 1st few weeks of life
chest, and back. Consider hyperandrogenism from polycystic ovary r Infantile acne:
syndrome or ovarian or adrenal tumor if the onset If all stages of lesions are in the typical facial
EPIDEMIOLOGY
r Acne occurs at some point in 8085% of all is rapid and/or the patient has virilization. distribution, diagnosis is straightforward.
For pustules, consider staphylococcal or candidal
adolescents/young adults:
infections.
It is the most common skin disease in this age DIAGNOSIS For papules, consider viral exanthem,
group.
r Neonatal acne occurs in 20% of infants, with onset Gianotti-Crosti syndrome, zinc deficiency, or
HISTORY irritant eczema.
at 3 wk of age and resolution by 4 mo of age. r Age at onset
r Infantile acne, with a male predominance, presents r Presence of fever, arthralgia, myalgia, or weight loss For nodules, consider pilomatrixoma, insect bites,
and idiopathic facial aseptic granuloma.
at 3 mo of age with resolution by 2 yr of age. r Family history of acne or endocrine disorders r Acne vulgaris, although generally a clinically
r Menstrual history: Menarche and regularity,
RISK FACTORS apparent diagnosis, can be confused with:
r Genetic oligomenorrhea Flat warts and molluscum contagiosum (both
r Medications: r Medication history including medications used for noninflammatory)
Glucocorticoids, anabolic steroids, isoniazid, acne (topical and systemic) Rosacea, which is usually after extended steroid
r Cosmetics/Pomades used therapy but has no comedones
phenytoin, iodides, bromides, cyclosporine,
azathioprine, and others r Workplace exposures (eg, fryers in fast-food Sebaceous hyperplasia (neonates and older
r Oily cosmetics, pomades, oil and coal tar exposure restaurants) teens): Forehead and cheeks.
r Hormonal changes related to androgen-producing Bacterial folliculitis: No comedones, and lesions
PHYSICAL EXAM are usually all in the same stage
tumors, menstrual periods, pregnancy, birth control r Type and distribution of lesions:
Pseudofolliculitis barbae (barbers itch): Related to
pills, or stress Open comedones (blackheads) secondary infection of ingrown hairs
GENERAL PREVENTION Closed comedones (whiteheads) Acnelike eruption of Apert syndrome: On arms,
r Avoid anabolic steroids, oily cosmetics, and Inflammatory papules and pustules legs, and buttocks
excessive scrubbing of skin. Nodules and cysts:
r Use powdered, water-based, or noncomedogenic Scarring and hyperpigmentation
r Fever or arthralgia TREATMENT
cosmetics.
r An association between acne and milk ingestion r Evidence of invasive infection (gram-negative
folliculitis and staphylococcal infections) MEDICATION
may possibly be related to hormones present in milk.
r In infants, look for signs of virilization including First Line
PATHOPHYSIOLOGY r Neonatal acne will resolve without treatment:
r Initially begins due to follicular plugging caused by body odor, axillary or pubic hair, and clitoromegaly.
r In adolescents, hyperandrogenism may manifest as Gentle washing with tepid water and cleanser
hyperkeratinization and abnormal desquamation of late-onset or resistant acne, hirsutism, acanthosis b.i.d.
pilosebaceous follicles (microcomedo) nigricans, alopecia, and deepened voice. Avoidance of oils and lotions
r Increased sebum production occurring in May use a keratolytic shampoo or a 2.5% benzoyl
adolescence and in infancy leads to sebum trapping DIAGNOSTIC TESTS & INTERPRETATION peroxide lotion
in follicles. Lab A mild nonfluorinated steroid (hydrocortisone 1%
r Follicle colonized by Propionibacterium acnes r Cultures are indicated only with suspicion of b.i.d.) may decrease erythema.
r P. acnes proliferate in an anaerobic setting, leading gram-negative folliculitis or staphylococcal or r Infantile acne will resolve but has rare potential for
to follicular wall rupture as well as a neutrophilic streptococcal infections. scarring:
r Consider obtaining free testosterone, serum Mild to moderate: Benzoyl peroxide (2.5%),
inflammatory response.
r Stimulation of toll-like receptors and cell surface dehydroepiandrosterone sulfate, luteinizing topical antibiotics (erythromycin or clindamycin),
receptors lead to the release of inflammatory hormone, and follicular-stimulating hormone levels topical retinoids
mediators, including cytokines, resulting in follicular in children who present with severe persistent Severe:
rupture. infantile acne or in acne vulgaris with virilization. Erythromycin 3050 mg/kg/day PO divided t.i.d.
Imaging
Children who present with virilization may require a
pelvic US or CT of the abdomen and pelvis.
26
ACNE
A
r Acne vulgaris (adolescents and young adults): Mild COMPLEMENTARY & ALTERNATIVE ADDITIONAL READING
to moderate acne (starting with 1st 2 and THERAPIES
progressing through therapeutic armamentarium Stress relief measures may be effective. r Cooper AJ. Systematic review of Propionibacterium
until there is improvement): acnes resistance to systemic antibiotics. Med J Aust.
Gentle cleansing with tepid water and mild DISPOSITION 1998;169:259.
cleanser such as a glycolic/salicylic acidbased Admission Criteria r El-Hallak M, Giani T, Yeniay BS, et al. Chronic
cleanser b.i.d. Secondary gram-negative, staphylococcal, or minocycline-induced autoimmunity in children.
Salicylic acid lotion: Thin layer applied to affected streptococcal infections leading to cellulitis or abscess J Pediatr. 2008;153:314319.
area b.i.d. with fever and toxicity r Haider A, Shaw JC. Treatment of acne vulgaris.
Benzoyl peroxide 2.5% daily to b.i.d. as tolerated Issues for Referral JAMA. 2004;292:726.
to entire involved area (not just lesions). r Referral to dermatology for treatment of: r Strauss JS, Krowchuk DP, Leyden JJ, et al.; American
Alternative is salicylic acid: Resistant and severe nodular acne Academy of Dermatology/American Academy of
Benzoyl peroxide bleaches fabrics and hair; in Severe pustular or cystic acne Dermatology Association. Guidelines of care for
dark-skinned patients, it may cause some Isotretinoin therapy acne vulgaris management. J Am Acad Dermatol.
lightening at higher concentrations. r Endocrinology: Rapid onset, atypical age, or 2007;56:651663.
Benzoyl peroxide also may cause excessive persistence
dryness of skin. See Also (Topic, Algorithm, Electronic
May increase concentration of benzoyl peroxide to Media Element)
5% if a lower concentration is tolerated FOLLOW-UP http://www.skincarephysicians.com/acnenet/
Topical antimicrobial (erythromycin or
clindamycin) containing benzoyl peroxide daily FOLLOW-UP RECOMMENDATIONS
Topical retinoid (adapalene or tretinoin) are Discharge instructions and medications: CODES
effective but not typically prescribed from the r Specific primary care or dermatology follow-up in a
emergency department. timely manner will reinforce instructions and ICD9
r Acne vulgaris (moderate to severe) or resistant encourage compliance. 706.1 Other acne
inflammatory acne: r Improvement in lesions with any therapy takes
Add to the above regimen: 48 wk.
Tetracycline 500 mg PO b.i.d. OR r Avoid an excessively complex initial program, PEARLS AND PITFALLS
Doxycycline 100 mg PO b.i.d. especially in boys. r Pearls:
Doxycycline is more effective but can cause r Application of topical medications should be done
photosensitivity or nausea. Time-honored dietary restrictions are not
about 15 min after facial cleansing and drying to
If failure of above, switch to: supported by best evidence.
avoid excessive absorption with increased side r Pitfalls:
Minocycline 50100 mg PO b.i.d. effects.
Minocycline can cause pseudotumor cerebri, r Warn about the possibility of initial worsening of Failing to recognize the profound psychosocial
autoimmune reactions, and blue pigmentation implications of acne for the suffering teen
symptoms, erythema, and scaling with therapy.
of skin and teeth. Missing signs of virilization or atypical
Erythromycin base 3050 mg/kg/day PO divided DIET presentation suggesting an androgen-producing
t.i.d. Dietary restrictions are ineffective. tumor
Trimethoprim (TMP)/Sulfamethoxazole 612 mg Failure to counsel, prevent, and monitor for
PROGNOSIS
TMP/kg/day PO divided b.i.d. pregnancy in females on systemic medications or
With optimal therapy and compliance, acne is a
topical retinoids
Second Line controllable disease.
Use of topical antibiotics not in combination with
The following therapies should be instituted by a COMPLICATIONS benzoyl peroxide can lead to bacterial resistance.
dermatologist: r Acne fulminans:
r Isotretinoin:
Sudden flare in males of severe acne of the chest
Drug is teratogenic. and back with associated fever, myalgia, and
Other possible side effects include headaches, arthralgia
nosebleed, paronychia, depression, elevated liver May occur during early isotretinoin therapy or with
enzymes, and possibly inflammatory bowel testosterone therapy
disease. Treatment includes systemic steroids and oral
r Consider oral contraceptives [norgestimate with antibiotics; after 4 wk, low-dose isotretinoin is
ethinyl estradiol (Ortho Tri-cyclin) or norethindrone used (see Medication section).
acetate with ethinyl estradiol (Estrostep)]. r Gram-negative folliculitis:
r Class B (level II evidence) drugs: Spironolactone, May develop after long-term antibiotic use
antiandrogens, and oral corticosteroids Suspect with flaring and worsening of acne on
Pregnancy Considerations antibiotic therapy
r Oral isotretinoin therapy is highly teratogenic. Use is Treatment with gram-negative antibiotics
r Staphylococcal (MRSA) secondary infections
restricted to prescription by dermatologists under r Excoriated acne: More common in females and
the stringently regulated FDA program iPledge:
Available in unregulated countries consists of compulsive picking at lesions resulting in
r Oral tetracyclines, topical retinoids, and hormonal infection and scarring.
therapy are all contraindicated during pregnancy.
27
ACUTE HEMOLYTIC ANEMIA

Angela M. Ellison
ETIOLOGY
BASICS Hemolysis occurs secondary to either an acquired or DIAGNOSIS
inherited cause:
DESCRIPTION r Acquired: HISTORY
r Hemolysis is the destruction or removal of RBCs r Dyspnea, fatigue, weakness, or angina may occur in
AIHA occurs when the body forms antibodies
before their normal life span of 90120 days. the presence of abrupt hemolysis and severe anemia.
against its own RBCs surface antigens. r Acute onset of pallor may be reported in cases of
r Hemolytic anemia occurs when the rate of hemolysis
Primary AIHA: Autoantibodies are present, but
exceeds the ability of the bone marrow to there is no evidence of systemic disease. It can be brisk hemolysis:
adequately compensate for the loss of RBCs. categorized as warm-reactive AIHA (IgG Slow onset of pallor usually suggests diminished
r This topic focuses on the identification and autoantibodies maximally bind RBCs at 37 C) or RBC production.
r Back pain and dark urine may be reported by
treatment of acute hemolytic anemia. cold-reactive AIHA (autoantibodies preferentially
bind RBCs at 4 C) (2). patients with intravascular hemolysis.
EPIDEMIOLOGY r Jaundice may be present because of an increase in
Cold-reactive AIHA includes cold agglutinin
Incidence disease (IgM autoantibodies) and paroxysmal cold indirect bilirubin.
r The incidence and prevalence of hemolytic anemia r Family history of anemia or autoimmune diseases
hemoglobinuria (IgG autoantibodies).
depends on the etiology. Secondary AIHA: Immune-mediated hemolytic should be illicited.
r Autoimmune-mediated hemolytic anemia (AIHA) is r Family history of splenectomy or cholecystectomy
anemia is only a manifestation of a broader
rare, with an estimated annual incidence of 1 in systemic disorder. Teenagers who present with suggests an inherited hemolytic disorder such as
80,000 persons (1). AIHA are more likely to have an underlying hereditary spherocytosis or pyruvate kinase
RISK FACTORS systemic illness (3). deficiency.
r AIHA is more likely to occur in females. Microangiopathic anemia results from the r Transfusion history should be obtained.
r G6PD deficiency is an X-linked recessive disorder: mechanical destruction of RBCs in circulation r Current and previous medication history should be
Individuals with this disorder are at risk of (eg, disseminated intravascular coagulation [DIC], documented.
developing acute hemolytic anemia when exposed hemolytic uremic syndrome [HUS], thrombotic r Exposure to other agents that may cause abrupt
to certain foods, drugs, and other substances. thrombocytopenia purpura [TTP]). hemolysis in patients with G6PD deficiency (eg,
r Individuals with inherited disorders that cause r Inherited:
naphthalene-containing mothballs, fava beans)
chronic hemolysis during steady-state conditions Enzymopathies (G6PD deficiency, pyruvate kinase should be explored.
(eg, sickle cell anemia [SCA], hereditary deficiency)
Membranopathies (hereditary spherocytosis, PHYSICAL EXAM
spherocytosis) are also at risk of developing acute r Evidence of CHF (tachycardia, gallop rhythm,
hemolytic episodes: hereditary elliptocytosis)
Hemoglobinopathies (thalassemia, SCA) cardiomegaly, and hepatomegaly) may be present.
These acute episodes may be triggered by the r Skin may appear jaundiced or pale:
onset of acute illness or infection. COMMONLY ASSOCIATED CONDITIONS
r Transfusion of incompatible blood products may also r Idiopathic Mucous membranes, conjunctivae, nail beds,
r Malignancy palms, and soles should be closely examined.
trigger an acute hemolytic reaction: r Lymphadenopathy suggests a malignancy.
May occur up to several weeks after the initial r Drugs r Splenomegaly suggests either malignancy or the
transfusion (delayed hemolytic reaction). r Autoimmune disorders
presence of other underlying disorder (eg, hereditary
GENERAL PREVENTION r Infections (viral and bacterial)
spherocytosis, SCA, or systemic lupus erythematosus
r Medications and chemicals that are likely to trigger r Transfusions [SLE]).
hemolysis in patients with G6PD deficiency should r SCA r Leg ulcers may be found in the presence of SCA or
be avoided. r TTP other chronic hemolytic states.
r Patients with chronic hemolytic diseases (eg, SCA, r HUS
hereditary spherocytosis) should be provided DIAGNOSTIC TESTS & INTERPRETATION
r DIC
anticipatory guidance regarding the signs and r Porphyria Lab
symptoms of acute hemolysis and worsening Initial Lab Tests
r Eclampsia r Complete blood and reticulocyte counts should be
anemia.
r Malignant HTN obtained to determine degree of anemia and if bone
PATHOPHYSIOLOGY r Prosthetic valves marrow response is adequate:
There are 2 mechanisms of hemolysis: Peripheral blood smear should be examined.
r Intravascular: Destruction of RBCs in the circulation
Spherocytes and schistocytes are pathognomonic
with release of cell contents into the plasma of hemolysis.
r Extravascular: Removal and destruction of RBCs Platelets and WBCs should also be examined to
with membrane alterations by the macrophages of evaluate for coexisting hematologic or malignant
the spleen and liver disorders.
Thrombocytopenia occurs in SLE and
microangiopathic hemolytic anemia.
r Indirect bilirubin, lactate dehydrogenase (LDH), and
haptoglobin levels should be obtained:
Indirect bilirubin and LDH levels are increased
while haptoglobin levels are usually decreased in
the presence of acute hemolysis.
28
ACUTE HEMOLYTIC ANEMIA

A
r Direct antiglobulin test (direct Coombs test) should Second Line COMPLICATIONS
be performed to determine if hemolysis is immune r Plasmapheresis or plasma exchange is another If severe:
mediated. therapeutic option in cases of suspected AIHA. r Cardiopulmonary compromise
r Urinalysis will reveal the presence of hemoglobinuria Patients with IgM autoantibodies respond better to r Congestive cardiac failure
in cases of intravascular hemolysis. The urine plasmapheresis than do those with IgG r Neurologic dysfunction
dipstick will identify the presence of blood in the autoantibodies (5). r Shock
absence of RBCs. r Although intravenous immunoglobulin (IVIG) is an
r Multiorgan system failure
Imaging attractive option for adults with AIHA, children with
Chest radiograph may be useful in the evaluation of AIHA usually do not respond to IVIG therapy.
cardiopulmonary status. SURGERY/OTHER PROCEDURES REFERENCES
Diagnostic Procedures/Other Splenectomy may be necessary in patients with
hereditary spherocytosis, hereditary elliptocytosis, or 1. Gehrs BC, Friedberg RC. Autoimmune hemolytic
Bone marrow aspiration may be indicated for the anemia. Am J Hematol. 2002;69:258271.
evaluation of possible bone marrow failure or refractory AIHA.
2. Vaglio S, Arista MC, Perrone MP, et al. Autoimmune
malignancy. DISPOSITION hemolytic anemia in childhood: Serologic features
DIFFERENTIAL DIAGNOSIS Admission Criteria in 100 cases. Transfusion. 2007;47:5054.
r Refer to Commonly Associated Conditions. Critical care admission criteria: 3. Heisel MA, Ortega JA. Factors influencing prognosis
r Other causes of anemia, including anemia r Patients with severe anemia and evidence of in childhood autoimmune hemolytic anemia. Am J
secondary to decreased production of RBCs or blood cardiopulmonary compromise require admission to Hematol Oncol. 1983;5:147152.
loss, should be considered. an ICU setting. 4. Meytes D, Adler M, Viraq I, et al. High-dose
r Patients who are severely anemic but stable should methylprednisolone in acute immune cold
be admitted for diagnostic workup. hemolysis. N Engl J Med. 1985;312:318.
TREATMENT 5. Silberstein LE, Berkman EM. Plasma exchange in
Issues for Referral
Hematology consultation should be obtained for all autoimmune hemolytic anemia. J Clin Apheresis.
INITIAL STABILIZATION/THERAPY
r Maintain the airway, and assure adequate patients with suspected acute hemolytic anemia. 1983;1:238242.
ventilation. Supplemental oxygen should be
administered to increase the oxygen-carrying ADDITIONAL READING
capacity. FOLLOW-UP
r Maintain adequate circulation. See Also (Topic, Algorithm, Electronic
FOLLOW-UP RECOMMENDATIONS
r Transfusions should be avoided unless absolutely Discharge instructions and medications: Media Element)
necessary: r Immunizations against encapsulated organisms and r Anemia
Blood transfusion in patients with AIHA is r Aplastic Anemia
prophylactic penicillin therapy should be
extremely challenging because type matching and r Hyperbilirubinemia, Direct
administered to those with splenectomy or
cross matching may be difficult and the risk of compromised splenic function. r Hyperbilirubinemia, Indirect
acute hemolysis of transfused blood is high. r Anticipatory guidance regarding the need for r Jaundice
r Patients with severely compromised
immediate evaluation and treatment of fever should
cardiopulmonary status or life-threatening anemia also be provided to patients with splenectomy or
should be transfused: compromised splenic function. CODES
The least incompatible blood available should be r All patients should be educated about the signs and
used if transfusion is indicated. ICD9
symptoms of recurrent acute hemolysis.
Packed RBCs should be administered slowly in an r Folic acid should be administered to children with r 282.2 Anemias due to disorders of glutathione
effort to decrease cardiac stress and, in the case metabolism
of AIHA, to decrease the rapid destruction of chronic hemolysis.
r Iron therapy is indicated in patients with iron r 283.0 Autoimmune hemolytic anemias
transfused blood. r 283.9 Acquired hemolytic anemia, unspecified
r Children with suspected cold-reactive AIHA should deficiency secondary to ongoing losses or low iron
be placed in a warm environment. stores.
r Medications and other agents that may be Patient Monitoring
contributing to acute hemolysis should be Hemoglobin level, reticulocyte count, indirect bilirubin, PEARLS AND PITFALLS
discontinued. LDH, and haptoglobin should be monitored closely to r Anemia associated with hemolysis is usually
determine response to therapy. normocytic, but a marked reticulocytosis can lead to
MEDICATION
DIET an elevated measurement of mean corpuscular
First Line
Patients with G6PD deficiency should avoid foods volume.
Corticosteroids represent the best primary therapy for r The concomitant presence of certain conditions (eg,
AIHA, particularly in children with IgG autoantibodies. containing fava beans.
Desirable dosing regimens are variable and should be infections, chronic hemolysis) may mask the
PROGNOSIS diagnosis of acute hemolysis by elevating
discussed with the hematology consultant: r Prognosis depends on the underlying cause and
r Corticosteroids are not as effective in cold agglutinin haptoglobin levels.
baseline health status of affected individuals. r The direct Coombs test may be falsely negative in
disease (4). r In general, death rarely occurs with prompt
r Paroxysmal cold hemoglobinuria is usually some patients with autoimmune hemolytic anemia.
diagnosis and appropriate treatment. r Myoglobinuria can mimic hemoglobinuria on urine
self-limited, but some patients may require a short
dipstick.
course of corticosteroids.
29
ACUTE RENAL FAILURE

Rahul Kaila
Nirupama Kannikeswaran
r Reversible in initial stages but if not treated can lead

BASICS to hypoxic-ischemic acute tubular necrosis (ATN). DIAGNOSIS
r Renal: Ischemia/toxic insultparenchymal injury
DESCRIPTION cellular destruction; tubular injury leading to tubular HISTORY
r Acute renal failure is more appropriately referred to Volume losses such as vomiting, diarrhea, preceding
obstruction or tubular backleak leading to decreased
as acute kidney injury (AKI). filtration pressure leading to decreased GFR sore throat or pyoderma, bloody diarrhea in HUS,
r Definition: Acute reduction in kidney function r Postrenal: Obstruction of the urethra, bladder, or fever, chills in patients with infection sepsis, history of
characterized by a rapid decrease in the glomerular previous surgery, nephrotoxic drugs, antibiotics,
ureter causes increase in fluid pressure proximally
function rate (GFR) diuretics, oliguria, or anuria
and hence tubular damage and decrease in renal
r Two typesoliguric and nonoliguric: function. PHYSICAL EXAM
Oliguric/Anuric AKI: r Assess vial signs with attention to indications of
Urine output <500 mL/24 hr in older children ETIOLOGY
r Prerenal (most common): shock.
and 1 mL/kg in infants and children r Signs of dehydration such as tachycardia, dry
Nonoliguric AKI: Normal urine output. It has less GI losses (acute gastroenteritis)
Increased urinary loss (diabetes insipidus, mucous membranes, shock, edema associated with
morbidity, and mortality is less than that found 3rd spacing of fluids or secondary to renal failure
with oliguric AKI. diuretics)
Vasodilation (sepsis) itself
r Clinically, AKI is divided into categories of prerenal, r Petechiae and bleeding in systemic vasculitis,
Blood loss (trauma, surgery)
renal, and postrenal. suprapubic mass in postrenal causes, HTN, seizures,
r It manifests as impairments of nitrogenous waste Redistribution of extracellular fluid (heart failure,
nephrotic syndrome, cirrhosis) uremic pericarditis
excretion (increase in BUN, acid-base regulation r Distinguishing between de novo acute renal failure
Skin losses (burns)
[metabolic acidosis]), and water and electrolyte r Renal: vs. acute renal failure superimposed on chronic renal
regulation (oliguria, anuria, hyperkalemia). failure by the presence of failure to thrive, anemia,
Acute glomerulonephritis (most commonly
EPIDEMIOLOGY poststreptococcal) evidence of renal rickets, and maintenance of urine
r Incidence in children is 0.8 per 100,000 population Intrarenal vascular diseases (hemolytic uremic output in acute renal failure superimposed on
(1). syndrome [HUS]), renal artery/vein thrombosis in chronic renal failure
r Incidence in children is about 1/5 that of adults, newborns DIAGNOSTIC TESTS & INTERPRETATION
although it is increasing due to an increase in the Acute interstitial nephritis: Pyelonephritis, drug Lab
number of surgeries for congenital heart diseases, induced (methicillin and beta-lactam antibiotics), Initial Lab Tests
solid organ and bone marrow transplantation, and NSAIDs, quinolones r CBC with differential and peripheral blood smear
improved survival of very low birth weight babies. ATN secondary to nephrotoxic drugs r Electrolytes, BUN, creatinine, calcium, magnesium,
r Estimated 20 cases/yr/100,000 neonates (2) (aminoglycosides, amphotericin B, contrast
phosphorus
r Estimated 2 cases/yr/100,000 adolescents (2) agents, ibuprofen, acyclovir) and uric acid in r Urine analysis, urine electrolytes, urine protein, urine
tumor lysis syndrome
RISK FACTORS r Postrenal: creatinine
r Intrinsic kidney disease r ASO titers, complement levels C3/C4, anti-DNase B
Congenital (posterior urethral valves, ureteropelvic
r Stem cell transplant recipient titers
junction obstruction) r Prerenal findings:
r Sepsis with and without multisystem organ failure Acquired (urolithiasis, tumors such as abdominal
r Tumor lysis syndrome lymphomas and rhabdomyosarcomas) Normal urinary sediments
r Hypoxic-ischemic injury r In developed countries, renal ischemia and Increased BUN/creatinine ratio
r Nephrotoxic insult nephrotoxins are the leading cause of AKI as Urine osmolality >400500 mosmol/L,
r Postoperative cardiac patients opposed to developing countries where primary >350 mosmo/L in neonates (urine concentration
renal disease is the most common cause. in view of hypovolemia)
PATHOPHYSIOLOGY r Factitious AKI: Use of creatine, a popular dietary Urine sodium <1020 mEq/L (sodium retention in
r Prerenal: Volume depletion or decrease in effective view of hypovolemia)
supplement, causes dramatic elevations in serum
circulating volume secondary to 3rd spacing of fluids FENa (fractional excretion of sodium): (UNa +
and urinary creatinine that meet definitions of
leads to acute decline in renal perfusion, which in UCr :PNa + PCr ) 100 <1% (child)
AKI:
turn causes ischemia of renal cells leading to a FENa <2.5% (neonates)
Failure to recognize this in patients who are
decrease in GFR. creatine users, typically young athletes, may result
r Compensation by dilation of afferent arterioles
in misdiagnosis.
through release of vasodilators such as
prostaglandins COMMONLY ASSOCIATED CONDITIONS
r Hyperkalemia
r HTN
30
ACUTE RENAL FAILURE

A
r Renal pathology findings: r Hypocalcemia/hyperphosphatemia: Treat with
Urinary sedimentsRBC casts and granular casts calcium gluconate (10%) 0.51 mL/kg up to 10 mL FOLLOW-UP
Urine osmolality <350 mosmol/L (inability to r Antihypertensives:
concentrate the urine) If increased vascular tone is causing HTN, FOLLOW-UP RECOMMENDATIONS
Urine sodium >3040 mEq/L (ability to reabsorb administer antihypertensives (2). Discharge instructions and medications:
the sodium) If volume overload is causing HTN, administer r Take medications as prescribed, and follow up with
FENa >2%, low C3 (systemic lupus furosemide. a nephrologist.
erythematosus, membranoproliferative and Nifedipine 0.251 mg/kg/dose PO/sublingual,
poststreptococcal glomerulonephritis); low C4, DIET
max single dose 10 mg r Infants with AKI: Formula low in phosphorus
ASO titers, anti-DNase B titers in patients with Labetalol 0.21 mg/kg IV q10min, max single r Older children: Protein with high biologic value
poststreptococcal glomerulonephritis dose 20 mg
Imaging Hydralazine 0.10.2 mg/kg IV q4h, max single PROGNOSIS
r Prerenal: Normal renal US and renal scan dose 40 mg Depends on need for dialysis, age of the patient, and
r Renal: Renal scandelay in accumulation and Sodium nitroprusside 0.050.1 g/kg/min IV, max underlying condition. Those of young age with
absence of excretion from collecting tubule of single dose 10 g/kg/min multisystem organ failure have a worse prognosis.
radioisotope in areas of parenchymal damage; SURGERY/OTHER PROCEDURES COMPLICATIONS
identifies areas of normal or poor perfusion and Renal replacement therapy: When medical r Seizures secondary to uremia
poor renal function management fails to restore kidney function, use r CHF secondary to HTN
r Postrenal: Renal US shows dilated renal pelvis. Use dialysis. Indications for initiating dialysis include: r Hypertensive encephalopathy
abdominal US in cases of suspected abdominal r Serum urea nitrogen >150 mg/dL r Hyperkalemia, dysrhythmia
mass. r Serum creatinine >10 mg/dL
r Voiding cystourethrogram for suspected posterior r Potassium >6.5 mEq/L (6.5 mmol/L), with T-wave
urethral valves elevation not corrected by medical means REFERENCES
r Renal scan shows isotopic collection at any level of r Severe metabolic acidosis with serum bicarbonate
ureter or bladder depending upon the obstruction 1. Moghal NE, Brocklebank JT, Meadow SR. A review
persistently <10 mEq/L and not relieved by of acute renal failure in children: Incidence, etiology
and absence/delay of excretion of the isotope. bicarbonate therapy and outcome. Clin Nephrol. 1998;49(2):9195.
DIFFERENTIAL DIAGNOSIS r CHF and fluid overload
2. Bunchman TE. Treatment of acute kidney injury in
Prerenal, renal, and postrenal acute renal failure are DISPOSITION children: From conservative management to renal
differentiated by using urinary indices, urine replacement therapy. Nat Clin Pract Nephrol.
osmolality, and imaging studies. Admission Criteria
r Any patient requiring dialysis 2008;4(9):510514.
r AKI patients who are hemodynamically unstable
TREATMENT r Electrolyte imbalances such as life-threatening
ADDITIONAL READING
hyperkalemia
INITIAL STABILIZATION/THERAPY r Hypertensive emergency or urgency Whyte DA, Fine RN. Acute renal failure in children.
r Fluid therapy: In an oliguric and hemodynamically r Multisystem organ failure Pediatr Rev. 2008;29(9):299307.
unstable patient, give 20 cc/kg of isotonic fluid in r Critical care admission criteria:
repeated boluses as necessary.
r Correct electrolytes. Unstable vital signs
CODES
r Hyperkalemia: ECGtall, peaked T waves: Discharge Criteria
r Follow up with nephrologist.
See Hyperkalemia topic for detailed management r Electrolyte abnormalities corrected within ICD9
instructions, including the use of calcium r 584.5 Acute kidney failure with lesion of tubular
gluconate, sodium bicarbonate, insulin/ acceptable limits
r Vital signs within acceptable limits necrosis
glucose, or albuterol. r 584.9 Acute kidney failure, unspecified
MEDICATION Issues for Referral
r Furosemide 2 mg/kg PO/IV q6h: Refer to nephrologist.
Indicated in edematous hypertensive child with COMPLEMENTARY & ALTERNATIVE PEARLS AND PITFALLS
signs of fluid overload needing immediate fluid THERAPIES r Hyperkalemia is the most common life-threatening
removal Use of mannitol or low-dose dopamine is still complication of AKI.
Use lower dose if patient is hypotensive controversial and clinically not recommended. r Diagnosing and treating severe hyperkalemia is
0.5 mg/kg initially; may repeat q2h until reaching
2 mg/kg q6h critical. Assess serum potassium and ECG.
r Sodium bicarbonate 0.51 mEq/kg IV given over r If there are elevations of serum and/or urinary
30 min; repeat PRN: creatinine in heathy persons, exclude use of creatine
May also calculate dose using 0.6 Body weight supplements as factious cause.
(Desired HCO3 Current HCO3 )/2. Monitor for
hypocalcemia.
Use to treat severe metabolic acidosis; pH <7.2
with inadequate respiratory compensation and
acidosis causing hyperkalemia
31
ACUTE RESPIRATORY FAILURE

Sean E. Button
Raymond Pitetti
ETIOLOGY PHYSICAL EXAM

BASICS r Chronic conditions that can lead to acute failure: r Assess vital signs with particular attention to
Poorly controlled asthma respiratory rate, oxygen saturation, and
DESCRIPTION CF temperature
Inability of the respiratory system to maintain Myopathy Measurement of oral temperature is not advised,
appropriate gas exchange to meet the metabolic Cardiac patients have difficulty keeping mouth closed for
demands of the body: Muscular dystrophy duration of time necessary to obtain sublingual
r Arterial oxygen tension falls below 60mm Hg (acute Acute conditions temperature reading
hypoxemia) r Failure of central nervous system drive: r General appearanceappears well or sick, work of
r CO tension rises above 50mm Hg (acute Drug intoxication (eg opioids, alcohol) breathing, GCS.
2
hypercarbia) Head trauma r Vitals: Respiratory rate, blood pressure, pulse
r With history of chronic respiratory failure an acute Intracranial hemorrhage oximetry.
r Pulmonary embolism r HEENT: Grunting, nasal flaring, stridor, head
respiratory failure is diagnosed by an increase in
PCO2 of 20 mm Hg from baseline r Inborn errors of metabolism bobbing.
r Arterial pH drops below 7.35 r Airway obstruction: r Cardiac: Murmur, muffled heart sounds, gallop
Croup r Lungs: Aeration, symmetry, stridor, stertor, wheeze,
EPIDEMIOLOGY
Epiglottitis rales, rhonchi, work of breathing and accessory
Inversely related to age: 2/3 of cases occur during
Anaphylaxis muscle use,
infancy1/2 of which are in neonatal period. r Skin: Skin temperature, color, perfusion of skin,
Bronchoconstriction
RISK FACTORS Foreign body aspiration capillary refill.
r Young age: Airway burn
Size of airway: Smaller in younger children Drowning DIAGNOSTIC TESTS & INTERPRETATION
Infants and young children have a large tongue r Lung/Alveolar injury: Lab
that can fill the oropharynx Septic shock/Systemic Inflammatory Response Initial Lab Tests
Respiratory center is immature in infants and r Blood gas:
Syndrome
younger children Pulmonary contusion Venous or capillary blood gas is less invasive, but
Greater compliance of thoracic cage relative to Airway burn is only useful if parameters are within normal or
older children/adults leads to a lower functional Drowning acceptable limits; useful for negative predictive
residual capacity r Pulmonary embolism value of respiratory failure
Marginal energy stores in infantsdiaphragm r Mechanical: Arterial blood gas- optimal measurement but
fatigues easily. Flail chest invasive and greater risk of injury
r Prematurity r Hemoglobin cooximetry:
Pneumothorax/Hemothorax
r Chronic lung disease (eg, CF, myopathy, asthma, Carboxyhemoglobin
RSV) COMMONLY ASSOCIATED CONDITIONS Methemoglobin
r Prematurity r CBC and differential
r Cardiac disease
r Lower respiratory infections: r CRP
GENERAL PREVENTION Pneumonia r Basic chemistry assay
Use of corticosteroids prior to delivery in preterm Bronchiolitis r Ammonia: Inborn error of metabolism
patients r Asthma
r Blood culture
PATHOPHYSIOLOGY r Respiratory viral Panel
r Inability of respiratory system to provide sufficient r Sputum culture
DIAGNOSIS
oxygen to meet metabolic needs or to excrete
enough CO2 produced by body. HISTORY Imaging
r 3 basic abnormalities account for most cases of r Pre-existing conditions r CXR: Pneumonia, pulmonary edema, pleural
acute respiratory failure: r Onset of symptoms effusion, pneumothorax, rib fractures
r Events surrounding onset of symptoms: r CT chest: Empyema, pulmonary embolism,
V/Q mismatch: determines adequacy of gas
exchange in the lung. V/Q ratio <1 throughout r Sudden or progressive onset of symptoms r Airway CT scanning, MRI and angiography can be
the lung results in hypoxemia r Systemic signs such as fever, cough, respiratory used to differentiate deep-tissue structures, bony
Intrapulmonary shunt distress, stridor, apnea, color changes, weakness, lesions and vascular abnormalities
Hypoventilation paralysis, headache Diagnostic Procedures/Other
r Pain r Bronchoalveolar lavage: Identify specific infectious
pathogen
r Lung biopsy
r Bronchoscopy
r Thoracentesis
r Pneumogram
Extensivesee Etiology.
32
ACUTE RESPIRATORY FAILURE

A
Discharge Criteria
r Resolution of underlying illness to acceptable degree
ADDITIONAL READING
TREATMENT r Ability for independent respirations or adequate Nitu ME, Eigen H. Respiratory failure. Pediatrics Rev.
PRE HOSPITAL respiratory status with mechanically assisted 2009;30(12):470478.
r Assess and stabilize airway, breathing, and respiration as outpatient (home oxygen, nasal See Also (Topic, Algorithm, Electronic
circulation CPAPA/BiPAPA) Media Element)
r Administer supplemental oxygen r Bronchiolitis
Issues for Referral
r Consider nasal or oral airway r Patients with acute respiratory failure should be r Croup
r Administer necessary medications as per local referred to an institution capable of the continuous r Epiglottitis
protocol (eg, Albuterol for wheezing, nebulized management, ongoing evaluation, and level of r Pneumonia
epinephrine for croup, parenteral epinephrine for expertise that will be necessary to care for such r Pneumothorax
anaphylaxis or severe asthma) patients. r Trauma-Chest
r The underlying diagnosis may necessitate
r Assess and stabilize airway, breathing, and subspecialist consultation (eg, neurology,
circulation cardiology, pulmonology, and ENT) CODES
r Treatment partly determined by underlying diagnosis
r Close ongoing monitoring is necessary:
FOLLOW-UP ICD9
r 518.81 Acute respiratory failure
Pulse oximetry and capnography
Respiratory status, including respiratory rate and FOLLOW-UP RECOMMENDATIONS r 770.84 Respiratory failure of newborn
work of breathing Discharge instructions and medications
Cardiovascular status, including perfusion, heart r Vary according to condition.
rate and capillary refill rate r Certain conditions will require continued use of PEARLS AND PITFALLS
Neurologic status medication:
Serial blood gas analysis r Pearls:
Bronchodilators, corticosteroids for asthma
exacerbations Prompt recognition of acute respiratory failure and
MEDICATION appropriate intervention can prevent the
First Line Oral antibiotic therapy for pneumonia
progression to cardiopulmonary arrest.
r Depends on working diagnosissee specific PROGNOSIS Always anticipate a difficult airway prior to
algorithm. Dependent on diagnosis and/or response to intubation
r Bronchoconstriction: treatment Use of venous or capillary blood gas is less
Albuterol, ipratropium, racemic epinephrine, invasive and if normal or acceptable values,
COMPLICATIONS
terbutaline, corticosteroid, magnesium as r Shock arterial blood gas sampling may be avoided
appropriate for condition r Long-term need for ventilatory support r Pitfalls:
Asthma r Permanent neurologic injury Failing to recognize impending respiratory failure.
Reactive airway disease Failure to aggressively manage acute respiratory
r Death
Bronchiolitis failure with assisted ventilations.
Allergic reaction Failure to provide continuous evaluation, and
r Stridor: treatment.
Racemic epinephrine, corticosteroid, parenteral
REFERENCES
Failure to recognize reversible causes of acute
epinephrine, heliox as appropriate for condition 1. Priestley MA, Helfaer MA. Approaches in the respiratory failure.
Croup management of acute respiratory failure in
Epiglottitis children. Curr Opin Pediatr. 2004;16:293298.
Allergic reaction 2. Schramm CM. Current concepts of respiratory
r Pneumonia
complications of neuromuscular disease in children.
r Parenteral antibiotic Curr Opin Pediatr. 2000;12:203207.
COMPLEMENTARY & ALTERNATIVE 3. Brochard L. Noninvasive ventilation for acute
THERAPIES respiratory failure. JAMA. 2002;288:932935.
r BiPAP 4. Cheifetz I. Invasive and noninvasive pediatric
r Nasal CPAP mechanical ventilation. Respir Care. 2003;48:
442458.
SURGERY/OTHER PROCEDURES 5. Arnold J. High-frequency ventilation in the pediatric
r Arterial catheter placement for frequent atrial blood
intensive care unit. Pediatr Crit Care Med. 2000;1:
sampling 9399.
r Nasal suction (deep, bulb)
r Needle thoracostomy
r Chest Tube
r Cricothyroidotomy
DISPOSITION
Admission Criteria
r Critical care admission criteria
r All patients with acute respiratory failure should be
admitted to the intensive care unit
33
ADRENAL INSUFFICIENCY
Kevin Ching
r Adrenal medulla:
BASICS Epinephrine and norepinephrinemediated by DIAGNOSIS
sympathetic stimulation
DESCRIPTION HISTORY
r Adrenal insufficiency is characterized by a deficiency ETIOLOGY r Chronic adrenal insufficiency:
r Primary adrenal insufficiency (2):
in the production and availability of adrenocortical Fatigue and weakness
hormones: CAH: Anorexia
21-hydroxylase deficiency: Neonates often Weight loss
In primary adrenal insufficiency, adrenal
dysfunction impairs glucocorticoid and present with salt-wasting CAH (hyponatremia, Nausea and vomiting
mineralocorticoid production. hyperkalemia, acidosis, and hypotension, with Recurrent abdominal pain
In secondary adrenal insufficiency, deficient ambiguous genitalia in females), while Skin pigmentation
corticotropin-releasing hormone (CRH) from the prepubertal children present with virilizing CAH. r Acute adrenal insufficiency (adrenal crisis):
Several other forms of CAH exist, including salt Neonates:
hypothalamus or adrenocorticotropic hormone
(ACTH) from the pituitary impairs adrenal wasting and nonsalt wasting. Lethargy
glucocorticoid production (mineralocorticoid Infection: Vomiting and diarrhea
Tuberculosis (TB), HIV, cryptococcosis, or fungal Weight loss
production is preserved).
r Acute adrenal insufficiency (adrenal crisis) is a infections (histoplasmosis, blastomycosis, or Seizures
coccidiomycosis) Children:
life-threatening emergency involving hypotensive
Autoimmune disease (Addison): Altered mental status
shock that ensues primarily from mineralocorticoid Comorbid autoimmune polyglandular
deficiency: Syncope
syndromes (type 1 diabetes, hypothyroidism, Seizures
Rare in children
etc.) Weakness
Nonspecific presentation often leads to delay in
Adrenal hemorrhage or infarction: Fever
diagnosis and treatment. Waterhouse-Friderichsen syndrome (Neisseria Severe abdominal pain
EPIDEMIOLOGY meningitidis, Streptococcus pneumoniae, Vomiting and diarrhea
Incidence Staphylococcus aureus, Pseudomonas Weight loss
r Incidence of primary adrenal insufficiency is aeruginosa) Skin pigmentation
unknown: Anticoagulant use
Congenital adrenal hyperplasia (CAH), the most Antiphospholipid syndrome PHYSICAL EXAM
r Chronic adrenal insufficiency:
common form of primary adrenal insufficiency, Septic shock:
occurs in 1 of 15,000 births (1). Critically ill patients may develop a relative Often subtle and nonspecific
r Although the incidence of secondary adrenal adrenal insufficiency (3). r Acute adrenal insufficiency (adrenal crisis):
insufficiency is also unknown, iatrogenic Etomidate: Fever
suppression of the hypothalamic-pituitary axis from Sedation agent used in rapid sequence Tachycardia
corticosteroid therapy is more common. induction and procedural sedation Dehydration
Reversible inhibition of cortisol production Hypotension
PATHOPHYSIOLOGY Unclear clinical significance in critically injured Shock
r Adrenal cortex: Altered mental status
trauma patients and critically ill patients with
Aldosteroneprimarily mediated by septic shock (4,5) Coma
renin-angiotensin system: r Secondary adrenal insufficiency:
Also stimulated by hyperkalemia DIAGNOSTIC TESTS & INTERPRETATION
Suppression by exogenous corticosteroid therapy
Aldosterone deficiency leads to hyponatremia, or endogenous steroid production (tumor)
Lab
hyperkalemia, and acidosis. Initial Lab Tests
Hypothalamic-pituitary disease: r Serum chemistries:
Cortisol and androgensmediated by ACTH and Trauma
CRH: Pituitary surgery Hyponatremia, hyperkalemia, metabolic acidosis,
Cortisol, in turn, inhibits both CRH and ACTH. Neoplasm (eg, craniopharyngioma) and hypoglycemia
Glucocorticoid (cortisol) deficiency can lead to r Cortisol level:
Congenital aplasia
hypoglycemia, hypotension, and shock. Obtain early morning sample, if possible.
Upregulation of ACTH increases Under conditions of severe stress, levels
melanocyte-stimulating hormone. <20 g/dL indicate adrenal insufficiency.
Androgen deficiency leads to diminished axillary r Serum ACTH
and pubic hair. r Plasma renin activity
r Serum aldosterone
r Thyroid studies
r CBC
r Blood cultures as indicated
34
ADRENAL INSUFFICIENCY
A
Imaging r Administer glucocorticoid: COMPLICATIONS
r Consider abdominal CT scan: Hydrocortisone: r Hypoglycemia
Identify adrenal hemorrhage, calcifications, and If acute adrenal insufficiency suspected, r Hypotension
infiltrative and metastatic diseases. administer stress dose immediately. r Shock
r Consider chest radiograph: Provides both glucocorticoid and r Sepsis
Identify TB, fungal pneumonias mineralocorticoid activity
Infants/toddlers (<3 yr): 25 mg IV/IM
Diagnostic Procedures/Other Children: 50 mg IV/IM
r ECG: REFERENCES
Adolescents (>12 yr): 100 mg IV/IM
Hyperkalemia may manifest as peaked T waves, Follow with 150 mg/day divided q68h 1. Perry R, Kecha O, Paquette J, et al. Primary adrenal
shortened QTc. Maintenance dosing in consultation with an insufficiency in children: Twenty years experience at
r ACTH stimulation test:
endocrinologist the Sainte-Justine Hospital, Montreal. J Clin
Obtain baseline serum cortisol and ACTH levels. Dexamethasone: Endocrinol Metab. 2005;90:32433250.
Administer 250 g IV cosyntropin (synthetic May be administered without interfering with 2. Arlt W, Allolio B. Adrenal insufficiency. Lancet.
ACTH). ACTH stimulation test 2003;361:18811893.
Check serum cortisol levels every 30 min. Negligible mineralocorticoid activity 3. Sarthi M, Lodha R, Vivekanandhan S, et al. Adrenal
Failure of cortisol to rise appropriately indicates 0.030.15 mg/kg/day IV divided q612h status in children with septic shock using low-dose
insufficiency.
Pregnancy Considerations stimulation test. Pediatr Crit Care Med. 2007;8:
DIFFERENTIAL DIAGNOSIS Crosses placenta and suppresses fetal adrenal 2328.
r CAH 4. Cotton BA, Guillamondequi OD, Fleming SB, et al.
r Infectious adrenalitis function:
r Consider fludrocortisone at 0.10.2 mg PO. Increased risk of adrenal insufficiency following
r Autoimmune polyglandular syndrome etomidate exposure in critically injured patients.
r Necessary if dexamethasone is given
r Adrenal hemorrhage Arch Surg. 2008;143:6267.
r Mineralocorticoid dose is NOT weight based.
r Hypopituitarism 5. Jackson WL. Should we use etomidate as an
r Sepsis Second Line induction agent for endotracheal intubation in
r Differential for abdominal pain (eg, acute Vasopressors for refractory hypotension: patients with septic shock? A critical appraisal.
r Dopamine 120 g/kg/min IV Chest. 2005;127:10311038.
appendicitis)
r Epinephrine 0.11 g/kg/min IV
r Norepinephrine 0.11 g/kg/min IV ADDITIONAL READING
TREATMENT
DISPOSITION Oelkers W. Adrenal insufficiency. N Engl J Med.
INITIAL STABILIZATION/THERAPY Admission Criteria 1996;335:12061212.
Critical care admission criteria:
circulation. r Necessary for all presentations of acute adrenal See Also (Topic, Algorithm, Electronic
r Aggressive volume resuscitation: Media Element)
insufficiency (adrenal crisis) Congenital Adrenal Hyperplasia
Bolus of 20 cc/kg of isotonic crystalloid; may
repeat as needed Issues for Referral
r Dextrose: Manage in consultation with an endocrinologist.
0.51 g/kg IV (2 mL/kg of 25% dextrose or CODES
5 mL/kg of 10% dextrose) if hypoglycemic
r Identify precipitant, and consider empiric antibiotics. FOLLOW-UP ICD9
r 255.2 Adrenogenital disorders
MEDICATION FOLLOW-UP RECOMMENDATIONS
r 255.41 Glucocorticoid deficiency
First Line Patient Monitoring
r Correct hyperkalemia: r Monitor and correct hypoglycemia and electrolyte
Calcium: abnormalities.
Calcium gluconate 100 mg/kg/dose IV of 10%
r Ensure appropriate fluid replacement therapy. PEARLS AND PITFALLS
r Monitor and adjust glucocorticoid maintenance r Immediate therapeutic intervention is frequently
solution over 35 min
Calcium chloride 20 mg/kg/dose IV of 10% dosing. necessary prior to diagnostic confirmation.
solution over 5 min (requires central venous r Presentation may be similar in sepsis or
access) disseminated intravascular coagulation.
Insulin and glucose: r Consider in critically ill patients with
Insulin 0.1 units/kg IV over 30 min
pressor-dependent or refractory shock.
Dextrose 0.5 g/kg IV over 30 min r As little as 2 wk of exogenous corticosteroid therapy
Sodium bicarbonate:
12 mEq/kg IV can suppress the hypothalamic-pituitary axis.
35
AGITATION
Marsha Ayzen Elkhunovich
Emily L. Willner
r Psychiatric: r Neurologic exam (as complete as patient

BASICS Manic episode in patient with bipolar disorder cooperation allows). Important elements include:
Severe depression (particularly if actively suicidal) Pupil size and reactivity
DESCRIPTION Acute psychosis in patient with schizophrenia; Gross neurologic abnormalities
r Agitation is restlessness, increased tension, and/or delusional disorder; or antisocial, paranoid, or Nuchal rigidity
irritability that can present with psychomotor borderline personality disorder Cognitive function
disturbances ranging from twitching or pacing to Severe anxiety r Look for signs of physical injury/trauma (especially
violent behavior, with or without altered level of Posttraumatic stress disorder to the head).
awareness. Autism r If possible, perform ophthalmologic and funduscopic
r It may occur in patients with an intoxication, a ADHD exams to assess vision and check for increased ICP.
psychiatric condition, as a result of an organic Conduct disorder or reaction to an acute stressor r Thorough cardiac, respiratory, abdominal, and skin
cause, or, in the case of developmentally Night terrors (common in normal children) exams to look for signs of systemic illness
delayed/minimally verbal children, as a r In a developmentally delayed or preverbal child, all r Psychiatric evaluation to assess for
manifestation of pain or distress. of the above etiologies are possible, but consider suicidal/homicidal ideation, psychosis, and level of
PATHOPHYSIOLOGY other disturbances that the child might be unable to awareness
r The unifying pathophysiology corresponds to the communicate: r Agitated children with developmental delay need an
precipitating etiology. Pain due to fracture, corneal abrasion, hair
especially detailed physical exam, including
r The current understanding is that psychomotor tourniquet, testicular torsion, renal stone, etc.
extremities (for fracture, hair tourniquet), HEENT
Infection due to pharyngitis, otitis media,
agitation results from dysregulation of the (ear or dental infection), abdomen (infection,
appendicitis, meningitis, urinary tract infection,
dopaminergic, noradrenergic, GABAergic, and constipation), and genitalia (hernia, torsion). See
etc.
serotonergic systems, the combination of which Crying/Colic topic.
Child abuse
causes these symptoms (1). However, sometimes an DIAGNOSTIC TESTS & INTERPRETATION
Change in the home/school environment
agitated state can result from an inability to
communicate, as in the example of a Lab
The extent of lab evaluation will depend on the clinical
developmentally delayed child. DIAGNOSIS presentation. Consider any of the following lab tests
ETIOLOGY HISTORY initially, depending on the clinical presentation.
r Toxicologic:
r Acute or chronic/recurrent (duration of symptoms) Initial Lab Tests
Alcohol r Underlying conditions (eg, developmental delay, r Dextrose stick
Cocaine, methamphetamines r Blood alcohol level
Hallucinogens such as PCP, Ecstasy (MDMA), autism, psychiatric condition, diabetes, SLE)
r Possible ingestions/exposures r Basic metabolic panel to look for electrolyte
jimson weed, etc.
r Current medications derangements associated with poisoning or
Postanesthesia emergence
Akathisia or paradoxical reaction (eg, to r Recent illness: SIADH/cerebral salt wasting associated with various
Streptococcal infection might suggest Sydenham neurologic conditions
metoclopramide, benzodiazepines, r LFTs and ammonia level if suspicious for hepatic
diphenhydramine) chorea or PANDAS.
Ingestion/Overdose (eg, to psychoactive drugs, Sinusitis might raise concern for intracranial encephalopathy
r Rapid strep test, anti streptolysin-O titers
amphetamine derivatives, NSAIDs, amantadine, extension/infection.
and many others) Viral symptoms might suggest ADEM or viral r Thyroid function tests
Medication side effects (eg, antipsychotics) encephalitis/meningitis. r Testing of carbon monoxide level
Withdrawal (eg, opiates) r Systemic symptoms: Fevers, vomiting, rash, arthritis, r CBC and blood culture if meningitis is suspected
r Medical: respiratory distress r Lumbar puncture if febrile or suspicious for
Encephalitis: Viral, autoimmune, paraneoplastic, r Neurologic symptoms: Gait changes, headache, encephalitis/meningitis:
or antibody mediated, such as anti-NMDA weakness Bacterial cultures, Lyme titers, and viral
receptor r Family history PCR/cultures for potential causes of viral
Meningitis r Allergies meningoencephalitis
Seizure (especially frontal or temporal lobe) See Meningitis, Lyme Disease, and Encephalitis
Atypical migraine: Confusional PHYSICAL EXAM topics for details.
r During the initial evaluation, make sure to assess if
Acute disseminated encephalomyelitis (ADEM) r If performing a lumbar puncture, consider consulting
Hypoglycemia the patient is a threat to himself or others.
r Vital signs: a neurologist regarding specific tests to be sent from
Hypoxemia or hypercarbia the spinal fluid.
Carbon monoxide poisoning Tachypnea is likely to be present in an agitated
Hyperthyroidism state, but frank respiratory distress and/or Imaging
Encephalopathy: Hypertensive, hepatic, systemic hypoxemia suggest an underlying cardiac or Imaging may be indicated based on clinical
lupus erythematosus (SLE) respiratory etiology. presentation:
Tachycardia is common in agitated patients but r Consider urgent head CT if concerned about
Poststreptococcal: Sydenham chorea, pediatric
autoimmune neuropsychiatric disorders associated may be seen with a toxidrome or a physical increased ICP or intracranial mass, hemorrhage, or
with streptococcus (PANDAS) illness: injury.
Traumatic brain injury Tachyarrhythmias may cause agitation in a r Consider ordering an MRI if a brain lesion or
preverbal or developmentally delayed child. autoimmune process is suspected.
Fever may indicate febrile delirium or an infectious r Nonverbal/Delayed children may need additional
or autoimmune cause. imaging to evaluate for painful or infectious
HTN is common in agitated patients. However, it conditions.
can also be caused by pain, toxic
exposures/ingestions, or increased intracranial Diagnostic Procedures/Other
pressure (ICP). Consider co-oximetry if carbon monoxide poisoning is
suspected.
36
AGITATION
A
DISPOSITION
TREATMENT Admission Criteria FOLLOW-UP
r Significant vital sign abnormalities
PRE HOSPITAL r Respiratory distress FOLLOW-UP RECOMMENDATIONS
Advise EMS personnel to: r Risk of harm to self/others Follow-up recommendations depend on the etiology
r Try to reassure the patient with calm voices and r Inability of caretaker to care for patient of the patients agitated state. Most patients who
present to the emergency department with agitation
decrease stimulation if at all possible. r Impaired neurologic state
r Decrease risk of harm to the patient and others. due to psychiatric or behavioral causes will require
r Need for further diagnostic or therapeutic follow-up with psychiatric or behavioral services.
EMS protocols may include IM sedation with procedures
benzodiazepines. r Critical care admission criteria:
INITIAL STABILIZATION/THERAPY Need for ventilator support because of inability to REFERENCES
r ABCs: Ensure that the patient is adequately control airway or need for significant sedation 1. Lindenmayer JP. The pathophysiology of agitation. J
protecting his or her airway, and stabilize breathing Deteriorating neurologic status Clin Psychiatry. 2000;61(Suppl 14):510.
and circulation abnormalities. Risk of cardiovascular depression or arrhythmia 2. Yildiz A, Sachs S, Turgay A. Pharmacological
r Ensure physical safety of patient, caregiver, and from an ingestion management of agitation in emergency settings.
medical staff. Issues for Referral Emerg Med J. 2003;20(4):339346.
r Verbal reassurance and redirection should be used r If an ingestion is suspected, consultation with a 3. Sorrentino A. Chemical restraints for the agitated,
for all patients. toxicologist or the poison control center is crucial for violent, or psychotic pediatric patient in the
r Chemical restraints can and should be used to identifying optimal treatment. emergency department: Controversies and
protect the patient and health care staff and allow r Consultation with a neurologist is indicated in recommendations. Curr Opin Pediatr. 2004;16(2):
for patient exam and treatment when verbal instances of abnormal neurologic exams and when 201205.
redirection is not adequate. ADEM or encephalitis are suspected. 4. Hilt RJ, Woodward TA. Agitation treatment for
r Consultation with social work services and/or pediatric emergency patients. J Am Acad Child
MEDICATION
r Consider options for chemical restraint as needed. psychiatry is indicated for patients with ingestion, Adolesc Psychiatry. 2008;47(2):132138.
r Benzodiazepines, alone or in combination with overdose, a psychiatric condition, or homicidal or
suicidal ideation for further investigation and
antipsychotics (2): ADDITIONAL READING
potential need for placement in protective care.
Midazolam PO dosing 0.250.5 mg/kg, max
single dose 10 mg, IM/IV dosing 0.1 mg/kg, max COMPLEMENTARY & ALTERNATIVE Dorfman DH. The use of physical and chemical
single dose 6 mg THERAPIES restraints in the pediatric emergency department.
Lorazepam PO/IM/IV 0.05 mg/kg/dose, max single r Physical restraints can be used if alternate measures Pediatr Emerg Care. 2000;16(5):355360.
dose 2 mg are ineffective:
r Atypical antipsychotics: Preferred over classical 4-point physical restraint is optimal.
antipsychotics due to more favorable side effect Subdue the patient with 45 staff members, with CODES
profile one restraining each extremity and one securing
Risperidone (Risperdal): the head. ICD9
PO dosing: 0.25 mg/dose in children 614 yr; It is essential to continually reassess the need for 307.9 Other and unspecified special symptoms or
0.5 mg >14 yr restraints and frequently monitor restrained syndromes, not elsewhere classified
r Classical antipsychotics: Haloperidol IM/IV/PO: patients, as there are risks for further harm with
IM dosing: 612 yr, 13 mg IM/IV; >12 yr, their use.
25 mg IM/IV r Further therapy depends on the etiology of the PEARLS AND PITFALLS
PO dosing: 0.25 mg/dose agitated state.
r Agitated behavior can be caused by a large number
Ziprasidone (Geodon) IM (4): Pregnancy Considerations
IM dosing: Children >12 yr, 1020 mg, dose r Haloperidol (Haldol) is potentially embryotoxic in of organic and psychiatric etiologies, and a detailed
may be repeated q2h (max daily dose 40 mg) history and physical exam is essential to limit the
high doses, so this drug should be avoided in considerations and to direct evaluation and
Olanzapine (Zyprexa) PO/IM (4): pregnancy if possible.
PO dosing: 2.55 mg in children >12 yr treatment.
r There is little literature on the safety of atypical r A developmentally delayed child with agitation
IM dosing: Children >12 yr, 5 mg; consider
using 2.5 mg dose in children <40 kg antipsychotics in those who are pregnant/lactating, needs broad consideration of medical etiologies that
Olanzapine and risperidone are available in oral but no evidence of teratogenicity has been found. may be causing distress prior to diagnosing a
disintergrating wafers that can be administered to primarily behavioral or psychiatric condition.
minimally cooperative patients without the need r All patients with acute agitation should be under
for IM or IV access close supervision. Proper documentation and use of
institution-specific protocol for restraints is
ALERT mandated by the Joint Commission.
r Use with caution when chemically restraining
patients with developmental delay and no prior
psychiatric diagnoses.
r These patients need a thorough medical
evaluation even if agitation improves with
chemical restraint.
37
ALTERED LEVEL OF CONSCIOUSNESS/COMA

Vincent J. Wang
r Infectious: r Mnemonic to remember the broad differential listed

BASICS Meningitis: Bacterial, viral, fungal, parasitic, and aboveMOVESTUPID (adapted from adult version):
mycobacterial Metabolicinborn errors of metabolism, Reye
DESCRIPTION Encephalitis: Bacterial and viral syndrome, etc.
r Altered level of consciousness (ALOC): Intracranial abscess or empyema Oxygen insufficiencypulmonary, cardiac,
Depressed level of consciousness (LOC) rather Tickborne illnesses (eg, Rocky Mountain spotted anemia; also, hypercarbia
than increased alertness fever) Vascular/Cardiac causeshypertensive
See Crying/Colic and Agitation topics for other Meningococcemia, disseminated intravascular emergency, ischemic/hemorrhagic CVA, Vasculitis;
changes in behavior. coagulation VPS malfunction; Vitamin deficiency
r ALOC is a spectrum: r Vascular/Cardiac: Endocrinehypo- or hyperglycemia, DKA;
Confusion: Disoriented with delayed or impaired Bradyarrhythmias may result in inadequate heart Electrolyte abnormalities; Envenomations
thinking or responses, but awake rate, leading to hypotension or shock. Seizuresactive, postictal, and nonconvulsive
Lethargy/Somnolence: Mild depressed LOC, but Tachyarrhythmias may result in ineffective cardiac status epilepticus
the patient remains easily arousable contractions and resultant shock. Tumor; Trauma; Temperature; Toxins
Obtundation: Increasing depression of LOC, Myocardial infarction Uremiarenal or hepatic dysfunction with
significant difficulty to arouse Hypotension hepatic encephalopathy
Coma: Alteration in LOC with no purposeful HTN Psychiatric; Porphyria
movement or awareness; not arousable Vasculitis: Henoch-Schonlein purpura, systemic Infection; Intussusception
r Objective measures to describe LOC: lupus erythematosus Drugs, including withdrawal
Glasgow Coma Scale (GCS): 15-point scale r Metabolic: r Other mnemonics: DPT OPV HIB MMR (1) or AEIOU
quantifying eye opening, verbal, and motor Hyperglycemia: Diabetic ketoacidosis (DKA) TIPS
responses: Hypoglycemia: Sepsis, toxicologic ingestion
Modifications for preverbal children Metabolic acidosis/alkalosis
AVPU: Alert, responsive to Verbal stimuli, Dehydration
DIAGNOSIS
responsive to Painful stimuli, Unresponsive Electrolyte abnormalities: Sodium, potassium, HISTORY
calcium, magnesium, and phosphorous r Obtain history of the patients baseline activity.
GENERAL PREVENTION
r Wearing helmets and protective gear in appropriate Hyperammonemia: Urea cycle defects r Trauma time and mechanism if applicable
physical activity Renal failure r Toxicologic exposure if applicable:
r Secure storage of medications Hepatic failure: Toxic, drug induced, Reye Time and exposure
syndrome, infectious, obstructive, inborn errors of History of unsupervised periods of time
PATHOPHYSIOLOGY metabolism, etc. r Environmental exposure:
Neurons in the ascending reticular activating system Hyperthyroidism/Hypothyroidism
r Respiratory: Temperature extremes
mediate the state of wakefulness in the brainstem and
Exposure to carbon monoxide
pons, connecting to the cerebral cortex, which Hypoxemia r General symptoms:
mediates awareness: Hypercarbia
r Disruption in the normal function of these areas r Environmental: Fever and other constitutional symptoms
Neck pain
leads to ALOC and coma (see below). Carbon monoxide poisoning Photophobia
Hypothermia Vomiting and/or abdominal pain
ETIOLOGY
r Trauma: Hyperthermia Incontinence of bowel or bladder
Envenomations (eg, snakes, spiders) Dietary history
Intracranial hemorrhage: Subarachnoid r Neurologic:
hemorrhage, epidural hemorrhage, subdural r Neurologic:
hemorrhage, cerebral contusion: Seizures: Headache
Hemorrhage may be worse with underlying Generalized or complex
Lethargy
Postictal period following seizures
bleeding disorders such as von Willebrand Changes in gait
Nonconvulsive status epilepticus
disease, hemophilia, etc. Seizure activity
Diffuse cerebral edema Vascular: r Cardiac:
Cerebrovascular accident (CVA): Thrombotic,
Concussion Chest pain
Anoxic brain injury hemorrhagic, embolic
Arteriovascular malformation: Bleeding Palpitations
Diffuse axonal injury Syncope
r Toxicologic: Aneurysm: Rupture r Dermatologic exam
Hemangiomas
Any agent causing hypoglycemia, such as r Neoplastic:
beta-blockers, oral hypoglycemic agents, isoniazid, PHYSICAL EXAM
Tumor growth r Vital signs including pulse oximetry
ethanol, salicylates r A thorough but rapid physical exam should be
Ethanol and other alcohols Hemorrhage from tumor
Narcotics Seizures secondary to tumor performed but may be tailored to the suspected
Substances of abuse, such as opioids, Increased intracranial pressure cause.
r Psychiatric r Maintain cervical spine precautions during the
hallucinogens, marijuana, heroin, LSD
r Other: physical exam for suspected traumatic injuries.
Psychotropic medications
Sedatives (eg, diazepam, chloral hydrate) Ventriculoperitoneal shunt (VPS) malfunction r Assess for odors (eg, DKA and some exposures or
Others (eg, clonidine, cyanide, Methemoglobinemia ingestions)
gamma-hydroxybutyrate, organophosphates, iron) Severe anemia r Neurologic assessment including:
Intussusception: Lethargy can be the sole GCS
presenting sign, rather than crying Presence of meningismus (Kernig or Brudzinski
Vitamin B12 deficiency signs, photophobia)
Neurologic exam
Limb movement (eg, focal or generalized shaking,
flexion/extension of extremities)
38
ALTERED LEVEL OF CONSCIOUSNESS/COMA

A
r HEENT:
Presence of hemotympanum, Battle sign, TREATMENT FOLLOW-UP
periorbital hematoma, CSF rhinorrhea or otorrhea,
retinal hemorrhages r Treatments for the diverse etiologies of ALOC are FOLLOW-UP RECOMMENDATIONS
Eyes: beyond the scope of this topic. Discharge instructions and medications:
Miosis or mydriasis r The following sections emphasize the initial r Avoid cause of symptoms.
Anisocoria suggests focal intracranial lesion. r Follow up closely with the primary care provider.
treatment and management. The reader is
Eye movements
encouraged to refer elsewhere for further details. Patient Monitoring
Oculocephalic reflexes r If discharged: Recurrence of symptoms
Corneal reflex PRE HOSPITAL
r Address ABCs per Pediatric Advanced Life Support r If admitted:
Presence of nystagmus
Cyanosis of the lips (PALS) or Advanced Trauma Life Support (ATLS) Cardiorespiratory status
Scalp deformities, lacerations protocols. Recurrence or worsening of symptoms
Facial swelling r Maintain cervical spine alignment for suspected
PROGNOSIS
Papilledema traumatic injury. Depends on the underlying cause
r Cardiac:
INITIAL STABILIZATION/THERAPY COMPLICATIONS
Bradycardia or tachycardia r Rapid assessment of ABCs:
r Respiratory: Depends on the underlying cause
Control airway as indicated:
Respiratory rate (hyper- or hypoventilation) Rapid sequence endotracheal intubation with
Breathing pattern GCS <8, significant hypoxemia, inability to REFERENCE
r Abdominal: control airway
Abdominal tenderness Normalize PCO2 1. Schunk JE. The pediatric patient with altered level of
Hepatomegaly Supplemental oxygen as needed consciousness: Remember your immunizations.
Presence of blood in the stool J Emerg Nurs. 1992;18(5):419421.
Maintain perfusion:
r Dermatologic: Establish vascular access.
Presence of bruising Administer isotonic solutions to avoid ADDITIONAL READING
Vesicular lesions hypotension and treat dehydration.
Cherry red, blue, or pale-colored lips r Maintain cervical spine precautions. Nelson DS. Coma and altered level of consciousness.
r Once stabilized, a methodical approach to the In Fleisher GR, Ludwig S, eds. Textbook of Pediatric
evaluation and treatment of the likely diagnosis Emergency Medicine. 6th ed. Philadelphia, PA:
Lab Lippincott Williams & Wilkins; 2010:176186.
Initial Lab Tests
should ensue.
r Bedside capillary glucose MEDICATION See Also (Topic, Algorithm, Electronic
r Consider any of the following, selectively: r Dextrose 0.251 g/kg IV for suspected or proven Media Element)
r Conversion Disorder
Serum electrolyte panel hypoglycemia
BUN, creatinine, AST, ALT, ammonia level r Consider naloxone 0.1 mg/kg IV/IM (max single r Trauma, Head
Serum osmolality dose 2 mg) for suspected narcotic ingestion.
Serum ethanol level r Activated charcoal 1 g/kg PO/NG (max single dose
Serum aspirin level 50 g) for suspected toxic ingestions except alcohols, CODES
Blood gas measurement iron
Urine toxicologic screening: Positive results ICD9
indicate either recent usage or usage within days SURGERY/OTHER PROCEDURES r 780.01 Coma
r Emergent neurosurgical intervention may be
to weeks of testing. r 780.09 Alteration of consciousness, other
required for intracranial lesions or hematomas.
Imaging r Hemodialysis may be required for some toxic
r Abdominal radiographs may reveal:
ingestions.
Signs of intussusception PEARLS AND PITFALLS
Radiopaque pills (eg, iron ingestion) DISPOSITION
r Pearls:
r Noncontrast CT brain may reveal: Admission Criteria
Intracranial hemorrhage r Persistence of ALOC with stable airway and Avoid use of atropine in rapid sequence induction
circulatory status since atropine causes pupillary dilation,
Intracranial mass, sulcular effacement, herniation,
r Admission for ALOC without a clear etiology eliminating the ability to assess pupillary reactivity
cerebral edema, hydrocephalus
r US, abdomen: r Critical care admission criteria: on physical exam.
r Pitfalls:
Intussusception Coma
r MRI may be necessary for infarction or thromboses Not recognizing that intracranial injury may occur
Respiratory failure or significant distress
in association with other causes of ALOC
as well as for improved imaging of the posterior Hemodynamic compromise requiring ongoing
Not suspecting child abuse: Numerous etiologies
fossa. resuscitation
may be secondary.
Diagnostic Procedures/Other Discharge Criteria Assuming that a toxicologic ingestion has not
r ECG as indicated r Resolved or self-limited changes in LOC occurred if tox screen is negative:
r EEG as indicated r Elimination of cause of symptoms Many ingestions require specific assays for
r Appropriate follow-up detection.
DIFFERENTIAL DIAGNOSIS Assuming that a toxicologic ingestion is the
r Munchausen syndrome Issues for Referral
r Autism or other neuropsychiatric disorders etiology for ALOC if tox screen is positive:
Depends on the underlying cause: Surgery, toxicology, The screen typically is positive for up to a week
r Death neurosurgery, neurology, social work, or psychiatry
after ingestion and may be unrelated to ALOC.
39
ALTITUDE SICKNESS
David O. Kessler

BASICS r Use of supplemental oxygen by tourists ascending to No physical signs are diagnostic of acute mountain
altitude may prevent altitude sickness. This is sickness:
DESCRIPTION particularly helpful during rapid ascent or a brief r Peripheral edema may be present in some cases.
r Altitude sickness comprises several different visit to a high altitude. r Rales may be heard with acute mountain sickness or
altitude-related illnesses, all of which are r Controlling the rate of ascent over a period of days
high altitude pulmonary edema.
preventable: will help prevent symptoms of altitude sickness. r Neurologic signs such as ataxia, altered mental
Acute mountain sickness r Children <2 yr of age should sleep below
status, paralysis, and paresthesia may suggest a
High altitude cerebral edema 2,000 meters. more serious cause such as high altitude cerebral
High altitude pulmonary edema r Children <10 yr of age should sleep below edema.
r Though these illnesses probably represent a
3,000 meters. r Retinal hemorrhages are extremely common, seen in
spectrum of similar pathophysiology, this topic will
PATHOPHYSIOLOGY 33% of climbers who do not live at high altitude:
mainly focus on acute mountain sickness.
r Altitude sickness increases with altitude and may be r The symptoms of acute mountain sickness are These are usually asymptomatic and are an
thought to occur secondary to cerebral swelling incidental finding.
seen in unacclimated people who climb to as low as
8,000 feet (2,400 meters). secondary to impaired cerebral autoregulation and DIAGNOSTIC TESTS & INTERPRETATION
hypoxia-induced vasodilation (3). Lab
EPIDEMIOLOGY r Vasogenic cerebral edema causes the symptoms of
Labs are not usually required as part of the workup for
Incidence acute mountain sickness. altitude sickness.
The incidence and severity of altitude sickness varies
with altitude and the rate of ascent (1): ETIOLOGY DIFFERENTIAL DIAGNOSIS
r Normally, an increase in altitude will cause increased
r 28% of children climbing to 2,835 meters from The symptoms of acute mountain sickness are
ventilation in response to relative hypoxemia. This nonspecific, and other illnesses may cause a similar
1,600 meters will experience symptoms of altitude leads temporarily to an alkalosis, but eventually the
sickness: cluster of symptoms, including:
body will equilibrate to the new environment. r Acute gastritis
21% experience symptoms traveling from sea r Rapid increases in altitude do not allow the acid
level (2). r Labyrinthitis
r Adult tourists traveling to 2,500 meters have similar base and volume status of the cerebral circulation to r Migraine headache
acclimatize slowly, which subsequently leads to r Meningitis
rates of symptoms (2025%). vasogenic edema.
r This increases to 4050% of people climbing to r Encephalitis
4,000 meters. r Intoxication
r If the ascent is made in hours as opposed to days, DIAGNOSIS r Psychiatric illness
the incidence rises to 90% (1). r Dehydration
HISTORY
RISK FACTORS r Acute mountain sickness is a clinical diagnosis:
r Rate of ascent and altitude itself are the biggest risk
Headache
factors for developing disease. Other factors that Poor sleep
TREATMENT
may contribute to ones risk include: Nausea
Poor hypoxemic ventilatory response PRE HOSPITAL
Vomiting IV hydration should be initiated, which protects
Genetic predisposition Anorexia
Degree of exertion against symptoms and works to combat
Dizziness altitude-related diuresis.
Altitude where one sleeps Fatigue
Use of sedatives r In preverbal children, this may manifest as crying or INITIAL STABILIZATION/THERAPY
r Infants are more susceptible to hypoxemia for r Assess and stabilize airway, breathing, and
fussiness.
multiple reasons, including: r Symptoms usually begin within 612 hr of a rapid circulation.
Increased rib cage compliance r The immediate treatment for those experiencing
ascent but may occur up to 4 days later.
Smaller airway diameter altitude sickness is to bring them down to a lower
Reduced alveoli elevation.
Persistent fetal hemoglobin r For high altitude pulmonary edema, assisted
Paradoxical inhibition of respiratory drive ventilation by endotracheal intubation and
mechanical ventilation or noninvasive ventilatory
support by BiPAP may be necessary:
Hyperventilation may lower intracranial pressure,
but excessive hyperventilation may paradoxically
decrease cerebral perfusion.
40
ALTITUDE SICKNESS
A
MEDICATION COMPLEMENTARY & ALTERNATIVE REFERENCES
r Oxygen is the primary treatment for altitude THERAPIES
sickness. Supplemental oxygen often dramatically Gingko biloba has been found to be more effective 1. Gallagher SA, Hackett PH. High-altitude illness.
improves symptoms: than placebo for reducing acute mountain sickness in Emerg Med Clin North Am. 2004;22:329355.
Oxygen, including hyperbaric oxygen, is small studies (3). 2. Samuels MP. The effects of flight and altitude. Arch
particularly useful for acute mountain sickness, Dis Child. 2004;89:448455.
high altitude cerebral edema, and high altitude DISPOSITION 3. Barry PW, Pollard AJ. Altitude Illness. BMJ. 2003;
pulmonary edema. Admission Criteria 326(7395):915919.
r Nifedipine 0.250.5 mg/kg/day PO in children r Patients who have altered mental status or
<40 kg, 10 mg PO per day in children >40 kg: neurologic signs should be evaluated for more
Improves overall symptoms; particularly useful in serious etiologies, such as high altitude cerebral CODES
improving pulmonary function in high altitude edema, and admitted for further management.
r Critical care admission criteria:
pulmonary edema ICD9
r Acetazolamide has been used successfully in adults Patients requiring mechanical ventilation 993.2 Other and unspecified effects of high altitude
to help mitigate symptoms of acute mountain Patients with severe symptoms, including
sickness: pulmonary edema, should be admitted to a critical
Acetazolamide 510 mg/kg/day divided t.i.d., or care unit. PEARLS AND PITFALLS
250 mg PO b.i.d. in adults, is typically started Discharge Criteria r Altitude sickness can be prevented by a slow rate of
1 day before ascent and is continued until Patients with acute mountain sickness who return to a
acclimatization is achieved. lower elevation will often return to baseline ascent or by avoiding very high altitudes.
r Children are more susceptible to hypoxemia-related
Acetazolamide is used only to prevent altitude spontaneously and may be safely discharged.
sickness, whereas dexamethasone is used to treat illnesses, such as acute mountain sickness.
r Oxygen is useful for all forms of altitude sickness.
once illness occurs.
Side effects include diuresis, paresthesia, FOLLOW-UP r Though acetazolamide has been traditionally used,
headache, nausea, and vomiting. patients tolerate it less than dexamethasone.
r Dexamethasone: FOLLOW-UP RECOMMENDATIONS
Patients with acute mountain sickness are at risk for
Treatment of altitude sickness: future events and should be counseled regarding
0.51.5 mg/kg IV/IM/SC/PO to a max of 48 mg
prophylaxis and preventative measures.
loading dose followed by 0.5 mg/kg to a max of
4 mg q6h. This is continued for 4872 hr. PROGNOSIS
Should be initiated at 1st suspicion or symptoms r Patients with acute mountain sickness typically
of altitude sickness improve completely without sequelae within several
Prevention of altitude sickness: Lower dosage and days.
frequency: r High altitude pulmonary edema and high altitude
0.05 mg/kg/dose PO q412h. Lesser frequency cerebral edema vary with severity, duration, and
of q12h may be used in children being passively appropriate medical therapy.
taken to altitude who are sedentary, such as
COMPLICATIONS
infants.
In more serious altitude-related illnesses, high altitude
Useful for acute mountain sickness, high altitude
cerebral or pulmonary edema or even death may
pulmonary edema, and high altitude cerebral
occur:
edema r Patients with comorbid pulmonary or cardiac risk
Dexamethasone is typically tolerated much better
than acetazolamide. factors are at greater risk from hypoxemia-related
Dexamethasone is used in both the prevention complications.
and treatment of altitude sickness.
r Ibuprofen 10 mg/kd/dose PO q6h may prevent or
treat headache associated with altitude sickness.
41
AMENORRHEA
William I. Krief
Cara Bornstein
r Secondary amenorrhea: PHYSICAL EXAM

BASICS Pregnancy r Vital signs, including height and weight
Functional: Weight loss, exercise, stress, chronic r BMI
DESCRIPTION illness r Evaluation for dysmorphic features (webbed neck,
r Primary amenorrhea is defined as the absence of CNS tumors: Craniopharyngioma, pituitary short stature, low hairline)
menses by the age of 14 yr in patients with no adenomas r Ophthalmologic exam looking for papilledema,
secondary sexual characteristics (ie, breast Medications: Antipsychotics, oral contraceptive visual field defects, and cranial nerve palsy in cases
development) or by the age of 16 yr in patients with pills, antihypertensives, steroids, chemotherapy of CNS tumors.
development of secondary sexual characteristics. Polycystic ovarian syndrome (PCOS) r Skin exam: Acne, acanthosis nigricans
r Secondary amenorrhea is the absence of menses for Endocrinopathies: Thyroid disease, diabetes r Tanner staging
3 consecutive months with previously normal mellitus r Breast findings: Underdeveloped, galactorrhea
menstruation or absence of menses for at least 6 mo Premature ovarian failure: Autoimmune, genetic
r Pubic hair development, facial hair: Too much or too
in females with previous oligomenorrhea. Female athlete triad (eating disorder, amenorrhea,
r Amenorrhea is a normal state prior to puberty and osteoporosis) little
r Genital exam: Clitoromegaly, virilization,
during pregnancy and lactation: COMMONLY ASSOCIATED CONDITIONS
The most common cause of secondary r Pregnancy imperforate hymen (bulging of external vagina),
amenorrhea is pregnancy. r Eating disorders vaginal agenesis, pelvic fullness (pregnancy or
tumor), cervical mucus production
EPIDEMIOLOGY r Stress, depression r Thyroid exam
r <1% of adolescent girls have primary amenorrhea. r PCOS
r The prevalence of secondary amenorrhea in the r Lactation DIAGNOSTIC TESTS & INTERPRETATION
general population has been reported to be as high r Chronic diseases Lab
as 5%: r Medication use Initial Lab Tests
May be as high as 80% in competitive athletes r Pregnancy test
r No other lab tests are required emergently, but they
RISK FACTORS
r Eating disorder DIAGNOSIS can be performed to be followed by the primary care
r Excessive exercising physician or subspecialist:
HISTORY Thyroid-stimulating hormone, follicle-stimulating
r Psychosocial stress r In cases of primary amenorrhea, a thorough history
hormone (FSH), luteinizing hormone (LH), and
of childhood growth and development, including prolactin are performed as part of the initial
GENERAL PREVENTION
growth charts and age of sexual development, is evaluation if the exam is suggestive of an
Maintaining an appropriate body mass index (BMI)
imperative: ovarian-axis problem.
PATHOPHYSIOLOGY Family history, including age of mother and sister If hirsutism is present, androgen testing should be
Any disruption of the complex interaction between the pubertal development performed (testosterone, DHEAS,
hypothalamic-pituitary-ovarian axis as well as outflow r Details about menstrual cycle, including last
androstenedione, 17-OH progesterone)
tract obstruction can cause amenorrhea. menstrual period (if applicable), flow, amount of If the exam suggests chronic disease: CBC, BUN,
ETIOLOGY days of flow, and cycle time. creatinine, LFTs, ESR
r Primary amenorrhea: r Sexual activity
r Any history of trauma or chronic illness Imaging
Mullerian agenesis (agenesis of the uterus and r Neuroimaging (CT/MRI) to evaluate the CNS for
upper 2/3 of vagina) r Substance abuse
tumors:
Imperforate hymen r Dietary history, exercise
MRI is preferred to visualize the sella turcica.
Turner syndrome r Psychosocial stressors r US to evaluate the ovaries and uterus
Constitutional delay of growth or puberty r Review of symptoms should include history of
Kallmann syndrome (facial abnormalities, vasomotor symptoms, palpitations, dizziness fatigue,
anosmia) hearing loss, visual changes, breast changes, and
All etiologies of secondary amenorrhea headache.
42
AMENORRHEA
A
Diagnostic Procedures/Other DISPOSITION ADDITIONAL READING
Probing the introitus with a moist cotton-tipped swab Admission Criteria
or soft catheter to verify patency of the hymen and r CNS tumors requiring acute management r Emans SJ. Amenorrhea in the adolescent. In Emans
vagina r Symptomatic eating disorder: SJ, Laufer MR, Goldstein DP, et al., eds. Pediatric
Pathological Findings Bradycardia, orthostatic BP, hypothermia, altered and Adolescent Gynecology. 5th ed. Philadelphia,
Depends on underlying cause mental status, syncope, electrolyte imbalance PA: Lippincott Williams & Wilkins; 2005.
r Master-Hunter T, Heiman D. Amenorrhea:
DIFFERENTIAL DIAGNOSIS Discharge Criteria Evaluation and treatment. Am Fam Physician.
r Hyperprolactinemia-altered metabolism, ectopic All patients who do not meet admission criteria can 2006;73(8):13741382.
production, breast-feeding, hypothyroidism, safely be discharged with appropriate outpatient
medications, pituitary adenoma follow-up. See Also (Topic, Algorithm, Electronic
r Hypergonadotropic hypogonadism (elevated LH and Issues for Referral Media Element)
r Patients should be referred to an endocrinologist Pregnancy
FSH): Gonadal dysgenesis (Turner syndrome),
premature ovarian failure and/or gynecologist for further evaluation.
r Hypogonadotropic hypogonadism (normal or low LH r Patients with an eating disorder require a
and FSH): Eating disorders, constitutional delays of multidisciplinary approach with adolescent CODES
growth or puberty, CNS tumor, chronic illness, medicine, a nutritionist, and a psychologist.
severe depression, cranial radiation, excessive r Counseling is important in adolescents whose ICD9
exercise, Kallmann syndrome, Sheehan syndrome diagnosis will make them unable to conceive. 626.0 Absence of menstruation
r Normogonadotropic: Congenital, hyperandrogenic
anovulation (PCOS, Cushing disease), outflow tract
obstruction (imperforate hymen, transverse vaginal FOLLOW-UP PEARLS AND PITFALLS
septum) FOLLOW-UP RECOMMENDATIONS r If secondary sexual characteristics are present,
r Pregnancy r Discharge instructions and medications: amenorrhea is due to pregnancy until proven
r Thyroid disease Refer for follow-up to a specialist. otherwise.
r Activity: r Important to remember the psychological effects of
Reducing activity if amenorrhea is secondary to impaired body image and self-esteem issues.
TREATMENT excessive exercising
Treatment should be directed toward the underlying DIET
cause of amenorrhea. Increasing caloric intake in patients with an eating
disorder and exercise-induced amenorrhea
MEDICATION
Medical treatment should be initiated following PROGNOSIS
diagnostic workup in the outpatient setting. In most instances, amenorrhea is not life threatening
and patients do well with medical management.
Excision of the hymen for imperforate hymen under COMPLICATIONS
sedation r Wrist and hip fractures when older due to poor bone
mineralization
r Infertility
43
ANAL FISSURE
Gregory Garra
BASICS DIAGNOSIS r Multiple fissure or nonmidline fissures can be the
result of perianal abscess.
DESCRIPTION HISTORY r Hemorrhoid
r Anal pain during or after defecation accompanied by
An anal fissure is a linear tear or tears in the lining of r Inflammatory bowel disease
lower half of the anal canal. the passage of blood-streaked stools or bright red r HIV
blood per the rectum r Immunosuppression
PATHOPHYSIOLOGY r Pain is typically severe and may last minutes to
r The pathogenesis is poorly understood: r Anal trauma:
hours.
Typically, the anoderm is resistant to abrasions r Infants may present with inconsolable crying. Child sexual abuse
and lacerations. r Children may volitionally withhold stool to prevent
Commonly associated with the passage of hard
stool the pain associated with stool passage. TREATMENT
r History of constipation is elicited in only 25% of PHYSICAL EXAM
cases. However, diarrhea is a predisposing factor in r Linear or pear-shaped split in the lining of the anal INITIAL STABILIZATION/THERAPY
Most anal fissures resolve spontaneously with dietary
47%. canal
r Associated pain may promote stool retention, thus r >90% of anal fissures are identified in the posterior modification and stool softeners.
increasing constipation and establishing a cycle of midline. MEDICATION
worsening pain or chronic fissure. r Spasm of the anal sphincter may obscure First Line
r Most occur in the posterior midline: visualization. r The primary treatment of anal fissures consists of
Rarely in the anterior midline r An anoscope or other clear plastic tubing, such as a anal hygiene, warm water sitz baths to relieve anal
chest tube, may be used to assist in dilating the sphincter spasm, and a stool softener.
ETIOLOGY r Long-term care and resolution may require use of a
r Anal fissures are the result of mechanical disruption anus for improved visualization.
of the anal mucosa or skin external to the anus. stool-softening agent or lubricant, such as
DIAGNOSTIC TESTS & INTERPRETATION polyethylene glycol (eg, Miralax) or mineral oil to
r This is almost exclusively the result of hard stools r Anal fissure is a clinical diagnosis.
r If causes other than constipation or hard stool are a keep the stool soft.
abrading or lacerating the epidermis.
possibility, consider the following: Second Line
COMMONLY ASSOCIATED CONDITIONS Topical anesthetics may be used but are associated
r Anal fissures can be seen in association with CBC
C-reactive protein with delayed healing and skin sensitization.
inflammatory bowel disease, immunosuppression,
and HIV infection. Stool culture, Gram stain, and ova/parasite DISPOSITION
r Anal fissures can result from sexual abuse. evaluation Patients with uncomplicated midline fissures not
Hepatic enzyme testing, total protein, and albumin suggestive of an alternate condition should be
discharged home with appropriate management
advice.
44
ANAL FISSURE
A
COMPLEMENTARY & ALTERNATIVE ADDITIONAL READING PEARLS AND PITFALLS
THERAPIES
r Ayantunde AA, Debrah SA. Current concepts in anal r Anal fissures in children typically result from hard
Other methods to soften or bulk stool to relieve
constipation include: fissures. World J Surg. 2006;30:22462260. stools. Education about dietary and, if necessary,
r Increasing water intake r Jonas MJ, Scholefield JH. Anal fissure. Gastroenterol medicinal/therapeutic stool softening can prevent
r Use of a high-fiber or high-bran diet Clin North Am. 2001;30:167181. recurrence.
r Consider the possibility of sexual abuse or an
r Psyllium seeds See Also (Topic, Algorithm, Electronic
alternate condition.
Issues for Referral Media Element) r Patients with multiple fissures, fissures not in the
r Children suspected of sexual abuse should be r Gastrointestinal Bleeding: Lower
r Inflammatory Bowel Disease midline, or other tissue abnormalities in the perineal
referred to the child protective services. or anal area should be evaluated for more serious
r Children with suspected inflammatory bowel disease r Rectal Bleeding
disease.
should be referred to gastroenterology for
evaluation.
CODES
FOLLOW-UP
ICD9
FOLLOW-UP RECOMMENDATIONS 565.0 Anal fissure
Discharge instructions and medications:
r All patients should be referred to their primary care
provider for follow-up evaluation if the condition
does not resolve.
DIET
Increased fluids and high-fiber diet
PROGNOSIS
>90% heal spontaneously or with simple measures
within 12 wk.
COMPLICATIONS
Chronic fissure
45
ANAPHYLAXIS
Christopher G. Strother
2. Two or more of the following that occur rapidly

BASICS DIAGNOSIS after exposure to a likely allergen for that
patient:
DESCRIPTION HISTORY Involvement of the skin or mucosal tissue
r Anaphylaxis is a severe, potentially lethal, allergic r Anaphylaxis is a clinical diagnosis, but no single
Respiratory compromise
reaction involving multiple systems that results from finding is always present. Reduced BP or associated symptoms
the sudden release of mast cell- and r Always inquire about possible allergen exposures Persistent GI symptoms (eg, crampy abdominal
basophil-derived mediators (1). and history of previous reactions. pain, vomiting)
r Classic immunologic anaphylaxis refers to IgE- or r Symptom progression and time from exposure are 3. Reduced BP following exposure to a known
IgG-mediated reactions. Anaphylaxis can also be important historical details. allergen for that patient:
nonimmunologic or anaphylactoid. r Symptomatology can include the following: Infants and children: Low systolic BP (age
Sense of impending doom specific) or >30% decrease from baseline
EPIDEMIOLOGY
Hives systolic BP
Incidence Generalized itching Adults: Systolic BP <90 mm Hg or >30%
r The rate of occurrence in children is difficult to
Cough decreases from baseline
precisely define but appears to be increasing (2). Nasal congestion
r Allergy-related conditions account for 0.21% of DIAGNOSTIC TESTS & INTERPRETATION
Shortness of breath
emergency visits. Wheezing Lab
r Anaphylaxis causes death in 0.652% of patients r Lab testing and imaging is not generally helpful in
Sore throat
(3). Laryngitis diagnosis nor prognosis for acute anaphylactic
Nausea reactions.
RISK FACTORS r Plasma histamine can be measured and peaks
r Previous allergic reactions to food Vomiting
r Atopic dermatitis Diarrhea 515 min following a reaction but returns to normal
Eye itching within 60 min.
r History of respiratory diseases such as asthma, r Serum tryptase can be elevated in the first few hours
Eye tearing
bronchiolitis, and croup Eye redness and may aid an unclear diagnosis but is not helpful
GENERAL PREVENTION Increased salivation in most cases.
r Avoidance of known allergens is essential but can Diaphoresis r Radioallergosorbent (RAST) testing or other allergy
be difficult, especially with food allergens. Seizures tests are essential in patients after recovery in order
r Allergen testing for patients with previous severe to identify allergens and prevent future reactions.
PHYSICAL EXAM
reactions can help patients avoid triggers. r Vital signs: Hypotension, tachycardia Initial Lab Tests
r HEENT: r The diagnosis of anaphylaxis is clinical. Laboratory
PATHOPHYSIOLOGY
r Immunologic anaphylaxis is an Stridor, dysphonia, aphonia, tearing, eye itching or testing is generally not helpful in the emergency
redness, nasal congestion, salivation department for diagnosing anaphylaxis.
immunoglobulin-mediated severe allergic reaction. r Laboratory testing may help in the management of
r An allergen reacts with IgE or IgG, which stimulates r GI:
Vomiting, diarrhea the complications of anaphylaxis. Such testing might
B and T cells, which in turn signal mast cells,
r Respiratory: include:
basophils, and eosinophils to degranulate.
r Mediators such as histamine, tryptase, Arterial or venous blood gas
Stridor, cough, wheezing, dyspnea, hypotension
r Dermatologic: CBC
histamine-releasing factor, and other cytokines are Basic metabolic panel
released. Urticaria, pruritus, flushing, diaphoresis
r Mediators have either direct effects on the r 1020% of patients with anaphylaxis will not have DIFFERENTIAL DIAGNOSIS
r Allergic reaction that is a type I hypersensitivity but
cardiovascular, GI, respiratory, or skin systems, skin findings.
creating symptoms or further promoting the release r 1 criteria set created by experts for diagnosing does not fully meet diagnostic criteria for
of mediators from other cells. anaphylaxis includes any one of the following (1): anaphylaxis
r Type I hypersensitivity reactions that are mild or r Vasovagal syncope, urticaria, angioedema, asthma,
1. Acute onset of an illness (minutes to several
moderate without developing fully to anaphylaxis hours) with involvement of the skin, mucosal anxiety, and other forms of shock can all mimic
are common. tissue, or both (eg, hives, pruritus, or flushing) and aspects of anaphylaxis.
at least one of the following: r Medications that cause flushing, such as
ETIOLOGY Respiratory compromise (eg, dyspnea, vancomycin, can mimic skin findings.
r Most anaphylactic reactions in children occur as a
bronchospasm, stridor, hypoxemia) r Overdose of medications such as anticholinergics
result of food allergy. Reduced BP or associated symptoms of
r Other common triggers include: can cause skin findings and cardiovascular changes.
end-organ dysfunction (eg, hypotonia, syncope, r Food syndromes like scombroid that involve
Insect bites incontinence) nonimmunoglobulin-mediated histamine release can
Drugs
appear very similar in clinical appearance though are
Exercise
usually not life threatening.
Latex r Serum sickness (transfusion reactions) is another
Immunotherapy
Environmental allergens such as pollen type of serious immune-mediated reaction (immune
complex or type III reaction).
COMMONLY ASSOCIATED CONDITIONS
Urticaria
46
ANAPHYLAXIS
A
DISPOSITION COMPLICATIONS
r Respiratory failure
r Shock
r Intubated patients
PRE HOSPITAL r Patients in respiratory distress r Multisystem organ failure
r Assess and stabilize airway, breathing, and r Significant generalized reactions and/or persistence r Disseminated intravascular coagulation
circulation. of symptoms
r Administer high-flow oxygen. r Persistent abnormal vital signs
r Obtain IV access and administer IV fluid. r Critical care admission criteria: REFERENCES
r Administer epinephrine, albuterol, and/or
Intubated patients 1. Sampson HA, Munoz-Furlong A, Campbell RL,
diphenhydramine as per local protocol. Persistent hypotension or respiratory distress et al. Second symposium on the definition and
r Cardiac and pulse oximetry monitoring despite adequate therapy requires continuous management of anaphylaxis: Summary
monitoring. reportSecond National Institute of Allergy and
r Assess and stabilize airway, breathing, and Discharge Criteria Infectious Disease/Food Allergy and Anaphylaxis
circulation. r Patients with complete resolution of symptoms may Network symposium. J Allergy Clin Immunol.
r Consider early intubation if loss of airway access be discharged following a period of observation in 2006;117:391.
from swelling is a possibility. the emergency department (generally 48 hr) 2. Ross MP, Ferguon M, Street D, et al. Analysis of
r Epinephrine is a key part of management. r Patients who receive epinephrine should be food-allergic and anaphylactic events in the
r Volume resuscitation with crystalloids or colloids observed 48 hr for biphasic reactions, which usually National Electronic Injury Surveillance System.
occur within 8 hr but can occur as late as 72 hr. J Allergy Clin Immunol. 2008;121:166.
MEDICATION 3. Moneret-Vautrin DA, Morisset M, Flabbee J, et al.
Issues for Referral
First Line r Patients without previous evaluation by an allergist Epidemiology of life-threatening and lethal
r Epinephrine is the mainstay of treatment: anaphylaxis: A review. Allergy. 2005;60(4):
should be referred as soon as possible for skin
0.01 mg/kg up to 0.5 mg IM/SC q35min: testing. 443451.
Epinephrine IM has the therapeutic advantage r Consultation with an allergist or immunologist can
of SC, and is the preferred route.
May give as an infusion (0.1 g/kg/min up to
be considered for desensitization therapy. ADDITIONAL READING
1 g/kg/min) if needed for persistent hypotension
or severe respiratory symptoms: See Also (Topic, Algorithm, Electronic
IV use is recommended only when absolutely
FOLLOW-UP Media Element)
necessary to maintain BP. Adverse events such FOLLOW-UP RECOMMENDATIONS Rash, Urticaria
as stroke and MI resulting from IV r Discharge instructions and medications:
administration are well reported. Typically, patients are discharged with prescribed
r Albuterol for wheezing: Adjunct to epinephrine for corticosteroid burst dose, diphenhydramine, and CODES
relief of bronchospasm (2.55 mg by nebulizer) an EpiPen.
r IV fluids for hypotension: 20 mL/kg normal saline Follow-up allergy testing should be arranged. ICD9
Consider steroids for up to 72 hr to prevent r 989.5 Toxic effect of venom
per bolus
biphasic reactions. r 995.0 Other anaphylactic shock, not elsewhere
Second Line Consider symptomatic treatment with classified
r Steroids:
diphenhydramine with or without an H2 blocker r 995.60 Anaphylactic shock due to unspecified food
Not helpful in acute management but do help to for up to 72 hr.
prevent progression of symptoms as well as r Activity:
rebound or biphasic symptoms
Methylprednisolone 12 mg/kg q6h, max single
As tolerated PEARLS AND PITFALLS
Avoid activities that might bring a patient into
dose 125 mg IV r IM-administered epinephrine is the mainstay and
contact with potential triggers (ie, bees and bee
Dexamethasone 0.3 mg/kg IV/IM q12h, max drug of choice for treating anaphylaxis.
stings)
single dose 10 mg IV/IM q12h r Up to 20% of patients will not have skin findings.
Prednisone 1 mg/kg/dose PO q12h, max single Patient Monitoring r Diphenhydramine will not treat the cardiovascular
dose 30 mg PO q12h Cardiovascular monitoring is essential in anyone with
r Diphenhydramine: respiratory distress or abnormal vital signs. effects of anaphylaxis.
r Failing to recognize the possibility of a biphasic
Relieves itching and flushing but does NOT DIET reaction and discharging too soon after stabilization
improve cardiovascular or respiratory effects of r Patients should be kept NPO during observation.
can be dangerous (most biphasic reactions occur
anaphylaxis and should not take priority over r Avoid foods allergens. within 8 hr).
epinephrine
12 mg/kg/dose IV/IM/PO q6h, max single dose PROGNOSIS
50 mg IV/IM/PO q6h r Prognosis is generally good if anaphylaxis is
r H2 blockers: recognized and treated early.
Can be used as supplement to diphenhydramine r Development of shock is a poor prognostic indicator.
Ranitidine 1 mg/kg/dose q6h, max single dose r Delay in the administration of epinephrine has been
50 mg IV q6h associated with poor outcomes.
Famotidine 1 mg/kg/dose q12h, max single dose
40 mg IV q12h
r Vasopressors: Can be used for persistent
hypotension despite epinephrine and fluids.
Dopamine, norepinephrine, or phenylephrine can be
used.
47
ANEMIA
Eyal Ben-Isaac
Vincent J. Wang
GENERAL PREVENTION r Diagnosis based on mean corpuscular volume

BASICS r Appropriate nutrition and iron intake (MCV):
r Screening hemoglobin at well-child visits Microcytic:
DESCRIPTION r Possible supplementation with iron and vitamins if Iron deficiency
r Anemia is defined by an abnormally low hemoglobin Thalassemias
at risk
(Hgb), hematocrit (Hct), or number of RBCs per Sideroblastic (eg, lead poisoning)
mm3 . PATHOPHYSIOLOGY Acute and chronic inflammation (can be
r A significant drop in Hgb may be important even if r Physiologic anemia:
normocytic)
the current value is normal. Relative polycythemia in utero stimulates Normocytic with low reticulocyte count:
r Black children have Hgb levels 0.3 g/dL lower erythropoietin; PaO2 rise after birth leads to Pancytopenias
than those of white or Asian children of comparable decreased erythropoiesis. Bacterial or viral suppression
age and socioeconomic status. Neonates have an increased rate of destruction of Pure RBC aplasia: Diamond-Blackfan, transient
r Normal (and lower limit) Hgb values by age: RBCs and a shortened RBC life span. erythroblastopenia of childhood (TEC)
Hgb and Hct values decrease during the 1st Normocytic with normal or high reticulocyte
Cord blood, 16.8 (13.7) g/dL
68 wk of life; may be low until 3 mo. count:
2 wk, 16.5 (13.0) g/dL
In premature infants, the decline in Hgb is more Antibody mediated (Coombs positive):
3 mo, 12.0 (9.5) g/dL
extreme and more rapid. Isoimmune (ABO/Rh incompatibility) or
6 mo to 6 yr, 12.0 (10.5) g/dL r Iron deficiency: Insufficient iron leads to depleted
712 yr, 13.0 (11.0) g/dL autoimmune etiologies such as infections (eg,
Adult female, 14.0 (12.0) g/dL RBC mass, decreased Hgb. mycoplasma, Epstein-Barr virus, HIV),
r Vitamin B and folate deficiencies lead to inhibited lymphomas, disorders of immune regulation (eg,
Adult male, 16.0 (14.0) g/dL 12
r This topic focuses on nontraumatic anemia. cell growth. systemic lupus erythematosus), drugs (eg,
r Lead interferes with heme synthesis. methyldopa or other drugs such as
EPIDEMIOLOGY r Reticulocytes: antihistamines, sulfonamides, insulin, penicillin,
Incidence Elevated in response to acute blood loss, etc., that can cause immune hemolysis that is
Iron deficiency: 1 in 24, or 11.2 million per year in hemolysis, or with initial iron replacement not autoimmune)
the U.S. Calculate the reticulocyte index (RI; or corrected Hemorrhagic disorder (blood loss)
reticulocyte count) as follows: RI = reticulocyte Microangiopathic hemolytic anemia
Prevalence
r Up to 20% of American children and 80% of (patient Hct normal Hct). (eg, artificial heart valves, hemolytic uremic
children in developing countries become anemic at RI should typically be between 1.0 and 2.0. syndrome [HUS; see Hemolytic Uremic
some point during their childhood. RI <2 with anemia indicates decreased Syndrome topic], disseminated intravascular
r Iron deficiency is the most common etiology of production of reticulocytes and therefore RBCs: coagulation [DIC], Kasabach-Merritt syndrome)
May indicate bone marrows inability to produce Membrane defects (eg, spherocytosis,
anemia: Toddlers 7%, adolescent and adult women
new blood cells elliptocytosis, paroxysmal nocturnal
916%.
hemoglobinuria)
RISK FACTORS ETIOLOGY Hemoglobinopathies
r Nutritional deficiencies: r Blood loss:
Enzyme defects (eg, G6PD deficiency, pyruvate
Iron deficiency (eg, excessive milk intake) Trauma kinase deficiency)
Vitamin B12 (eg, exclusively breast-fed by GI losses (ulcer, Meckel diverticulum, polyp, Macrocytic:
vegetarian mother) hemangioma, inflammatory bowel disease) Megaloblastic: Folate deficiency, vitamin B12
Folic acid (eg, impaired absorption) Menorrhagia/Dysfunctional uterine bleeding deficiency, hereditary orotic aciduria
r Age: r Increased RBC destruction Nonmegaloblastic: Liver disease,
r Decreased RBC production hypothyroidism, myelodysplasia, preleukemia,
Congenital or early onset (eg, Diamond-Blackfan,
r Nutritional deficiencies: Diamond-Blackfan, Fanconi anemia
enzyme deficiencies)
Late infancy (eg, hemoglobinopathies) Iron, vitamin B12 , folate
Late infancy/Toddlers (eg, iron deficiency, lead Chronic illnesses involving deficiencies of vitamin
poisoning) B6 , copper DIAGNOSIS
r Sex: Malabsorptive conditions
r Congenital: HISTORY
Males more likely to have G6PD deficiency r Symptoms: Pallor, fatigue, exercise intolerance
Immune hemolytic anemias are more common in Inherited bone marrow failure disorders (eg, r Sudden onset may represent an acute event.
adolescent females. Diamond-Blackfan, Fanconi anemia) r Syncope or palpitations
r Ethnicity: Hemolytic processes r Bone pain (eg, SCD, infiltrative disorders)
Thalassemias: Much of Africa, the Middle East, Infections (eg, cytomegalovirus, toxoplasmosis,
r Blood loss (eg, trauma, menstrual history,
the Indian subcontinent, Southeast Asia, areas syphilis, rubella, herpes, group B streptococcus,
parvovirus) hematochezia, melena)
bordering the Mediterranean Sea r Ethnic origin
r RBC defects: Membrane, enzymes, and
Hemoglobinopathies: r Diet: Initiation and current intake of milk
Hgb S syndromes in Central African origin hemoglobinopathies (eg, sickle cell disease [SCD])
Hgb E syndromes in Southeast Asia r Anemia in the immediate newborn period: Consider r Jaundice: Timing, recurrence
G6PD deficiency in Mediterranean or Southeast hemorrhagic and isoimmune causes, congenital r Exposures:
Asian origin infections, sepsis, and congenital disorders of the Toxins: Insecticides, benzene, nitrogen mustards
RBC. Medications:
Immune mediated (eg, penicillin, quinidine,
methyldopa)
Aplastic crises due to chemotherapeutic agents,
chloramphenicol, sulfonamides, anticonvulsants,
cimetidine, and others
48
ANEMIA
A
Lead (old paint, pica, foreign
medications/foods/pottery) TREATMENT FOLLOW-UP
G6PD deficiency: May be precipitated by
antimalarials, sulfonamides, nitrofurantoin, PRE HOSPITAL FOLLOW-UP RECOMMENDATIONS
naphthalene (moth balls), fava beans r Assess and stabilize airway, breathing, and Discharge instructions and medications:
r Family history of anemia, splenectomy, gallstones circulation. r Return for increased pallor, fatigue, or blood loss
r Assessment for trauma: r Iron supplementation (see Medication)
PHYSICAL EXAM r Timing of follow-up CBC depending on etiology and
r Vital signs (including orthostatics): Tachycardia, IV fluid resuscitation if tachycardic or hypotensive
hypotension, tachypnea Supplemental oxygen usually appropriate severity
r Pallor, heart murmur, hepatosplenomegaly INITIAL STABILIZATION/THERAPY DIET
r Lymphadenopathy: Neoplastic process r Assess and stabilize airway, breathing, and Iron deficiency: Increase dietary iron such as red meat,
r Glossitis: B deficiency circulation. beans, green leafy vegetables, blackstrap molasses,
12
r Dactylitis: SCD r Exclude traumatic etiologies. enriched breakfast cereals, and some sea foods.
r Purpura: Infections, DIC r Evaluate nature of anemia, estimate of blood loss,
PROGNOSIS
r Petechiae: HUS, DIC, pancytopenia and presence of other illnesses. r The prognosis generally is good but overall depends
r Signs of extramedullary hematopoiesis (eg, frontal r Supplemental oxygen usually is appropriate.
on underlying cause and severity.
r Transfusion criteria: Severe hypoxemia, significant r Iron-deficiency anemia resolves with treatment.
bossing)
r Syndromic features: Limb anomalies in Fanconi, ongoing losses, significant tachycardia, and/or
hypotension: COMPLICATIONS
Diamond-Blackfan Chronic anemia can lead to cardiac problems
10 cc/kg packed RBCs over 34 hr (faster if active
DIAGNOSTIC TESTS & INTERPRETATION hemorrhage) (arrhythmia, high output failure) and poor growth.
Lab 1 cc/kg per Hgb level over 34 hr if severely
Initial Lab Tests anemic or any signs/suspicion of CHF on history or
r CBC with differential and smear: exam
ADDITIONAL READING
Mentzer index (MCV/RBC) may suggest iron Use caution if suspecting a hemolytic process. r Aslan D, Altay. Incidence of high erythrocyte count
deficiency (ratio >13) vs. thalassemia (<13). Discuss with the hematologist first if suspecting in infants and young children with iron deficiency
Clues on the smear: an oncologic process. anemia: Re-evaluation of an old parameter.
Acanthocytes: Vitamin E deficiency, liver disease r See Aplastic Anemia topic for aplastic crises and J Pediatr Hematol Oncol. 2003;25(4):303306.
Bizarre shapes: RBC membrane defects, Sickle Cell Disease and Acute Hemolytic Anemia r Cohen AR. Hematologic emergencies. In Fleisher
thalassemia syndromes topics for specifics on these diseases. GR, Ludwig S, eds. Textbook of Pediatric Emergency
Blister or bite cells: G6PD deficiency
MEDICATION Medicine. 6th ed. Baltimore, MD: Lippincott
Helmet cells (fragmented cells): r Oral iron supplementation for deficiency: Williams & Wilkins; 2010.
Microangiopathic anemia r Glader B. The anemias. In Kliegman RM, Behrman
Rouleaux: Inflammation or immune hemolytic Prophylaxis: 12 mg of elemental iron/kg/day
Mild to moderate anemia: 3 mg of elemental RE, Jenson HB, et al., eds. Nelson Textbook of
anemia
Stomatocytes: Liver disease, stomatocytosis iron/kg/day Pediatrics. 18th ed. Philadelphia, PA: Saunders;
Target cells: Iron deficiency, hemoglobinopathy, Severe anemia: 46 mg of elemental iron/kg/day. 2007:20032006.
liver disease Parenteral iron may be indicated for specific
Tear drop cells: Bone marrow failure, burns etiologies: Iron deficiency with inflammatory
Basophilic stippling: Lead toxicity, thalassemia bowel disease and dialysis and oncology patients. CODES
r Reticulocyte count Consultation with the hematologist is
r Consider type and cross-matching blood recommended before such administration. ICD9
r Autoimmune causes: See specific topics. r 280.9 Iron deficiency anemia, unspecified
r Consider heme testing the stool r 283.0 Autoimmune hemolytic anemias
r Other tests depending on initial labs and possible DISPOSITION r 285.9 Anemia, unspecified
etiologies: Admission Criteria
Coombs/Direct antibody test r Admit for anemia requiring inpatient evaluation or
Iron studies (iron, ferritin, total iron-binding for severe symptomatic anemia.
capacity, % saturation) r Critical care admission criteria: PEARLS AND PITFALLS
Hemoglobin electrophoresis Unstable vital signs despite resuscitation r In the immediate newborn period, consider
DIC panel Ongoing blood loss with unstable vital signs hemorrhagic and isoimmune causes, congenital
Tumor lysis labs Discharge Criteria infections, sepsis, and disorders of RBCs.
Diagnostic Procedures/Other r Stable vital signs r Iron deficiency is the most common childhood
Bone marrow aspirate or biopsy may be indicated to r Asymptomatic anemia.
evaluate for an infiltrative process and/or marrow r Able to tolerate oral therapy if needed r CBC and smear typically allow definitive diagnosis
arrest: r Close follow-up is assured of the etiology of anemia.
r Persistent severe normocytic anemia (evaluate for
TEC, Diamond-Blackfan)
Issues for Referral
r Macrocytic anemia without obvious etiology Hematology referral for:
r Aplastic anemia and disorders of RBCs, including
(evaluate for myeloproliferative syndromes,
Diamond-Blackfan) autoimmune hemolytic anemia, heredity
r Blasts on smear (evaluate for leukemia) spherocytosis, hemoglobinopathies, thalassemia,
r Pancytopenias and G6PD deficiency
r CBC suggestive of leukocyte disorders and/or
DIFFERENTIAL DIAGNOSIS thrombocytopenia
See Etiology section. r Evidence of bone marrow failure
49
ANGIOEDEMA
Rahul Kaila

BASICS r Idiopathic: Most common r Nonpitting edema of the face, lip, hands, feet, GI
r Food induced: Eggs, peanuts, cows milk, shellfish tract, or any part of the skin:
DESCRIPTION r Medication induced: Nonpitting edema has ill-defined margins.
r Angioedema is self-limited localized swelling Edema of the GI tract can present with acute
Trimethoprim/sulfamethoxazole, other sulfa
resulting from extravasation of fluid into interstitial derivatives, penicillins, cephalosporins, and NSAIDs abdominal pain, nausea, and vomiting without
tissues. r Insects causing angioedema: Fire ants, venomous cutaneous features.
r Nonpitting edema involves the deeper layers of the r Associated urticaria and flushing may be seen.
insects
dermis and subcutaneous tissues. r Latex allergy: Especially in children with r Skin may be warm and tender.
r Most commonly involves head, neck, hand and GI r Angioedema of the throat can cause airway
myelomeningocele and in children with multiple
tract: surgical procedures obstruction.
Involvement of the larynx is life threatening. r Physically induced: Heat, cold, vibration, ultraviolet r Hereditary angioedema3 common forms:
r As compared to other forms of edema, which are
radiation, and pressure Subcutaneous edema:
symmetric, angioedema is: r Infection induced: Nonerythematous, nonpruritic, and
Asymmetric Viral most common: Herpes simplex virus, circumscribed
Has a rapid onset coxsackievirus, Epstein-Barr virus, and viral upper Not associated with urticaria
Occurs in nondependent areas respiratory tract infection can cause angioedema Abdominal edema:
EPIDEMIOLOGY and urticaria. Attack can mimic a surgical abdomen.
r 2nd most common allergic disease leading to Bacterial infections such as otitis media, sinusitis, Present with vomiting, diarrhea, ileus, and
hospitalization, next only to asthma and tonsillitis and urinary tract infection are diffuse abdominal pain
r The exact incidence is unknown. associated with angioedema. It can be the 1st and only presenting sign (4)
r Prevalence is higher in children with atopic r Hereditary angioedema: C1 esterase inhibitor Laryngeal edema:
Life-threatening presentation
dermatitis. deficiency is a rare autosomal dominant condition,
r Hereditary angioedema (C1 esterase inhibitor Present with stridor, dyspnea, hoarseness, and
which occurs result of kinin pathway activation:
Type 1 occurs in 85% of patients with C1 esterase dysphagia
deficiency) occurs 1 in 50,000 (1).
inhibitor deficiency. DIAGNOSTIC TESTS & INTERPRETATION
RISK FACTORS Type 2 occurs in 15% (3).
Angioedema occurs with higher frequency in children r Acquired angioedema:
Lab
r No lab test is recommended routinely, and no test is
with history of food allergy, allergic rhinitis, asthma, or Increased destruction or metabolism of C1 diagnostic.
atopic dermatitis. esterase inhibitor r Avoid challenging a patient with a specific food or
GENERAL PREVENTION Clinically apparent after 4050 yr of age drug to confirm suspected allergy.
Avoidance of trigger agents Associated with rheumatologic conditions and r Elevated tryptase level: Marker of mast cell
lymphomas
PATHOPHYSIOLOGY degranulation can be elevated for few hours after
r Mast cell activation following contact with IgE Resembles hereditary angioedema but
the reaction, but normal values do not exclude
distinguished by low C1q levels
cross-linking antigen leads to release of histamine, angioedema.
r Patients with chronic, recurrent, unexplained
which in turn increases the vascular permeability,
and leakage of fluid into the skin: DIAGNOSIS episodes of angioedema should undergo evaluation
IgE cross-linking with the mast cell also releases to rule out connective tissue disorders as well as
prostaglandin D2 and leukotrienes, activates the HISTORY autoimmune and thyroid problems.
r Focus on agents likely to cause angioedema (eg, r It is not necessary to perform this in the emergency
complement system, and releases several other
vasodilators. foods such as shellfish, peanuts, wheat, eggs): department setting:
r Non-IgE: Kinin-mediated pathway: If history of new food/exposure time, note when Workup should include CBC, ESR, antinuclear
Kallikrein enzyme converts kininogen to the consumption or contact occurred. antibody, thyroid function testing, and
r All medications including over-the-counter antithyroglobulin and antimicrosomal antibody.
bradykinin, a potent vasodilator, which increases
vascular permeability and causes edema. medications r Hereditary angioedema:
Andioedema caused by the use of r Family history of angioedema, autoimmune Complement C4 level is usually low during the
angiotensin-converting enzyme (ACE) inhibitors is problems attack as well as between acute episodes.
a typical example using this mechanism (2). r Swelling: C1 esterase inhibitor levels help distinguish
r Mast cell angioedema (IgE mediated): Onset between various types of hereditary
90% associated with urticaria Location angioedema:
In kinin pathway activation (non-IgE mediated), Associated symptoms: In type 1, there is quantitative deficiency of C1
urticaria usually is absent (1). Pruritus esterase inhibitor.
r Direct, nonimmunologic mechanisms include radio Dyspnea In type 2, there is a functional defect in C1
contrast dyes, physical stimuli like thermal and Dysphagia inhibitor.
mechanical, medications like vancomycin and Vomiting
Imaging
opioids, and foods like strawberries and shellfish. Diarrhea r Imaging is usually not indicated.
Nausea r US of the abdomen is helpful to differentiate
Edema of the GI tract can present with acute
surgical abdomen from abdominal angioedema:
abdominal pain, nausea, and vomiting without
In angioedema, 80% have ascites and edema of
cutaneous features.
intestinal wall (5).
50
ANGIOEDEMA
A
Diagnostic Procedures/Other r Hereditary angioedema: During an acute attack, REFERENCES
Radioallergosorbent testing (RAST) if food allergy is patients should be treated with fresh frozen plasma
suspected in an outpatient setting (FFP) or C1 inhibitor concentrate: 1. Krishnamurthy A, Naguwa SM, Gershwin ME.
Plasma: 2 units of FFP given IV, may be repeated Pediatric angioedema. Clinic Rev Allergy Immunol.
DIFFERENTIAL DIAGNOSIS 2008;34:250259.
in 2 hr
Myxedema, facial cellulitis, superior vena cava 2. Ferdman RM. Urticaria and angioedema. Clin
Kallikrein inhibitor (Ecallantide):
syndrome, dermatomyositis, facial lymphedema, 30 mg IM given in 3 different injection sites, Pediatr Emerg Med. 2007;8(2):7280.
allergic contact dermatitis, and idiopathic edema
usually both arms and 1 thigh 3. Frigas E, Nzeako UC. Angioedema: Pathogenesis,
Only approved in patients >16 yr differential diagnosis, and treatment. Clin Rev
TREATMENT C1 inhibitor concentrates 1020 U/kg Allergy Immunol. 2002;23:217231.
(alternatively: <50 kg, 500 U; 50100 kg, 4. Soccorsa S, Casali A, Bolondi L. Sonographic
PRE HOSPITAL 1000 U; >100 kg, 1500 U) (4) findings in abdominal hereditary angioedema.
r Assess and stabilize airway, breathing, and J Clin Ultrasound. 1999;27:537540.
DISPOSITION
circulation. 5. Farkas H, Varga L, Szeplaki G, et al. Management
r In children with angioedema of the larynx, Admission Criteria
r Patients with no systemic symptoms and localized of hereditary angioedema in pediatric patients.
administration of epinephrine IM is of utmost angioedema without progression of symptoms may Pediatrics. 2007;120:e713e722.
importance. be discharged home.
r Discontinue exposure to any triggering agent. r Patients with systemic symptoms, diffuse
ADDITIONAL READING
INITIAL STABILIZATION/THERAPY angioedema, and/or progression of symptoms
r Assess and stabilize airway, breathing, and should be admitted to the hospital for close See Also (Topic, Algorithm, Electronic
circulation. monitoring and follow up. Media Element)
r Epinephrine is the drug of choice for patients with r Critical care admission criteria: r Anaphylaxis
anaphylaxis or angioedema with upper airway Patients with laryngeal edema or impending r Asthma
involvement. airway compromise r Atopic Dermatitis
Patients with signs and symptoms of anaphlyaxis r Rash, Urticaria
MEDICATION
r Medication will depend on whether or not the Discharge Criteria
r Patients with no sign of airway compromise can be
patient has hereditary angioedema.
r For hereditary angioedema, standard therapies of managed on an outpatient basis. CODES
r Patients should be discharged home on a short
epinephrine, steroids, and antihistamines are
ineffective and not recommended. course of antihistamines and oral steroids. ICD9
r See treatment of hereditary angioedema below. r 277.6 Other deficiencies of circulating enzymes
r Epinephrine is the drug of choice for patients with r 995.1 Angioneurotic edema, not elsewhere
FOLLOW-UP
anaphylaxis or angioedema with upper airway classified
involvement: FOLLOW-UP RECOMMENDATIONS
r Discharge instructions and medications
Dose = 1:1,000 concentration: 0.01 mg/kg IM,
max single dose 0.5 mg All patients should be discharged with an PEARLS AND PITFALLS
Dose can be repeated in 515 min intervals as epinephrine autoinjector: r Pearls:
needed. Patients with a weight <30 kg require an
r Antihistamines: EpiPen Jr. Early recognition of laryngeal edema to prevent
Avoid medications, food, physical agents and impending airway obstruction
Typically, both an H1 blocker and H2 blocker are Early administration of epinephrine in
used. allergens that cause angioedema.
r For hereditary angioedema: life-threatening angioedema
H1 blockers: Patients with hereditary angioedema require
Diphenhydramine 1 mg/kg IM/IV/PO q6h, max Follow up with an experienced allergist.
Register at the hereditary angioedema different therapy than anaphylaxis, including
50 mg plasma, Ecallantide, or C1 inhibitor concentrate.
Hydroxyzine 0.51 mg/kg IM/IV/PO q6h, max international database at www.haeregister.org.
Discharge patients with a prescription for an
50 mg DIET EpiPen.
H2 blockers: Avoid triggers (food products) that cause r Pitfalls:
Theoretically may be beneficial and are angioedema. Missing hoarseness as a sign of impending airway
commonly used
Famotidine 0.5 mg/kg IV, max single dose 40 mg PROGNOSIS obstruction
Ranitidine 24 mg IV, max single dose 100 mg Hereditary angioedema is incurable, but acute attacks Failure to recognize the potentially progressive
r Steroids: can be treated, and prophylaxis is available. nature of angioedema
For hereditary angioedema, epinephrine, steroids,
Indicated if airway involvement or extensive and antihistamines are not useful.
cutaneous involvement Administering epinephrine solution of 1:10,000
Dexamethasone 0.2 mg/kg IV/IM/PO (max single instead of 1:1,000
dose 10 mg) may be repeated q612h if
necessary.
Methylprednisolone 12 mg/kg IV q6h
Prednisone 2 mg/kg PO (max single 60 mg)
loading dose can be used, followed by 1
mg/kg/dose b.i.d. for 5 days (max 60 mg/day)
51
ANKLE SPRAIN
Megan E. Lavoie
Marc Gorelick
Grade II (moderate)partial ligament tear: r Inversion stress test (for integrity of CFL):
BASICS Moderate pain Hold foot in neutral, stabilize tibia/fibula above
Swelling with possible ecchymosis ankle joint, invert ankle with other hand to assess
DESCRIPTION Pain with weight bearing or ambulation talar tilt and inversion of midfoot. Compare
r Ankle injury is a musculoskeletal injury where Some joint instability on testing relative to uninjured side.
ligaments of ankle are injured due to stretching or Grade III (severe)complete ligament tear or r Squeeze test (assessing for syndesmosis injury):
tearing, typically from inversion injury. rupture: Compress the tibia and fibula at the level of the
r The major concern is differentiating sprain from Severe pain or occasionally painless midcalf. The test is positive if there is pain distally
fracture. Significant swelling (>4 cm about fibula) over tibia and fibula with calf squeezing.
Unable to bear weight or ambulate r External rotation test (assessing for syndesmosis
EPIDEMIOLOGY Mechanically unstable ankle on testing
r The ankle is the most commonly injured joint among injury):
athletes (1): ETIOLOGY Stabilize leg proximal to ankle joint, grasp plantar
3040% of all athletic injuries Trauma to ankle, typically by inversion or eversion aspect of foot, and rotate it externally. The test is
r Most frequently seen musculoskeletal injury in the positive if there is pain with external rotation.
emergency department or primary care setting: Fracture DIAGNOSTIC TESTS & INTERPRETATION
75% of all ankle injuries are sprains.. Imaging
85% of sprains are inversion injuries. r If there is concern for fracture, obtain ankle x-rays.
r Incidence is equal in males and females. DIAGNOSIS r Ottawa ankle rules (2,3):
RISK FACTORS HISTORY Obtain AP, lateral, and mortise x-rays of ankle if
Previous ankle sprain or injury r Mechanism of injury patient presents within 10 days of injury with any
r Activity at time of injury of the following:
PATHOPHYSIOLOGY r Previous injury to ankle Bony tenderness in posterior aspect of distal 6
r The ankle is a hinge joint composed of the tibia,
r Location, duration, and quality of pain cm of malleolus of tibia or fibula
fibula, and talus, which in turn are stabilized by Unable to walk for 4 steps immediately after
ligaments medially and laterally: r Bearing weight or ambulatory after injury
injury or in emergency department
Lateral ligaments: Anterior talofibular ligament r Presence of swelling or bruising
If there is bony tenderness over the navicular bone
(ATFL), calcaneofibular ligament (CFL), posterior r Pop or snap in ankle at time of injury or base of the 5th metatarsal, obtain foot x-rays.
talofibular ligament (PTFL): Ottawa ankle rules were not developed for use in
The ATFL is the most commonly injured. PHYSICAL EXAM
r Inspect for swelling, bruising, and deformity. children; if there is concern for fracture involving
The PTFL is the strongest of the lateral ligaments the growth plate, obtain x-rays.
and is rarely injured with inversion injury. Compare with contralateral ankle. r If the sprain is symptomatic >6 wk, or if there is
r Assess passive and active range of motion.
Medial support is from the deltoid complex: crepitus, catching, or locking of the joint, obtain CT
Medial ligament sprain with eversion injury, r Palpate for tenderness along entire length of fibula,
or MRI.
which is commonly associated with lateral tibia, and base of 5th metatarsal.
malleolus fracture r Palpate for tenderness along ligaments. DIFFERENTIAL DIAGNOSIS
r Several types of ligamentous injuries: r Anterior drawer test (for integrity of ATFL): r Fracture of lateral, medial, or posterior malleolus
r Fracture of proximal fibula:
Grade I (mild)ligament stretch: Hold ankle in slight plantar flexion, grasping heel
Mild pain with one hand, holding tibia/fibula above joint Maisonneuve fracture involves a syndesmosis
Minimal if any swelling line, trying to pull foot forward with anterior force injury to the interosseus membrane, which results
Can bear weight or ambulate with minimal pain on heel. Compare laxity relative to uninjured side. in a proximal fibular fracture.
No joint instability on testing
52
ANKLE SPRAIN
A
r Fracture of lateral process of talus r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN REFERENCES
r Fracture of anterior process of calcaneus r Opioids:
r Fracture of base of 5th metatarsal Morphine 0.1 mg/kg IV/IM/SC q2h PRN: 1. DiGiovanni BF, Partal G, Baumhauer JF. Acute ankle
r Navicular or midtarsal fracture Initial morphine dose of 0.1 mg/kg IV/SC may injury and chronic instability in the athlete. Clin
r Salter I distal fibula fracture be repeated q1520min until pain is controlled, Sports Med. 2004;23:119.
r Hindfoot sprain then q2h PRN. 2. Steill, IG, McKnight, RD, Greenberg GH, et al.
r Tear of peroneal brevis or longus tendon Codeine or codeine/acetaminophen dosed as Decisions rules for use of radiography in acute
0.51 mg/kg of codeine component PO q4h PRN ankle injuries: Refinement and prospective
r Superficial peroneal nerve injury
Hydrocodone or hydrocodone/acetaminophen validation. JAMA. 1993;269:11271132.
r Osteochondral talar dome injury
dosed as 0.1 mg/kg of hydrocodone component 3. Gravel J, Hedrei P, Grimard G, et al. Prospective
r Syndesmosis (high) sprain PO q46h PRN validation and head-to-head comparison of 3 ankle
r Ankle impingement syndrome rules in a pediatric population. Ann Emerg Med.
SURGERY/OTHER PROCEDURES 2009;54:534540.
Surgery is not needed in the acute setting but may
4. Chorley JN. Ankle sprain discharge instructions
TREATMENT ultimately be indicated by the consulting orthopedic
from the emergency department. Pediatr Emerg
surgeons for grade III sprains.
Care. 2005;21(8):498501.
PRE HOSPITAL Issues for Referral
r Rest, ice, compression, and elevation of affected r Follow up with primary physician, sports medicine,
extremity (RICE) or orthopedics if pain is not improving in 47 days. ADDITIONAL READING
r Avoid weight bearing if painful. r Refer to orthopedics from the emergency
r Pain control department if: Wolfe MH, Uhl TL, Mattacola CG, et al. Management
Fracture or dislocation of ankle sprains. Am Fam Physician. 2001;63(1):
INITIAL STABILIZATION/THERAPY Neurovascular compromise 93104.
r RICE
r Adequate pain control Tendon rupture or subluxation See Also (Topic, Algorithm, Electronic
Wound penetrating joint space Media Element)
r Crutches during initial period, with weight bearing
Locking of joint r Fracture, Foot
as tolerating Syndesmosis sprain r Trauma, Foot/Toe
r Plastic ankle-foot orthotic, walking boot, or Symptoms out of proportion to degree of trauma
posterior splint if severe sprain; air or gel-filled ankle
brace if mild or moderate sprain
r Early mobilization and range-of-motion exercises FOLLOW-UP CODES
r Return to athletics only when jogging is pain free
FOLLOW-UP RECOMMENDATIONS ICD9
and the affected ankle has full range of motion. r Discharge instructions and medications: r 845.00 Unspecified site of ankle sprain
MEDICATION RICE r 845.01 Deltoid (ligament), ankle sprain
r NSAIDs: Analgesic medication r 845.02 Calcaneofibular (ligament) ankle sprain
Consider NSAID medication in anticipation of r Activity:
prolonged pain and inflammation: Weight bearing when pain free
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN No return to athletics until pain free PEARLS AND PITFALLS
Naproxen 5 mg/kg PO q8h PRN
PROGNOSIS r If growth plates are open, the clinician must
Some clinicians prefer to avoid NSAIDs due to Most patients will be back to playing sports by 6 wk,
theoretical concern over influence of callus but up to 50% will have symptomatic complaints for consider a possible Salter-Harris type I fracture.
formation if fracture is present. r Premature return to activity can cause chronic ankle
up to a year after injury (4).
instability and pain. Patients should be counseled
not to return to activity until their injured ankle has
full range of motion and can tolerate weight bearing
without pain.
53
ANTERIOR UVEITIS (IRITIS)

Maria Carmen G. Diaz
PATHOPHYSIOLOGY r Slit lamp exam:

BASICS Inflammation of the uveal tract Inflammatory cells
Proteinaceous flare
DESCRIPTION ETIOLOGY
r Traumatic: In cases of severe inflammation, leukocytes may
r The uveal tract is comprised of the iris, ciliary body, settle in the anterior chamber, forming a
and choroid. The iris and ciliary body are found in Direct blow from blunt object
r Infectious: hypopyona white or yellowish accumulation of
the anterior portion of the uveal tract, and the purulent material
choroid is in the posterior portion. Herpes Keratitic precipitates: WBCs on endothelium. Small
r Uveitis is an inflammation of the uveal tract. Syphilis precipitates are nongranulomatous. Large ones
r Anterior uveitis is an inflammation of the iris and/or r Inflammatory:
are granulomatous and often seen in sarcoidosis.
ciliary body. It is often referred to as iridocyclitis or HLA-B27 r Traumatic iritis: Aqueous cells and flare with normal,
iritis depending on the part of the uveal tract that is Sarcoidosis low, or elevated intraocular pressure. Assess
inflamed. JRA carefully for hyphema.
r Posterior uveitis includes choroiditis and retinitis. r Idiopathic r Chronic anterior uveitis: May have minimal
r Uveitis may be classified by location, chronicity, or COMMONLY ASSOCIATED CONDITIONS symptoms but may have severe inflammation on
etiology. When classified by etiology, it is generally r JRA exam
identified as traumatic, infectious, inflammatory, or r HLA-B27 r Specific physical exam findings may help to uncover
idiopathic. r Sarcoidosis an underlying etiology or associated condition:
r Herpes HLA-B27 associated uveitis:
EPIDEMIOLOGY Ankylosing spondylitis
Incidence Iritis with hypopyon in anterior chamber
r The annual incidence of uveitis is 17 in 100,000
DIAGNOSIS Lower extremity pain
people (1). Back pain
r Anterior uveitis occurs most commonly in patients HISTORY Reiter syndrome:
between the ages of 20 and 50 yr (1). r Always ask about history of trauma. Iritis
r 2950% of cases of pediatric anterior uveitis are r Acute anterior uveitis: Sudden onset of Associated arthritis and urethritis
idiopathic. photophobia, pain, redness, decreased vision, and Inflammatory bowel disease:
r 16% of cases of anterior uveitis in children are tearing (2). Deep aching pain that may radiate to Iridocyclitis
related to the human leukocyte antigen B27 the periorbital or temporal area. Pain is worse with GI symptoms
(HLA-B27). eye movement and accommodation (4). Joint inflammation
r Traumatic iritis: Photophobia, redness, and pain of Psoriasis:
Prevalence
r Pediatric uveitis comprises 510% of all cases of the affected eye 13 days after injury, usually a Chronic anterior uveitis
direct blow to the eye Pauciarticular or polyarticular arthritis of distal
uveitis (2). r Chronic anterior uveitis: May have minimal
r 1 study from the United Kingdom described a joints of hands/feet and sacroiliac joints
symptoms. Will often have other symptoms of Rash
prevalence of 4.9 in 100,000 children (3).
r Iritis is seen in 25% of pediatric patients with underlying disease. Sarcoidosis-associated uveitis:
Chronic anterior uveitis
ankylosing spondylitis. PHYSICAL EXAM Large keratitic precipitates
r Iritis is seen in 312% of patients with Reiter r Assess visual acuity.
Iris nodules
syndrome. r Perilimbal or circumcorneal injection (ciliary flush) Aqueous cells
r Iridocyclitis occurs in 211% of patients with r Tearing but no purulent discharge Patients with onset at 8 and 15 yr of age will
inflammatory bowel disease. r Pupil is constricted and may be irregular. often have pulmonary involvement,
r Uveitis occurs in 20% of patients with juvenile r Pupillary response to light is sluggish compared to lymphadenopathy/hepatosplenomegaly.
rheumatoid arthritis (JRA) (2). unaffected eye. Those with onset of disease at <5 yr of age will
r May have direct photophobia also have arthritis and skin rash.
RISK FACTORS
r May have consensual photophobia (photophobia of
JRA is the most common condition associated with
anterior uveitis in the pediatric population: affected eye when light shines in unaffected eye) (4)
r Uveitis is most prevalent in the pauciarticular form
of JRA.
r Females who are antinuclear antibody positive and
Rh negative are at the highest risk for developing
uveitis (2).
54
ANTERIOR UVEITIS (IRITIS)

A
Herpes-associated uveitis: PROGNOSIS
Iridocyclitis TREATMENT Idiopathic cases of anterior uveitis usually resolve in 6
Aqueous cells wk. Most cases will not recur (1).
Posterior synechiae INITIAL STABILIZATION/THERAPY
Keratitic precipitates COMPLICATIONS
In cases of traumatic iritis, careful primary and r Synechia: Adhesions of the posterior iris to the
Hypopyon secondary surveys should be conducted to rule out
Hyphema anterior capsule of the lens
other concomitant traumatic injuries. r Angle closure glaucoma
May have elevated intraocular pressures
MEDICATION r Cataract formation (6)
May have associated keratitis
Skin vesicles First Line r Band keratopathy
JRA-associated uveitis: Cycloplegics and topical corticosteroids: r Visual loss (2)
Pauciarticular or polyarticular arthritis (usually r Corticosteroid therapy should only be initiated after
precedes the onset of uveitis) consultation with ophthalmology.
r Prednisone: 2 drops in affected eye q.i.d.: REFERENCES
Patients with idiopathic anterior uveitis may 1. Dargin JM, Lowenstein RA. The painful eye. Emerg
Lab require a corticosteroid taper lasting several
Initial Lab Tests Med Clin North Am. 2008;26:199216.
r Lab work is often not indicated in the emergent weeks.
2. Patel H, Goldstein D. Pediatric uveitis. Pediatr Clin
Corticosteroids may worsen symptoms in certain
setting. North Am. 2003;50:125136.
r Infectious uveitis can be difficult to diagnose and infectious etiologies of anterior uveitis (4).
r Tropicamide 1%: 12 drops in affected eye t.i.d.: 3. Edelsten C, Reddy MA, Stanford MR, et al. Visual
may require specific serology testing if the patient loss associated with pediatric uveitis in English
Good cycloplegic choice because of its short
does not respond to conventional therapy. primary and referral centers. Am J Ophthalmol.
r Patients with a suspected systemic condition will (46 hr) duration of action. In contrast, atropine
2003;135:676680.
lasts 57 days.
require further testing. This may often be done as an 4. Mahmood AR, Narang AT. Diagnosis and
outpatient. Second Line management of the acute red eye. Emerg Med Clin
Treat underlying disorder in nontraumatic cases. North Am. 2008;26:3555.
Imaging
r Consider CXR or CT of the chest if there is suspicion SURGERY/OTHER PROCEDURES 5. Levine L. Pediatric ocular trauma and shaken infant
for sarcoidosis. Surgery is generally only indicated if complications syndrome. Pediatr Clin North Am. 2003;50:
r Consider obtaining images of the sacroiliac joints if develop. 137148.
there is suspicion of HLA-B27 disease. 6. Wagner RS, Aquino M. Pediatric ocular
DISPOSITION inflammation. Immunol Allergy Clin North Am.
DIFFERENTIAL DIAGNOSIS Admission Criteria 2008;28:169188.
r Retinoblastoma: Systemic illness or trauma requiring inpatient therapy
May cause intraocular inflammation in a patient Discharge Criteria
<5 yr of age Most patients may be discharged home with close CODES
May occasionally present with red, painful eye outpatient follow-up.
May see pseudohypopyonlayering of tumor Issues for Referral ICD9
cells in anterior chamber r All patients with anterior uveitis should be referred 364.3 Unspecified iridocyclitis
r Leukemia:
to an ophthalmologist.
Also causes ocular inflammation r Consider referral to a rheumatologist if an
Will see heterochromia, iris infiltrates, associated rheumatologic disease is suspected. PEARLS AND PITFALLS
spontaneous hyphema, leukemic cells in the
r Patients with anterior uveitis will have hyperemia
aqueous, or pseudohypopyon in the anterior
segment FOLLOW-UP adjacent to the limbus. In contrast, hyperemia in
r Juvenile xanthogranuloma: those with conjunctivitis is maximal on the
Nonneoplastic histiocytic proliferation that usually FOLLOW-UP RECOMMENDATIONS periphery, farther from the limbus.
r Discharge instructions and medications: r Consensual photophobia is another distinguishing
develops in children <2 yr of age
Present with anterior chamber cells or Follow-up with an ophthalmologist. feature of anterior uveitis. This is not seen in other
spontaneous hyphema. There also may be iris Use medication as prescribed. superficial causes of photophobia.
heterochromia. Traumatic iritis: r Floaters and decreased visual acuity are
The condition is self-limited and remits by 5 yr of Avoid bright lights. symptoms of posterior uveitis.
age (2). Use sunglasses (5). r All patients with anterior uveitis require referral to
r Activity: an ophthalmologist.
Traumatic iritis: Avoid strenuous activity and
contact sports until cleared by an ophthalmologist.
55
ANTICHOLINERGIC POISONING
David H. Jang
Lewis S. Nelson
r Tricyclic antidepressants (TCAs): r Mental status changes are common:

BASICS Amitriptyline Patients are often confused and may also display
Doxepin agitated delirium.
DESCRIPTION Imipramine Seizure may rarely occur.
r Anticholinergic poisoning occurs with the inhibition r Neuroleptics: r Inability for eyes to accommodate and mydriasis
of muscarinic cholinergic transmission at muscarinic Chlorpromazine (often does not respond to light as opposed to
receptors that often manifest as an anticholinergic Clozapine mydriasis that occurs with sympathomimetics)
syndrome. Olanzapine r Skin is dry and flushed.
r Overdose from anticholinergic agents often occur Quetiapine r Often will have accompanying decreased GI motility
secondary to prescription medications, r Plants: as well as urinary retention
nonprescription medications, and plants. Atropa belladonna (deadly nightshade)
r Severe problems include seizures and agitated Datura stramonium (jimson weed) DIAGNOSTIC TESTS & INTERPRETATION
delirium. Lab
COMMONLY ASSOCIATED CONDITIONS Initial Lab Tests
RISK FACTORS Ingestion of other drugs or alcohol r Anticholinergic syndrome is a clinical diagnosis, and
r Use of multiple anticholinergic medications
assays are only adjunctive.
simultaneously, such as over-the-counter (OTC) r Acetaminophen level:
cough/cold preparations DIAGNOSIS
r Repeated high-dose anticholinergic use, such as The serum acetaminophen level should be
HISTORY considered in patients with intentional ingestion.
diphenhydramine for allergy or ipratropium for r A history of exposure may be helpful but may not be OTC products often contain acetaminophen.
status asthmaticus r The measurement of electrolytes, BUN, creatinine,
r Adolescents who use substances like cough syrups available or forthcoming.
r The use of OTC medicines, such as multisymptom and blood sugar may be useful to differentiate from
or hallucinogenic plants recreationally other etiologies.
cold preparations or dietary supplements, may be
PATHOPHYSIOLOGY obtained. r Measurement of creatine phosphokinase for
r Anticholinergic symptoms result from muscarinic r Onset of symptoms is usually within 1 hr. suspected rhabdomyolysis that can occur with
receptor antagonism. r Anticholinergic toxicity following ingestion typically agitation, seizures, or certain overdoses (doxylamine
r Atropine is the prototypical muscarinic receptor peaks in 14 hr and lasts 48 hr, but this largely can cause rhabdomyolysis in overdose)
antagonist. depends on the agent and dose. Imaging
r Antagonism of central and peripheral muscarinic r Symptoms include altered mental status: A noncontrast head CT should be obtained in
cholinergic receptors Confusion unresponsive patients or those with focal neurologic
r Antagonism of central muscarinic receptors often Garbled, pressured, nonsensical speech deficits.
will produce delirium, agitation, or seizures. Classically will display picking behavior where
r Antagonism of peripheral muscarinic receptors will Diagnostic Procedures/Other
patients will pick at imaginary objects near them. r Obtain ECG.
often produce tachycardia, decreased GI motility, Lilliputian hallucinations in which patients have r Strongly consider lumbar puncture in patients who
and flushed skin. distortion of sense of scale, perceiving that objects
or persons are extremely small or extremely large have signs and symptoms of meningitis or
ETIOLOGY relative to themselves encephalitis (more likely; seizure, fever, altered
r Anticholinergics: mental status, etc.) where a history of an overdose
Atropine PHYSICAL EXAM may not be forthcoming.
r Anticholinergic syndrome is a clinical diagnosis.
Benztropine DIFFERENTIAL DIAGNOSIS
r Vital sign abnormalities are common:
Scopolamine r Sympathomimetic poisoning
r Antihistamines: Tachycardia is typical, and mild hyperthermia may r Malignant hyperthermia
Chlorpheniramine occur. r Neuroleptic malignant syndrome
Diphenhydramine r Hyperthyroidism/Thyroid storm
Doxylamine
r Subarachnoid hemorrhage
r Serotonin syndrome
r Withdrawal syndromes
r Encephalitis
r Sepsis
56
ANTICHOLINERGIC POISONING
A
When administered, the patient should be on a ADDITIONAL READING
TREATMENT cardiopulmonary monitor, with atropine at the
r Howland MA. Antidotes in depth: Physostigmine. In
bedside to give for immediate.
INITIAL STABILIZATION/THERAPY Should not be used in patients with suspected Goldfrank LR, Flomenbaum NE, Lewin NA, et al.,
r Assess and stabilize airway, breathing, and TCA overdose eds. Goldfranks Toxicologic Emergencies. 8th ed.
circulation. Relative contraindications include reactive airway Stamford, CT: Appleton & Lange; 2006.
r Maintaining vital signs within acceptable limits and disease, atrioventricular block, and intraventricular r Koppel C, Ibe K, Tenczer J. Clinical symptomatology
controlling patient agitation are commonly required. conduction delays. of diphenhydramine overdose: An evaluation of 136
r Patients who are hyperthermic may require cooling Adverse reactions often include increased cases in 1982 to 1985. J Toxicol Clin Toxicol.
and sedation with a benzodiazepine. cholinergic symptoms, such as bradycardia, 1987;25:5370.
r Use of antipsychotics, such as haloperidol, is bronchorrhea, vomiting, and diaphoresis: r Burns MJ, Linden CH, Graudins A, et al. A
Monitoring for bradycardia and airway comparison of physostigmine and benzodiazepines
relatively contraindicated, as these medications may
secretions is especially important. for the treatment of anticholinergic poisoning. Ann
increase risk of cardiac dysrhythmia, lower seizure
Physostigmine when compared to Emerg Med. 2000;35:374381.
threshold, impair heat dissipation, and also have
benzodiazepines showed shorter time to recovery
anticholinergic effects. See Also (Topic, Algorithm, Electronic
from agitation, but length of stay was unchanged.
MEDICATION As a pure antidote, physostigmine is superior to Media Element)
r Activated charcoal: benzodiazepines, but clinician comfort and Sympathomimetic Toxicity
1 g/kg may be administered in cooperative familiarity should determine whether
patients to bind drug in the GI tract. physostigmine or benzodiazepines are used for
Typically, charcoal is used only if ingestion treating anticholinergic symptoms. CODES
occurred <1 hr previously, but anticholinergic
DISPOSITION
medications slowing GI motility and charcoal may ICD9
be administered later than 1 hr after ingestion. Admission Criteria 971.1 Poisoning by parasympatholytics
r Benzodiazepines: r Unstable vital signs, abnormal mental status, patient
(anticholinergics and antimuscarinics) and
Used to control agitation and delirium being a danger to self or others, end-organ toxicity spasmolytics
r If antidotal physostigmine or benzodiazepines are
Extremely favorable safety profile and clinician
familiarity usually indicate benzodiazepines as a needed to reverse anticholinergic symptoms,
first-line medication admission should be strongly considered. PEARLS AND PITFALLS
Diazepam: r Anticholinergic syndrome can be clinically diagnosed
0.1 mg/kg IV, max single dose 10 mg q520min Unstable vital signs, seizures, end-organ toxicity
with a good physical exam and history.
titrated to effect Discharge Criteria r It is important to be wary of medications that are
First line for agitation; faster and more Any patient with vital signs within normal limits, anticholinergic and also have other associated
predictable as a sedative normal mental status, and no evidence of end-organ toxicity, such as TCAs.
Lorazepam in doses of 0.05 mg/kg IV q15min damage may be discharged from the emergency r Use of benzodiazepines or physostigmine to control
titrated to effect is the preferred treatment for department.
seizures. agitation or other neurologic symptoms assists in
r Physostigmine: Issues for Referral management.
r Refer patients with intent of self harm to psychiatry. r Physostigmine is the preferred antidote because it
Dose 0.02 mg/kg, max single dose 0.5 mg in r Refer patients with substance abuse for drug
children <10 yr of age, 12 mg total dose in results in normalization of mental status and
counseling. reversal of other anticholinergic symptoms.
adults, given IV over 5 min
r Although benzodiazepines only result in sedation
Physostigmine is a cholinergic antidote used to
reverse central anticholinergic effects: FOLLOW-UP and do not improve other anticholinergic symptoms,
As such, physostigmine is the preferred clinician familiarity with benzodiazepines and their
medication since it normalizes anticholinergic PROGNOSIS excellent safety profile may warrant use.
symptoms and benzodiazepines only provide Patients who are anticholinergic typically do well with
sedation. good supportive care, with special attention to other
Physostigmine may allow restoration of normal medication effects such as sodium channel blockade.
mental status and avert the need for additional COMPLICATIONS
evaluation such as lumbar puncture or head CT. Complications of anticholinergic toxicity often can
Indications for physostigmine include the presence include seizures and injury to self.
of anticholinergic toxicity without any evidence of
QRS or QTc prolongation.
Half-life is approximately 15 min, but duration of
action may be over an hour. Redosing may be
required as indicated.
57
ANTICOAGULANT POISONING
Beth Y. Ginsburg
PATHOPHYSIOLOGY r Warfarin is also associated with nonhemorrhagic

BASICS r The mechanism of action of warfarin as an dermatologic complications:
anticoagulant involves its role in the inhibition of the Urticaria
DESCRIPTION vitamin K cycle: Purple toe syndrome, which is due to small
r Warfarin and heparin are the main anticoagulants Vitamin K is a cofactor in the synthesis of clotting atheroemboli that are no longer adherent to
available for medicinal use: factors II, VII, IX, and X and proteins C and S. It is plaque by clot
Warfarin is an oral anticoagulant. required for transforming clotting factor from their Warfarin skin necrosis, which is due to
Unfractionated heparin is administered IV or SC. inactive to active forms. microvascular thrombosis in dermal vessels as a
Low-molecular-weight heparins (LMWH; eg, Warfarin leads to inactivation of vitamin K. result of falling protein C levels with the onset of
dalteparin, enoxaparin) are administered SC. Vitamin K must be enzymatically reduced back to warfarin therapy
r Indications for use include coronary artery disease, its active form in order to resume function as a Treatment involves cessation of warfarin and
cerebrovascular events, venous thromboses, and cofactor. initiation of heparin.
pulmonary embolisms. Heparin is also used for Warfarin inhibits this enzymatic reaction, thereby r Heparin functions as an anticoagulant by
prevention of thrombosis after surgery and during interfering with coagulation. accelerating the binding to antithrombin III to
periods of immobilization (eg, hospitalization). r Toxicity is characterized by coagulopathy: thrombin. As a result, clotting factors IX to XII and
r Long-acting oral anticoagulants, or superwarfarins, The risk of hemorrhage depends on the intensity thrombin are inhibited.
are manufactured for use as rodenticides and of anticoagulation as well as the patients r Duration of action is usually 13 hr.
typically contain only a small concentration of comorbidities. r LMWHs have a similar mechanism of action with
anticoagulant. The most common sites of bleeding are the GI and some pharmacologic differences:
r Exposure to superwarfarin rodenticides are the most genitourinary tract. Patients may also present with Patients with renal insufficiency or failure are at
common pediatric anticoagulation issue seen in the bruising and menorrhagia. increased risk of toxicity.
pediatric emergency department. Most of these The most serious complication is an intracranial r Toxicity is characterized by coagulopathy that can
fortunately do not result in anticoagulation. hemorrhage, which is associated with a high result in various forms of bleeding.
r Superwarfarin exposures should be evaluated by lab mortality rate. r Heparin is also associated with a mild
r Anticoagulant effects can be potentiated by
assay due to fact that if anticoagulation occurs, it thrombocytopenia referred to as heparin-induced
will be present for weeks to months and may result coingestion of other drugs that inhibit warfarin thrombocytopenia (HIT) as well as a more severe
in death from minor trauma, such as intracranial metabolism or lead to increased free warfarin levels form referred to as heparin-induced
hemorrhage after minor head injury. by competing for binding to albumin: thrombocytopenia and thrombosis syndrome
Allopurinol, anabolic steroids, cephalosporins, (HITTS):
EPIDEMIOLOGY cimetidine, clofibrate, cyclic antidepressants, HIT and HITTS occur less frequently with LMWHs.
Incidence erythromycin, ethanol, NSAIDs, sulfonylureas
r There are many reported cases of intentional and r Anticoagulant effects are delayed until existing ETIOLOGY
unintentional overdoses of warfarin and r Heparin
stores of active vitamin K and coagulation factors
superwarfarins: r Warfarin (Coumadin)
are depleted. In most patients, effects are not
In children, these are typically exposure to apparent until at least 15 hr. r Rodenticides (superwarfarins):
superwarfarin rodenticides used in the home. r Duration of action is several days for warfarin. Brodifacoum
Most unintentional single ingestions of r Superwarfarins have a duration of action of weeks Difenacoum
superwarfarins are not associated with a large Chlorophacinone
to months depending on which agent is ingested.
enough dose to cause toxicity. Diphacinone
They are also more potent than warfarin:
Toxicity may potentially develop with repeated
They are designed as such to be lethal rodenticides
ingestions over time, even if small.
when ingested in a single, small dose by a rodent.
Intentional overdoses of superwarfarins are
associated with significant toxicity.
r Unfractionated heparin typically is administered to
hospitalized patients. Most overdoses involve
unintentional poisoning due to medication error.
r There is potential for intentional overdose with
self-administered LMWH.
58
A
r Elevated PTT is indicative of coagulopathy secondary r In cases of life-threatening hemorrhage secondary
DIAGNOSIS to heparin toxicity. LMWHs do not have an effect on to warfarin or superwarfarins, coagulopathy should
the PTT, and this test cannot be used to monitor for be reversed with a transfusion of fresh frozen
HISTORY LMWH toxicity. plasma (FFP), prothrombin complex concentrate, or
r In absence of a history of exposure, complaints of r Hemoglobin and hematocrit should be monitored in recombinant factor VIIa.
bleeding and/or bruising in conjunction with cases of bleeding. r Exchange transfusion may be used in neonates
abnormal laboratory values may be suggestive of an r Platelets should be monitored for development of following a heparin overdose.
exposure to an anticoagulant. r Oral activated charcoal (1 g/kg) may be administered
r Children with exposure to rodenticide HIT or HITTS.
r Urine and stool may be checked for occult blood. to patients with a recent (1 hr) potentially significant
anticoagulants typically have an exposure history of ingestion of oral anticoagulant as long as there are
possible ingestion of a small quantity of rodenticide. ALERT no contraindications such as altered mental status.
r In children, lab error resulting from inadequately
PHYSICAL EXAM MEDICATION
The physical exam should focus on uncovering filled blood vials to assay coagulation times r Vitamin K in the form of vitamin K (phytonadione)
1
evidence of coagulopathy and bleeding: commonly results from underfilling these tubes. is used to reverse coagulopathy in the setting of oral
r Vital sign abnormalities may include tachycardia and r When filling vacuum tubes, allow the tube to
anticoagulant toxicity.
hypotension depending on the degree of blood loss. aspirate precisely the quantity of blood taken by Vitamin K3 (menadione) is not appropriate for
r Evaluation of the mouth may reveal gingival its vacuum. use; only vitamin K1 (phytonadione) is used.
bleeding. r Even a slightly decreased amount may errantly It should be administered in any case of serious
r Rectal exam may uncover bright red blood or result in falsely prolonged coagulation times due bleeding regardless of the degree of elevation of
melena. Stool may be tested for occult blood. to inappropriate anticoagulant/blood ratio in the the PT or INR.
r A urine sample may reveal gross hematuria and may tube. r Chronic warfarin exposure:
be tested for microscopic hematuria. For patients with an elevated INR who require
r Dermatologic examination may reveal bruising. Imaging chronic anticoagulation, the use of vitamin K and
r Neuroimaging should be performed if there is
r Altered mental status, seizures, or any other transfusion depends on the degree of elevation of
concern for an intracranial hemorrhage. INR and whether or not there is bleeding:
neurologic deficits should elicit concern for r Imaging with CT and/or US may be used for
intracerebral hemorrhage. INR <5.0; no significant bleeding: Lower the
diagnosing hemorrhage into other tissues or warfarin dose, or omit next dose, of warfarin;
DIAGNOSTIC TESTS & INTERPRETATION compartments. monitor INR frequently; resume anticoagulation
Lab when INR reaches therapeutic range.
r Prolongation of the PT and elevation of the INR are INR 5.09.0; no significant bleeding: Omit
indicative of coagulopathy secondary to warfarin or TREATMENT next 12 doses of warfarin; monitor INR
a superwarfarin: frequently; resume anticoagulation when INR
Onset of PT prolongation and INR elevation is
r Assess and stabilize airway, breathing, and reaches therapeutic range. May administer
between 12 and 24 hr post ingestion. vitamin K 12.5 mg PO, especially if patient is
circulation.
It is not routinely necessary to obtain a PT or INR r Blood transfusion should be initiated in patients at increased risk for bleeding.
prior to this time frame. INR 9.0; no significant bleeding: Hold
If there is a concern for chronic or repeated with significant blood loss who are, or are expected warfarin; administer vitamin K1 2.55.0 mg PO;
exposures to a superwarfarin rodenticide to become, hemodynamically unstable: monitor INR frequently; administer additional
For the purpose of obtaining the baseline, PT and Packed RBCs are useful in replacing lost blood but vitamin K1 as needed; resume anticoagulation
INR are not required. cannot easily or fully correct coagulopathy. when INR reaches therapeutic range.
Serious or life-threatening bleeding and
elevated INR: Hold warfarin; administer vitamin
K1 10-mg slow IV infusion; supplement with
FFP, prothrombin complex concentrate, or
recombinant factor VIIa; administer additional
vitamin K1 as needed q12h.
59
r Warfarin (not superwarfarin) exposure: Following r Superwarfarin exposure: After exposure, PT and INR r Blood products:
exposure in asymptomatic patients not requiring should be monitored at 24 and 48 hr post exposure: Vitamin K1 will not begin to affect clotting for 6 hr.
anticoagulation, PT and INR should be monitored at Patients who develop coagulopathy will require Patients with active hemorrhage will require FFP or
24 and 48 hr post ingestion: high doses of vitamin K several times a day for whole blood. Recombinant factor VII (NovoSeven)
Vitamin K1 0.6 mg/kg/dose PO b.i.d.q.i.d, weeks to months. may be used as an alternative to FFP:
typically 510 mg PO b.i.d.q.i.d. 3 days in Vitamin K1 : Starting dose is typically 2550 mg FFP 1525 mL/kg IV; adult dose 24 units IV.
children; max single dose 1050 mg PO PO b.i.d.q.i.d. in adolescents/adults and Based on serial PR/INR, repeated doses may be
b.i.d.q.i.d. 3 days in adolescents 0.6 mg/kg/dose PO b.i.d.q.i.d. in children taken necessary.
Given if coagulation results reveal prolongation for an initial 4-wk period. NovoSeven 35120 g/kg IV
secondary to anticoagulant effects INR should be monitored frequently and the dose r Heparin has a relatively short duration of action.
3 days of therapy is dosing for warfarin titrated up or down according to the INR. Following an overdose, observation alone may be
(medicinal). Upon completion of treatment with vitamin K, INR sufficient if significant bleeding has not occurred:
r Vitamin K may be administered prophylactically should continue to be monitored frequently for Heparin infusion should be held. It may be
1
(without serial measurements of PT and INR) for several days to determine if it is safe to resumed when serial PTT levels reach the
3 days. Treatment for this time period will likely discontinue vitamin K1 therapy. therapeutic range.
cover the expected duration of action of r Parenteral vitamin K : r Protamine:
1
warfarin: Given SC or IV for severe warfarin or Used to reverse coagulopathy due to heparin
This is not recommended following large superwarfarin toxicity toxicity. It has a greater affinity for heparin than
ingestions since the duration of anticoagulation is Children 15 mg IV/SC, adults 1025 mg IV/SC; antithrombin III, thereby causing dissociation of
unpredictable. max volume 5 mL/50 mg per dose at SQ injection the heparin-antithrombin III complex
Treatment for prolonged coagulation due to a site 1 mg of protamine neutralizes 100 U of heparin.
rodenticide such as brodifacoum or difenacoum, IV: Given rarely due to risk of anaphylactoid The dose of protamine given should not exceed
etc., is a min of 4 wk and longer in some cases. reaction. Children dosed as 0.6 mg/kg/dose; max the amount of heparin expected to be found
r Vitamin K should not be given prophylactically single dose 1025 mg in older intravascularly at the time of protamine infusion.
1
following suspected ingestion of a superwarfarin. children/adolescents. Infuse at a rate of 1 mg/min Excess protamine administration may result in
r The duration of action is expected to be several or 5% of total dose/min, whichever is slower. paradoxical anticoagulation.
weeks to months. The administration of vitamin K Slow infusion immediately if there are The dose needed should be calculated from the
for several days will merely delay the onset of an INR anaphylactoid symptoms. dose of heparin administered and assuming a
abnormality and coagulopathy in cases in which a SC administration is reserved for cases in which heparin half-life of 6090 min:
significant amount of superwarfarin was ingested: oral administration is unlikely to be effective, such If 3060 min after heparin injection, give
In addition, most exposures to superwarfarins do as significant GI hemorrhage. 0.5 mg of protamine per 100 U of heparin
not result in anticoagulation since the amount IM administration should always be avoided in initially given.
ingested, if any, is not enough to cause toxicity. In patients with coagulopathy due to risk of If 2 hr after heparin injection, give 0.25 mg of
these cases, PT and INR will remain within normal developing hematomas. protamine per 100 U of heparin initially given.
range and treatment with vitamin K is not needed. IV administration is associated with a risk of
anaphylactoid reaction and even death. Slow IV
infusion of vitamin K1 should be limited to cases
of life-threatening bleeding.
60
A
Protamine use should be limited to cases of Issues for Referral r Howland MA. Antidotes in depth: Vitamin K . In
1
life-threatening hemorrhage. Patients who present following an intentional Flomenbaum NE, Goldfrank LR, Hoffman RS, et al.,
Protamine is associated with significant adverse overdose require a psychiatric evaluation. eds. Goldfranks Toxicologic Emergencies. 8th ed.
effects, including anaphylactic and anaphylactoid New York, NY: McGraw-Hill; 2006.
reactions, bradycardia, acute lung injury, and r Su M, Hoffman RS. Anticoagulants. In Flomenbaum
thrombocytopenia. FOLLOW-UP NE, Goldfrank LR, Hoffman RS, et al., eds.
Diabetic patients receiving protamine-containing PROGNOSIS Goldfranks Toxicologic Emergencies. 8th ed. New
insulin (NPH) are at increased risk of having an r There is potential for significant morbidity due to York, NY: McGraw-Hill; 2006.
adverse reaction. hemorrhage, particularly in cases of large intentional
Protamine is not recommended for use in cases of overdoses of superwarfarins.
bleeding secondary to LMWHs. r Due to its short duration of action, development of CODES
DISPOSITION significant morbidity secondary to heparin overdose
Admission Criteria is rare. ICD9
r Patients requiring ongoing care for hemorrhage or 964.2 Poisoning by anticoagulants
COMPLICATIONS
at risk for significant hemorrhage, including patients r Hemorrhage, particularly intracranial hemorrhage
with intentional ingestions of superwarfarins
r Critical care admission criteria: with permanent neurologic injury PEARLS AND PITFALLS
r Death
Unstable vital signs, life-threatening hemorrhage r Superwarfarin rodenticide exposure is the most
(eg, intracranial hemorrhage) common anticoagulant issue in pediatric patients.
Discharge Criteria ADDITIONAL READING r Usually, this is a single small exposure with low
r Patients usually may be safely discharged if they likelihood to result in anticoagulation. Due to length
r Ansell J, Hirsh J, Hylek E, et al. Pharmacology and
have a reliable history of an unintentional overdose, of anticoagulation (weeks to months) and potential
management of the vitamin K antagonists. Chest. for fatality, evaluation of PT/INR at 2448 hr is
are asymptomatic, and are not considered to be at
2008;133:160S198S. recommended.
risk for hemorrhage. r Bronstein AC, Spyker DA, Cantilena JR, et al. 2007
r For children with unintentional exposures to r Do not initially give prophylactically vitamin K , as
1
Annual Report of the American Association of this may mask prolonged coagulation that will occur
rodenticides, the chance of toxicity is small, but it
Poison Control Centers National Poison Data and be present for months.
is recommended that they follow up for repeat
PT/INR:
System (NPDS): 25th Annual Report. Clin Toxicol. r Only vitamin K (phytonadione), not vitamin, K is
1 3
2008;46:9271057.
These patients may complete their 24- and 48-hr r Howland MA. Antidotes in depth: Protamine. In useful.
PT and INR testing as outpatients. r Failure to thoroughly fill Vacutainer tubes sent for
Flomenbaum NE, Goldfrank LR, Hoffman RS, et al.,
coagulation profile is a common lab error.
eds. Goldfranks Toxicologic Emergencies. 8th ed. r Failure to aggressively reverse anticoagulated
New York, NY: McGraw-Hill; 2006.
patients with significant active bleeding may result
in severe morbidity and mortality.
r Protamine has anticoagulant properties itself.
61
ANTICONVULSANT POISONING
Beth Y. Ginsburg
Children with phenytoin toxicity may have atypical r Valproic acid:

BASICS presentations such as opisthotonos. Acute toxicity is seen at levels >100 g/mL, the
An overdose or rapid infusion of IV phenytoin may upper range of therapeutic.
DESCRIPTION result in cardiovascular toxicity (ie, impaired Associated with neurotoxicity characterized by
r Anticonvulsant toxicity falls broadly into several myocardial contractility and conduction, lethargy. Coma with cerebral edema may develop
categories. decreased peripheral vascular resistance). in cases of severe toxicity. GI effects may include
r Classically used anticonvulsants, such as phenytoin, Dysrhythmias may include asystole, ventricular nausea and vomiting.
phenobarbital, and carbamazepine, cause ataxia tachycardia, and ventricular fibrillation. ECG Associated with various metabolic effects:
and nystagmus. manifestations may include increased PR interval, Metabolic acidosis, hyperammonemia,
r Anticonvulsants working by GABA mechanism, such widened QRS interval, and alteration of ST hypocarnitinemia, hypernatremia, and
as phenobarbital, valproic acid, and topiramate, segments and T waves. hypocalcemia
cause dose-dependent CNS depression similar to These effects are partially due to the presence of Pancreatitis, hepatotoxicity, and renal insufficiency
sedative-hypnotic medications. propylene glycol and ethanol in the diluent used rarely occur after acute overdose of valproic acid.
r Unique toxicities, such as cardiotoxicity from in IV preparations and are therefore not Bone marrow suppression resulting in
carbamazepine and metabolic toxicity from valproic associated with overdoses of oral preparations. pancytopenia may occur following very large
acid or topiramate, also occur. These are more IV phenytoin also is associated with local skin overdoses.
common with newer anticonvulsants. irritation, and extravasation may cause necrosis. Chronic toxicity may result in hepatotoxicity due to
r The search for an effective anticonvulsant has led to This also is due to the presence of propylene altered fatty acid metabolism.
glycol. r Gabapentin: Overdose is characterized by lethargy,
the use of a variety of agents since the mid-1800s
with several new anticonvulsants having been Chronic phenytoin toxicity may be associated with slurred speech, ataxia, and movement disorders.
introduced starting in the 1990s. behavioral changes such as hyperactivity, GI symptoms may occur.
confusion, lethargy, and hallucinations as well as r Lamotrigine:
RISK FACTORS gingival hyperplasia, cerebellar effects, and Toxicity is associated with lethargy, nystagmus,
Anticonvulsant use as antiepileptic drug encephalopathy. and ataxia. Seizures have been reported in the
r Phenobarbital setting of overdose.
GENERAL PREVENTION
General poison prevention methods, such as keeping Toxicity is seen at levels >40 g/mL but may Associated cardiotoxicity may include QRS
medications inaccessible to children occur at lower levels with co-ingestants. prolongation. GI symptoms may occur.
Toxicity is typically dose dependent, similar to that Chronic lamotrigine toxicity may lead to rashes,
PATHOPHYSIOLOGY of other sedative hypnotic agents. rhabdomyolysis, and hepatotoxicity.
r Seizures result from one of several cellular
Typically is characterized by slurred speech, ataxia, r Topiramate:
mechanisms: and incoordination. Severe toxicity may lead to Lethargy, nystagmus, ataxia, and myoclonus.
The mechanism of action of anticonvulsants coma with respiratory depression, hypothermia, Seizures have been reported in the setting of
relates to one or more of the cellular mechanisms and loss of neurologic responses. overdose.
responsible for seizures: Phenobarbital toxicity also is associated with
Phenytoin and carbamazepine prolong Metabolic acidosis also has been reported in the
development of cutaneous bullae over setting of topiramate toxicity.
inactivation of sodium channels. pressure-point areas. r Tiagabine: Toxicity is associated with lethargy,
Lamotrigine inhibits glutamic acid activity. r Carbamazepine:
Phenobarbital, valproic acid, gabapentin, and nystagmus, facial myoclonus, and posturing.
Toxicity is seen at levels >612 g/dL. Seizures have been reported in cases with high
tiagabine enhance GABA activity. Overdose is associated with neurologic effects
Topiramate blocks sodium channels, modulates serum concentrations.
such as nystagmus, ataxia, and dysarthria. Large r Levetiracetam: Lethargy, coma, and respiratory
glutamic acid activity, and enhances GABA overdoses may be associated with a decreased
activity. depression were described in 1 case of overdose.
level of consciousness and even coma. Seizures
The mechanism of action of levetiracetam is not ETIOLOGY
may occur in patients both with and without
well defined. underlying seizure disorders. See Pathophysiology.
r Adverse effects and toxicity associated with
Carbamazepine also is associated with
anticonvulsant exposure depend on the particular cardiovascular toxicity due to anticholinergic
agent involved. activity. Effects may include sinus tachycardia, DIAGNOSIS
r Phenytoin:
hypotension as a result of myocardial depression, HISTORY
Toxicity is seen at levels above the therapeutic and conduction abnormalities such as QRS and r A history of exposure is usually available.
level of 1020 mg/L. QT. Other manifestations of anticholinergic toxicity r History of ataxia may be given.
Toxicity primarily affects the cerebellar and may occur, such as decreased GI motility and
vestibular systems and may be concentration urinary retention. PHYSICAL EXAM
dependent: Children are more likely to present with dystonic r Vital sign abnormalities are rare:
Nystagmus may occur at a concentration reactions, choreoathetosis, and seizures but are Bradycardia and/or hypotension may occur with IV
>15 mg/L. less likely to have cardiotoxicity. Children are at phenytoin or carbamazepine toxicity.
Ataxia may occur at a concentration >30 mg/L. risk for toxicity at lower serum drug Respiratory depression may develop with CNS
Lethargy, slurred speech, and pyramidal and concentrations. depression.
extrapyramidal effects may occur at a SIADH may occur with high concentrations. Hypothermia has been described in cases of
concentration >50 mg/L. Chronic toxicity may result in headaches, diplopia, phenobarbital toxicity.
Seizures rarely may occur in the setting of an and ataxia. Fever occurs with anticonvulsant hypersensitivity
acute overdose of phenytoin, typically in patients syndrome.
with a prior seizure disorder.
62
ANTICONVULSANT POISONING
A
r Ophthalmologic findings often include nystagmus. SURGERY/OTHER PROCEDURES
r Cardiac dysrhythmias may occur with TREATMENT Hemodialysis/hemoperfusion:
carbamazepine toxicity or IV phenytoin toxicity. r Valproic acid; hemodialysis/hemoperfusion; for rapid
r Nausea and vomiting are associated with phenytoin, INITIAL STABILIZATION/THERAPY clinical deterioration, hepatic dysfunction, continued
carbamazepine, gabapentin, valproic acid, and r Assess and stabilize airway, breathing, and drug absorption, and/or serum valproic acid
lamotrigine toxicity. circulation. concentration >1,000 mg/L
r Dermatologic findings include cutaneous bullae in r Assess bedside fingerstick blood glucose r Indications for phenobarbital toxicity are persistent
the setting of phenobarbital toxicity. Local skin concentration for altered mental status. severe hypotension.
irritation may develop in cases of IV phenytoin r Discontinue further dosing of anticonvulsant.
r GI decontamination: DISPOSITION
extravasation. Rash occurs with anticonvulsant
hypersensitivity syndrome. Activated charcoal may be considered in recent
Admission Criteria
r Neurologic findings are common. Ataxia, usually r Abnormal vital signs, metabolic derangements,
(<1 hr) ingestions.
with accompanying nystagmus, is typical with neurologic symptoms, or end-organ dysfunction
Multiple-dose activated charcoal may be r Ataxia resulting from phenytoin or carbamazepine
phenytoin, carbamazepine, and phenobarbital. considered for phenytoin, phenobarbital,
Altered mental status, confusion, lethargy, coma, carbamazepine, and valproic acid toxicity. toxicity. If only ataxia, cardiac monitoring is not
slurred speech, myoclonus, posturing, ataxia, r Phenytoin: required.
r Admission for extended-release valproic acid. Peak
incoordination, and seizures may also result from Cardiac dysrhythmias and hypotension from IV
anticonvulsants generally. phenytoin toxicity usually resolve within an hour. concentrations may take 24 hr to occur.
DIAGNOSTIC TESTS & INTERPRETATION Hypotension generally responds to an IV fluid. The
phenytoin infusion should be stopped for a few Cardiac dysrhythmia, unstable vital signs
Lab minutes and may be restarted at half the initial
Initial Lab Tests Discharge Criteria
r Assess bedside fingerstick blood glucose in all rate. Asymptomatic after a period of observation or if signs
Use of multiple-dose activated charcoal 1 mg/kg and symptoms of toxicity resolve
patients with altered mental status. orally q24h may be indicated.
r CBC is generally recommended. r Phenobarbital:
r Serum electrolytes are genally recommended. FOLLOW-UP
In toxicity, alkalinization with a sodium
r Serum drug concentration for phenytoin,
bicarbonate infusion is an effective means of
phenobarbital, carbamazepine, orvalproic acid: PROGNOSIS
elimination of phenobarbital. r Significant toxicity associated with anticonvulsant
An elevated serum drug concentration may help Multiple-dose activated charcoal is more effective
confirm toxicity and in some cases may help guide exposure is rare.
and safer (recommended). r Potential for significant morbidity and mortality with
management. Use of multiple-dose activated charcoal 1 mg/kg
Serial drug concentrations should be obtained in orally q24h may be indicated. severe toxicity exists.
cases of overdose of phenytoin and r Carbamazepine:
carbamazepine since there may be prolonged or Assess for cardiac dysrhythmia, which may require
delayed absorption. ADDITIONAL READING
treatment with sodium bicarbonate.
Serial drug concentrations also should be Use of multiple-dose activated charcoal 1 mg/kg r Craig S. Phenytoin poisoning. Neurocrit Care.
obtained in cases of overdose of extended-release orally q24h may be indicated. 2005;3:161170.
preparations of valproic acid. r Valproic acid: Use of L-carnitine, possible r Doyon S. Anticonvulsants. In Flomenbaum NE,
r Carbamazepine: Assay serum electrolytes.
hemodialysis or hemoperfusion Goldfrank LR, Hoffman RS, et al., eds. Goldfranks
r Valproic acid:
Toxicologic Emergencies. 8th ed. New York, NY:
Specific lab assays are indicated. In addition to MEDICATION
r Activated charcoal: McGraw-Hill; 2006.
CBC and serum electrolytes, assay LFTs r Lheureux PER, Hantson P. Carnitine in the treatment
andammonia concentration, lipase, and venous 1 mg/kg PO, may be repeated q24h if multidose
activated charcoal is needed. of valproic acid-induced toxicity. Clin Toxicol.
blood gas. 2009;47:101111.
r Lamotrigine: LFTs and serum creatine Do not give multiple doses of charcoal with
r Spiller HA. Management of carbamazepine
phosphokinase sorbitol; severe abdominal bloating and pain may
r Topiramate: Electrolytes, serum bicarbonate, and occur overdose. Pediatr Emerg Care. 2001;17:452456.
Multidose charcoal; useful for phenytoin,
blood gas analysis should be obtained in cases of
phenobarbital, carbamazepine, and possibly
topiramate toxicity. CODES
valproic acid
Diagnostic Procedures/Other r Sodium bicarbonate:
r ECGs in cases of carbamazepine toxicity may
If cardiotoxicity is due to carbamazepine, sodium ICD9
demonstrate QRS widening, QT prolongation, bicarbonate bolus and infusion should be 966.3 Poisoning by other and unspecified
atrioventricular block, and ventricular dysrhythmias. administered for widening of the QRS interval anticonvulsants
r Lamotrigine toxicity may also be associated with >100 msec.
QRS widening. If wide QRS >100 msec, give 1 mEq/kg IV push,
DIFFERENTIAL DIAGNOSIS then repeat ECG 10 min later to assess response. PEARLS AND PITFALLS
r Hypoglycemia If QRS narrowing resulted, bicarbonate infusion of r Common presenting problems are ataxia and
r Sedative-hypnotic intoxication 2 ampules of sodium bicarbonate in 1 L of D5W
nystagmus as well as impaired consciousness or
r Ethanol intoxication may be infused.
r L-carnitine: neurologic function.
r Acute cerebellar ataxia r Newer anticonvulsants have unique toxicities that
r Vertigo The loading dose is 100 mg/kg IV (max single
may require specific treatment.
dose 6 g) over 30 min, followed by 15 mg/kg IV r Multiple-dose activated charcoal may be useful for
r Encephalopathy of other etiology
over 1030 min q4h until clinical improvement is
evident. phenytoin, phenobarbital, carbamazepine, and
Oral dosing of 100 mg/kg/day (up to 3 g/day) possibly valproic acid.
r Phenobarbital coma can mimic brain death.
divided q6h may be given following an acute
overdose without hepatotoxicity or symptomatic
hyperammonemia.
Should be administered in cases of
hyperammonemia or hepatotoxicity.
63
APHTHOUS STOMATITIS
Helene Tigchelaar
PATHOPHYSIOLOGY
BASICS r Conflicting theories increasingly support immune DIAGNOSIS
dysregulation.
DESCRIPTION r Cells in an area of diminished mucosal barrier may HISTORY
r Aphthous stomatitis (canker sores) are: r History of lesions:
become the targets of a cell-mediated immune
Recurrent reaction: Prodrome of tingling or burning at site
Painful Targeted by lymphocytes and Langerhans cells Erythematous papule forms
Solitary or occasionally multiple r Antibody formation and complement fixation Develops into a painful ulcer
Limited to the nonkeratinized mucous membranes Length of healing stage depends on severity
induced by L-forms of streptococci may play a role in r Age at onset of lesions
of the mouth (ventral tongue, buccal mucosa, pathophysiology.
labial mucosa, floor of the mouth) r Apparent provocative and relieving factors including
Yellow or gray, shallow, round or oval ulcers, ETIOLOGY emotional stressors and menstrual cycle
r Current evidence suggests a genetic and r Frequency of episodes
sharply demarcated, with an erythematous border
r Discussed are minor recurrent aphthous stomatitis immunologic predisposition. r Impact on quality of life
r Most cases are idiopathic: r Known underlying health conditions
(RAS), major RAS (10%), and herpetiform aphthous
ulceration: No proven viral associations r Associated symptoms: Fever, malaise, genital ulcers,
Minor aphthous stomatitis: COMMONLY ASSOCIATED CONDITIONS ocular and musculoskeletal involvement
Lesions are <1 cm in diameter. r Behcet disease:
Lesions heal in 1 wk without scarring. Vasculitis:
PHYSICAL EXAM
Usually starts in adolescence and improves with r Vital signs
Diagnostic criteria include a min of 3 oral
age r Toxicity
outbreaks per year plus 2 additional extraoral
Major aphthous stomatitis is more severe r Hydration and nutrition
areas of involvement.
(<10%): Findings may not be present simultaneously but r Location, size, number and appearance of lesions:
Ulcers are larger, deeper, more frequent, and may be elicited by history. Minor RAS: Lesions limited to the floor of mouth,
associated with severe pain. Oral and genital lesions similar to all 3 types of tongue, soft palate, and buccal and labial mucosa
Lesions can last weeks to months. RAS r Submental adenopathy is common.
Lesions scar. Cutaneous lesions r Facial edema:
Presents at puberty and does not remit Uveitis, retinal vasculitis, optic neuritis, and Seen with major RAS
Herpetiform ulceration: vascular occlusion may lead to blindness. r Findings outside the oral mucosa suggest the
More frequent in females Arthralgia
Clusters of small lesions (up to 100) throughout possibility of other associated diseases.
Progressive neurologic involvement in 20% of
the mouth patients DIAGNOSTIC TESTS & INTERPRETATION
Herpesvirus is not isolated from these lesions, r Inflammatory bowel disease (IBD): Lab
and there is no initial vesicle. Crohn disease can involve any portion of the GI May occasionally be indicated to look for etiology for
Onset in adulthood RAS:
tract, including the mouth.
EPIDEMIOLOGY r HIV and AIDS: r CBC with differential to rule out cyclic neutropenia
Gingival involvement is a differentiating feature. r Consider serum ferritin, folate, and B vitamin levels
Incidence
r Lifetime risk of a single episode up to 50% May have severe debilitating RAS r Biopsy for recalcitrant atypical lesions
r 20% of the population has RAS: r Periodic fever with aphthous stomatitis, pharyngitis, r Tzanck smear to rule out herpes simplex
Female preponderance and adenitis (PFAPA syndrome):
Pathological Findings
Onset 25 yr with slight male predominance r Biopsy rarely is required and is not diagnostic:
RISK FACTORS Cyclic event of 36-wk intervals with fever lasting
r Genetics: 3040% of patients with RAS have a May be required if suspicion of granulomatous
5 days
family history of aphthous ulcers: infection or inflammatory disease
Otherwise healthy child r Lesions have an ulcer base covered by a
Multiple gene inheritance pattern, penetrance Dramatic defervescence and symptomatic relief
affected by multiple factors with 1 dose of prednisone fibrinopurulent pseudomembrane:
r Dental appliances (braces) can cause mouth trauma, Lymphocytosis and mononuclear cells at the
Mouth lesions are small and few and involve the
increasing the frequency of ulcers lips and buccal mucosa margins of the lesion
r See Commonly Associated Conditions. Superficial tissue necrosis
Pharyngitis and cervical adenopathy
Syndrome generally resolves within 5 yr Neutrophils and debris cover the area of necrosis.
GENERAL PREVENTION r Celiac disease: Dilated blood vessels
r Prevention of mouth trauma:
Dental wax on braces Adherence to a glutenfree diet may promote DIFFERENTIAL DIAGNOSIS
resolution. r Geographic tongue:
Avoid toothbrush abrasions.
r Cyclic neutropenia Migratory glossitis in a maplike pattern
Avoid abrasive foods and citrus fruits.
Avoid chemical irritants, including toothpaste r Iron and possibly zinc deficiency Rarely painful
r Trauma:
containing sodium lauryl sulfate.
r Decreasing physical and emotional stress and Burns from hot foods or caustics
improving rest may decrease the frequency of Biting or sucking injuries to the buccal mucosa
episodes. and palate
r Consider treating deficiencies in iron, zinc, folate,
and B vitamins.
64
APHTHOUS STOMATITIS
A
r Herpes simplex gingivostomatitis: COMPLEMENTARY & ALTERNATIVE COMPLICATIONS
Fever (primary herpes infection) THERAPIES Major RAS and associated conditions:
Initial lesions are vesicular. r Topical and systemic tetracycline is a traditional r Scarring
Lesions may be extraoral. therapy with questionable efficacy. r Dehydration and weight loss secondary to decreased
Lesions occur on keratinized mucosa such as the r No support for use of antivirals
oral intake
hard palate and gingiva in addition to distribution r Levamisole, colchicine, gamma globulin, dapsone, r Chronic pain with decreased quality of life
of aphthous ulcers. estrogen replacement, empirical zinc replacement,
r Herpangina (coxsackie A virus):
and monoamine oxidase inhibitors are all therapies
Fever with limited data to support their use. ADDITIONAL READING
Multiple lesions r Vitamin B : Empirical or with documented
12 r Eisenberg E. Diagnosis and treatment of recurrent
Initially vesicular and then ulcerative with an deficiency
erythematous base, limited to the posterior r Licorice root extract (eg, paste or CankerMelts discs, aphthous stomatitis. Oral Maxillofac Surg Clin North
pharynx, uvula, and soft palate Am. 2003;15:111122.
r Hand-foot-and-mouth disease (HFMD; coxsackie A OTC patches) may heal or reduce extension of r Holbrook WP, Kristmundsdottir T, Loftsson T.
existing lesions.
16): r Barrier-protective gels like cyanoacrylate (Orabase Aqueous hydrocortisone mouthwash solution:
Fever Clinical evaluation. Acta Odontol Scand. 1998;
Sooth-N-Seal) protect ulcers from acidic foods and
Vesicles that progress to ulcers on an 56(3):157160.
trauma. r Natah SS, Konttinen YT, Enattah NS, et al. Recurrent
erythematous base limited to the anterior buccal r Debacterol, a topic sulfuric acid/phenolic solution
mucosa, tongue, and hard palate aphthous ulcers today: A review of the growing
(cauterizing agent) that is not FDA approved
Papules and vesicles on hands, feet, knees, r Thalidomide: knowledge. Int J Oral Maxillofac Surg. 2004;33:
elbows, and buttocks 221234.
Other enteroviruses can cause both herpangina Inhibits the production of cytokines r Patel N, Sciubba J. Oral lesions in young children.
and HFMD Found to be effective in numerous studies of HIV
Pediatr Clin North Am. 2003;50(2):469486.
r Oral lichen planus: with severe RAS as well as Behcet disease and
major RAS See Also (Topic, Algorithm, Electronic
White patches on buccal mucosa, plaque on tip of
Teratogenic: Media Element)
the tongue, erosions of gingiva May only be prescribed under FDA-mandated r Hand-Foot-and-Mouth Disease
May be associated with cutaneous or genital r Herpes Simplex
System for Thalidomide Education and
involvement r Inflammatory Bowel Disease
Prescribing Safety (STEPS)
Oral lesions are rare in children.
Additional side effects of rash and somnolence r Oral Lesions
SURGERY/OTHER PROCEDURES r Stomatitis
TREATMENT Silver nitrate cautery improves pain but not healing
time.
MEDICATION CODES
First Line DISPOSITION
r Antimicrobial mouth rinses r The vast majority of patients with RAS can be
r Topical anesthetics: managed as outpatients. ICD9
r Severe outbreaks of major RAS and associated 528.2 Oral aphthae
Topical benzocaine available in gel, liquid
(Anbesol or Orajel), or adhesive disc (Orajel conditions may rarely require hospitalization for IV
protective discs) 4 times a day hydration and parenteral analgesia. PEARLS AND PITFALLS
r Topical steroids:
Discharge Criteria r Pearls:
For symptomatic relief of severe or recurrent Ability to remain hydrated and nourished
outbreaks Recent alternative therapies provide the potential
Topical triamcinolone acetonide or hydrocortisone
Issues for Referral for control of RAS symptoms.
r Severe RAS requires referral to a dermatologist or r Pitfalls:
hemisuccinate cream or ointment applied
oral maxillofacial surgeon. Failure to obtain an adequate history and perform
sparingly b.i.d. r Suspicion for Behcet disease or HIV disease may
Steroid rinses can be used for posterior lesions, an adequate physical exam to identify associated
prednisolone 1 mg/kg/day swish and spit 2 times require referral to an immunologist. conditions such as Behcet disease and
r Suspicion for IBD may require referral to a
a day predisposing conditions such as AIDS and IBD
May predispose to candidal overgrowth gastroenterologist. Failure to recognize the impact on quality of life
r Menthol: for patients with major RAS
Short-acting local anesthetic: FOLLOW-UP
Lozenges
Over-the-counter Canker Cover is menthol in an FOLLOW-UP RECOMMENDATIONS
adhesive disc. Patient Monitoring
Second Line Pregnancy monitoring for females on systemic
r Intra- and perilesional glucocorticoids for deep or medications
prolonged major lesions as a single intramucosal DIET
injection Avoid acidic, spicy, salty, or abrasive foods.
r Oral steroids:
Prednisone 1 mg/kg/day tapered over 2 wk PROGNOSIS
r Episodes of minor RAS become less frequent as the
May also use rinse and swallow prednisolone
1 mg/kg/day b.i.d. for combined topical and patient ages.
systemic treatment r Major RAS and herpetiform RAS are chronic health
problems that may be controllable with appropriate
medications but do not remit.
65
APLASTIC ANEMIA
Dana Aronson Schinasi
Imaging
BASICS DIAGNOSIS No imaging is needed to establish the diagnosis of
aplastic anemia.
DESCRIPTION HISTORY
r Aplastic anemia is characterized by pancytopenia r Clinical presentation is variable and is based on the Diagnostic Procedures/Other
degree of pancytopenia, and specific cell lines that Bone marrow aspiration and biopsy:
and a hypocellular bone marrow. r Staging is based on exam of peripheral blood and
r May be inherited (congenital) or acquired: are depleted:
>80% of cases are acquired. Progressive anemia: Suggested by history of marrow and has implications for treatment and
fatigue, pallor, dyspnea, headache outcome.
EPIDEMIOLOGY Neutropenia: Suggested by history of fever, Pathological Findings
Incidence mucosal ulcerations, recurrent bacterial infections Bone marrow aspiration and biopsy:
r Incidence is 2 per million people per year in the Thrombocytopenia: Suggested by easy bruising, r Hypocellular marrow with fatty replacement
U.S. (1). petechiae, jaundice, mucous membrane bleeding r Absence of abnormal infiltrates or fibrosis
r Incidence is triphasic, with peaks at (2): r Recent infection, medication use, radiation
25 yr of age, due to inherited causes treatment or exposure DIFFERENTIAL DIAGNOSIS
2025 yr r History of failure to thrive, short stature, and nail, r Acute lymphoblastic leukemia
>60 yr skin, or hair anomalies may point to an underlying r Acute myelogenous leukemia
inherited syndrome. r Bone marrow infiltration
RISK FACTORS r Family history of anemia
r No age, sex, or racial predominance r Chemotherapy effects
r Risk for acquired aplastic anemia is higher in the r Human herpesvirus 6
PHYSICAL EXAM
setting of: r Pallor is usually the first sign of aplastic anemia: r Megaloblastic anemia
Viral infection (Epstein-Barr virus, parvovirus B19, May be accompanied on skin exam by bruising, r Multiple myeloma
hepatitis, HIV) petechiae, purpura r Myelodysplastic syndrome
Drugs (NSAIDs, chloramphenicol, sulfonamides, r Findings on cardiovascular exam range from r Non-Hodgkin lymphoma
carbamazepine, cimetidine, nifedipine) tachycardia and systolic flow murmur to overt signs r Osteopetrosis
Toxins (nitrous oxide, radiation, benzene) of heart failure such as weak pulses, prolonged r Splenic sequestration
Autoimmune disease (systemic lupus capillary refill, pulmonary congestion, and
erythematosus) hepatomegaly.
Pregnancy r Jaundice and tender hepatomegaly may be seen in TREATMENT
Graft vs. host disease (GVHD) some patients.
GENERAL PREVENTION r Splenomegaly may be present. PRE HOSPITAL
r Specific findings of certain inherited syndromes (5): r Assess and stabilize airway, breathing, and
Avoidance of risk factors, if known
Fanconi anemia: Microcephaly, strabismus, short circulation.
PATHOPHYSIOLOGY r Stop exposure to possible offending agent, if known.
r Mostly unknown, although immune dysfunction has stature, mental retardation, hyperpigmentation,
been implicated in the pathogenesis (3) hypopigmentation, thumb anomalies, skeletal INITIAL STABILIZATION/THERAPY
r Involves loss of, or injury to, pluripotent anomalies r Support hemodynamics:
Shwachman-Diamond syndrome: Eczema, skeletal Crystalloid IV fluids are the initial fluids of choice
hematopoietic stem cells (4):
anomalies to support circulation.
In absence of infiltrative bone marrow process
Dyskeratosis congenita: Oral leukoplakia, Since aplastic anemia is usually of gradual onset,
ETIOLOGY dysmorphic nails, dental anomalies, exudative most patients are well compensated and can
r Inherited (congenital): retinopathy tolerate moderate levels of anemia.
See Commonly Associated Conditions. Amegakaryocytic thrombocytopenia: Absent radii Blood and platelet transfusions: Goal is relief of
Familial aplastic anemia Diamond-Blackfan syndrome: Cleft palate, symptoms of poor tissue oxygenation or CHF, not
r Acquired: micrognathia, thumb anomalies restoration of normal hemoglobin levels.
Idiopathic: No clear etiology is identified in the DIAGNOSTIC TESTS & INTERPRETATION Exposure to HLA may adversely affect future
majority of children with acquired aplastic anemia. engraftment of transplanted bone marrow;
Lab
Following orthotopic liver transplantation therefore, transfusions should be used judiciously.
Initial Lab Tests
COMMONLY ASSOCIATED CONDITIONS r CBC: Irradiated, cytomegalovirus-negative blood
r Fanconi anemia Anemia: Usually normocytic, may be macrocytic products should be used to minimize
r Shwachman-Diamond syndrome Neutropenia, with toxic granulation alloimmunization
r Spontaneous bleeding may occur with platelet
r Dyskeratosis congenita Absence of blast cells
r Amegakaryocytic thrombocytopenia Thrombocytopenia counts <10,000/L; consider transfusion at these
Normal morphology on peripheral smear; no levels.
(thrombocytopenia-absent radius syndrome)
r Diamond-Blackfan syndrome suggestion of leukemia
r Cartilage-hair hypoplasia Reticulocyte count <1%
r Coombs test, lactate dehydrogenase, renal and
r Pearson syndrome
r Dubowitz syndrome hepatic function tests may be useful in evaluating
r Paroxysmal nocturnal hemoglobinuria the etiology
r Serologic viral testing for Epstein-Barr virus,
parvovirus, hepatitis, and HIV, as indicated
66
APLASTIC ANEMIA
A
MEDICATION REFERENCES
First Line FOLLOW-UP
Broad-spectrum antibiotics to cover potentially 1. Young NS, Kaufman DW. The epidemiology of
life-threatening infections in the setting of fever with FOLLOW-UP RECOMMENDATIONS acquired aplastic anemia. Haematologica.
r Discharge instructions and medications: 2008;93(4):489.
neutropenia:
r Vancomycin 10 mg/kg/dose IV q6h Patients should return to the emergency 2. Shimamura A, Guinan EA. Acquired aplastic
r Ceftriaxone 5075 mg/kg/dose IV q24h department if they develop fever, prolonged anemia. In Nathan DG, Orkin SH, eds. Hematology
bleeding, or signs of heart failure. of Infancy and Childhood. Philadelphia, PA: WB
r No role for prophylactic antibiotics with neutropenia
Medications vary based on severity and should be Saunders; 2003:256.
in the absence of fever prescribed in conjunction with a pediatric 3. Nakao S. Immune mechanism of aplastic anemia.
Second Line hematologist. Int J Hematol. 1997;66(2):127134.
r Immunosuppressive therapy (when no HLA-matched r Activity:
4. Young NS, Maciejewski J. The pathophysiology of
sibling is available): Patients with splenomegaly or thrombocytopenia acquired aplastic anemia. N Engl J Med.
Antithymocyte globulin 40 mg/kg/day for 4 days should avoid contact sports. 1997;336:1365.
Cyclosporine 12 mg/kg/day IV starting on day 5 Dental work should be postponed until the patient 5. Shimamura A. Clinical approach to marrow failure.
for 36 mo is no longer neutropenic. Hematology. 2009;329337.
Prednisone 40 mg/m2 /day (max single dose Patient Monitoring 6. Fuhrer M, Rampf U, Baumann I, et al.
60 mg/day) PO for 2 wk r Blood counts should be monitored on a regular Immunosuppressive therapy for aplastic anemia in
Recombinant human granulocyte basis. children: A more severe disease predicts better
colony-stimulating factor 5 g/kg/day SC for r Patients should be monitored for adverse effects of survival. Blood. 2005;106:2102.
28 days
r HLA-matched unrelated donor hematopoietic cell immunosuppressive therapies. 7. Davies JK, Guinan EC. An update on the
DIET management of severe idiopathic aplastic anaemia
transplantation
r Avoid potential causative agents. in children. Br J Haematol. 2007;136:549.
SURGERY/OTHER PROCEDURES r Neutropenic patients should avoid raw meats, dairy
A central venous catheter is required for the
products, and certain fruits and vegetables. ADDITIONAL READING
administration of immunosuppressive therapy and r Salt restriction is recommended while on
hematopoietic cell transplantation.
cyclosporine or steroid therapy. See Also (Topic, Algorithm, Electronic
DISPOSITION Media Element)
PROGNOSIS r Acute Hemolytic Anemia
Admission Criteria Depends on severity of pancytopenia (7):
Critical care admission criteria: r Anemia
r The spontaneous recovery rate is not well
r Hemodynamic instability, persistent or uncontrolled r Leukemia
established (1). r Lymphoma
bleeding, septic shock r Estimated 5-yr survival rate for patients receiving an
r All patients with neutropenia and fever require
HLA-matched sibling donor hematopoietic stem cell
admission for broad-spectrum antibiotics, while transplant is >90% (6).
awaiting culture and sensitivity results. r Estimated 5-yr survival rate for patients receiving CODES
r All patients with a new diagnosis require admission
immunosuppression is 75% (1).
for further diagnostic testing and for initiation of ICD9
therapy. COMPLICATIONS r 284.01 Constitutional red blood cell aplasia
r Complications of aplastic anemia include infections r 284.89 Other specified aplastic anemias
Discharge Criteria
r Patients should not be discharged from the and bleeding. r 284.9 Aplastic anemia, unspecified
r Complications related to immunosuppressive
emergency department without consultation with a
pediatric hematologist. therapies and conditioning regimens for stem cell
r Patients deemed eligible for discharge by a pediatric transplantation include GVHD and graft failure. PEARLS AND PITFALLS
hematologist must have normal vital signs, be r In contrast to those with leukemia, children with
afebrile, and be without signs of CHF or bleeding.
aplastic anemia should have WBCs of normal
Issues for Referral morphology on the peripheral smear.
Diagnostic and management decisions should r Patients with fever and neutropenia require
always be made in consultation with a pediatric broad-spectrum antibiotics and admission.
hematologist.
COMPLEMENTARY & ALTERNATIVE
THERAPIES
HLA-matched sibling donor hematopoietic cell
transplantation is the treatment of choice for children
with severe or very severe disease (6):
r Survival rates are better than using
immunosuppression alone.
67
APNEA
Robin L. Altman
Ilene A. Claudius
GENERAL PREVENTION DIAGNOSTIC TESTS & INTERPRETATION

BASICS r Risk factors identified to decrease the incidence of
Lab
sudden infant death syndrome (SIDS) do not seem r Oxygen saturation or arterial blood gas, especially if
DESCRIPTION to impact infantile apnea (5). suspecting acidosis
r Apnea of infancy is an unexplained episode of r Measures to decrease premature delivery r Consider complete sepsis evaluation if ill appearing
cessation of breathing either 20 sec duration or or <60 days old with history of prematurity (7).
accompanied by bradycardia, cyanosis, pallor, or PATHOPHYSIOLOGY r Consider urinalysis and urine culture in all-aged
r Central apnea: Disruption of respiratory signals from
marked hypotonia (1).
r Apnea of prematurity is the cessation of breathing the CNS patients (8,9).
r Obstructive apnea: Attempt at breathing through an r RSV, influenza, or pertussis testing if clinically
for 20 sec or accompanied by a decrease in heart
occluded airway indicated
rate of at least 30 bpm or oxygen desaturation r Consider urine toxicology testing if poisoning, either
r Cyanosis: Hemoglobin desaturation from impaired
below 85% in an infant <37 wks PCA. Apnea of
prematurity usually resolves by 43 wks oxygen exchange or distribution intentional or unintentional, is suspected (10),
postconceptual age (2,3). r Altered muscle tone can be CNS or vasovagally though urine toxicology testing is center dependent
r Periodic breathing is a normal immature respiratory mediated processes. and usually limited to drugs of abuse.
r Apnea of prematurity: Immaturity of breathing r Consider glucose and electrolytes if the history is
pattern in which infants pause in breathing for
several seconds without cyanosis. Parents may easily responses to hypoxia, hypercarbia, and inhibition of suggestive (acute gastroenteritis, dehydration,
mistake this for true apnea (4). airway receptors (6) underlying medical problem, inappropriate formula
r Apnea can be part of an apparent life-threatening mixing, seizures, medication use).
COMMONLY ASSOCIATED CONDITIONS r Additional labs if clinically indicated only
event (ALTE). (See Apparent Life-Threatening Event See Differential Diagnosis.
topic.) Imaging
r 3 categories of apnea: r Chest radiograph
Central: Absence of respiratory effort DIAGNOSIS r Head neuroimaging as indicated based on the
Obstructive: Breaths associated with no air history and suspicion of injury (including
movement or with paradoxical inverse movements HISTORY nonaccidental trauma)
r Birth history
of the chest wall and abdomen Diagnostic Procedures/Other
r Central vs. obstructive
Mixed: Features of both r Workup for GERD or seizures (if clinically indicated)
r Thorough description of the apnea, including who
EPIDEMIOLOGY can be performed on either an inpatient or
witnessed it
Incidence r Feeding and growth history outpatient basis.
r Pneumocardiogram may be performed for patients
2,00010,000 episodes of acute infantile apnea per r Fever
year in the U.S. without a clear etiology felt to be at high risk of
r Respiratory symptoms
recurrent apnea (eg, premature infants, patients
Prevalence r Seizure activity with recurrent apneas or subsequent apneas in the
r 0.20.9% of infants have apnea leading to r History of previous ALTEs emergency department, significant apneic event
admission. r Family history of SIDS requiring substantial resuscitation).
r Up to 5.3% of all parents report periods of infantile r Consider ECG or Holter testing for suspicion of
r Medication use (including over the counter)
apnea >20 sec when questioned. r Trauma (accidental or suspected nonaccidental) arrhythmia, QT prolongation, or cardiac history.
r 210% of the pediatric population has obstructive
r Degree of resuscitation required
sleep apnea in the U.S. (See Obstructive Sleep DIFFERENTIAL DIAGNOSIS
r Proximity to feeds r Seizure
Apnea topic.)
r 70% of infants born at <34 wk estimated r GERD
PHYSICAL EXAM r Lower respiratory tract infection
gestational age experience apnea of prematurity. r Toxic or ill appearing
r Vital signs r Bronchiolitis
RISK FACTORS r Pertussis
r Infants <1 yr, especially between 1 and 3 mo of age r Signs of distress
r Prematurity r Cyanosis r Upper respiratory tract infection
r Respiratory infection, especially respiratory syncytial r Pallor r Nonaccidental head injury, intentional poisoning,
virus (RSV) r Respiratory findings intentional suffocation
r GERD or other feeding difficulties r Cardiac findings r Coughing or gagging on mucus
r Congenital upper airway compromise r Mental status r Breath-holding or other vasovagal episode
r Neuromuscular disorder r Muscle tone (limpness or stiffness) r Acute hypoglycemia or electrolyte abnormality
r Head trauma r Focal neurologic findings r Sepsis or serious bacterial infection, including
r Sepsis r Skin lesions urinary tract infection
r Any evidence of trauma, including retinal r Arrhythmia
r Risk of apnea of prematurity increases with
decreasing gestational age at birth. hemorrhages
r Blood in nares
r Recurrent episodes
68
APNEA
A
Discharge Criteria 6. Abu-Shaweesh J, Martin R. Neonatal apnea:
r Well appearing
TREATMENT r Normal physical exam
Whats new? Pediatr Pulmonol. 2008;43:
937944.
PRE HOSPITAL r Single episode of apnea without high-risk features 7. Zuckerbraun NS, Zomorrodi A, Pitetti RD.
Assess and stabilize airway, breathing, and r >4348 wk postconceptual age Occurrence of serious bacterial infection in infants
circulation. r Abuse is not suspected. aged 60 days or younger with an apparent
INITIAL STABILIZATION/THERAPY r Follow-up is ensured. life-threatening event. Pediatr Emerg Care.
r Assess and stabilize airway, breathing, and r Family is comfortable with discharge. 2009;25(1):1925.
circulation. 8. Altman RL, Li KI, Brand DA. Infections and
r For recurring apneas or an ill-appearing patient, Issues for Referral apparent life-threatening events. Clin Pediatr.
r Patients diagnosed with or suspected to have
2008;47(4):372378.
rapid stabilization and initial therapies focus on seizures should be referred to neurology. 9. Brand DA, Altman RL, Purtill K, et al. Yield of
airway control, respiratory support as needed, and r Patients with GERD should be referred to their
consideration of sepsis or other life-threatening diagnostic testing in infants who had an apparent
primary care provider or gastroenterology. life-threatening event. Pediatrics. 2005;
conditions such as head injury. r Patients with recurrent apneas or apnea of
r For the child with recurrent apneas, consider a 115(4):885893.
prematurity should be referred to pulmonology. 10. Pittetti RD, Whitman A, Zaylor D. Accidental and
targeted workup of the potential underlying cause.
nonaccidental poisonings as a cause of apparent
MEDICATION life-threatening events in infants. Pediatrics.
First Line
FOLLOW-UP 2008;122:e359e362.
r Oxygen may be needed with significant apnea
and/or cyanosis. r Discharge instructions and medications are guided
r If a cause is identified or suspected, targeted therapy by the cause and use of xanthine therapy.
ADDITIONAL READING
should be initiated (eg, anticonvulsant for suspected r No activity restrictions r Hall KL, Zalman B. Evaluation and management of
seizure or bronchodilator for bronchoconstriction). r Parents should be taught infant CPR apparent life-threatening events in children. Am
r Further therapy should be determined based on the
Patient Monitoring Fam Physician. 2005;71(12):23012308.
suspected etiology. r Close primary care provider follow-up is required. r Kiechl-Kohlendorfer U, Hof D, Peglow UP, et al.
Second Line r Consider consultation by pulmonology for home Epidemiology of apparent life threatening events.
r For apnea of prematurity, methylxanthines and Arch Dis Child. 2005;90:297300.
monitoring of preterm infants with extreme apnea, r Southall DP, Plunkett CB, Banks MW, et al. Covert
CPAP are the mainstays of therapy: infants with anatomic abnormalities susceptible to
Aminophylline: airway compromise, infants with neurologic or video recordings of life-threatening child abuse:
Loading dose: 5 mg/kg PO/IV Lessons for child protection. Pediatrics. 1997;
metabolic disorders affecting respiratory control,
Maintenance dose: 12 mg/kg/dose q68h 100(5):735760.
and infants with chronic lung disease (1).
Caffeine:
Loading dose: 10 mg/kg PO/IV PROGNOSIS See Also (Topic, Algorithm, Electronic
Maintenance dose: 510 mg/kg PO/IV per day r Apnea of prematurity typically resolves by 43 wk Media Element)
Theophylline: postconceptual age. Obstructive Sleep Apnea
Loading dose: 5 mg/kg PO r Risk of SIDS after an uncomplicated ALTE is 03%.
Maintenance dose: 36 mg/kg/day PO divided Children with recurrent ALTEs or those requiring
q68h significant resuscitation may have an increased risk CODES
r Further therapy should be determined based on the of future SIDS. This data can be applied to apnea as
suspected etiology. well. ICD9
r 770.81 Primary apnea of newborn
DISPOSITION r 770.82 Other apnea of newborn
Admission Criteria REFERENCES
r Floor admission:
Ill appearance 1. Committee on Fetus and Newborn. American
Academy of Pediatrics. Apnea, sudden infant PEARLS AND PITFALLS
Condition (eg, sepsis) requiring admission
Age <4348 wk postconceptual age death syndrome, and home monitoring. r A good history is key to determining the cause.
Consider admission for high-risk apneic event (eg, Pediatrics. 2003;111(4):914917. r Consider occult child abuse.
multiple apneas, bradycardia, significant and 2. Finer N, Higgins R, Kattwinkel J, et al. Summary r It is essential to address parental concerns. If apneic
prolonged change in tone and color) proceedings from the apnea-of-prematurity
events are recurrent, ensure that parents have been
Respiratory acidosis group. Pediatrics. 2006;117(3):S47S51.
trained in infant CPR.
Risk for child abuse 3. Nimavet D, Sherman M, Santin R, et al. Apnea of
Physical exam findings, lab testing, or medical or prematurity. eMedicine. Available at http://
family history that is concerning enough to the emedicine.medscape.com/article/974971-
health care provider to necessitate admission overview. Accessed September 13, 2010.
Marked obstructive apnea with associated hypoxia 4. DeWolfe CD. Apparent life-threatening event: A
or hypercarbia review. Pediatr Clin North Am. 2005;52(4):
Physician or parental concern regarding severity of 11271146.
event, degree of resuscitation needed, medical 5. Davis N, Bossung-Sweeney L, Peterson DR.
history Epidemiological comparisons of sudden death
Apnea of prematurity requiring initiation of syndrome with infant apnoea. Aust Paediatr J.
methylxanthines 1986;22(Suppl 1):2932.
Need for intubation or recurrent apneic episodes
that might portend the need for intubation
Identification of underlying disease requiring
critical care monitoring
69
APPARENT LIFE-THREATENING EVENT

Kevin Ching
ETIOLOGY
BASICS An underlying diagnosis is identified in only 50% of DIAGNOSIS
cases (50% are idiopathic):
DESCRIPTION r GI: HISTORY
r According to the NIH, an infant apparent Detailed accounts from witnesses (caretaker) and
Gastroesophageal reflux
life-threatening event (ALTE) is an unexpected, emergency prehospital personnel may provide
Intussusception
frightening episode that is characterized by some important insight on nature of event:
Volvulus r Condition:
combination of (1): Swallowing incoordination
Apnea (central, obstructive, or mixed) r Neurologic: Awake, asleep, crying, position (prone vs. supine)
Color change (cyanosis, pallor, redness, or r Activity during event:
Seizure
plethora) CNS hemorrhage Coughing, feeding, vomiting, gagging
Marked change in muscle tone (limpness or r Respiratory effort:
Hydrocephalus
rigidity) Chiari malformation Fast, slow, shallow, stridor, gasping, choking, none
Choking or gagging Central hypoventilation syndrome r Color:
Fear (in some cases) that the infant has died Vasovagal syncope Red, blue, purple, pale
r An ALTE may prompt the caregiver to stimulate or r Respiratory: r Tone and movement:
resuscitate the infant before recovery. Laryngotracheomalacia Limp, rigid, convulsions
EPIDEMIOLOGY Vocal cord dysfunction r Duration:
Incidence Vascular ring Time to recovery (eg, normal respiratory pattern or
Unknown, though estimates range from 0.56% Obstructive sleep apnea tone)
(2): Foreign body aspiration r Interventions (and duration):
r Most occur in infants <1 yr of age, peaking at 1 wk Congenital airway anomalies None, gentle or vigorous stimulation, artificial
Stimulation of laryngeal chemoreceptors respirations, CPR
to 2 mo of age (3).
Breath-holding spell r Recent illnesses
RISK FACTORS r Cardiac: r Past medical history:
r Prematurity
Congenital heart disease (eg, ductal-dependent Prenatal care
r Infection with respiratory syncytial virus (RSV) lesion) Prematurity
r Male gender Dysrhythmia (eg, long QT, Wolff-Parkinson-White Developmental history
r Prone sleeping position syndrome) Feeding history
r Feeding difficulties Cardiomyopathy Sleep habits
r History of apnea, cyanosis, or pallor Myocarditis Prior events
r Metabolic/Endocrine: r Family/Social history:
PATHOPHYSIOLOGY Inborn error of metabolism Siblings with sudden infant death syndrome (SIDS)
r The pathophysiology of ALTE in infants is unclear.
Endocrine disorder Dysrhythmias
r Apnea (1): r Infection:
Medications in home
Cessation of respiratory airflow for any reason: Sepsis or meningitis Smoking, alcohol, or substance abuse
In central apnea, respiratory pauses may be RSV
caused by CNS immaturity, seizures, or tumors. Pertussis PHYSICAL EXAM
In obstructive apnea, breathing may be r Infants may appear well without any signs or
Croup
obstructed by a laryngeal web, vascular ring, Pneumonia symptoms of pathology:
tracheoesophageal fistula, or foreign body. r Child abuse: In 1 study, 83% of infants evaluated by
In pathologic apnea, there is a respiratory pause paramedics had unremarkable physical exams
Physical abuse
>20 sec accompanied by bradycardia, cyanosis, Munchausen by proxy (eg, suffocation, intentional
after an ALTE (4).
pallor, hypotonia, or other signs of compromise. poisoning, head trauma)
In apnea of infancy, there is an unexplained r Normal:
respiratory pause >20 sec, or <20 sec when Respiratory pauses
accompanied by bradycardia, cyanosis, pallor, Periodic breathing
hypotonia, or other signs of compromise.
Periodic breathing is a normal respiratory pattern
involving 3 brief pauses interrupted by <20 sec
of normal respirations in between (no bradycardia,
cyanosis, or hypotonia).
70
APPARENT LIFE-THREATENING EVENT

A
r Thorough exam: PROGNOSIS
r Highly variable: Dependent on underlying condition
General: TREATMENT r The recurrence rate for severe ALTE is as high as
Height, weight, head circumference (compared
to norms) INITIAL STABILIZATION/THERAPY 68%.
Dysmorphisms r Assess and stabilize airway, breathing, and r Overall risk of death is <1% (2).
Vital signs circulation.
Neurologic assessment: r Management is dependent on presentation and
Muscle tone, posture condition. REFERENCES
Developmental assessment: r Most infants appear well on presentation, and
Age-appropriate milestones 1. Infantile apnea and home monitoring. NIH
minimal stabilization and therapy will be required. Consensus Statement. 1986;6:110.
Respiratory and cardiac:
Stridor, wheezes, rales DISPOSITION 2. Brooks JG. Apparent life-threatening events and
Murmurs Admission Criteria apnea of infancy. Clin Perinatol. 1992;19:809838.
BP differential r Admission criteria vary: Some institutions routinely 3. Davies F, Gupta R. Apparent life threatening events
Signs of trauma: admit patients with ALTE and perform extensive in infants presenting to an emergency department.
Consider dilated funduscopy. workup; others do not admit patients and do not Emerg Med J. 2002;19:1116.
routinely conduct lab testing or imaging: 4. Stratton SJ, Taves A, Lewis RJ, et al. Apparent
It is unclear if there is any superiority of routine life-threatening event in infants: High risk in the
Lab admission or routine discharge. out-of-hospital environment. Ann Emerg Med.
r Lab testing should be guided by the history and
r Any infant who has required resuscitation or whose 2004;43:711717.
physical exam findings.
r No standard for the minimum lab and radiographic history, exam, or diagnostic studies suggest any 5. Kahn A. Recommended clinical evaluation of
potential abnormalities should be hospitalized for infants with an apparent life threatening event.
testing exists (5). further workup and monitoring. Consensus document of the European Society for
Initial Lab Tests the Study and Prevention of Infant Death, 2003.
r High-yield studies include: Discharge Criteria
Patients with normal physical exam and no apparent Eur J Pediatr. 2004;163:108115.
Bedside glucometry
underlying medical problem requiring treatment are
CBC
potential candidates for discharge:
Urinalysis r In particular, children >30 days old with a single ADDITIONAL READING
Electrolytes, BUN, calcium, magnesium r American Academy of Pediatrics Task Force on
Serum bicarbonate ALTE may be discharged safely from the hospital.
Serum lactate Issues for Referral Sudden Infant Death Syndrome. The changing
r Other tests to consider: Subspecialty referral is determined by historical and concept of sudden infant death syndrome:
Toxicology screen physical exam findings as well as lab and radiographic Diagnostic coding shifts, controversies regarding the
Metabolic screening (eg, ammonia) findings. sleeping environment, and new variables to consider
Respiratory virus screens (eg, RSV, pertussis) in reducing risk. Pediatrics. 2005;116:12451255.
r Shah S, Sharieff GQ. An update on the approach to
CSF analysis
Blood and urine cultures FOLLOW-UP apparent life-threatening events. Curr Opin Pediatr.
2007;19:288294.
Imaging FOLLOW-UP RECOMMENDATIONS
r CXR: High yield Discharge instructions and medications:
r Neuroimaging r If there is any problem for which medication
r Skeletal survey
CODES
prescription is required, take the prescription
Diagnostic Procedures/Other compliantly. ICD9
r ECG r Use a supine sleep position.
799.82 Apparent life threatening event in infant
r Screen for gastroesophageal reflux (eg, esophageal r Discourage cosleeping.
pH probe or upper GI series) r Avoid overheating (overbundling).
r Echo r Encourage breast-feeding. PEARLS AND PITFALLS
r Multichannel polysomnography r Avoid overfeeding. r Infants typically are well appearing with a normal
r Ensure timely vaccinations.
DIFFERENTIAL DIAGNOSIS physical exam after ALTE.
r Eliminate any exposure to tobacco smoke. r There is a lack of evidence supporting or refuting
See Etiology. r Seek training in CPR. management styles. The range of appropriate
Patient Monitoring management is a spectrum from no lab or imaging
r Cardiopulmonary monitoring, such as an apnea evaluation and routine discharge to routine
alarm, is of no proven benefit. admission and lab investigations.
r Parents should monitor for recurrent episodes of r Children >30 days old with a single ALTE and
ALTE or other illness. normal exam are particular candidates for safe
home discharge.
r Child abuse can present as an ALTE.
r Studies have not confirmed a link between ALTE and
SIDS.
71
APPENDICITIS
Lindsey Tilt
Anupam Kharbanda
Progression to suppurative appendicitis occurs Rovsing sign: Pushing on the abdomen in the left
BASICS when bacteria and inflammation spread lower quadrant elicits pain in the RLQ
transmurally to the serosa of the appendix and Obturator sign: Pain on passive internal rotation
DESCRIPTION inflammatory exudate irritates neighboring of the flexed right thigh
r Appendicitis is an inflammation of the appendix, a tissues. This surrounding tissue is innervated by Psoas sign: Pain on passive extension of the right
blind-ending structure that arises from the cecum. the T12 and L1 spinal nerves, which causes thigh with the patient lying on the left side
r Occurs in 1 in 15 individuals (7%) somatic pain that the patient localizes in the right Since these maneuvers can be painful to an
r Males > females (3:2) lower quadrant (RLQ). already uncomfortable child, less forceful
r Familial predisposition Ultimately, gangrenous appendicitis may occur, alternatives include asking the child to walk or
r Seasonal peak: Spring and fall which involves necrosis of the appendiceal wall hop and whether that causes pain.
r Diet may influence frequency of appendicitis: and can rapidly progress to perforation if r A pelvic exam should be considered in teenage
untreated. female patients due to the overlap in presentation of
Countries with high-fiber diets have a lower
incidence of appendicitis as compared to those ETIOLOGY many gynecologic processes.
with lower-fiber diets (1). r Luminal obstruction: Lymphoid follicle hyperplasia, DIAGNOSTIC TESTS & INTERPRETATION
r Mortality is low (<1%), but morbidity is high and fecalith, foreign bodies, parasites Lab
mostly associated with perforation. r Direct invasion:
Initial Lab Tests
r Perforation occurs in 1530% of patients but is not Enteric infection leads to ulceration of the mucosa. r WBC: The likelihood of appendicitis is greatly
evenly distributed through age groups: Superinfection leads to inflammation and necrosis. decreased if the WBC is <10,000/L (2).
Greatest in children <4 yr; this is thought to be, in The most common bacteria responsible are r C-reactive protein (CRP): Combining use of WBC
part, due to patients inability to communicate Escherichia coli, Bacteroides fragilis, and and CRP increases sensitivity of laboratory
their symptoms. Peptostreptococcus and Pseudomonas species. evaluation of possible appendicitis.
Perforation usually occurs within 3648 hr of r Urinalysis:
onset of symptoms. May be useful in differentiating appendicitis from
Prevalence of perforation with symptoms >36 hr DIAGNOSIS
a urinary tract infection
is as high as 65% (2). HISTORY Sterile pyuria may occur with appendicitis due to
EPIDEMIOLOGY r Classic presentation: the proximity of the inflamed appendix to the
Incidence Abdominal pain: bladder. Bacteria and nitrates should be absent in
r 12 in 10,000 children per year <4 yr of age Vague, periumbilical pain develops first. the urine.
r 25 in 10,000 children per year in 1017 yr olds (1) Colicky r Urine pregnancy test: Useful in ruling out pregnancy
r Most common in the 2nd decade of life (2) Unrelated to activity or position as a cause as well as recognition in the event a CT
Nausea and/or anorexia: scan is considered
GENERAL PREVENTION Follows the abdominal pain r Serum chemistry: If local practice involves
In any child having abdominal surgery, elective Food refusal is a useful surrogate in children. documentation of renal function prior to use of IV
appendectomy should be considered to obviate the Migration of pain to the RLQ: contrast with CT scan, obtaining these lab values
future risk of appendicitis. Occurs 612 hr following onset of pain early may decrease time to CT imaging.
Pain is exacerbated by movement.
PATHOPHYSIOLOGY Imaging
r The 2 leading hypotheses are: Vomiting: r X-rays are not routinely useful in the diagnosis of
Often occurs as the infection progresses
Luminal obstruction: Nausea/Vomiting is present in more than half of appendicitis, but recognition of a fecalith or free air
Obstruction trapping mucus in the appendix, under the diaphragm may quickly provide radiologic
patients with appendicitis.
leading to elevated intraluminal pressure Classically follows the onset of pain evidence necessary for the decision to undergo
Increased pressure leading to impaired surgery.
Fever: r US:
perfusion and venous drainage and thus Common but nonspecific finding in children
ischemia of the appendix Findings of appendicitis include a nonperistalsing,
Bacteria entering the compromised tissue, presenting with appendicitis
r <50% of pediatric patients will present with the noncompressible, blind-ending tubular structure
leading to inflammatory infiltrate and eventually >6 mm in diameter
necrosis classic presentation. Women and toddlers are most
Strengths:
Direct invasion: likely to have atypical presentations (1), including Low cost, no radiation, and requires little
Direct bacterial invasion of the ulcerated diffuse abdominal pain, vomiting, or fever.
preparation time
mucosa of the appendix after enteric infections PHYSICAL EXAM Provides dynamic images
May explain why appendicitis is more common r Observe the patient. Especially useful in females, where acute
in the spring and fall, when enteric infections r Begin with a component of the physical exam that is gynecologic disease can often be confused with
are at a peak (1,3) not painful (cardiac/pulmonary). appendicitis
r Appendicitis and perforation represent a continuum r Assess for difficulty with walking, jumping, or Limitations:
of disease. positioning. Operator dependent, low negative predictive
r Patient signs and symptoms correlate with degree r Auscultate bowel sounds, which may be normal, value
and timing of inflammation: hyperactive, or hypoactive depending on stage of
Initially, isolated inflammation within the appendix disease.
causes edema and inflammatory infiltration of the r Palpate at McBurney point: 1/3 the distance from
appendiceal wall. Early distention of the appendix the right anterior superior iliac spine to the umbilicus
triggers visceral pain, which is transmitted r Assess for specific signs for appendicitis:
primarily through sympathetic fibers traveling to
Rebound tenderness: Pain that is elicited on
the spinal cord along T10, so pain is appreciated
release of pressure after deep palpation of the
as periumbilical and vague.
abdomen
72
APPENDICITIS
A
r CT scan: r Complicated/Advanced appendicitis: PROGNOSIS
Findings of appendicitis include a fluid-filled Select antibiotics that cover Gram-negative rods Patients do well after an appendectomy, with most
tubular structure >6 mm in diameter with and anerobes. Length of treatment is often children going home in 2448 hr. In comparison, in
periappendiceal inflammation. influenced by normalization of inflammatory cases of complicated appendicitis, one case study
Choice of contrast: markers and temperature (typically 1 wk). reported a mean hospital length of stay of 61/2
Rectal contrast alone is sufficient for the Piperacillin/Tazobactam: days (7).
diagnosis of appendicitis (4) but is difficult to >9 mo of age, <40 kg: 300 mg piperacillin
COMPLICATIONS
administer in young children. component/kg/day in divided doses q8h r Abscess, phlegmon, diffuse peritonitis, cellulitis,
Recent literature suggests that CT with IV >40 kg: 3 g piperacillin/0.375 g tazobactam
small bowel obstruction, ileus, wound infections,
contrast alone is useful and sufficient (5). q6h
fistulas, sepsis, death
Strengths: Second Line r Complications are more common in perforated
Not operator dependent r 2nd-generation cephalosporin:
No decrease in quality of image with obesity appendicitis.
Cefoxitin 100 mg/kg/day divided q6h, max single r Decreased fertility in females with appendicitis is
Provides a better view of the extent of disease,
dose 12 g/day recognized.
which can guide drainage of fluid collections or Cefotetan 4080 mg/kg/day divided q12h, max
alternative diagnoses single dose 6 g/day
Limitations: Radiation exposure, contrast r If penicillin allergic: Gentamicin (22.5 mg/kg/dose
exposure, higher cost
REFERENCES
r A negative or equivocal result on US should be q8h or 5 mg/kg/dose per day) and metronidazole
(30 mg/kg/day in divided doses q6h, max single 1. Rothrock SG, Pagane J. Acute appendicitis in
followed with the more sensitive CT scan to reliably dose 4 g/day) children: Emergency department diagnosis and
exclude appendicitis or to identify those patients management. Ann Emerg Med. 2000;36:3951.
with appendicitis missed by US (4). SURGERY/OTHER PROCEDURES 2. Bundy DG. Does this child have appendicitis?
r Acute appendicitis:
DIFFERENTIAL DIAGNOSIS JAMA. 2007;298(4):438451.
r General: Surgical treatment is indicated for acute
3. Carr NJ. The pathology of acute appendicitis. Ann
appendicitis.
Gastroenteritis, mesenteric adenitis, constipation, Diagn Pathol. 2000;4(1):4658.
Surgical timing: The choice of when to go to the
acute pancreatitis, peptic ulcer, Henoch-Schonlein operating room is variable among individual 4. Garcia Pena BM, Mandl KD, Kraus SJ, et al.
purpura, cholecystitis, inflammatory bowel surgeons/institutions. Debate exists over the risks Ultrasound and limited computed tomography in
disease, septic arthritis of delaying surgery in patients who are candidates the diagnosis and management of appendicitis in
Meckel diverticulitis, volvulus, referred pain from for appendectomy (eg, delays >8 hr). children. JAMA. 1999;282:10411046.
pneumonia/pleuritis r Complicated/Advanced appendicitis (appendicitis 5. Kharbanda AB, Taylor GA, Bachur RG. Suspected
r Genitourinary: appendicitis in children: Rectal and intravenous
with gangrene or perforation of the appendix):
Pregnancy/Ectopic pregnancy, pelvic inflammatory Acute presentation of advanced appendicitis contrast-enhanced versus intravenous contrast-
disease, ovarian torsion, follicular rupture, (ie, perforation with signs and symptoms <96 hr, enhanced CT. Radiology. 2007;243(2):520526.
endometriosis without a well-organized abscess on CT) and 6. Green R, Bulloch B, Kabani A, et al. Early analgesia
Urinary tract infection, nephrolithiasis patients who remain unstable despite for children with acute abdominal pain. Pediatrics.
Testicular torsion, orchitis, hernia resuscitation will go to the operating room for an 2005;166:978983.
appendectomy. 7. St Peter SD, Tsao K, Spilde TL, et al. Single daily
Patients with stable perforations such as with a dosing ceftriaxone and metronidazole vs standard
TREATMENT triple antibiotic regimen for perforated appendicitis
well-formed abscess or phlegmons may be
INITIAL STABILIZATION/THERAPY observed initially on antibiotics. in children: A prospective randomized trial.
r NPO, provide IV fluids, correct any electrolyte Some surgeons elect for 1014 days of outpatient J Pediatr Surg. 2008;43:981.
abnormalities antibiotics followed by an interval appendectomy
r NG tube if there is concern for obstruction or ileus in 68 wk.
Interval appendectomy is an increasingly common CODES
MEDICATION practice despite the lack of randomized clinical
First Line trials comparing this with standard appendectomy. ICD9
r Early analgesia is recommended. There is no r 540.0 Acute appendicitis with generalized peritonitis
DISPOSITION r 540.1 Acute appendicitis with peritoneal abscess
increase in missed appendicitis or in negative
All patients with acute appendicitis should be
appendectomies after analgesia (6):
admitted from the emergency department. r 541 Appendicitis, unqualified
Morphine 0.1 mg/kg IV/IM/SC q2h PRN
Initial morphine dose 0.1 mg/kg IV/SC may be
repeated q1520min until pain is controlled FOLLOW-UP PEARLS AND PITFALLS
then q2h PRN
r For acute appendicitis, antibiotics are usually given FOLLOW-UP RECOMMENDATIONS r Failure to diagnose appendicitis is one of the most
preoperatively to decrease the risk of abscess Postoperatively, patients should return if they develop common causes for malpractice lawsuits in pediatric
formation and wound infection: any symptoms of an abdominal abscess, such as emergency medicine.
Ampicillin/Sulbactam 100200 mg abdominal pain, vomiting, or fever. r Younger children, particularly of toddler age, are at
ampicillin/kg/day divided q6h to a max of 12 g increased risk for perforated appendicitis, probably
q6h due to inability to communicate pain sensation.
73
ARTHRITIS, RHEUMATOID
Helene Tigchelaar
Usha Sethuraman
r Enthesitis-related JIA: r Pattern of pain:

BASICS Pain at tendon insertion and joints Onset, duration; frequency; severity; timing;
In addition, two of the following: migration; spinal, muscle, or jaw pain
DESCRIPTION Sacroiliac tenderness Location and number of joints, symmetry,
r Juvenile rheumatoid arthritis, or juvenile idiopathic Inflammatory spinal pain swelling, warmth or redness
arthritis (JIA), is the most common rheumatic Anterior uveitis r Stiffness in morning or with immobility
disease of childhood. Positive family history
r Definition: Onset >8 yr of age PHYSICAL EXAM
r Vital signs, general appearance, gait
Arthritis in at least 1 joint for >6 wk in a child Positive HLA-B27 (8592% of cases)
r Psoriatic arthritis: r Examine heart, lungs, eyes, and skin.
<16 yr of age after other causes have been
r Examine all joints for symmetry, swelling, redness,
excluded Arthritis and definite psoriasis or two of the
r Has a highly variable disease course following: tenderness, warmth, pain to palpation or
r Persists into adulthood in many children Dactylitis, nail pitting, onycholysis PLUS movement, and full range of motion and mobility.
r International League of Associations for Family history r Muscle strength
Rheumatology (ILAR) classification system: Clinically similar to early-onset oligoarticular
7 clinical subtypes defined HLA-B27 positive: Axial arthritis with psoriasis
r Undifferentiated: Lab
Subtypes are different diseases with different Initial Lab Tests
genetics, presentations, and clinical features. Arthritis that does not fit current classifications r Perform limited, focused diagnostic studies.
r Systemic arthritis JIA (10% of JIA): r CBC with differential, ESR, C-reactive protein:
EPIDEMIOLOGY
Peak onset between 1 and 6 yr of age r Studies suggest that JIA is underreported. Nonspecific and frequently normal in JIA
Affects boys and girls equally r Prevalence is 0.074.01 per 1,000 children. r Urinalysis, LFTs, BUN, and serum creatinine:
Arthritis plus daily spiking (intermittent) fevers for r Lower (26/100,00) in urban African Americans Alternative diagnosis of systemic lupus
>2 wk with toxicity plus 1 of the following: r Incidence is 0.0080.226 per 1,000 children. erythematosus (SLE) or vasculitis
Macular pink rash with fever r Ferritin levels for systemic JIA
r Distribution of subtypes varies with population.
Serositis, lymphadenopathy, anemia r Acute joint pain: Consider:
Hepatosplenomegaly, pericarditis RISK FACTORS
Extra-articular symptoms precede arthritis by r Genetic predisposition Cultures of throat, blood, stool, joint aspirate
weeks or months and are self-limiting. r Female (in most types) Inflammatory joint aspirate: 50075,000
Laboratory findings: WBC/mm3 ; glucose >50% of serum
Antinuclear antibody (ANA) negative PATHOPHYSIOLOGY Septic arthritis: >50,000 WBC/mm3 ; glucose
Rheumatoid factor (RF) negative r Synovium infiltrated by lymphocytes, plasma cells, <50% of serum; Gram stain and/or culture
Elevated ferritin may occur. macrophages, and dendritic cells positive
In persistent disease, short stature, brachydactyly, r Fibroblast and synoviocytes proliferate. Serologic testing for Lyme disease and
and micrognathia can occur. r Different autoantigens are targeted. antistreptolysin O (ASO) titer
r Fibrin deposits on/in the synovium r Chronic joint pain: ANA and RF:
Life-threatening complications like tamponade,
vasculitis, and macrophage-activating syndrome r Joint effusions, erosion, and destruction Often negative in JIA and false positive in general
(MAS) may occur. r Ends in deformity, subluxation, and ankylosis population
r Oligoarthritis JIA (50% of all cases): HLA-B27 (associated with IBD, reactive arthritis,
<5 joints in 1st 6 mo ETIOLOGY psoriatic arthritis, juvenile ankylosing spondylitis)
r Poorly understood
Large lower joints but rarely hips Imaging
r Abnormal autoimmunity involved r X-ray for arthritis of single joint:
2 additional types after 6 mo:
Persistent: 4 joints always r Genetic factors play a strong role Consider x-ray of contralateral joint
Extended: >4 joints always r Specific HLAs identified Early findings:
Females > males Effusion
Disease onset between 1 and 5 yr of age Soft tissue swelling
Uveitis only systemic symptom (2025%) DIAGNOSIS Osteoporosis, periostitis, new bone formation
ANA positive in 7585% Late findings:
High risk of uveitis when ANA is positive HISTORY Subchondral erosions
r History is key to proper diagnosis.
r Polyarticular JIA (25% of all cases): Narrowing of cartilage space
r Family history (including siblings):
5 joints within 1st 6 mo Bony destruction and fusion
Females > males Psoriasis, hypermobility syndromes, inflammatory r US for effusion if isolated hip pain or knee pain and
Morning stiffness, joint swelling bowel disease (IBD), uveitis, other autoimmune swelling
Systemic findings are less diseases
r RF negative polyarticular JIA: r Patient history (as above) DIFFERENTIAL DIAGNOSIS
r Precipitating factors: r Trauma
<10 yr of age, fewer joints r Infection:
No systemic features Trauma
Recent illness (upper respiratory infection, sore Sepsis, bacterial endocarditis, septic arthritis,
Asymmetric joint arthritis
throat, enteritis) osteomyelitis, Lyme disease, postinfectious and
Often ANA positive (uveitis)
r Polyarticular JIA (RF positive): Medications, activity viral arthritis (Parvovirus), malaria
r Alleviating factors: Medications, heat, cold r Reactive arthritis:
>8 yr of age
r Review of systems: Patterns of fever, rash, loss of Neisseria and streptococcal infections
Females, more severe disease
weight, abdominal pain, eye symptoms Rapid onset of multiple joint involvement more
Symmetric small joint polyarthritis
typical of reactive than JIA
Usually HLA DR4 positive:
Progressive, unremitting, adult counterpart
Early, aggressive treatment required
74
ARTHRITIS, RHEUMATOID
A
r Rheumatic fever DISPOSITION r Pericarditis:
r Other immune-mediated diseases: Admission Criteria Presenting symptom or accompany systemic JIA
Henoch-Schonlein purpura, SLE, Kawasaki r Pericarditis/Symptomatic pericardial effusion Subclinical pericardial effusion or pericarditis
disease, polyarteritis r MAS or toxic appearing Chest pain, tachycardia, dyspnea, cardiomegaly,
Drug reaction, serum sickness friction rubs
r Hematologic/Oncologic: Issues for Referral CXR, ECG, echo
r Rheumatology referral for suspected JIA
Leukemia, lymphoma, neuroblastoma, bone Treatment:
r Ophthalmology for suspicion of uveitis ABCs
tumor, hemoglobinopathies, and hemophilia r Hematology/Oncology referral for suspected
r IBD Systemic steroids
malignancy Quality-of-life issues include depression, lower
r Orthopedic/Infectious disease for septic joint rate of marriage, increased unemployment as
TREATMENT COMPLEMENTARY & ALTERNATIVE
patients enter adulthood, and limited
socialization.
MEDICATION THERAPIES
r Physical and occupational therapy, splinting
First Line r Emotional support with counseling or therapy
NSAIDs: ADDITIONAL READING
r Inhibit COX-1 and COX-2 in the inflammatory r Borchers AT, Selmi C, Cheema G, et al. Juvenile
response
r For mild cases, response in 6 wk
FOLLOW-UP idiopathic arthritis. Autoimmun Rev. 2006;5:
279298.
r 50% respond to the 1st NSAID FOLLOW-UP RECOMMENDATIONS r DeWitt EM, Sherry DD, Cron RQ. Pediatric
r Another 50% respond to a 2nd NSAID Patient Monitoring rheumatology for the adult rheumatologist: Therapy
r Ibuprofen 10 mg/kg/dose PO/IV q6h PRN r Patients on MTX and biologic agents require close
and dosing for pediatric rheumatic disorders. J Clin
r Ketorolac 0.5 mg/kg IV/IM q6h PRN monitoring of CBC and LFTs. Rheumatol. 2005;11(1):2133.
r Naproxen 5 mg/kg PO q8h PRN r Patients on etanercept require monitoring for r Giannini EH, Ilowite NT, Lovell DJ, et al. Long-term
neurologic complications including neuropathy. safety and effectiveness of etanercept in children
Second Line r All patients with JIA require monitoring for
r Disease-modifying antirheumatic drugs with selected categories of juvenile idiopathic
ophthalmic complications. arthritis. Arthritis Rheum. 2009;60(9):27942804.
r Required in 2/3 of persistent joint disease
r Goldmuntz EA, White PH. Juvenile idiopathic
r Retards progression of disease: PROGNOSIS
r Mortality reported is 0.291.1%. arthritis. A review for the pediatrician. Pediatr Rev.
Methotrexate (MTX) 515 mg/m2 once weekly r 60% of deaths are due to systemic type. 2006;27:2432.
PO, IM or SC: r Ravelli A, Martini A. Juvenile idiopathic arthritis.
Used for systemic/polyarticular forms r Spontaneous remission varies by subtype:
Requires folic acid supplementation Systemic onset: Lancet. 2007;369:767778.
Requires lab monitoring 50% remit in 1 yr, 25% joint destruction
Improvement after 612 wk Oligoarticular: Best prognosis of all:
Combination therapy with leflunomide has 3550% remission rates CODES
better outcome when monotherapy fails. Chronic uveitis has high morbidity; extended
Sulfasalazine, hydroxychloroquine type has worse prognosis. ICD9
r Biologic agent: Tumor necrosis factor (TNF) receptor RF-positive polyarticular disease has a 6% 10-yr r 714.30 Chronic or unspecified polyarticular juvenile
antagonists: remission rate: rheumatoid arthritis
Generally chronic and progressive r 714.31 Acute polyarticular juvenile rheumatoid
Rapid improvement in MTX resistance cases
Etanercept 0.4 mg/kg SC biweekly or 0.8 mg/kg Psoriatic arthritis is chronic and destructive. arthritis
r Biologic agents are continuing to improve functional r 714.32 Pauciarticular juvenile rheumatoid arthritis
SC once weekly
Other TNF-alpha antagonists used are infliximab outcome.
and adalimumab. r Predictors of progressive disability: Female sex,
r Oral or IV steroids 0.52.0 mg/kg/day PO: early-onset symmetric disease, hip involvement, PEARLS AND PITFALLS
Systemic JIA, rarely used for other subtypes positive RF, and prolonged elevation of ESR
r Pearls:
Not for long-term therapy COMPLICATIONS
r Uveitis (may be presenting complaint): Increased use of disease-modifying antirheumatic
Early use of MTX to allow weaning of steroids
r Corticosteroid joint injection: drugs and biologic agents is dramatically
Common in pauciarticular with positive ANA improving outcome.
Most commonly used in pauciarticular Red eye, tearing, pain, decreased vision r Pitfalls:
Prevents use of systemic drugs Permanent damage may have occurred.
r All patients with JIA require emergent Severe pain, refusal to bear weight, or a red hot
Triamcinolone hexacetonide
r Treatment of uveitis: severely painful joint suggests infection or
ophthalmology exam for eye complaints: malignancy rather than JIA.
Frequent eye exams Regular slit lamp exam on a set schedule: Normal laboratory studies including negative ANA
Topical corticosteroids and mydriatics Frequency based on duration, age at onset, and and acute phase reactants do not rule out JIA.
Systemic steroids and sub-Tenon injections ANA status of disease Patients on immunosuppressive therapy may not
r Macrophage activation syndrome (58%):
SURGERY/OTHER PROCEDURES demonstrate normal serologic or clinical response
r Release of joint contractures Systemic onset highest risk to infection.
r Joint replacement Fever, hepatosplenomegaly, anemia, Failure to entertain the diagnosis of uveitis in any
r Autologous stem cell transplants lymphadenopathy, thrombocytopenia and child with a red, painful, or tearing eye
leukopenia, neurologic abnormalities
May follow infection or due to drugs (MTX,
sulfasalazine, NSAIDs)
Treatment:
High-dose IV corticosteroids
Cyclosporin
75
ARTHRITIS, SEPTIC
Rebecca L. Vieira
Nikhil B. Shah
r Kingella kingae DIAGNOSTIC TESTS & INTERPRETATION

BASICS Increasingly recognized causative agent (2) Lab
r N. gonorrhoeae and meningitidis Initial Lab Tests
DESCRIPTION r H. influenzae type B (Hib) r WBC, ESR, and C-reactive protein typically reveal
r Septic arthritis refers to inflammation of a joint
More common in under- or nonimmunized children elevations consistent with infection.
caused by a bacterial infection r Salmonella Elevations are not always present
r Most commonly bacterial in origin r Blood cultures are positive in 3040% of patients
Seen in children with hemoglobinopathy such as
r 90% are monoarticular
sickle-cell disease with septic arthritis
r Hip and knee joints affected most frequently r Other: r Blood culture (aerobic and anaerobic)
r Early recognition and treatment are critical to Pseudomonas aeruginosa (from puncture wounds r Kochers criteria (4) can be used to clinically predict
prevent joint damage and permanent disability or injectable drug use) septic arthritis in a child with painful hip:
r Septic arthritis of the hip is a surgical emergency Nonsalmonella gram negative rods (Serratia, Non-weight bearing on affected side
and requires immediate drainage Enterobacter, Campylobacter) ESR >40
r Septic arthritis is distinct from joint infections caused Anaerobes (Bacteroides, Fusobacterium spp., etc.) Fever
by viral or fungal pathogens (referred to as aseptic WBC count >12,000
arthritis) r When 4/4 criteria are met, there is a 99%
r Septic arthritis includes suppurative arthritis, DIAGNOSIS probability of septic arthritis
bacterial arthritis, pyogenic arthritis, purulent HISTORY 3/4 = 93%; 2/4 = 40%; 1/4 = 3%; 0/4 = 0.2%
arthritis and pyarthrosis r Fever, joint pain, restricted range of motion r CRP and ESR can be used to monitor disease course
r Pain is progressive, does not wax and wane and response to treatment
EPIDEMIOLOGY r Additional tests may be necessary when specific
r Reported incidence: 537 per 100,000 (1,2) r Decreased limb use, particularly limping, is the most
r Most frequently affects children <3 years old common manifestation pathogens are suspected:
r Males affected more than females (1.2-2 to 1) r Findings are nonspecific in neonates and young Throat culture (GAS, N. gonorrhoeae)
r Hip and knee joints most frequently involved infants (<23 months): Eye and CSF (neonatal gonococcal infection)
ASO (GAS)
r Majority are monoarticular Presents similar to sepsis, i.e., irritability, poor
feeding, or fever without a focus Lyme titer
RISK FACTORS Subtle findings include: Stool and/or urine (for septic or reactive arthritis
r Neonates: umbilical vessel catheterization; central Positional preference (eg, leg abducted and secondary to gastrointestinal infection)
r Arthrocentesis fluid
venous catheter, femoral venipuncture, osteomyelitis externally rotated in septic hip)
r Older children: immunodeficiency, joint surgery, Lack of use of the involved extremity Synovial WBC >50,000 with >90% PMN
hemoglobinopathy, underlying arthritis, diabetes, (pseudoparalysis) suggests septic arthritis
sexual activity Evidence of discomfort when handled Pathologic organisms in the synovial fluid on
r Preexisting arthropathy (which may delay the (paradoxical irritability) or having the diaper Gram stain or culture confirms diagnosis
diagnosis) (3) changed Gram stain and culture are negative in 4050% of
r Most patients have no underlying medical conditions r Findings in older children and adolescents: patients with other findings suggestive of septic
Fever and other constitutional symptoms (eg, arthritis
PATHOPHYSIOLOGY malaise, poor appetite) Imaging
r Most cases result from hematogenous dissemination r X-rays are rarely diagnostic, can be used to rule out
Swelling of affected joint
of an organism into either the joint or metaphysis Pain with movement osteomyelitis or other causes of pain and swelling,
r Rarely can occur from direct inoculation (i.e,
Limp, refusal to walk or bear weight sometimes show evidence of joint effusion
penetrating injury) or contiguous extension (eg, joint r Hip involvement may cause referred pain in adjacent Findings suggestive of septic arthritis include
involvement during osteomyelitis) structures such as the knee or abdomen (may mimic displacement of muscle surrounding the joint,
r Bacteria spread through metaphyseal capillaries
an acute abdomen or UTI) distension of joint capsule, joint space widening,
to epiphyseal plate, allowing invasion into joint r Unusual worsening of one joint in patients with subluxation or dislocation (rarely), and bony
space underlying arthropathy (eg, juvenile idiopathic erosion (late finding)
Inflammatory response with neutrophilic r Ultrasound
arthritis [JIA, formerly JRA]) should arouse suspicion
infiltration occurs for septic arthritis Can identify and quantify joint effusion
Pus accumulation leads to distension of joint High negative predictive value for septic hip
capsule producing the characteristic clinical and PHYSICAL EXAM Joint aspiration should be performed if ultrasound
radiographic findings r Patients with septic arthritis often appear ill
r Fever may or may not be present demonstrates an effusion
ETIOLOGY Can be used to guide diagnostic aspiration
r Bacterial etiology confirmed by appropriate culture r Joint may be warm, erythematous, swollen and r CT scan
(blood, synovial fluid, and/or other sites) in 5070% tender (swelling rare in hip & shoulder) Not routinely used in diagnostic evaluation
r Active & passive range of motion elicit pain r Bone scan/scintigraphy
of cases
r Staphylococcus aureus r Range of motion may be decreased
Generally only used if concomitant osteomyelitis
r Patients with septic arthritis of the hip will suspected or if a deep joint (eg, hip or sacroiliac)
Most common cause across all age groups
Increasing prevalence of community-acquired preferentially hold leg flexed & externally rotated is affected
methicillin-resistant S. aureus (CA-MRSA) r In adolescent, perform GU exam to evaluate for GC r MRI
r Streptococci infection. More sensitive imaging modality
Includes Group A and B streptococci (GAS and Also evaluates concomitant osteomyelitis or
GBS, respectively) and pneumococcus osteomyelitis-associated abscess
GAS seen primarily in children >5 years
GBS in infants <3 months
Pneumococcus in children <2 years
76
ARTHRITIS, SEPTIC
A
Diagnostic Procedures/Other r Ciprofloxacin 10 mg/kg/dose q12h up to max COMPLICATIONS
r Arthrocentesis is necessary 400 mg IV q12h r Osteomyelitis
r Orthopedic consultation if uncomfortable or For use if suspected GC arthritis, only appropriate r Bacteremia or sepsis
inexperience performing arthrocentesis in areas without GC quinolone resistance r 1040% will have the following:
r Oxacillin 50 mg/kg/dose IV q68h up to max Decreased joint function(restriction, increased
r Fracture, sprain, soft tissue traumatic injury 1 g/dose IV q6h laxity
r Nafcillin 25 mg/kg/dose IV q46h up to max 2 g IV Limb length discrepancy
r Other orthopedic conditions (eg, slipped capital
q46h Avascular necrosis
femoral epiphysis, Legg-Calve-Perthes disease) r Clindamycin 10 mg/kg/dose IV q8h
r Oncologic processes (eg, leukemia, osteosarcoma, Enlargement of the femoral head (in septic
r Vancomycin 10 mg/kg/dose IV q12h up to max arthritis of the hip)
osteoid osteoma)
r Aseptic arthritis single dose 1 g IV q12h
r Sexually active adolescents: Anti-staph and strep
r Reactive arthritis REFERENCES
r Lyme disease agent plus coverage for N. gonorrhoeae
r Cellulitis (3rd-generation cephalosporin or quinolone if in 1. Riise OR, Handeland KS, Cvancarova M, et al.
nonquinolone-resistant geographic area) Incidence and characteristics of arthritis in
r Osteomyelitis
SURGERY/OTHER PROCEDURES Norwegian children: A population-based study.
r Transient synovitis
Septic hip usually mandates surgical irrigation: Pediatrics. 2008;121(2):e299306.
r Arthroscopy and needle aspiration may be 2. Yagupsky P, Bar-Ziv Y, Howard CB, et al.
Epidemiology, etiology, and clinical features of
TREATMENT considered in certain circumstances, but this
septic arthritis in children younger than 24 months.
decision is made by orthopedic surgeon.
MEDICATION Arch Pediatr Adolesc Med. 1995;149(5):53740.
DISPOSITION 3. Sauer ST, Farrell E, Gellar E, et al. Septic arthritis in
First Line
r Analgesics, antipyretics, and antibiotics are the Admission Criteria a patient with juvenile rheumatoid arthritis. Clin
r All patients are admitted Orthop Relat Res. 2004;(418):21921.
mainstay pharmacologic agents. r If findings are equivocal, arthrocentesis or
r Opioids 4. Mathews CJ, Coakley G. Septic arthritis: Current
Morphine 0.1 mg/kg IV/IM/SC q2h PRN: orthopedic consultation cannot occur in ED, admit diagnostic and therapeutic algorithm. Curr Opin
Initial morphine dose 0.1 mg/kg IV/SC may be patient for inpatient therapy and observation. Rheumatol. 2008;20:457.
repeated q1520min until pain is controlled Discharge Criteria 5. Luhmann JD, Luhmann SJ. Etiology of septic
then q2h PRN r Well-appearing arthritis in children: An update for the 1990s.
Codeine codeine/acetaminophen dosed as r No fever, normal WBC, normal ESR and CRP, able to Pediatr Emerg Care. 1999;15:40.
0.51 mg/kg of codeine component PO q4h PRN bear weight (if lower limb joint)
Hydrocodone or hydrocodone/acetaminophen r Synovial fluid analysis with WBC <50,000 cells/
dosed as 0.1 mg/kg of hydrocodone component microL and negative Gram stain in well-appearing CODES
PO q46 h PRN child with good follow-up
r NSAIDs ICD9
Issues for Referral r 711.40 Arthropathy, site unspecified, associated
Consider NSAID medication in anticipation of r Refer to orthopedic surgeon
prolonged pain and inflammation r Refer to infectious disease specialist for unusual with other bacterial diseases
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN. r 711.45 Arthropathy involving pelvic region and
Ketorolac 0.5 mg/kg IV/IM q6h PRN pathogens or therapy failure
thigh associated with other bacterial diseases
Naproxen 5 mg/kg PO q8h PRN r 711.46 Arthropathy involving lower leg associated
r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN
r Septic arthritis is a surgical emergency that requires
FOLLOW-UP with other bacterial diseases
prompt joint irrigation by an orthopedic surgeon. FOLLOW-UP RECOMMENDATIONS

Systemic antibiotics should be started immediately Follow up at 1-wk intervals PEARLS AND PITFALLS
after synovial fluid analysis, awaiting surgical Patient Monitoring r Early diagnosis and treatment is critical for best
irrigation. r Monitoring response to therapy (serial examination,
r Antibiotics should be chosen to cover the most likely outcome
WBC count, ESR and/or CRP, and synovial fluid WBC r Initiation of antibiotics prior to synovial fluid analysis
causative organisms based on age and risk factors. and culture)
r Birth3 mo: Combination of anti-staphylococcal r Radiographs 23 wk into the course to look for confounds diagnosis
r Goals of treatment are to sterilize and decompress
agent (eg, oxacillin or vancomycin) plus gentamicin evidence of osteomyelitis
or cefotaxime r Drug monitoring (antibiotic levels, serum bactericidal the joint
r Failure to perform synovial fluid analysis in a timely
Oxacillin 50 mg/kg/dose IV q6h titers, adverse effects) has been suggested
Gentamicin 57 mg/kg IV q24h or divided q8h r Long-term monitoring for joint dysfunction and manner can delay diagnosis and treatment, leading
Cefotaxime 50 mg/kg/dose IV q6h to worse outcomes
limb-length discrepancy
Ceftriaxone 50 mg/kg/dose IV daily
r Older than 3 mo: Antistaphylococcal and PROGNOSIS
r Varies by pathogen, joint involvement, and time to
streptococcal agent (nafcillin, clindamycin, or
vancomycin, depending on prevalence and diagnosis
susceptibilities of CA-MRSA) in combination with r Factors related to poor outcome include:
gram-negative coverage if clinical situation suggests Greater duration before treatment
possible gram-negative organism (eg, direct Involvement of the hip joint
inoculation, gram negatives seen on Gram stain) Age less than one year old
r Cefotaxime 50 mg/kg/dose q68h up to max dose S. aureus or Enterobacteriaceae
1 g IV q8h
r Ceftriaxone 50 mg/kg/dose IV daily, up to max dose
2 g IV daily
77
ASCARIS LUMBRICOIDES
Ami P. Shah
Raymond Pitetti
r They further mature in the lungs for 1014 days. PHYSICAL EXAM
BASICS r Larvae then penetrate the alveolar walls and enter r Most patients are asymptomatic.
the tracheobronchial tree. From this site, they are r The patient may be malnourished.
DESCRIPTION coughed up, swallowed, and reach the small r Nonspecific GI symptoms, including abdominal pain
r Ascaris lumbricoides is the largest small intestinal r Heavy worm load may present as intestinal
intestine:
parasite, growing up to 40 cm. Loffler syndrome: Acute transient pneumonitis obstruction.
r It is a roundworm (nematode) that is the most may occur during the larval migratory phase, r May present with signs of biliary obstruction and
common cause of helminth infections in humans. presenting with fever, cough, and marked peritonitis, including:
EPIDEMIOLOGY eosinophilia. Abdominal distention
r >1 billion people are infected with this worm r In the small intestine, they mature into adult worms,
Decreased bowel sounds
annually. where they then reside. Scleral icterus
r Most common in tropical and subtropical areas r Adult female worms lay 200,000 eggs per day. Jaundice
r Uncommon in the U.S., found predominantly in rural r Eggs are passed in the feces. They need to incubate Pallor
southeastern parts of the U.S. for 23 wk in the soil to become infectious.
r Global distribution ETIOLOGY Lab
r 1/41/3 of the worlds population is infected with A. lumbricoides, or roundworm: A small intestinal r Stool for ova and parasites:
this worm. parasite Infection is confirmed by identification of eggs in
r School-aged children have highest incidence. the stool sample.
COMMONLY ASSOCIATED CONDITIONS r Peripheral blood can be tested to look for
RISK FACTORS Malnutrition
r Poor hygiene and sanitation eosinophilia in severe cases or suspected case of
r Unwashed vegetables and fruits Loffler syndrome.
r Children playing in soil
DIAGNOSIS Imaging
r Not routinely required
HISTORY
GENERAL PREVENTION r Patients may present with nonspecific GI and r X-ray, US, and CT scan of the abdomen may be
r Routine sanitary hygiene, especially good hand
pulmonary symptoms, such as: required based on the clinical presentation.
washing
r Washing vegetables and fruits well, especially if Nausea
Vomiting r Acute appendicitis
grown in soil that uses human feces as a fertilizer Abdominal pain r Cholangitis
PATHOPHYSIOLOGY Diarrhea r Hepatitis
r Infection starts with ingestion of fertilized eggs. Cough
r Pancreatitis
Unfertilized eggs are not infective: Nasal congestion
r Patients may cough up round white strings or r Other helminth or tropical parasitic infections, such
Ingestion of eggs is typically from unwashed fruits
or vegetables that contain eggs. noodlelike material. as strongyloides and hookworm
Children may become infected directly from their r Travel to tropical areas or living on a farm are crucial
hands when playing in soil or sand containing the components of the history.
parasite.
r The larvae then hatch in the small intestine, from
where they enter the portal circulation and reach the
lungs via systemic circulation.
78
ASCARIS LUMBRICOIDES
A
SURGERY/OTHER PROCEDURES COMPLICATIONS
r May be required to relieve obstruction caused by a r Loffler syndrome
TREATMENT r Small bowel obstruction
heavy worm load
INITIAL STABILIZATION/THERAPY r Endoscopic retrograde cholangiopancreatography r Small bowel perforation and peritonitis
r Assess and stabilize airway, breathing, and may help relieve biliary obstruction. r Biliary tract obstruction
circulation.
r Symptomatic care unless signs of intestinal DISPOSITION
obstruction are present
Admission Criteria ADDITIONAL READING
r Secondary intestinal obstruction, peritonitis, bowel
r Emergent surgical consultation if intestinal
perforation, or biliary tract obstruction American Academy of Pediatrics. Ascaris lumbricoides
obstruction r Critical care admission criteria: infections. In Pickering LK, Baker CJ, Kimberlin DW,
MEDICATION If unstable vital signs, particularly due to et al., eds. Red Book: 2009 Report of the Committee
First Line pulmonary compromise on Infectious Diseases. 28th ed. Elk Grove Village, IL:
r Treatment should be instituted for all cases, both Author; 2009:221222.
Discharge Criteria
asymptomatic. Appropriate antihelminth therapy has been initiated See Also (Topic, Algorithm, Electronic
r Benzimidazoles (albendazole and mebendazole) are
Issues for Referral Media Element)
wormicidals. These agents act by blocking the Infectious disease referral may be required in the U.S. http://www.dpd.cdc.gov/dpdx/html/Ascariasis.htm
energy/adenosine triphosphate production of the since the infection is infrequent.
worms, leading to their death:
Albendazole: <2 yr of age, 200 mg PO as a single CODES
dose; >2 yr of age, 400 mg PO as a single dose FOLLOW-UP
Mebendazole: >2 yr of age 100 mg PO b.i.d.
3 days: FOLLOW-UP RECOMMENDATIONS ICD9
Used in children >2 yr Discharge instructions and medications: 127.0 Ascariasis
r Ivermectin 150200 g/kg PO once, max single r Emphasize personal hygiene and hand washing.
dose 400 mg: r Although not necessary, it is recommended to
PEARLS AND PITFALLS
Used in children >15 kg repeat the stool sample for ova and parasites
Do not use during lactation. 23 wk after antihelminth therapy. r Pearls:
A 2nd course of antihelminth therapy may be Though rarely encountered in the U.S., Ascaris
ALERT necessary if the sample is positive. should be considered in any child with suggestive
For all medications above, safety not established in signs or symptoms.
Patient Monitoring
children <2 yr of age. r Inspect stools every day for worm passage. Antihelminth therapy is generally effective and
Pregnancy Considerations r If coughing, inspect the sputum for worms. safe.
r Pitfalls:
Safety not established in pregnant patients.
PROGNOSIS Delay in diagnosis can lead to serious
Second Line Unless there are rare complications such as bowel complications, including intestinal obstruction,
For cases of partial or complete intestinal and biliary obstruction or Loffler syndrome, the prognosis with peritonitis, bowel perforation, or biliary tract
tract obstruction: treatment is excellent. obstruction.
r Piperazine is a helminth paralytic. It causes flaccid
paralysis of the worms and thus facilitates their
passage from the small intestine (75 mg/kg PO per
day 2 days).
r Pyrantel pamoate is a neuromuscular depolarizing
agent that can be used alternatively (11 mg/kg/dose
PO as a single dose).
79
ASCITES
r Infectious: TB, schistosomiasis, chlamydia Ascitic fluid polymorphonuclear count 250/mm3

BASICS r Neoplastic: Neuroblastoma, lymphoma, ovarian indicates infection.
tumors Ascitic fluid is classified as an exudate if the total
DESCRIPTION r GI: Infarcted bowel, perforation, pancreatitis protein concentration is 2.5 or 3 g/dL, but this
r Ascites is the pathologic accumulation of fluid in the r Others: Ventriculoperitoneal shunt, chylous ascites, has low sensitivity of 59%.
peritoneal cavity. systemic lupus erythematosus (SLE) Serum to ascites albumin gradient (SAAG): This is
r Liver, kidney, and cardiac diseases are common calculated as the difference between serum
causes of ascites in children. albumin value and ascitic fluid albumin:
r Can be classified as (1): DIAGNOSIS The presence of SAAG 1.1 g/dL indicates that
Grade 1: Detected only by US exam the patient has portal HTN with 97% sensitivity
Grade 2: Moderate ascites manifested by HISTORY (3).
r Increase in belt or clothing size, inappropriate A high SAAG (>1.1 g/dL) is associated with
moderate symmetrical distension of abdomen
Grade 3: Gross ascites with marked abdominal weight gain diffuse parenchymal liver disease and occlusive
r Abdominal pain or sensation of fullness portal and hepatic venous disease, liver
distension
r Yellow discoloration of eyes metastasis, and hypothyroidism.
EPIDEMIOLOGY r Easy fatigability Milky fluid indicates chylous ascites, usually
r 44% of children with cirrhosis have ascites (2).
r Shortness of breath having a triglyceride concentration >200 mg/dL.
r 16.555% of patients with subacute hepatic failure,
r History of pre-existing liver disease, heart disease, Ascitic fluid glucose concentration is similar to
acute hepatitis, or fulminant hepatic failure have that of serum:
and kidney disease
ascites. r Risk factors: History of IV drug use or repeated Low levels indicate infection.
RISK FACTORS Levels are undetectable in gut perforation.
r Children with liver disease, heart failure, nephrotic blood transfusions
The ascitic fluid/serum ratio of LDH is 0.4 in
syndrome, ventriculoperitoneal shunt PHYSICAL EXAM uncomplicated ascites. The ratio:
r IV drug use, unprotected sex, recurrent transfusion r Abdominal distension with or without an everted Approaches 1 in cases of spontaneous bacterial
of blood or blood products umbilicus peritonitis (SBP)
r Evaluate for hepatosplenomegaly, consistency of >1 in cases of tumor
PATHOPHYSIOLOGY liver (soft vs. firm vs. hard), abdominal masses Ascitic fluid amylase concentration is 40 IU/L in
r Underfilling theory: Portal HTN leads to r Presence of shifting dullness, flank dullness, fluid uncomplicated ascites and is increased in the
inappropriate sequestration of fluid in the wave setting of ascites secondary to pancreatitis or gut
splanchnic vasculature: r Stigmata of liver disease and cirrhosis: Jaundice, perforation.
This leads to decreased effective circulating
palmar erythema, abdominal wall collaterals Imaging
volume causing activation of renin-angiotensin r Presence of venous hum at umbilicus in portal HTN r US of the abdomen is the diagnostic modality of
and aldosterone pathways, leading to sodium and r Sister Mary Joseph nodule: A hard periumbilical choice to confirm ascites, determining the presence
water retention
r Overfill theory: Primary abnormality is inappropriate nodule indicative of metastatic disease from a pelvic of a mass, and evaluating the size of the liver and
or GI primary tumor spleen.
sodium and water retention, leading to r Presence of cardiac disease: Jugular venous r CT scan is helpful if a focal lesion such as
hypervolemia rather than hypovolemia.
r Peripheral arterial vasodilation theory: Cirrhosis distension, gallop, rales in chest malignancy is visualized on the US.
r Extremity edema, anasarca in nonhepatic causes of r Upright and supine films of the abdomen may
causes distortion of liver architecture and hepatic
ascites demonstrate diffuse abdominal haziness and loss of
fibrosis:
psoas margins.
This leads to increased intrahepatic resistance to DIAGNOSTIC TESTS & INTERPRETATION r Consider CXR and/or echo to evaluate for cardiac
blood flow causing portal HTN, which leads to Lab
shunting of blood to systemic circulation. r CBC with platelet count causes of ascites.
Vasodilators like nitric oxide are produced, leading r Evaluation of liver disease: AST, ALT, alkaline Diagnostic Procedures/Other
to splanchnic arterial vasodilation, which Abdominal paracentesis may be performed to confirm
phosphatase, serum total and direct bilirubin, total
decreases effective circulating volume. the presence of ascites, diagnose its cause, or
protein, albumin, PT, hepatitis profile
This theory is the most widely accepted. r Evaluation of renal disease: Electrolytes, BUN and determine the nature of the fluid (and if it is
infected):
ETIOLOGY creatinine, urinalysis, urine protein creatinine ratio r Left lower quadrant paracentesis site may be
r Liver disease: Cirrhosis, fulminant hepatic failure, r Ascitic fluid analysis: Cell count, total protein,
congenital hepatic fibrosis, portal vein obstruction, albumin, glucose, lactate dehydrogenase (LDH), preferred over midline location since the abdominal
lysosomal storage disorders amylase, triglycerides, bacterial culture, and wall is relatively thinner and the depth of fluid is
r Kidney disease: Nephrotic syndrome, obstructive cytology: greater.
r Tap 2 fingerbreadths cephalad and 2 fingerbreadths
uropathy, peritoneal dialysis, perforated urinary tract Normal ascitic fluid is transparent, yellow, and
r Cardiac: CHF, constrictive pericarditis contains <500 WBC/mm3 with medial to the anterior superior iliac spine.
polymorphonuclear count <250/mm3 .
80
ASCITES
A
r US-guided paracentesis is preferred to reduce the SURGERY/OTHER PROCEDURES DIET
incidence of complications. r Large-volume paracentesis with albumin infusion: r Salt-restricted diet
r Removal of >100 mL/kg of ascitic fluid is considered For diuretic resistant ascites, tense ascites, or those r Maintain calorie intake at goal.
large-volume paracentesis, and albumin with respiratory distress secondary to ascites r Protein intake (1 g/kg/day) unless patient is severely
replacement in addition to IV fluid replacement r Definitive therapy may involve: catabolic
typically accompanies such paracentesis. Transjugular intrahepatic portasystemic shunts
(TIPS) and peritoneovenous shunts for refractory PROGNOSIS
DIFFERENTIAL DIAGNOSIS Variable depending on the cause and extent of
r Obesity ascites
Liver transplantation underlying disease
r Abdominal masses (eg, neuroblastoma,
hepatoblastoma, Wilms tumor) r Respiratory distress
r Pregnancy Admission Criteria
r Ascites resistant to oral diuretic therapy r SBP
r Urine and fecal retention
r If SBP is suspected r Complications of portal HTN: Variceal hemorrhage,
r Critical care admission criteria: hepatorenal syndrome, liver failure
TREATMENT Ascites causing significant respiratory distress
PRE HOSPITAL Complications of underlying disease: Liver failure, REFERENCES
variceal hemorrhage, hepatic encephalopathy
Assess and stabilize airway, breathing, and circulation.
Discharge Criteria 1. Moore KP, Wong F, Gines P, et al. The
INITIAL STABILIZATION/THERAPY r Uncomplicated, small-volume ascites management of ascites in cirrhosis: Report on the
r Assess and stabilize airway, breathing, and consensus conference of the International Ascites
r Stable vital signs
circulation. r No airway or hemodynamic compromise Club. Hepatology. 2003;38:258266.
r Ascites with respiratory compromise should be 2. Peter L, Dadhich SK, Yachha SK. Clinical and
treated with paracentesis. Issues for Referral laboratory differentiation of cirrhosis and
r Dietary sodium restriction to 12 mEq/kg/day: r All patients with ascites require referral to a extrahepatic portal venous obstruction in children.
Effective in reducing the dose of diuretics and subspecialist for determination of the extent of J Gastroenterol Hepatol. 2003;18:185189.
leads to shorter hospital stay; effective only if underlying disease and its management. 3. Runyon BA, Montano AA, Akriviadis EA, et al. The
urinary sodium >15 mEq/24 hr r Referral to dietician to set caloric goal and serum-ascites albumin gradient is superior to the
r Water restriction is not recommended unless there sodium-restricted diet exudates-transudate concept in the differential
is associated hyponatremia (serum sodium diagnosis of ascites. Ann Intern Med. 1992;117:
<130 mmol/L). FOLLOW-UP 215220.
MEDICATION
r Diuretics are used to produce a negative fluid FOLLOW-UP RECOMMENDATIONS
r Discharge instructions and medications: CODES
balance of 10 mL/kg/day. Spironolactone and
furosemide are preferred diuretics. Steady gradual Sodium restricted diet:
12 mEq/kg/day for infants and children ICD9
loss is preferred. Oral diuretics are preferred
12 g/day (4488 mEq of sodium per day) in 789.59 Other ascites
compared to IV diuretics:
Spironolactone 1.53.3 mg/kg/day PO/IV in adolescents
r Consider combination oral diuretic therapy:
divided doses b.i.d.q.i.d. PEARLS AND PITFALLS
Furosemide 0.51 mg/kg/dose PO/IV q8h PRN Single morning dose of spironolactone
r For suspected or culture proven SBP: (0.33 mg/kg) along with furosemide (0.5 mg/kg) r Paracentesis is the gold standard to detect the
Cefotaxime 50 mg/kg/dose IV q8h, max single in the ratio of 5:2 underlying cause of ascites.
r Follow up with an appropriate specialist based on r Urgent paracentesis is indicated in patients with
dose 2 g/day
Ceftriaxone 50 mg/kg IV per day the etiology of ascites. ascites and fever or those with acute
r To prevent SBP: r Activity:
decompensation or significant respiratory distress
Penicillin 50 mg/kg/day PO divided b.i.d.q.i.d. Bed rest is not recommended in children with secondary to ascites.
may be used to prevent SBP in patients with uncomplicated ascites. r Prompt initiation of broad-spectrum antibiotic
ascites. This practice is losing prevalence due to Patient Monitoring therapy is indicated if SBP is suspected.
poor penicillin sensitivity of streptococcal bacteria. r Strict intake and output
r Weight
81
ASTHMA
Catherine H. Chung
Airway hyperresponsiveness: IgE-mediated Moderate: Normal or slightly agitated alertness,

BASICS response leading to bronchoconstriction pale color, speaks in short phrases, 3050%
Bronchial constriction: Stimulation of smooth increase in respiratory rate, moderate dyspnea,
DESCRIPTION muscle and endogenous stimulation of mast cells moderate intercostal retractions with suprasternal
r Asthma is a chronic, reversible, recurrent r Results in progressive air trapping, poor retractions/chest hyperinflation, wheeze
inflammatory disease of the airways resulting in oxygenation, poor ventilation, and throughout expiration, 9195% oxygen
airway obstruction, bronchial hyperresponsiveness, ventilation/perfusion mismatch. saturation in room air, PaCO2 <42 mm Hg
and inflammation. r After recurrent episodes, sensory nerves may Severe: Agitated or somnolent; cyanotic; difficulty
r Acute exacerbations result from inflammation, speaking; respiratory rate >50% increase; severe
become hypersensitive with hyperreactivity.
typically due to viral infection. r Progressively over the years, patients may lose the dyspnea, deep intercostal and tracheosternal
r Common environmental triggers include cigarette retractions; chest hyperinflation; wheeze
perception of dyspnea, increasing the chance of
smoke, house dust mites, and animal dander. inadequate self-treatment of exacerbations. throughout inhalation/exhalation; poor aeration;
<91% oxygen saturation in room air;
EPIDEMIOLOGY ETIOLOGY PaCO2 42 mm Hg
r Most prevalent chronic disease in childhood
Genetic and environmental components: r Associated conditions such as rhinitis, eczema, or
r 9% (6 million) of children in the U.S. have asthma. r Genetic: Multiple genetic defects have been linked
r Male prevalence higher than females (10% vs. sinusitis may be found on physical exam.
to asthma, and twin studies have found high
7.8%) concordance rates.
r Black and Hispanic children have higher prevalence r Environment: Common triggers (ie, dust, pollen, Lab
rates. dander, smoke, viral infections) often result in Initial Lab Tests
r Prevalence has doubled from 19801990. r Venous or arterial blood gas may be useful in severe
increased IgE-specific response.
r In 2004, asthma was responsible for 760,000 exacerbations to objectively measure oxygenation
COMMONLY ASSOCIATED CONDITIONS and ventilation.
emergency department visits. r Atopy (allergies, eczema) in patient or family r Initial use of venous blood gas is preferable. If
RISK FACTORS r Upper respiratory infections further information is required, arterial sampling
r Atopy
may be performed.
r Low birth weight
r Frequent respiratory infections DIAGNOSIS Imaging
r Obesity Chest radiograph rarely uncovers an unsuspected
HISTORY alternative diagnosis:
r Race: Black and Hispanic populations, due to either r Focus on onset, duration, progression, and severity r CXR should not be routinely performed on patients
genetic and/or environmental factors: of symptoms: presenting with 1st episode of wheezing.
In teenage years, these patients have a high risk How does the severity of this attack compare to r Most films will show hyperinflation and flatted
of mortality of acute asphyxial asthma. other exacerbations?
r Exposure to triggers diaphragms from air trapping, increased bronchial
GENERAL PREVENTION wall markings from inflammation, and/or atelectasis.
r Recent febrile respiratory illnesses r CXR may be useful if alternate problems such as
Avoidance of triggers:
r Common triggers: Upper respiratory infections, r Ask about medication dose, route, frequency and
pneumonia, pneumothorax, etc. are suspected.
tobacco smoke, weather changes, dust mites, air time since last dose.
r Inquire about compliance with controller Diagnostic Procedures/Other
pollution, cockroaches, animal dander, mold r Asthma is a clinical diagnosis; however, spirometry
r Less common triggers: Cold, foods, emotional stress, medication.
r Frequency, severity, and management of past may be used to help establish the diagnosis:
exercise Spirometry, also known as pulmonary function
exacerbations: Number of emergency department testing, evaluates for signs of reversible
PATHOPHYSIOLOGY visits, hospitalizations, ICU admissions, and previous
r A multifactorial and complex disease involving the obstruction.
intubations Difficult to perform before 5 yr of age
immunologic response of airways to infectious r Smoking or drug use
and/or environmental triggers If clinical suspicion is high in a child with normal
r Comorbid conditions such as cardiac, chronic lung,
r Cause of airway hyperresponsiveness is unknown in or near normal spirometry, bronchoprovocation
or psychiatric disease with methacholine, histamine, cold air, or exercise
most patients.
r Numerous environmental exposures may cause PHYSICAL EXAM may show airway hyperresponsiveness.
r Vital signs: Tachypnea, hypoxia r Allergy testing to identify potential allergens
asthma to develop: Cigarette smoke, lacquer,
isocyanates, acrylates, varied wood dusts, ivory dust, r Focus on general appearance, mental status, color, DIFFERENTIAL DIAGNOSIS
aldehydes, metals, preservatives, plastic and rubber and accessory muscle use and work of breathing r Acute wheezing: Bronchiolitis, foreign body
dust, fungicides, and numerous other chemicals: r Lack of wheeze may be due to poor aeration: aspiration, pneumonia, anaphylaxis, tracheitis,
Low-molecular-weight agents act as haptens. Cough-variant asthma will present with cough but laryngotracheobronchitis, bronchitis, cholinergic
Higher-molecular-weight products are directly no or minimal wheeze. toxicity, pulmonary edema, cardiac failure
immunogenic. r Degree of respiratory distress is determined by r Chronic or recurrent wheezing: Gastroesophageal
Exposure to these may cause permanent injury assessing lung auscultation for aeration, symmetry, reflux, recurrent aspiration, cystic fibrosis,
and sensitize the patient and induce asthma in a wheeze in inspiratory/expiratory phase, ability to immunodeficiency, primary ciliary dyskinesia,
previously nonasthmatic patient. speak, accessory muscle use, and oxygen bronchopulmonary dysplasia, foreign body
This is distinct from allergens that trigger an requirement. aspiration, bronchiolitis obliterans, pulmonary
exacerbation of asthma in asthmatic patients. r Estimation of severity: edema, vocal cord dysfunction, interstitial lung
r Three components of asthma: disease, tracheobronchomalacia, vascular
Mild: Normal alertness, color, and speech; normal
Airway edema: Regulated by mast cells, to 30% increase in respiratory rate; absent to mild rings/compression, tracheal stenosis/webs, cystic
eosinophils, macrophages, epithelial cells and dyspnea; no to mild intercostal retractions; lesions/masses, cardiac disease,
activated T lymphocytes causing inflammation, end-expiratory wheeze; >95% oxygen saturation tumors/lymphadenopathy
mucus production, and edema in room air, PaCO2 <42 mm Hg
82
ASTHMA
A
r Ketamine 0.252 mg/kg IV/IM loading dose: PROGNOSIS
r Improvement of an asthma exacerbation can be
TREATMENT May be followed with infusion
Ketamine may be used in an attempt to avert expected in 2448 hr.
PRE HOSPITAL intubation or as sedation prior to endotracheal r Long-term control of asthma symptoms can be
r Assess and stabilize airway, breathing, and intubation. expected in 24 wk.
circulation. r Noninvasive positive pressure ventilation: r 50% of children with asthma will be asymptomatic
r Administer supplemental oxygen. BiPAP/CPAP: as adults.
r Administer bronchodilators as appropriate protocol. Use in an attempt to avert endotracheal intubation
COMPLICATIONS
MEDICATION DISPOSITION r Cardiorespiratory arrest
Admission Criteria r Pneumothorax
First Line
r Mild to moderate exacerbations: Critical care admission criteria: r Pneumomediastinum
Oxygen to achieve oxygen saturation >90% r Altered mental status, need for ventilation support r Pneumonia
Inhaled beta2 -agonist, with or without (BiPAP/CPAP, mechanical ventilation), need for r Cardiac dysrhythmias
ipratropium, up to 3 treatments in 1st hr adrenergic infusion, need for very frequent (eg,
Inhaled beta2 -agonist may be either albuterol or q60min nebulization, significant respiratory acidosis,
levalbuterol: severe hypoxia, hypercarbia, respiratory failure, ADDITIONAL READING
Albuterol 0.15 mg/kg/dose by intermittent or complications (pneumothorax, dysrhythmias), or r Camargo CA Jr, Spooner CH, Rowe BH. Continuous
continuous nebulization (0.5 mg/kg/hr) comorbidities (pneumonia, cystic fibrosis)
Continuous nebulization has similar efficacy and r Admit less severely ill patients to the general versus intermittent beta-agonists in the treatment of
side effects as intermittent dosing. inpatient unit. acute asthma. Cochrane Database Syst Rev.
Levalbuterol (0.075 mg/kg) by intermittent 2003:cd001115.
Discharge Criteria r Craven D, Kercsmar CM, Myers TR, et al.
or continuous nebulization r Good clinical response to treatment that is sustained
Ipratropium bromide (0.250.5 mg), up to Ipratropium bromide plus nebulized albuterol for the
60 min after last treatment treatment of hospitalized children with acute
3 treatments in 1st hr, given concurrently with r Peak flowmeter >80% predicated
inhaled beta2 -agonist asthma. J Pediatr. 2001;138:51.
r Caregiver and patient competence in proper use of r Kulick R, Ruddy R. Allergic emergencies. In Fleisher
Systemic corticosteroids if no immediate
improvement or prolonged symptoms prior to inhaler G, Ludwig S, eds. Textbook of Pediatric Emergency
r Reliable caregivers to provide continual observation Medicine. 4th ed. Philadelphia, PA: Lippincott
arrival:
Prednisone or prednisolone 12 mg/kg PO, max and management of medication Williams & Wilkins; 2000;9991016.
single dose 60 mg r National Asthma Education and Prevention
Issues for Referral
Methylprednisolone 2 mg/kg Refer to an allergist or pulmonologist if: Program. Expert Panel Report 3: Guidelines for the
Dexamethasone 0.6 mg/kg IV/IM/PO, max r Atypical symptoms or questionable diagnosis Diagnosis and Management of Asthma. NIH-NHLBI
single dose 12 mg r Comorbid conditions (sinusitis, nasal polyps, severe publication. Washington, DC: U.S. Government
Single-dose dexamethasone equivalent to burst Printing Office. October 2007.
rhinitis, vocal cord dysfunction)
dose of prednisone; may be used without r Specialized treatment for immunotherapy See Also (Topic, Algorithm, Electronic
subsequent steroid treatment
r Severe exacerbations: r Poor control of asthma symptoms Media Element)
r Patient requires additional education and guidance r Bronchiolitis
As outlined for mild to moderate exacerbations, r Wheezing
plus consider: on complications of therapy, medication adherence,
Nonrebreathing mask to deliver supplemental or allergen avoidance
oxygen r Life-threatening asthma exacerbation
Epinephrine 1:1000, 0.01 cc/kg/dose (max r >2 oral corticosteroid courses per year CODES
single dose 0.5 cc) SC or IM
Indicated for those with very tight wheezing with ICD9
impaired delivery of inhaled beta-agonists. FOLLOW-UP r 493.00 Extrinsic asthma, unspecified
IV magnesium sulfate 5075 mg/kg over 20 min, r 493.02 Extrinsic asthma, with (acute) exacerbation
r Discharge instructions and medications:
max single dose 2.5 g r 493.81 Exercise induced bronchospasm
Terbutaline 10 g/kg SC/IV bolus: Provide an asthma action plan detailing when and
May follow with infusion of 0.4 g/kg/min; how to escalate therapy.
increase by increments of 0.30.5 g/kg/min Patients with persistent asthma should be started
on a daily inhaled corticosteroid. PEARLS AND PITFALLS
q30min as needed for respiratory distress r Activity: r Albuterol and levalbuterol, at equipotent doses,
Second Line Avoid exercise or pollen if these are triggers. have similar efficacy and safety profiles.
Adjunctive therapies, with largely unproven benefit, Patient monitoring r In severe asthma with very poor aeration, wheezing
may be considered for severely ill children who are Use peak flowmeter to monitor lung function.
unresponsive to more conventional treatment: may not be heard.
Provide asthma action plan to clarify medication r Ketamine is the sedative of choice for endotracheal
r Heliox (mixture of oxygen and helium) to reduce plan and warning signs. intubation due to bronchodilatory properties.
turbulent airflow and resistance
83
ASYSTOLE
Mioara D. Manole
Robert W. Hickey
r Post ROSC phase: PHYSICAL EXAM

BASICS Oxygen delivery is restored. r Primary survey: ABCDE
Reactive oxygen species are produced. r Secondary survey:
DESCRIPTION Inflammatory mediators are released. Identify signs of:
r Asystole is characterized by: Pathologies include: Treatable potential causes: 6Hs, 5Ts, trauma
Cessation of cardiac mechanical activity Myocardial dysfunction (hypotension, (accidental and nonaccidental)
Absence of perfusion to vital organs bradycardia, tachycardia, or tachyarrhythmia) Signs of futile resuscitation efforts (dependent
Absence of central pulses, loss of consciousness, Hypoxic-ischemic encephalopathy (cerebral cyanosis, rigidity)
and apnea or gasping respirations edema, seizures) r Airway:
r ECG shows flat line, pulseless electrical activity Metabolic acidosis and electrolyte abnormalities If artificial airway is established, check:
(PEA), ventricular tachycardia, or ventricular (hyperkalemia, hypocalcemia, Tracheal tube position: End-tidal CO2 , lung
fibrillation (VF). hypomagnesemia) sounds, or direct visualization of tube between
r This topic covers asystolic cardiac arrest (CA). VF CA Coagulation abnormalities vocal cords (End-tidal CO2 can be absent due to
is covered in a separate topic. Renal failure absence of CO2 production during CA.)
r 4 phases of CA are described: Prearrest, no flow, Adrenal insufficiency Tracheal tube patency and size
r 1st monitored rhythm (2): If artificial airway is not established:
low flow (CPR), and post return of spontaneous
circulation (ROSC) (1). Out-of-hospital CA: Assess for airway patency.
r 2 categories of CA exist, with different etiology, Asystole (46%) r Breathing:
pathophysiology, and outcome (2): Bradycardia (10%) Check for adequacy and symmetry of ventilation
Out-of-hospital CA PEA (10%) (identify pneumothorax, tracheal tube
In-hospital CA (occurs in the hospital setting: VF (7%) malposition).
Emergency department, pediatric ICU, operating In-hospital CA: r Circulation:
room, pediatric wards) Bradycardia (49%)
Assess quality of pulse after ROSC.
Asystole (16%) r Disability:
EPIDEMIOLOGY VF (10%)
PEA (9%) Assess for spontaneous movement after ROSC.
Incidence r Exposure:
r Out-of-hospital CA occurs in 8.04/100,000 persons
per year (72.71 in infants, 3.73 in children, 6.37 in ETIOLOGY Signs of physical abuse (bruises, petechiae)
r Out-of-hospital CA (2): r Secondary survey
adolescents) (3).
r In-hospital CA occurs in 3% of the children Respiratory (asphyxia, respiratory failure) Glasgow Coma Score
Cardiac (arrhythmias, shock) Neck: Check for venous distention (identify
admitted to the hospital (4).
Trauma cardiac tamponade).
RISK FACTORS r In-hospital CA: Chest: Respiratory disease, pulmonary edema
Congenital abnormalities, ex-premature children, birth Cardiac (arrhythmias, shock, congenital heart Cardiovascular: Perfusion, heart sounds, rhythm
asphyxia, chronic illness, cancer treatment, transplant disease) Extremities: Intraosseous (IO) accessnote sites
patients (1) Respiratory (respiratory failure, tracheal tube of previous IO attempts, and check patency of IO
GENERAL PREVENTION displacement, airway obstruction) and signs of infiltration.
r Trauma prevention: Car seats, seat belts, drowning Trauma
r Potential treatable causes of CA: 6Hs and 5Ts DIAGNOSTIC TESTS & INTERPRETATION
prevention Lab
r Infants: Back to sleep program Hypoxia, Hypovolemia, Hypo-/Hyperkalemia,
Metabolic acidosis (Hydrogen ions), Initial Lab Tests
r Chronic conditions: Early treatment of shock and r During CA:
Hypoglycemia, Hypothermia
respiratory failure Check for treatable causes of CA: 6Hs, 5Ts.
r CPR training for parents of high-risk children Trauma, Toxins, Tamponade (cardiac), Tension
pneumothorax, Thromboembolism Obtain bedside capillary glucose level, ABG,
electrolytes, and hemoglobin level. Consider
PATHOPHYSIOLOGY
r Prearrest phase: obtaining a specimen for toxicology screen.
DIAGNOSIS r Post ROSC: CBC, electrolytes, lactate, glucose,
Asphyxial CA: Hypoxemia, followed by arterial
hypotension, bradycardia, PEA, and asystole toxicology screen, ABG
HISTORY
VF CA: VF, followed by asystole r Events leading to CA: Sudden collapse vs. Imaging
Asystole is the common terminal rhythm for both r CXR: Confirm tracheal tube placement.
progressive deterioration, trauma r Consider head CT for suspicion of trauma.
VF and PEA. r Past medical history: Chronic condition, medications
r No flow phase: r Consider skeletal survey if suspicious for
r ROSC: Obtained in the field, hospital, no ROSC
Oxygen delivery ceases. r Bystander CPR nonaccidental trauma.
Tissue hypoxia results in anaerobic metabolism, r Family history of sudden death (inheritable cardiac Diagnostic Procedures/Other
lactate production, and acidosis. r ECG
r Low flow (CPR) phase disease)
r Consider echo post ROSC to evaluate cardiac
contractility and pericardial effusion.
r Asystole, VF, PEA
r Determine rhythm in 2 different leads to assure no
faulty lead placement.
84
ASYSTOLE
A
TREATMENT Administration routes:
r IV or IO is preferable. 1. Topjian AA, Berg RA, Nadkarni VM. Pediatric
PRE HOSPITAL r Absorption of medication through a tracheal tube is cardiopulmonary resuscitation: Advances in
r Activate EMS (5). science, techniques, and outcomes. Pediatrics.
uncertain.
r Get automated defibrillation (automatic external r Epinephrine: 2008;122:10861098.
defibrillator) (5). 0.01 mg/kg of 1:10 000 for the 1st and 2. Moler FW, Meert K, Donaldson AE, et al.
r Start CPR (5). subsequent doses IV or IO: In-hospital versus out-of-hospital pediatric cardiac
r Airway management (5): Higher doses (IV or IO) are no longer arrest: A multicenter cohort study. Crit Care Med.
Short transport time: Bag-mask ventilation recommended and may be harmful. 2009;37:22592267.
Long transport time: Placement of advanced If administered via tracheal tube, use a dose of 3. Atkins DL, Everson-Stewart S, Sears GK, et al.
airway depends on the level of training, 0.1 mg/kg to compensate for lower absorption. Epidemiology and outcomes from out-of-hospital
experience, and availability of end-tidal CO2 r Magnesium sulfate for hypomagnesemia or torsades cardiac arrest in children: The Resuscitation
detector. de pointes: Outcomes Consortium EpistryCardiac Arrest.
If airway is obstructed, reposition (jaw thrust, 2550 mg/kg, max 2 g IV or IO Circulation. 2009;119:14841491.
head tilt chin lift) and look for foreign body in the r Dextrose if glucose is <50 mg/dL: 4. Reis AG, Nadkarni V, Perondi MB, et al. A
oropharynx. 0.25 g/kg rapid IV infusion (2.5 cc/kg D10) prospective investigation into the epidemiology of
in-hospital pediatric cardiopulmonary resuscitation
INITIAL STABILIZATION/THERAPY SURGERY/OTHER PROCEDURES using the international Utstein reporting style.
r Airway and breathing (5):
Extracorporeal membrane oxygenation (ECMO): Pediatrics. 2002;109:200209.
Tracheal intubation r Consider ECMO-CPR (E-CPR) for selected patients in 5. The International Liaison Committee on
Use capnography or an end-tidal CO2 detector. which ROSC cannot be achieved (eg, in-hospital CA, Resuscitation (ILCOR) consensus on science with
Resuscitation with 100% O2 . witnessed arrests with bystander CPR and short treatment recommendations for pediatric and
After ROSC: Titration of FiO2 to ensure adequate transport time, in select patients with reversible neonatal patients: Pediatric basic and advanced life
oxygenation while avoiding hyperoxia pathologic processes).
r Compression technique: Push hard, push fast, support. Pediatrics. 2006;117:e955e977.
r Consider ECMO for patients with hemodynamic
minimize interruptions (5): instability after ROSC.
Push hard: 1/3 of the depth of the chest
Infant: Chest compressions with 2 thumbs DISPOSITION CODES
encircling hands technique (2 rescuers), or Admission Criteria
2-finger technique (1 rescuer) Critical care admission criteria: ICD9
Children: 1- or 2-hand technique r All patients who have sustained CA 427.5 Cardiac arrest
r Compression/Ventilation ratio (5):
Lay rescuers 30:2 for single responder PEARLS AND PITFALLS
Health care providers 15:2 FOLLOW-UP
After advanced airway is placed (eg, endotracheal r Pearls:
tube, laryngeal mask airway, Combitube, etc.), FOLLOW-UP RECOMMENDATIONS ECMO-CPR should be considered for selected
ventilations are given without interrupting chest PROGNOSIS patients.
r Survival is lower for the following categories:
compressions at a rate of 810/min (compressions Check for potential causes of CA (6Hs, 5Ts).
give at 100/min). Infants r Pitfalls:
r Treatment algorithm (5): Congenital abnormalities (cardiac, chromosomal
Inadvertent hyperventilation during CPR is
CPR abnormalities)
common and harmful.
Epinephrine every 35 min Chronic conditions (malignancy, transplant,
Check pulse and cardiac rhythm every 2 min. pulmonary, renal)
r Survival is higher for the following categories:
Rotate compressors every 2 min.
Check for potential causes (6Hs and 5Ts). Bystander CPR was administered.
r Postresuscitation care (5): ROSC was obtained in the field or before arrival to
Ventilation: the hospital.
Target normocapnia: Hospitals staffed with pediatric physicians
Hyperventilation can cause hypocapnia and In-hospital CA vs. out-of-hospital CA (2)
cerebral vasoconstriction, causing secondary Children compared with adolescents
r Survival to hospital discharge for all cases of
brain insult.
Hyperventilate only for impending herniation. pediatric CA:
Temperature: Out-of-hospital CA: 12%
Avoid hyperthermia. In-hospital CA: 27%
Therapeutic hypothermia may be beneficial for r Good neurologic outcome in children who gain
neurologic outcome. ROSC (2):
Consider inducing therapeutic hypothermia for Out-of-hospital CA: 24%
1224 hr for comatose patients. In-hospital CA: 47%
Hemodynamic support: COMPLICATIONS
Vasoactive drugs to improve hemodynamics and r Hypoxic-ischemic encephalopathy
maintain normotension: Epinephrine, r Seizures
norepinephrine, dopamine r Death
Glucose control:
Avoid hyperglycemia or hypoglycemia.
Glucose-containing fluids are not recommended
during resuscitation unless hypoglycemia is
present.
85
ATAXIA
Steven Krebs
Faye Doerhoff
ETIOLOGY
BASICS r Acute ataxia: DIAGNOSIS
Acute cerebellar ataxia:
DESCRIPTION Historically, primary varicella was the most HISTORY
r Ataxia is a disturbance in making coordinated r Duration/progression of symptoms
common etiology of acute cerebellar ataxia,
movements. r Identify any previous similar or related episodes.
preceding as many as 26% of cases (2).
r Ataxias may be generalized, affecting gait or Generally considered postinfectious; commonly r Identify recent illnesses (weeks to months).
affecting extremities alone. occurs 2 wk following viral illness r Associated vertigo or otalgia
r Acquired ataxia is commonly differentiated into Infectious/Immune-mediated conditions for which r Recent head or neck trauma
acute, recurrent, or chronic: directed therapy may be required: r Recent immunizations
Acute ataxia in children is uncommon, and Brainstem encephalitis; pneumococcal or r Constitutional symptoms
life-threatening causes of pure ataxia are rare: meningococcal meningitis; herpes simplex virus r Access or exposure (witnessed or suspected) to
The most common cause is acute cerebellar (HSV)-1; acute demyelinating encephalomyelitis
medication, alcohol, or household chemicals
ataxia (40% of all cases) (1). (ADEM); mycoplasma pneumonia; legionella; r Changes in gait, speech, general coordination
Most common in younger children (24 yr of malaria; MS; systemic infections such as r Changes in cognitive function (in conjunction with
age) but may affect older children typhoid, scarlet fever, diptheria, leptospirosis,
70% have a history of antecedent infection and coxiella (Q fever) motor findings may suggest toxic/acquired
13 wk prior to ataxia. Infectious/Immune-mediated conditions for which pathology)
r Changes in personality or behavior
Toxic exposures account for 30% of acute supportive care is primary treatment:
Direct infection by echovirus, coxsackie B; post- r Recurrent or persistent headache, vomiting, and/or
cases.
Most commonly, it is a poisoning in children or parainfectious cerebellitis by Epstein-Barr diplopia suggest intracranial mass lesion and
6 yr of age. virus, hepatitis A, influenza A and B, coxsackie possible elevated ICP
2nd peak in adolescence, associated with A, parvovirus B19, measles, mumps, enterovirus r Delay or loss of developmental milestones in infants
intentional ingestion or drug abuse Toxic exposure/ingestion: Alcohol, ethylene glycol, and toddlers
Chronic ataxias can be further classified as anticonvulsants, dextromethorphan, r Repeated bronchopulmonary infections
progressive or nonprogressive: antihistamines, risperidone, phenothiazines (ataxia-telangiectasia)
Episodic and chronically progressive ataxias are Mass lesions: Tumor, vascular malformation, r Family history of ataxia (episodic ataxia)
uncommon and usually are caused by inherited abscess (cerebellar, cerebral, epidural)
metabolic or genetic disorders. Head or neck trauma: Cerebellar PHYSICAL EXAM
r Signs of increased ICP must be evaluated: Bulging
contusion/hemorrhage, posterior fossa
RISK FACTORS hematoma, postconcussion syndrome, fontanelle in infants, papilledema, Cushing triad
Access or exposure to toxic substances that may cause vertebrobasilar dissection (bradycardia, HTN, abnormal or irregular
ataxia Vertigo or vestibular pathology respirations)
Postictal r Meningismus including nuchal rigidity, Brudzinski
GENERAL PREVENTION
Poison prevention education is the most effective way Stroke and Kernig signs
Paraneoplastic syndrome: Opsoclonus-myoclonus r Neurologic exam may be difficult depending on
to prevent toxic exposures:
r Emphasize childproof containers and safe storage of syndrome (neuroblastoma) age/cooperation of the child: Include general
prescription medications so that they are Sensory ataxia: Guillian-Barre syndrome (GBS), consciousness, cranial nerve function, strength,
inaccessible to children. Miller-Fisher syndrome (MFS) tone, deep tendon reflexes (hyper- or areflexia),
Other: Nonconvulsive seizures/epilepsy, central proprioception, noting symmetry with all:
PATHOPHYSIOLOGY pontine myelinolysis, conversion disorder, paretic Patients with chronic lesions usually have normal
r Complex movements and activities are coordinated tone and reflexes.
ataxia of upper or lower motor neurons
by the cerebellum: r Recurrent ataxia: In infants, check for decreased truncal and/or
The cerebellum lies in the posterior cranial fossa Recurrence of acute cerebellar ataxia extremity tone, areflexia, decreased deep tendon
beneath the tentorium. Migraine or equivalents: Basilar migraine, benign reflexes
Lesions in the cerebellum, its afferent, and/or paroxysmal positional vertigo (BPPV) r Detailed cerebellar examination: Difficult to
efferent pathways can cause ataxia: Metabolic disorders: Mitochondrial disorders, urea impossible in younger children:
Midline lesions affect truncal gait with swaying cycle defects, amino/organic acidopathies, Observe posture and gait for wide base,
during walking, sitting or standing, or Hartnup disease staggering, zig-zag course, short unequal steps,
head/neck bobbing (titubations) Genetic: Episodic ataxia types 14 inability to sit/stand unsupported
Unilateral hemisphere lesions cause movement r Chronic ataxia: Swaying provoked with eye closure (Romberg
disturbance in the ipsilateral side Progressive ataxia: sign) may or may not be present depending on the
Acute cerebellar ataxia usually results from Brain tumor: Astrocytoma, pontine glioma, site of the lesion (lower vermis lesions cause
postinfectious cerebellar demyelination. medulloblastoma, ependymoma postural tremor not enhanced with eye closure)
r Hydrocephalus and increased intracranial pressure
Genetic: Friedrich ataxia, ataxia telangiectasia, Limb ataxia more marked in:
(ICP) from space-occupying lesions (posterior fossa spinocerebellar degeneration, Refsum disease Upper than lower extremities
tumors, cerebellar hemorrhage) may cause ataxia. Metabolic: Abetalipoproteinemia, liposomal Complex than simple movements
r Pathology of the inner ear or proprioceptive sensory Fast then slow movements (finger-to-nose,
storage disease, mitochondrial defects
dysfunction may also cause ataxia. Nonprogressive ataxia: heel-to-shin, rapid alternating movements)
Head trauma, cerebral palsy, kernicterus Distal movements are typically more affected than
Congenital malformations: Arnold-Chiari, proximal movements.
cerebellar agenesis/hypoplasia, Dandy-Walker Oculomotor signs such as rebound nystagmus,
opsoclonus
86
ATAXIA
A
DIAGNOSTIC TESTS & INTERPRETATION Acyclovir IV q8h: 20 mg/kg <12 yr old; 10 mg/kg PROGNOSIS
12 yr old r Outcome is largely determined by etiology.
Lab
r Bedside serum glucose testing If immunocompromised, cover for Listeria r Acute cerebellar ataxia has an excellent prognosis,
r Lumbar puncture (LP) if febrile, toxic appearing, or monocytogenes with most patients recovering completely without
meningitic: Ampicillin 50 mg/kg IV q6h plus aminoglycoside intervention within 2 wk to 3 mo.
r Consider mannitol or hypertonic saline for increased r With or without specific treatment, >90% of GBS
CSF studies including culture with Gram stain,
protein, glucose, cell count, and viral studies: HSV, ICP: and MFS patients recover fully within 612 mo.
enterovirus, etc. Neurosurgery consultation is necessary for any
patient with evidence of increased ICP. COMPLICATIONS
Obtain opening pressures when possible.
Tumors, stroke, traumatic brain injury, and brainstem
CSF examination is routinely normal in Second Line encephalitis are commonly complicated by significant
postinfectious acute cerebellar ataxia. r GBS and MFS may be treated with intravenous
r Urine/serum toxicology screens: neurologic sequelae.
immunoglobulin (IVIG) and/or plasmaphoresis.
Drug level should be obtained where a specific r ADEM/inflammatory conditions may be treated with
intoxicant is identified. methylprednisolone or IVIG (specialty consultation REFERENCES
r Urinary catecholamine metabolites for suspicion of recommended). 1. Gierhon-Korthals MA, Westberry KR, Emmanuel PJ.
neuroblastoma
r Serologic evaluation for suspected inborn error of DISPOSITION Acute childhood ataxia: 10-year experience. J Child
Admission Criteria Neurol. 1994;9(4):381384.
metabolism includes CBC, transaminases, ammonia, r Inpatient admission criteria: 2. Connolly AM, Dodson WE, Prensky AL, et al.
lactate, pyruvate, and ketone levels.
Any acute ataxia without established etiology Course and outcome of acute cerebellar ataxia.
Imaging Concern for active infectious etiology requiring IV Ann Neurol. 1994;35(6):673679.
r Urgent head/brain imaging (usually CT) in any
antibiotic/antiviral treatment
patient with acute presentation of unknown Suspicion of GBS/MFS
etiology, focal neurologic deficits, altered Known or suspected ingestion of toxic substance ADDITIONAL READING
consciousness, recent head trauma, signs of requiring prolonged monitoring for clearance r Friday JH. Ataxia. In Fleischer GR, Ludwig S,
increased ICP, or persistent ataxia for >1 wk: r Critical care admission criteria:
Any patient having LP performed should first have Henretig FM, et al., eds. Textbook of Pediatric
Cases requiring advanced airway support Emergency Medicine. 6th ed. Philadelphia, PA:
head imaging to rule out obstruction or cerebellar Evidence of increased ICP, for neurosurgical
herniation. Lippincott Williams & Wilkins; 2010.
intervention, or for monitoring of treatment r Johnston MV. Movement disorders. In Kleigman RM,
MRI can detect inflammation/encephalitis, and is
better at posterior fossa imaging but is slower Discharge Criteria Behrman RE, Jenson HB, et al., eds. Nelson
r Well-appearing patients with acute cerebellar ataxia Textbook of Pediatrics. 8th ed. Philadelphia, PA:
than CT; need for stat MRI may be discussed with
neurologist and/or radiologist. r Toxic substance ingestions with short half-life and Saunders; 2007.
r If nuchal rigidity or pain or headache, consider return to baseline function r Ryan MM, Engle EC. Acute ataxia in childhood.
urgent CT or MRI; cerebellar herniation may cause Issues for Referral J Child Neurol. 2003;18(5):308316.
these symptoms. r Consider emergency department or inpatient
Diagnostic Procedures/Other neurology consultation especially when no clear
Further diagnostic testing may be indicated after etiology is readily identified. CODES
consultation with neurology: r Consider infectious disease consultation for
r EEG in patients with altered consciousness and inpatients with suspected infectious etiology. ICD9
r Local or regional poison control center and/or r 334.3 Other cerebellar ataxia
fluctuating clinical signs r 781.2 Abnormality of gait
r Electromyography in patients with sensory ataxia toxicology consultation for management
recommendations of known or suspected ingestion r 781.3 Lack of coordination
may help diagnose or confirm GBS or MFS.
r Inpatient cardiology evaluation if suspicion or
DIFFERENTIAL DIAGNOSIS diagnosis of Friedrich ataxia
See Etiology. r Inpatient genetics evaluation if suspicion of inborn PEARLS AND PITFALLS
error of metabolism r Failure to recognize signs of increased ICP may
TREATMENT result in worse neurologic outcomes or delay of
FOLLOW-UP lifesaving intervention.
PRE HOSPITAL r Acute cerebellar ataxia generally has no other
In the setting of recent trauma, cervical spine FOLLOW-UP RECOMMENDATIONS symptoms outside of incoordination, unsteady gait,
stabilization and evaluation of ABCs r Discharge instructions and medications:
or tremorany other findings require investigation
Supportive care and reassurance are the of alternate etiologies.
r Prompt evaluation of ABCs mainstays in the majority of cases. r MFS is characterized by triad of ataxia, areflexia,
r Appropriate immobilization in cases of trauma For significant ataxia, head protection may be and opthalmoplegia (usually diplopia).
indicated due to risk of fall.
MEDICATION r Activity:
First Line Strenuous activities such as sports or those
r Suspicion of active infectious etiology (meningitis, requiring complex coordination (eg, bicycling)
encephalitis) warrants coverage with should be avoided until all symptoms resolve.
broad-spectrum antibiotics pending identification of
a causative organism. Consider acyclovir as well:
Ceftriaxone 50 mg/kg IV (max single dose 2 g)
q12h (meningitic dosing)
87
ATLANTOAXIAL INSTABILITY
Joni E. Rabiner
Jeffrey R. Avner

BASICS r Recommendations vary and should be r Vital signs
individualized. r Thorough neurologic exam for:
DESCRIPTION r The Special Olympics requires radiologic screening Upper motor neuron signs: Hyperreflexia, clonus,
r Atlantoaxial instability (AAI) is characterized by
for all athletes with Down syndrome prior to sports Babinski
excessive mobility at the articulation between C1 participation. Posterior column signs: Diminished touch,
(atlas) and C2 (axis): r The American Academy of Pediatrics recommends proprioception
AAI is due to bony abnormality and/or the use of history and physical examination to r Neck exam for tenderness over the cervical spinous
ligamentous laxity or defect. screen for symptomatic AAI in patients with Down processes
Considered symptomatic if there are neurologic syndrome but does not support routine radiologic r Torticollis or cock-robin deformity of the neck
symptoms consistent with spinal cord compression screening for asymptomatic AAI (1). (seen in rotary subluxation):
The atlantodens interval (ADI) is the predental Sudeck sign in rotary subluxation: Chin and
space between the anterior aspect of the dens and PATHOPHYSIOLOGY
r The atlantoaxial articulation depends on the stability spinous process of C2 point to the same side.
the posterior border of the anterior arch of C1. Complete physical exam looking for evidence of
AAI may be defined as an ADI on lateral cervical of the odontoid process and the surrounding
ligaments: congenital syndromes.
spine x-ray of greater than:
45 mm in children <8 yr of age Any laxity, injury, and/or disruption of the spinal DIAGNOSTIC TESTS & INTERPRETATION
3 mm in older children and adults ligaments or bony structures may cause AAI. Lab
r Atlantoaxial rotary subluxation: r Spinal ligaments:
Initial Lab Tests
A form of AAI that results in forced rotation of the The transverse ligament is a strong ligament that Consider CBC, ESR/C-reactive protein, and rapid strep
neck with lateral tilt (torticollis) keeps the odontoid process in contact with C1 test for Grisel syndrome.
Usually due to laxity or disruption of the alar and prevents AP displacement.
The paired alar check ligaments attach the Imaging
ligaments r Radiographic imaging is indicated for patients with
May occur spontaneously or in association with odontoid process to the occipital condyles and
prevent rotary displacement. neck pain and/or neurologic symptoms in the setting
trauma or neck infection of trauma or other risk factors for AAI.
r The Steele rule of 3rds: Spinal cord, odontoid
EPIDEMIOLOGY r X-rays of the cervical spine:
r Rare in absence of risk factors such as trauma or process, and empty space each account for 1/3 of
the diameter of the C1 ring: AP, lateral, and open-mouth odontoid views (or
Down syndrome: With AAI, the odontoid process loses contact with Waters view for children unable to cooperate with
Trauma: 10% of cervical spine fractures involve C1, moves posteriorly, and approaches the spinal open mouth view)
C1-2 cord (especially with neck flexion). ADI should be measured on the lateral view:
Down syndrome: Maximal ADI occurs in flexion.
The presence of empty space within the ring of C1
Asymptomatic AAI in 1020% Posterior ADI, the distance between the
allows for some pathologic displacement of the
Symptomatic AAI in 12% posterior aspect of the dens and anterior aspect
r There is no evidence that asymptomatic AAI odontoid process posteriorly without impinging on
the spinal cord. of the posterior portion of C1, correlates with
increases the risk of developing symptomatic AAI r In the skeletally mature spine, the atlantoaxial joint neurologic deficits.
(1). In young children, the posterior ADI should be
has 10 degrees of flexion and extension and 50
greater than the transverse diameter of the
RISK FACTORS degrees of rotation with minimal lateral bending (2).
r Trauma: Flexion with axial load displaces the dens.
ETIOLOGY In teenagers, the posterior ADI should be
odontoid process posteriorly and injures the r Trauma >1314 mm.
transverse ligament. r Rotary subluxation can occur following an upper Shortening of the posterior ADI reflects
r Down syndrome: Associated with laxity of the
respiratory infection, head/neck surgery, or minor narrowing of the spinal canal with likely
transverse ligament trauma. impingement of the spinal cord.
r Odontoid process abnormalities: Aplasia, r Occurs primarily in children Flexion and extension views if cervical spine is
hypoplasia, fracture: stable:
Os odontoideum (failure of the odontoid process COMMONLY ASSOCIATED CONDITIONS Do not attempt flexion and extension views if
to fuse with the body of C2) See Risk Factors. there are neurologic symptoms.
r Congenital syndromes affecting bones and/or soft Flexion and extension views should never be
tissues of the neck: Congenital scoliosis, DIAGNOSIS forced, as pain will limit flexion of the neck to
osteogenesis imperfecta, neurofibromatosis, prevent the odontoid process from impinging on
spondyloepiphyseal dysplasia congenita (40% risk HISTORY the spinal cord.
of AAI), Morquio syndrome (due to odontoid r Trauma: Widening of the ADI in flexion is a sign of occult
hypoplasia/aplasia), Larsen syndrome, Klippel-Feil Head or facial injury associated with neck flexion instability.
syndrome, chondrodysplasia punctata and axial load (eg, head hitting a car windshield r Radiographic results are often poorly reproducible
r Infections or surgery of the head/neck: or a diving accident) and can change over time from abnormal to normal
Grisel syndrome: A form of AAI due to r Down syndrome or from normal to abnormal.
ligamentous laxity as result of an infectious or r Other congenital syndromes (see Risk Factors) r Further diagnostic imaging (CT or MRI) is indicated:
inflammatory process of the head and neck region r Recent infection or surgery If the initial cervical spine x-ray is abnormal
r Rheumatoid arthritis r Neurologic symptoms: Easily fatigued, changes in If the initial cervical spine x-ray is normal, consider
r Degenerative spinal disease further imaging for persistent torticollis, neck pain,
gait, changes in bowel or bladder function,
clumsiness limitation of neck movement (especially if
r Neck: Pain, decreased range of motion, head tilt, or associated with trauma or a recent head/neck
torticollis infection), or neurologic symptoms.
CT: Dynamic CT scanning with flexion and
extension
MRI to evaluate ligaments, spinal cord
88
ATLANTOAXIAL INSTABILITY
A
DIFFERENTIAL DIAGNOSIS DISPOSITION ADDITIONAL READING
r Atlantoaxial dislocation
Admission Criteria
r Os odontoideum r Admit patients with suspected AAI. r Avner JR. Evaluation of the cervical spine. In
r Critical care admission criteria: Wolfson AB, Hendey GW, Ling LJ, et al., eds.
Symptoms of spinal cord compression Harwood-Nuss Clinical Practice of Emergency
TREATMENT Medicine. 5th ed. Philadelphia, PA: Lippincott
Discharge Criteria Williams & Wilkins; 2009:11001105.
PRE HOSPITAL Stable cervical spine without neurologic symptoms r Loder RT. The cervical spine. In Morrissy R, Weinstein
Cervical spine immobilization if: Issues for Referral
r Trauma with the presence of neck pain, limitation of S, eds. Lovell and Winters Pediatric Orthopedics.
Consult neurosurgery and/or orthopedic surgery for 6th ed. Philadelphia, PA: Lippincott Williams &
neck movement, neurologic symptoms, distracting symptomatic AAI. Wilkins; 2006:871920.
injury r Rahimi SY, Stevens EA, Yeh DJ, et al. Treatment of
r Known AAI with neurologic symptoms
FOLLOW-UP atlantoaxial instability in pediatric patients.
INITIAL STABILIZATION/THERAPY Neurosurg Focus. 2003;15(6):14.
r Maintain cervical spine stabilization with a hard FOLLOW-UP RECOMMENDATIONS r Shetty A, Kini A, Prabhu J. Odontoid fracture: A
r Discharge instructions and medications: retrospective analysis of 53 cases. Indian J Orthop.
cervical collar until a thorough neurologic exam is
completed and appropriate imaging, if indicated, is Follow-up for repeat imaging as directed 2009;43(4):352360.
obtained and reviewed. Neurologic consultation and close follow-up r Swischuk LE. Emergency Imaging of the Acutely Ill
r Asymptomatic AAI: No treatment should be assured if there is any radiographic or Injured Child. 4th ed. Baltimore, MD: Lippincott
r Symptomatic AAI: Cervical spine stabilization abnormality or if there is high suspicion of injury Williams & Wilkins; 2000.
maintaining the spine in a neutral position (eg, persistent neck pain, neurologic symptoms)
regardless of radiographic results. See Also (Topic, Algorithm, Electronic
r Rotary subluxation: Most resolve spontaneously;
r Activity: Media Element)
antibiotics to treat associated infections as r Fracture, Cervical spine
needed: Activity recommendations are made on an r Spinal Cord Compression
<1 wk of symptoms: Soft collar, rest for a week, individual basis.
r Trauma, Neck
physical therapy In general, avoid contact sports or sports with
>1 wk of symptoms: Halo traction high risk of neck flexion in patients with:
Postsurgical stabilization
MEDICATION Down syndrome with ADI >5 mm CODES
First Line High-risk sports include gymnastics, diving,
Consider NSAIDs to reduce inflammation in rotary pentathlon, butterfly stroke, high jump, and soccer. ICD9
subluxation: Patient Monitoring 718.88 Other joint derangement, not elsewhere
r Ibuprofen 10 mg/kg/dose PO/IV q6h PRN, max dose Observe for neurologic symptoms. classified, involving other specified sites
800 mg PO, 2.4 g/24 hr
r Ketorolac 0.5 mg/kg IV/IM q6h PRN, max dose PROGNOSIS
30 mg/dose, 120 mg/24 hr
Depends on cause of AAI and neurologic PEARLS AND PITFALLS
r Naproxen 5 mg/kg PO q8h PRN, max dose involvement: r Pearls:
r Good prognosis for those with symptomatic AAI
500 mg/dose, 1,250 mg/24 hr Down syndrome is an important associated
treated with surgery
Second Line condition that increases the risk of AAI and
r Methylprednisolone 30 mg/kg IV over 15 min COMPLICATIONS resultant spinal cord compression.
r Subluxation Any patient with an increased predental space on
followed by an infusion of 5.4 mg/kg over the next
r Spinal cord compression with excessive range of lateral cervical spine x-ray should have additional
23 hr:
Indicated for neoplastic or inflammatory etiology motion in AAI radiographic imaging (CT or MRI) to delineate the
of spinal cord compression presence and/or extent of injury, regardless of the
Dosage derived from adult guidelines due to lack presence or absence of neurologic symptoms.
of high-level evidence in pediatrics REFERENCES Persistent torticollis, neck pain, or limitation of
Steroids are no longer routinely used for spinal neck movement (especially if associated with
1. American Academy of Pediatrics Committee on trauma or a recent head/neck infection) may be a
cord trauma, as current data has led to its Sports Medicine and Fitness. Atlantoaxial instability
withdrawal from Advanced Trauma Life Support sign of atlantoaxial rotary subluxation.
in Down syndrome: Subject review. Pediatrics. r Pitfalls:
(ATLS) guidelines. 1995;96:151154.
r Dexamethasone may be used for spinal cord Forcing the neck into a neutral position during
2. Willis BPD, Dormans JP. Nontraumatic upper clinical evaluation if there is resistance to
compression: cervical spine instability in children. J Am Acad
Numerous dosing regimens exist, with no very movement, increased pain, or torticollis
Orthop Surg. 2006;14:233245. Inaccurate measurement of the predental space
definitive benefit of a specific regimen. Refer to
the consulting neurologist and/or neurosurgeon on a lateral cervical spine x-ray
for dosing recommendations. Attempting and/or forcing flexion and extension
views of the cervical spine if there are neurologic
SURGERY/OTHER PROCEDURES symptoms
Posterior C1-2 fusion for unstable displacement,
neurologic involvement, or transverse ligament
injuries, as they are unlikely to heal
89
ATOPIC DERMATITIS
Desiree M. Seeyave

BASICS DIAGNOSIS Lab
r No diagnostic tests are available.
DESCRIPTION HISTORY Elevated IgE levels are common.
r Atopic dermatitis, also known as eczema, is a r History of atopy or atopic dermatitis
r Bacterial or viral cultures when lesions are
chronic, pruritic, relapsing skin eruption that is r Symptoms of:
superinfected during acute flares
worse in infants and toddlers and generally Acute waxing and waning of itchy, dry patches of r Tzanck smear and viral culture to confirm eczema
improves with age. skin
r Inflammation causes itching, scratching, and Weeping of skin herpeticum
scarring. Hyper- or hypopigmentation Diagnostic Procedures/Other
r Variants include: r Biopsy can be done to rule out other skin conditions.
PHYSICAL EXAM r Patch testing to differentiate atopic from contact or
Infantile eczema r Acute flares: Poorly demarcated erythema, with
Nummular eczema weeping, crusting, edema, exudation, allergic dermatitis
Dyshidrotic eczema papulovesicles, scaling, or crusting Pathological Findings
Eczema herpeticum r Chronic disease: Poorly defined hyper- or Biopsy may reveal:
Exfoliative erythroderma hypopigmentation, lichenification (thickened skin), r Nonspecific lymphocytic infiltration of epidermis and
EPIDEMIOLOGY scaling, and excoriation intercellular edema in acute flares
r Age-dependent distribution: r Hyperplasia and hyperkeratosis in chronic disease
Incidence
r 60% of children with atopic dermatitis develop it Infantile eczema:
Widespread disease involving cheeks, forehead, DIFFERENTIAL DIAGNOSIS
before 1 yr and 80% develop it by 5 yr of age. r Seborrheic and contact dermatitis
r Rarely, it can appear 1st at puberty or later. scalp, diaper area, and extensor surfaces r Psoriasis
Children 311 yr:
Prevalence Flexural surfaces (neck, antecubital and r Scabies
Occurs in 1020% of children popliteal fossae) with lichenification r Xerosis
Hands and feet may be involved. r Wiskott-Aldrich syndrome
RISK FACTORS
r Personal or family history of atopy: Asthma, allergic Adolescence to adulthood: Flexures, hands, feet, r Histiocytosis X
rhinitis, atopic dermatitis occasionally face, eyelids, and neck r Acrodermatitis enteropathica
r Excessive dryness of skin, exacerbated by winter, dry r Exfoliative erythroderma with diffuse scaling and r Hyper-IgE syndrome
air, and prolonged or frequent hot baths erythema in severe cases
r Stress r Nummular eczema: Single or multiple coin-shaped
r Sweating plaques on extensor surfaces of hands, arms, and TREATMENT
r Environmental allergens (eg, pollens or dust mite legs:
May have central clearing and round lesions INITIAL STABILIZATION/THERAPY
antigen) r If ill appearing, address ABCs per Pediatric
r Food allergen exposure (eg, milk protein, peanuts, similar to dermatophyte infections, impetigo, or
granuloma annulare Advanced Life Support (PALS) algorithm.
eggs) r Eczema herpeticum or Kaposi varicelliform r Infections of the skin, such as eczema herpeticum,
GENERAL PREVENTION eruption: are the most common emergencies associated with
Strategies to minimize rash in patients with eczema: Disseminated herpes simplex virus 1 or 2 atopic dermatitis.
r Keep skin lubricated often, and prevent excessive infection; also can be due to coxsackievirus A16 r Hydration status is especially important in severe
stripping of natural oils from skin. or vaccinia virus cases:
r Shorten bath times, use lukewarm instead of hot Umbilicated vesiculopustular eruption usually is May need fluid resuscitation similar to burn
water, and apply lubricant immediately after disseminated and widespread in areas of skin management
affected by atopic dermatitis. r Topical steroids to control inflammation. Begin with
washing.
r Use humidifiers during winter to prevent excessive Vesicles may become hemorrhagic and crusted, mid- to high-potency steroids per dayb.i.d. for
drying of skin. painful punched-out erosions. acute flares (no longer than 7 days) and taper to
r Avoid use of harsh soaps, cleansers, and other r Other associated findings: low-potency steroid.
chemicals. Xerosis (dry skin) MEDICATION
Geographic tongue
ETIOLOGY Dennie-Morgan folds (infraorbital eyelid folds) First Line
r Multifactorial etiology, with genetic, environmental, r High potency steroids:
Pityriasis alba (dry, scaly, hypopigmented patches)
physiologic, and immunologic factors influencing Ichthyosis vulgaris (inherited fishlike scaling) Halcinonide (Halog) 0.1% cream/ointment per day
acute and chronic flares Keratosis pilaris (chicken-skin appearance due to or b.i.d.
r Increased IgE levels and response to triggering cornified plugs in upper hair follicles) Fluocinonide (Lidex) 0.05% cream/ointment per
agents lead to release of histamine, prostaglandins, Hyperlinear palms day or b.i.d.
and cytokines. Facial pallor/infraorbital darkening Desoximetasone (Topicort) per day or b.i.d.
r Decreased cell-mediated immunity and impaired Keratosis pilaris (follicular accentuation on Betamethasone dipropionate (Diprosone) 0.05%
extensor surfaces of upper arms and thighs) per day or b.i.d.
neutrophil chemotaxis
r Asthma, allergic rhinitis
r Food allergies
r Early growth delay
90
ATOPIC DERMATITIS
A
r Mid-potency steroids: Second Line PROGNOSIS
Betamethasone valerate (Valisone) 0.1% Prednisone 12 mg/kg PO divided per dayb.i.d.: r Up to 50% of patients outgrow atopic dermatitis
cream/ointment b.i.d. r A short course may be given in disease that is after 5 yr of age.
Fluticasone (Cutivate) 0.05% cream/ointment difficult to control or hospitalized patients. r Can be a lifelong condition; tends to improve with
b.i.d. r Never use in any case of eczema herpeticum. age
Mometasone (Elocon) 0.1%
cream/ointment/lotion b.i.d. DISPOSITION COMPLICATIONS
r Hyper- or hypopigmentation of affected areas
Prednicarbate (Dermatop) 0.1% b.i.d. Admission Criteria r Sepsis from bacterial or viral superinfection
Triamcinolone acetonide (Aristocort) 0.1% r Ill appearing
r Extensive skin involvement with weeping, secondary r Localized abscess formation
cream/ointment b.i.d.
r Low-potency steroids: r Flexion contractures in severe cases
bacterial or viral superinfection
Hydrocortisone 12.5% cream/ointment/lotion r Dehydration from excessive loss of fluids from the r Overuse of potent topical steroids can result in
b.i.d.t.i.d. skin hypopigmentation, telangiectasias, atrophy, striae,
Desonide (DesOwen) 0.05% cream b.i.d. r Disseminated eczema herpeticum for IV antivirals and systemic absorption leading to
Fluocinolone acetonide (Synalar) 0.01% cream, hypothalamic-pituitary axis suppression and growth
apply sparingly b.i.d. Discharge Criteria retardation.
r Well appearing
r Low-cost generic steroids:
r Mild-moderate involvement of skin
Betamethasone dipropionate 0.05% r Reliable follow-up
ointment/cream REFERENCES
Mometasone 0.1% cream/ointment/lotion Issues for Referral 1. Paller A, Eichenfield LF, Leung DY, et al. A 12-week
Triamcinolone acetonide 0.1% ointment/cream Refer to dermatologist in severe cases, unresponsive study of tacrolimus ointment for the treatment of
Fluocinolone acetonide 0.01% to topical steroids, extensive lichenification, eczema atopic dermatitis in pediatric patients. J Am Acad
Hydrocortisone 1% cream/ointment/lotion herpeticum Dermatol. 2001;44(1 Suppl):S47S57.
r Bland emollients (eg, Aquaphor, Vaseline), apply
COMPLEMENTARY & ALTERNATIVE 2. Hoare C, Li Wan Po A, Williams H. Systematic
liberally several times a day review of treatments for atopic eczema. Health
r Antihistamines to control itching: THERAPIES
r Phototherapy with ultraviolet B for extensive and Technol Assess. 2000;4(37):1191.
Diphenhydramine 1.25 mg/kg/dose q6h PO/IM/IV 3. Isolauri E, Arvola T, Tas YS, et al. Probiotics in the
resistant disease (2)
(max 300 mg/day) r Probiotic-supplemented formula: Bifidobacterium management of atopic eczema. Clin Exp Allergy.
Hydroxyzine 2 mg/kg/day divided q68h PO; 2000;30(11):16041610.
0.51 mg/kg/dose q46h IM PRN lactis Bb-12 and Lactobacillus strain GG decrease
r Calcineurin phosphatase inhibitors: severity of atopic dermatitis in babies being weaned
off breast milk (3).
Suppresses T-cell function r Trim nails to prevent scratching. CODES
Safe and effective in children >2 yr of age with r Protective clothing while sleeping.
severe atopic dermatitis (1)
r Cold compresses q.i.d. for acute flares with oozing, ICD9
Tacrolimus 0.03% or 0.1% cream or pimecrolimus r 690.12 Seborrheic infantile dermatitis
1% cream: Apply a thin layer to the skin b.i.d. and crusting, and superinfection
r 691.8 Other atopic dermatitis and related conditions
continue for 1 wk after skin clearance.
r Antivirals for eczema herpeticum: r 705.81 Dyshidrosis
Acyclovir 15 mg/kg/day IV divided q8h or 1,200
FOLLOW-UP
mg/day PO (max 80 mg/kg/day) divided q68h FOLLOW-UP RECOMMENDATIONS
710 days Discharge instructions and medications:
PEARLS AND PITFALLS
Valacyclovir 20 mg/kg PO t.i.d. for 5 days (max r Frequent application of emollients for skin r Good skin care and lubrication are essential for
3 g/day) in children >2 yr r Limit length, frequency, and temperature of bathing. control of disease.
r Topical steroids for active lesions: Mild, mid-, high r Topical steroid overuse can lead to chronic skin
ALERT
r Use of corticosteroids on the face may produce potency changes and adrenal suppression.
r Primary care provider follow-up in 12 wk, sooner if r Eczema herpeticum and severe disease can lead to
permanent change in cosmetic appearance. Limit
corticosteroid use on the face to <35 days of culture of lesions was performed severe fluid loss from lack of a protective skin barrier.
r Return for pain or swelling, increasing discharge,
continuous use.
r Calcineurin phosphate inhibitors should not be fever, worsening of skin condition
used with occlusive dressings, and sun exposure DIET
should be avoided. Side effects include burning, Avoid known food allergies; in severe disease, avoid
pruritus, flulike symptoms, allergic reaction, common food allergens (eg, milk protein, peanuts,
erythema, and headache. eggs).
91
AVASCULAR NECROSIS OF THE FEMORAL HEAD

Louis A. Spina
PATHOPHYSIOLOGY r Review of systems is pertinent for:

BASICS Circulation to the femoral head is interrupted due to No isolated fever
traumatic or nontraumatic causes: Symptoms isolated to 1 or both lower extremities
DESCRIPTION r This leads to death of the bone marrow and No constitutional symptoms, such as weight loss,
r Avascular necrosis (AVN) is an aseptic necrosis myalgias, etc.
osteocytes, which leads to collapse of the involved
resulting from disrupted blood supply: segment. No significant medical problems, such as
The areas of dead bone are weakened and can leukemia, juvenile rheumatoid arthritis, etc.
lead to collapse. ETIOLOGY
r AVN may occur in any joint or bone and in any age r The cause of LCPD is unknown: PHYSICAL EXAM
r Patients are generally well appearing (nontoxic) and
group but is most common in the hip joint: Mechanical obstruction of extraosseous vessels
has not been demonstrated. afebrile.
In pediatrics, Legg-Calve-Perthes disease (LCPD), r An antalgic gait is usually present:
which is the main focus of this topic, is the most There is suggestion that LCPD is a local
common cause of AVN of the femoral head (hip manifestation of a generalized transient disorder In delayed presentation, a Trendelenburg gait may
joint). of the epiphyseal cartilage, rendering it avascular. be present.
r When associated with acquired abnormalities r Limitations in abduction and internal rotation of the
AVN may also occur as complications of:
Slipped capital femoral epiphysis (SCFE) such as SCFE and DDH, the etiology is better affected hip are usually present with the hip
Developmental dysplasia of the hip (DDH) understood: positioned in both flexion and extension.
r A high index of suspicion is usually necessary for In DDH, AVN is usually iatrogenic, secondary to r Shortening of the affected limb may be present.
cartilaginous compression during reduction of the r Atrophy of the proximal thigh on the affected limb
accurate early diagnosis.
joint. may be present.
EPIDEMIOLOGY In SCFE, AVN may result from injury to the r Pertinent negatives on physical exam:
r Usually occurs in children between 3 and 12 yr of
retinacular vessels, compression from an Normal range of motion of the knee(s)
age intrascapular hematoma, direct injury from No swelling or bruising
r Most commonly seen between 5 and 7 yr of age operative repair, or due to forced manipulation of
r Boys are affected 35 times as often as girls. an unstable or acute slippage. DIAGNOSTIC TESTS & INTERPRETATION
r 1020% of cases are bilateral. Imaging
r Uncommon in black and Hispanic populations COMMONLY ASSOCIATED CONDITIONS r Radiographic evaluation of bilateral hips with both
r Sickle cell disease/hemoglobinopathies:
AP and Lauenstein (frog) lateral views should be the
Incidence Sickling of RBCs leads to hyperviscosity and initial Imaging modality:
Occurs in 6 out of 100,000 children vascular occlusion in the intramedullary capillaries Often normal in early stages of the disease
and veins. In later stages, increased density of necrotic bone
RISK FACTORS r HIV infection
r Low birth weight will be seen.
r Chronic renal disease/dialysis:
r 2nd-hand smoke exposure as well as maternal Can show a flattened, fragmented, and small
Increased parathyroid hormone leads to increased femoral head
smoking during pregnancy (1)
r Steroid exposure bone turnover, disorganized bone matrix, and Mottled density may be present in areas of
r Birth via C-section (1) microfractures. osteoclastic activity with new bone formation.
r Systemic lupus erythematosus: The modified lateral pillar classification of the
r Delayed growth maturation
With high-dose corticosteroid therapy femoral head seen on x-ray has been developed to
r Other hip conditions: r HTN help determine the extent of disease (3):
SCFE r Alcoholism Group A: The height of the lateral pillar is
DDH normal.
r HTN Group B: There is reduction between 50% and
r HIV infection: DIAGNOSIS 100% of the original height of the lateral pillar.
Unclear if increased risk is from HIV infection Group B/C: There is reduction of exactly 50% of
HISTORY
itself, HIV-associated complications, or r The presenting complaint is usually a limp. the original height of the lateral pillar with a
complications of HIV-directed therapy (2) r There may or may not be associated pain: thin and poorly ossified lateral pillar.
Group C: There is reduction of >50% of the
GENERAL PREVENTION If pain is present, it may be in the affected hip, the
r Avoidance of known risk factors original height of the lateral pillar.
anterior ipsilateral thigh, or the ipsilateral knee r MRI is the most accurate modality and is the study
r Successful diagnosis and management of conditions (referred pain).
of choice in those with normal radiographs and
such as DDH and SCFE Pain is usually mild and/or intermittent.
r Identification and treatment of antithrombin factor r Parents sometimes report what they feel is an suspected AVN:
Double line sign in T2 images are classic:
deficiencies, hypofibrinolysis, and thrombophilia: associated injury. 2 concentric low- and high-signal bands
Protein-C deficiency r Parents or child may report complaints of growing
Useful for picking up bilateral cases of AVN
Protein-S deficiency pains. Smaller lesions (<1/4th the diameter of the radial
Antithrombin factor C or S deficiency head) and more medial lesions predict better
Resistance to activated protein-C outcomes.
92
AVASCULAR NECROSIS OF THE FEMORAL HEAD

A
r A bone scan may be obtained if radiography is DISPOSITION REFERENCES
indeterminate with high index of suspicion and MRI Admission Criteria
is either unavailable or contraindicated: r Admission is not usually necessary for LCPD. 1. Bahmanyar S, Montgomery SM, Weiss RJ, et al.
This will show decreased uptake/perfusion to the r Operative therapy can be scheduled electively as an Maternal smoking during pregnancy, other prenatal
femoral head. outpatient. and perinatal factors, and the risk of Legg-Calve-
Photopenic area surrounded by increased tracer Perthes disease. Pediatrics. 2008;122:e459e464.
uptake is typical. Discharge Criteria 2. Gaughan DM, Mofenson LM, Hughes MD, et al.
Less sensitive and less specific than MRI LCPD is managed as an outpatient provided that: Osteonecrosis of the hip (Legg-Calve-Perthes
r Orthopedic consultation has been obtained or close disease) in human immunodeficiency virus-infected
DIFFERENTIAL DIAGNOSIS follow-up with a pediatric orthopedist has been
r Trauma, fracture children. Pediatrics. 2002;109:874.
r Soft tissue injury arranged. 3. Herring JA, Kim HT, Browne R. Legg-Calve-Perthes
r Pain, if present, is well controlled. disease. Part I: Classification of radiographs with
r Transient synovitis
r Septic arthritis Issues for Referral use of the modified lateral pillar and Stulberg
All patients with the diagnosis of AVN of the femoral classifications. J Bone Joint Surg Am. 2004;86:
r Osteomyelitis
head should have urgent referral to a pediatric 21032120.
r Rheumatic disease, arthritis
orthopedist. 4. Herring JA, Kim HT, Browne R. Legg-Calve-Perthes
r Malignancy, tumor disease. Part II: Prospective multicenter study of
r Appendicitis effect of treatment on outcome. J Bone Joint Surg
r Testicular torsion FOLLOW-UP Am. 2004;86:21212134.
r Pelvic inflammatory disease 5. Yrjonen T. Long-term prognosis of Legg-Calve-
FOLLOW-UP RECOMMENDATIONS Perthes disease: A meta-analysis. J Pediatr Orthop
Activity:
B, 1999;8:169172.
r Recommended activity may vary dependent on
TREATMENT 6. Rosenfeld SB, Herring JA, Chao JC. Legg-Calve-
severity of the disease; treatment is still somewhat Perthes disease: A review of cases with onset
INITIAL STABILIZATION/THERAPY controversial. before six years of age. J Bone Joint Surg Am.
r Treatment is focused on removing pressure from the r Nonoperative treatment ranges from nonweight
2007;89(12):27122722.
joint and allowing the disease to run its course: bearing with a brace, weight bearing with a brace
Cannot cure the disease, but the goal is to allowing for limited movement, and weight bearing
minimize damage to and allow for remodeling of with a brace that allows full movement of the hip. ADDITIONAL READING
the femoral head. r Physical therapy is sometimes used to improve range
r Crutches and/or a cane may be useful in those old r Johannesen J, Briody J, McQuade M, et al. Systemic
of motion of the hip.
enough to use appropriately. effects of zoledronic acid in children with traumatic
r Avoidance of activities and sports that put pressure PROGNOSIS femoral head avascular necrosis and Legg-Calve-
r 2 factors that are of long-term prognostic value
Perthes disease. Bone. 2009;45(5):898902.
on the hip joint (5): r Wenger DR, Ward WT, Herring JA. Legg-Calve-
COMPLEMENTARY & ALTERNATIVE Age of the patient at the onset of disease Perthes disease. J Bone Joint Surg Am. 1991;
THERAPIES Shape of the femoral head at skeletal maturity 73(5):778788.
r IV bisphosphonate therapy has been associated with r Age at which long-term results are felt to worsen is
preserving the integrity of the femoral head in 89 yr.
children with traumatic AVN. r Lateral pillar classification has been shown to CODES
r IV zoledronic acid has been shown in a small study correlate with prognosis:
to reduce bone remodeling and turnover, especially Classifications B/C and C have been directly ICD9
in the LCPD group: correlated with poor prognosis (4,6). 733.42 Aseptic necrosis of head and neck of femur
Zoledronic acid requires further study to confirm r Most patients clinically do well in early adulthood.
patient safety and efficacy before its use can be r Radiographic osteoarthritis is increased in 20- and
widely recommended. 40-yr follow-ups. PEARLS AND PITFALLS
r Most patients who had poor results at skeletal
SURGERY/OTHER PROCEDURES r Pearls:
r An operative vs. nonoperative approach (with maturity develop osteoarthritis over 50 yr of life.
Requires high index of suspicion and should still
bracing) is still controversial. be considered even if radiographic investigation is
r Surgery may involve a pelvic osteotomy, a femoral
normal
osteotomy, or a combination of the two. MRI is the most sensitive and specific diagnostic
r Indication for surgical repair is based on disease modality for AVN.
category and age at presentation of disease: r Pitfalls:
Children 8 yr of age with group B classification Not recognizing those at increased risk for AVN
have been found to do equally as well with both (such as those with sickle cell disease, HIV, and
operative and nonoperative treatment (4). others)
Children 8 yr of age with group B or B/C disease
classification have been found to do significantly
better with surgical treatment (4).
Children with group C classification have the
poorest outcome regardless of the treatment
route (4).
93
LWBK822-driver-B LWBK822-Hoffman ch047.xml April 15, 2011 13:21
BACTEREMIA
Joni E. Rabiner
Jeffrey R. Avner
ETIOLOGY r If occult bacteremia is suspected:

BASICS r Bacteremia in well-appearing children 336 mo: Child with up-to-date immunizations (>6 mo of
Prevaccination: Streptococcus pneumoniae (80%) age): No lab tests indicated due to low rate of
DESCRIPTION and Hib (20%) were the primary causes of bacteremia and complications
r Bacteremia is defined as the presence of bacteria in bacteremia (5). Incompletely immunized child (ages 336 mo):
the blood. Postvaccination: Escherichia coli (1/3), nonvaccine CBC: Some sources suggest sending a blood
r Bacteremia may be transient and resolve serotypes of S. pneumoniae (1/3), Staphylococcus culture if screening WBC count >15,000/mm3
spontaneously or may lead to complications aureus, Neisseria meningitidis, group A WBC has a low positive predictive value for
including focal infections, meningitis, sepsis, or streptococcus, Salmonella species (2) occult bacteremia (2).
septic shock. r Bacteremia in children with sickle cell disease: Blood culture:
r Occult (or unsuspected) bacteremia is a term used to Bacteremia/Sepsis: S. pneumoniae (most Time to positive culture for pathogens: Mean
describe bacteremia in a well-appearing, previously common), Hib (if incomplete immunization) 15 hr (5)
healthy child (usually 336 mo of age) without a Bacteremia/Osteomyelitis: S. aureus, Salmonella Time to positive culture for contaminants:
source of infection on history or physical exam. r Bacteremia in children who are Mean 31 hr (5)
immunosuppressed: Contaminants: Slow growth, gram-positive
EPIDEMIOLOGY
S. aureus, Staphylococcus epidermidis (associated rods, coagulase-negative gram-positive cocci
Incidence with cellulitis, abrasion, indwelling catheters) C-reactive protein and ESR are nonspecific
r The incidence of bacteremia varies with a variety of
Streptococcus viridans (associated with mucosal inflammatory markers.
factors including: tenderness, mouth sores)
Exposure to a particular organism (ie, local Imaging
Gram-negative organisms (E. coli, Klebsiella, Consider CXR for occult pneumonia.
epidemiology) Pseudomonas)
The host immune status (eg, HIV, sickle cell S. pneumoniae Diagnostic Procedures/Other
disease, cancer) Salmonella Consider procedures related to complications of
Clinical appearance (well vs. ill) bacteremia:
Risk factors (eg, dental work, indwelling catheters) COMMONLY ASSOCIATED CONDITIONS r Bladder catheterization to evaluate for urinary tract
r Declining incidence of occult bacteremia: Complications include focal infections, meningitis, infection (UTI)
Routine Haemophilus influenzae type b (Hib) and sepsis, septic shock, pneumonia, and septic arthritis. r Lumbar puncture to evaluate for meningitis
heptavalent pneumococcal conjugate (PCV7) r Joint aspiration to evaluate for septic arthritis
vaccines have significantly decreased the
prevalence of occult bacteremia from 35% to DIAGNOSIS DIFFERENTIAL DIAGNOSIS
0.250.7% in vaccinated, nontoxic febrile r Viral illness
HISTORY r UTI
children (13). r Fever:
The risk of bacteremia in incompletely vaccinated r Occult pneumonia
>38 C (100.4 F) for infants <3 mo of age or
febrile children is likely <35% due to herd children with immunodeficiency r Sepsis
immunity. >39 C (102.2 F) for children 336 mo of age r Contaminated blood culture (false positive)
For vaccinated febrile children, the risk of serious who are well appearing and at risk for occult
complications is <0.05% (4). bacteremia
r The rate of contaminant isolation from blood r Risk factors: Chronic underlying illness, TREATMENT
cultures is 1.8% (2): immunodeficiency, recent antibiotic use
For example, with a bacteremia rate of 0.25%, r Immunization status INITIAL STABILIZATION/THERAPY
there would be 7 contaminated blood culture r Assess and manage ABCs per Pediatric Advanced
results for every 1 true positive blood culture (3). PHYSICAL EXAM Life Support (PALS) protocol.
r Vital signs r Patients with organisms other than S. pneumoniae
RISK FACTORS r General appearance:
r Chronic underlying medical conditions (such as S. aureus, N. meningitidis, H. influenzae)
r Immunodeficiency: HIV, chemotherapy Well appearing in occult bacteremia typically require hospital admission and parenteral
r Incomplete immunization: <6 mo of age or Ill appearance suggests a serious bacterial illness antibiotic therapy.
associated with the bacteremia. r If penicillin-susceptible bacterial growth, clinical
incomplete primary series of 3 vaccinations for both r Complete physical exam looking for source of signs and symptoms in the child guide
Hib and PCV7, although there may be effect with as infection: management:
few as 1 dose of vaccine (1) Petechiae, especially below the nipple line,
r Recent or current antibiotic use These patients may be appropriate candidates for
suggest the diagnosis of meningococcemia. outpatient therapy with amoxicillin, particularly if
GENERAL PREVENTION pathogen is S. pneumoniae.
DIAGNOSTIC TESTS & INTERPRETATION r Suspected occult bacteremia:
Routine vaccination with Hib, PCV7, and
Lab
meningococcal conjugate vaccine as per the Advisory Completely immunized child, no severe illness
Initial Lab Tests
Committee on Immunization Practices (ACIP) r If bacteremia is known from a prior blood culture other than fever, normal vital signs: No empiric
antibiotics are required.
PATHOPHYSIOLOGY result:
r Bacteria enter bloodstream: Repeat blood culture
Directly (eg, dental work, laceration, catheter Additional lab tests vary depending on:
placement) Age of the patient
Indirectly through disruption of normal mucosal Specific bacteria identified
barriers, usually following viral infection or other Host risk factors
focal infection: Appearance of the patient
Often associated with nasopharyngeal Persistence of fever
colonization or exposure (eg, meningococcemia, Other symptoms (nuchal rigidity, joint swelling,
invasive pneumococcal disease) respiratory distress, etc.)
r Bacteria in bloodstream are either cleared
spontaneously or cause focal infection or septicemia
94
BACTEREMIA
r For incompletely immunized children with elevated Issues for Referral ADDITIONAL READING
WBC >15,000/mm3 : Any child with persistent or recurrent bacteremia
Consider ceftriaxone. should be referred to, or have consultation with, an r Avner JR. Acute fever. Pediatr Rev.
r For immunocompromised patients or patients with infectious disease specialist. 2009;30(1):513.
r Baraff LJ. Management of infants and children with
B
systemic symptoms, particularly unstable vital
signs: fever without source. Pediatr Ann.
Consider ceftriaxone and vancomycin.
FOLLOW-UP 2008;37(10):673679.
r In specific circumstances, such as leukopenic FOLLOW-UP RECOMMENDATIONS See Also (Topic, Algorithm, Electronic
oncology patients, additional antibiotic coverage for Discharge instructions and medications: Media Element)
Pseudomonas may be indicated. r If the child is treated with antibiotics, follow-up r Fever in Children Older than 3 Months
r Known bacteremia from a prior blood culture r Fever in Infants 03 Months of Age
within 24 hr.
result: r If the child is not treated with antibiotics, follow-up r Meningococcemia
If bacteremia is thought to represent a true for persistent fever in 48 hr. r Sepsis
pathogen (ie, not a contaminant), antibiotic r If the child looks sicker, or if new signs or symptoms
administration should be determined on the basis develop, the patient should follow-up sooner.
of known or epidemiologically determined
bacterial sensitivities. Patient Monitoring CODES
Clinical symptoms:
MEDICATION r Fever ICD9
First Line r Appearance r 771.83 Bacteremia of newborn
r Ceftriaxone 50100 mg/kg/day IV/IM divided r 790.7 Bacteremia
q1224h PROGNOSIS
Vancomycin 4060 mg/kg/day divided q6h r Depends on age, severity, etiology, past medical
May be added based on local susceptibility history, and immunization status
patterns of S. pneumoniae and severity of illness if r For occult bacteremia, spontaneous resolution of PEARLS AND PITFALLS
present, and immune status of patient bacteremia occurs in >90% without antibiotic r Pearls:
r Amoxicillin 80 mg/kg PO divided b.i.d.t.i.d.: treatment. Occult (unsuspected) bacteremia occurs in
Used for patient with penicillin-sensitive well-appearing febrile children.
COMPLICATIONS
pathogens, particularly S. pneumoniae As the incidence of occult bacteremia has declined
r Antipyretics as needed: Pneumonia, septic arthritis, osteomyelitis, meningitis,
sepsis, septic shock, death below 0.5% (with universal PCV7 and Hib
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN vaccination), routine CBC and blood culture
Acetaminophen 15 mg/kg/dose PO/PR q4h PRN management strategies for febrile young children
Second Line REFERENCES should be abandoned.
r Pitfalls:
Clindamycin 10 mg/kg IV/PO q8h: 1. Carstairs KL, Tanen DA, Johnson AS, et al.
r May be appropriate as parenteral or oral therapy in Not assuring appropriate follow-up for a child
Pneumococcal bacteremia in febrile infants with suspected or documented bacteremia within
penicillin-allergic patients presenting to the emergency department before 2448 hr
DISPOSITION and after the introduction of the heptavalent
penumococcal vaccine. Ann Emerg Med.
Admission Criteria 2007;49:772777.
r Neonates <28 days
r Outpatient follow-up cannot be assured 2. Herz AM, Greenhow TL, Alcantara J, et al.
r Dehydration, lethargy, ill appearance Changing epidemiology of outpatient bacteremia in
3- to 36-month-old children after the introduction
r Immunocompromised patient with known or
of the heptavalent-conjugated pneumococcal
suspected bacteremia vaccine. Pediatr Infect Dis J. 2006;25:293300.
r Bacteremia with persistent fever
3. Wilkinson M, Bulloch B, Smith M. Prevalence of
r Critical care admission criteria: occult bacteremia in children aged 3 to 36 months
Sepsis presenting to the emergency department with fever
Meningitis with neurologic symptoms in the postpneumococcal conjugate vaccine era.
Discharge Criteria Acad Emerg Med. 2009;16:220225.
Children with occult bacteremia who return for 4. Meltzer AJ, Powell K, Avner JR., AJ, et al. Fever in
follow-up due to a positive blood culture for S. infants and children. Consensus in Pediatrics.
pneumoniae can be discharged home if the child 2005;1(7):119.
remains afebrile, well appearing, and has no evidence 5. Avner JR, Baker MD. Occult bacteremia in the
of serious bacterial infection (eg, meningitis): post-pneumococcal conjugate vaccine era: Does
r Patients with organisms other than S. pneumoniae the blood culture stop here? Acad Emerg Med.
(such as S. aureus, N. meningitidis, H. influenzae) 2009;16:258260.
typically require hospital admission and parenteral
antibiotic therapy.
95
BALANITIS/BALANOPOSTHITIS
Kerry Caperell
Raymond Pitetti

BASICS r Infectious:
Lab
Group A streptococcus Initial Lab Tests
DESCRIPTION Escherichia coli and fungi are common in r Typically, no lab testing is necessary.
r Balanitis is defined as inflammation of the glans diaper-wearing children. r A culture for group A streptococcus from the genital
penis. Enterococci and Staphylococcus aureus are more area may be performed in children with recent
r Balanoposthitis is defined as inflammation of the common in older children. phayngitis, impetigo, or other signs of possible strep
glans penis and foreskin. Neisseria gonorrhoeae and Chlamydia trachomatis infection.
EPIDEMIOLOGY
are possibilities in sexually active children. r Rapid antigen testing for group A streptococcus has
Viruses not been validated in this setting.
Incidence r Noninfectious inflammation:
r 2.97.6% in circumcised boys (1) r Patients suspected of having an STI should have
r 5.914.4% in uncircumcised boys (1) Irritant dermatitis swabs sent for chlamydia, gonorrhea, and herpes
Drug eruption
r More common in black and Hispanic boys simplex.
Local trauma r For patients without obvious balanitis, urinalysis and
r Peak age in children is 25 yr but can occur at any
age (2). COMMONLY ASSOCIATED CONDITIONS possibly urine culture to detect urinary tract infection
r Immunodeficient states, including AIDS may be necessary.
RISK FACTORS r Diabetes mellitus
r Uncircumcised male DIFFERENTIAL DIAGNOSIS
r Smegma
r Poor hygiene
DIAGNOSIS r Psoriasis
r Excessive washing
r Eczema
r Not yet toilet trained
HISTORY r Paraphimosis
r Recent antibiotics r Dysuria is a common complaint.
r Lichen planus
r Penile itching or pain
GENERAL PREVENTION r Human papillomavirus
r Good hygiene to the area r Penile discharge
r Balanitis xerotica obliterans
r Practicing gentle foreskin retraction (avoiding r Swelling or redness of the glans penis
r Herpes simplex
excessive force) PHYSICAL EXAM
r Erythema and swelling of the glans penis
PATHOPHYSIOLOGY
r Infections: r Occasionally, foul-smelling exudate is seen. TREATMENT
In uncircumcised boys, the potential space r Inguinal lymphadenopathy
r Phimosis INITIAL STABILIZATION/THERAPY
between the foreskin and glans may retain r Patients who are unable to void may require
moisture as well as bacteria. r The triad of pain, fiery erythema, and a thin
emergent bladder drainage.
Particularly when the foreskin begins separating transudate/exudate under the prepuce may indicate r Provide analgesia to patients with severe pain.
from the glans around the 2nd and 3rd yr of life, a group A streptococcus as the causative agent.
collection of moisture and bacteria may result in r Carefully evaluate the scrotum to determine if any MEDICATION
an infection that is often suppurative. evidence of testicular torsion is present: Scrotal First Line
Typically, local cellulitis as well as collection of pus appearance, cremasteric reflex, testicular position, r Oral antibiotic
in the potential space between the glans and testicular tenderness. r Amoxicillin 40 mg/kg/day PO divided b.i.d.t.i.d.,
foreskin occurs. r Evaluate for epididymitis by palpation of the max 500 mg/dose for 710 days
Since the potential space is not all contiguously r Cephalexin 50 mg/kg/day PO divided b.i.d.q.i.d.,
epididymis.
open to the meatus of the foreskin, pus collection
max 500 mg/dose for 710 days
may act as an abscess in this area, which is often
near the coronal sulcus.
r Irritant dermatitis due to soap or other cleaning
agent
r Trauma due to forceful foreskin retraction
96
BALANITIS/BALANOPOSTHITIS
r Most irritant and bacterial cases can be treated with See Also (Topic, Algorithm, Electronic
topical mupirocin b.i.d. for 1 wk FOLLOW-UP Media Element)
r If group A streptococcus is suspected, amoxicillin r Epididymitis/Orchitis
b.i.d. for 10 days is necessary.
r Cases due to STIs are treated in the same manner as
r Scrotal Pain
r Testicular Torsion
B
r Sitz baths 3 times daily until signs of inflammation r Urinary Tract Infection
the respective STI.
r Fungal infection can be treated with topical nystatin disappear
r Good hygiene
q.i.d. for 1 wk.
r Only use gentle force to retract the foreskin.
Second Line r Antibiotics as indicated
CODES
For group A streptococcal infections, any of the
r Follow up with the primary care physician as needed.
regimens for strep pharyngitis is adequate. ICD9
PROGNOSIS 607.1 Balanoposthitis
SURGERY/OTHER PROCEDURES r Most patients have an uneventful course.
r Forced retraction of the foreskin to release pus
followed by cleaning with chlorhexidine or Betadine r Up to 10% of patients will have a recurrence.
PEARLS AND PITFALLS
may be performed: COMPLICATIONS
This procedure is typically very painful and may be r Most cases resolve with only local care and
Balanitis xerotica obliterans, a chronic inflammatory
preceded with topical anesthetic such as EMLA or disease, is a separate entity that should be considered antibiotics.
another analgesic. r If there is significant swelling between the foreskin
in cases of balanitis that are refractory to conventional
If this is performed, instruct the parent to continue treatment (3). and glans, forced retraction of the foreskin to
retracting the foreskin multiple times daily to release pus may be highly beneficial.
ensure it remains retractible. r Balanitis suspected of being secondary to sexually
r A dorsal slit through the phimotic area performed REFERENCES transmitted pathogens should raise the possibility of
emergently if bladder drainage by catheterization or sexual abuse.
suprapubic aspiration is necessary but cannot be 1. Fergusson DM, Hons BA, Lawton JM, et al.
carried out. This procedure would usually be Neonatal circumcision and penile problems: An
performed by a urologist. 8-year longitudinal study. Pediatrics. 1988;81:
537541.
DISPOSITION 2. Kiss A, Kiraly L, Kutasy B, et al. High incidence of
Admission Criteria balanitis xerotica obliterans in boys with phimosis:
Patients with urinary obstruction requiring Prospective 10-year study. Pediatr Dermatol.
catheterization or surgery should be admitted. 2005;22:305308.
Discharge Criteria 3. Schwartz RH, Rushton HG. Acute balanoposthitis in
Uncomplicated cases can be discharged from the young boys. Pediatr Infect Dis J. 1996;15:176177.
emergency department.
Issues for Referral ADDITIONAL READING
r Patients with urinary retention who cannot be
catheterized should be seen by a urologist r Edwards SK. European guideline for the
emergently. management of balanoposthitis. Int J STD AIDS.
r Those who have urinary retention, phimosis, or 2001;12(Suppl 3):68.
disease that is refractory to treatment should be r Link R. Cutaneous diseases of the external genitalia.
seen by a urologist. In Wein AJ, Kavoussi LR, Novick AC, et al., eds.
r Suspicion of a sexually transmitted etiology in a Campbell-Walsh Urology. 9th ed. Philadelphia, PA:
young child should be further investigated for the Saunders; 2007.
possibility of sexual abuse.
97
BAROTRAUMA, SINUS
Curt Stankovic

BASICS Any situation that will expose someone to a pressure Imaging
gradient, such as ascent or decent in an airplane or r Barosinus is a clinical diagnosis, so no imaging is
DESCRIPTION scuba diving, skydiving, mountain climbing: required (3).
Barosinusitis is also known as aerosinusitis or sinus r The frontal sinus is most commonly affected, r However, sinus plain radiographs may reveal
squeeze: followed by the maxillary sinus. mucosal thickening and fluid in the sinus.
r It results in pain and occasionally bleeding into the r CT scan of the sinuses with coronal and axial views
sinus cavities as a result of exposure to pressure COMMONLY ASSOCIATED CONDITIONS
r Barodontalgia is recommended for patients with severe
gradients. r Barotitis barosinusitis (1).
EPIDEMIOLOGY r Pulmonary barotrauma Diagnostic Procedures/Other
r Barotrauma is much less common in children than
Barosinusitis can be classified into 3 grades:
adults. r Grade 1: Mild transient discomfort without
r 34 episodes per 100,000 adult exposures (1) DIAGNOSIS radiologic findings
r Middle ear barotrauma is 610 times more r Grade 2: Severe pain for <24 hr with mucosal
prevalent than barosinusitis (1). HISTORY
r Exposure to pressure gradients without pressure thickening on radiograph
r Grade 3: Severe pain for >24 hr, severe mucosal
RISK FACTORS equalization, such as diving, air travel
r Flying, scuba diving, skydiving, mountain climbing r Preceding upper respiratory tract infection or thickening, opacification on radiograph. Epistaxis
r Hyperbaric oxygen chamber seasonal allergies may be present. Sinusitis may occur.
r Presence of anatomic abnormalities of the nose and r Feeling of pressure in the affected sinus, worsening DIFFERENTIAL DIAGNOSIS
paranasal sinuses including polyps (2) congestion, sudden sharp facial pain, or frontal r Barodontalgia
headache r Sinusitis
GENERAL PREVENTION r Epistaxis, vertigo, nausea may be present. r Seasonal allergies
Avoid exposure to potential pressure gradients,
especially when suffering from upper respiratory tract r Cerebrovascular accident
PHYSICAL EXAM
infections or seasonal allergies. r Inspect nasal mucosa for evidence of infection, r Malignant tumors of nasal cavity and sinuses
PATHOPHYSIOLOGY polyp, allergies, or epistaxis.
r Barosinusitis is typically preceded by an upper r Tenderness over the sinus may be present, and sinus
transillumination may reveal fluid. TREATMENT
respiratory tract infection or seasonal allergies.
r In this setting, it occurs when the facial sinuses are r 5th cranial nerve or infraorbital nerve palsy may be
PRE HOSPITAL
unable to drain due to obstruction of ostia by mucus present in severe barosinusitis. r Remove patient from the source of barotrauma.
secretions or edema. This prevents the sinus to r Percuss maxillary teeth with tongue depressor to r Attempt to equalize pressure by swallowing or
equalize if exposed to a pressure gradient. inspect for tenderness. performing the Valsalva maneuver.
r The Boyle law (P1V1 = P2V2) can predict sinus r Rule out other injuries associated with barotrauma:
barotrauma. The volume of gas is inversely related Pulmonary barotrauma: Look for signs of a INITIAL STABILIZATION/THERAPY
to the amount of pressure on it. pneumothorax or subcutaneous emphysema.
r There are 2 types of barotraumasqueeze and Patient may complain of shortness of breath, circulation.
r Apply local pressure if epistaxis is present.
reverse squeeze: hemoptysis, and dysphagia.
Barotitis media: Which is associated with otalgia, r Use analgesics and nasal decongestants to relieve
Squeeze occurs when pressure is applied to air
that is trapped in a sinus. The volume of gas blood/fluid in the middle ear, ruptured tympanic pain and pressure.
reduces, resulting in negative pressure and the membrane.
influx of fluid and blood.
Reverse squeeze occurs when the pressure outside
of the sinus is low, resulting in the air within the
sinus to expand. If the sinus is obstructed,
preventing pressure equalization, pain, and
bleeding may occur.
98
BAROTRAUMA, SINUS
MEDICATION Issues for Referral 3. Weissman B, Green RS, Roberts PT. Frontal sinus
r Otorhinolaryngologist referral may be necessary for barotrauma. Laryngoscope. 1972;82(12):
First Line
r Nasal decongestants: severe or persistent symptoms. 21602168.
r Otorhinolaryngology or neurosurgery referral may be
Oxymetazoline 0.05%, 2 sprays in each nostril
necessary if the sphenoid sinus is involved and does
4. Setliff RC 3rd. Minimally invasive sinus surgery: The
rationale and the technique. Otolaryngol Clin North
B
b.i.d. for 35 days (1)
Phenylephrine not respond to first-line treatment. Am. 1996;29(1):115124.
r Analgesics (NSAIDs) at age-appropriate doses r Dental referral may be necessary if barodontalgia is
r Opioids: present. Barodontalgia may result in referred pain to
Morphine 0.1 mg/kg IV/IM/SC q2h PRN: face. ADDITIONAL READING
Initial morphine dose of 0.1 mg/kg IV/SC may r Brubakk AO, Neuman TS. Bennett and Elliotts
be repeated q1520min until pain is controlled, FOLLOW-UP Physiology and Medicine of Diving. 5th rev ed.
then q2h PRN. United States: Saunders Ltd.; 2003:800.
Codeine or codeine/acetaminophen dosed as FOLLOW-UP RECOMMENDATIONS r Hanna HH, Tarington CT. Otolaryngology in
0.51 mg/kg of codeine component PO q4h PRN r Discharge instructions and medications:
aerospace medicine. In DeHart RL, ed.
Hydrocodone or hydrocodone/acetaminophen Nasal decongestants and oral analgesics Fundamentals of Aerospace Medicine. Philadelphia,
dosed as 0.1 mg/kg of hydrocodone component Oral antibiotics if fluid is seen in the sinus cavity PA: Lippincott Williams & Wilkins; 1985:520530.
PO q46h PRN r Activity:
r NSAIDs: Avoid activities that may result in barotrauma See Also (Topic, Algorithm, Electronic
Consider NSAID medication in anticipation of until fully recovered. Media Element)
r Barotrauma, Ear
prolonged pain and inflammation. If undergoing endoscopic sinus surgery, the
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN r Sinusitis
patient may return to full activity in 13 wk.
Ketorolac 0.5 mg/kg IV/IM q6h PRN
Naproxen 5 mg/kg PO q8h PRN PROGNOSIS
r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN Generally considered good. Patients typically respond CODES
r Aspirin should be avoided due to the potential for to first-line medications:
r Recurrent barosinusitis may be secondary to
hematoma formation. ICD9
r If bleeding or sinus effusion is present, antibiotics anatomic pathology. These patients are more likely 993.1 Barotrauma, sinus
to need surgical drainage of the affected sinus.
are indicated (1): r Patients with uncontrolled or chronic sinusitis as
Amoxicillin 4080 mg/kg/day PO divided
b.i.d.t.i.d., max daily dose 2 g well as seasonal allergies may find more difficulty PEARLS AND PITFALLS
Clindamycin 30 mg/kg PO divided t.i.d., max daily returning to normal activities. r Treat patients who have blood or fluid in the sinus
dose 1.8 g COMPLICATIONS cavity with antibiotics to prevent infectious
Trimethoprim/Sulfamethoxazole (TMP/SMZ) r Rarely, a sinus may rupture and result in
complications.
10 mg/kg/day PO divided b.i.d., max single dose pneumocephalus causing vertigo, vomiting, r Refer patients with severe or unresponsive
320 mg TMP/1,600 mg SMZ headache, and pain. symptoms to otorhinolaryngology.
r Other complications include orbital cellulitis, r Recognize life-threatening complications of
Second Line
Pseudoephedrine 1 mg/kg/dose PO given b.i.d.q.i.d.; abscess, and hematoma formation. barotrauma.
adult dose 60120 mg PO (1)
r Surgery is used to restore sinus ventilation.
REFERENCES
r May be necessary if traditional medications fail and 1. Hamilton-Farrell M, Bhattacharyya A. Barotrauma.
symptoms persist Injury. 2004;25(4):359370.
r Endoscopic sinus surgery has improved efficacy 2. Baughman SM, Brennan J. Barotrauma secondary
when compared to conventional surgical options (4) to inflammatory maxillary sinus polyp: A case
report. Aviat Space Environ Med. 2002;73(11):
DISPOSITION 11271131.
Admission Criteria
Uncontrollable pain
Discharge Criteria
Ability to manage pain with oral analgesics or
opioids
99
BETA-BLOCKER POISONING
Amit K. Gupta
Mark Su
r Lipid-soluble agents (propranolol) may cause a DIFFERENTIAL DIAGNOSIS

BASICS depressed mental status by crossing the blood-brain r Calcium channel blocker toxicity
barrier and penetrating the CNS. r Digoxin toxicity
DESCRIPTION r Hypoglycemia may occur due to increased insulin r Clonidine toxicity
r There are 3 subtypes of beta receptors: r Cardiogenic shock
release from the beta islet cell of the pancreas.
Beta1 receptors located primarily on cardiac r A slight rise in serum potassium may occur due to r Hemorrhagic shock
cells: impaired uptake by skeletal muscle. r Septic shock
Blockade leads to bradycardia, hypotension,
ETIOLOGY r Acute myocardial infarction
decreased myocardial contractility, and reduced
r Numerous brands of beta-blockers are available.
myocardial oxygen consumption.
Beta2 receptors located primarily on smooth r Understanding the different characteristics of each
muscle; blockade leads to relaxation in arteries class may be helpful in evaluating the clinical TREATMENT
and pulmonary bronchi; also found on beta islet outcome and guiding therapy.
PRE HOSPITAL
cells of the pancreas, promoting insulin release COMMONLY ASSOCIATED CONDITIONS r Assess and stabilize airway, breathing, and
Beta3 receptors located on adipose tissue cause Congenital heart disease, CHF, cardiac dysrhythmia, circulation.
lipolysis. It is unclear if beta-blocker poisoning has essential tremor r Supplemental oxygen
any significant effect on these functions. r Establishment of an IV line with cardiac monitoring
r Consequential overdoses of beta-blockers can cause
severe hypotension and bradycardia and potentially DIAGNOSIS INITIAL STABILIZATION/THERAPY
death. r Assess and stabilize airway, breathing, and
HISTORY circulation.
EPIDEMIOLOGY r Obtain history of exposure, other possible
r Assess blood glucose level.
Incidence coingestants, and events that led to exposure. r Consultation with a medical toxicologist or poison
r Exposures to beta-blockers accounts for a large r Ask parents to bring in pill bottles if possible.
number of emergency department visits. control center is recommended.
r Pediatric deaths are exceedingly rare. PHYSICAL EXAM r Activated charcoal (1 g/kg) may be given if the
r Absorption of beta-blockers is rapid and occurs
r Propranolol is the most toxic beta-blocker and the patient is protecting the airway.
within 30 min. r Syrup of ipecac is contraindicated.
most frequently reported beta-blocker used in r Depressed mental status may be due to r Orogastric lavage may be considered if the patient
suicide attempts worldwide.
hypoglycemia or to lipid-soluble agents crossing the presents shortly after a potentially life-threatening
RISK FACTORS blood-brain barrier. overdose (usually within 1 hr) and the airway is
r Exposure to sustained-release preparations can lead r Cardiovascular effects may include bradycardia.
protected:
to delayed toxicity. r Pulmonary effects may include bronchospasm or This is predicated on having a clinician with
r Coingestants with other cardiotoxic agents such as pulmonary edema. experience performing orogastric lavage; NG
calcium channel blockers, cyclic antidepressants, and lavage is not indicated and not helpful.
neuroleptics may exacerbate toxicity. DIAGNOSTIC TESTS & INTERPRETATION
Lab MEDICATION
GENERAL PREVENTION r Immediate assessment of capillary blood glucose First Line
Poison proofing homes and giving parents poison r Hypoglycemia may result from beta-blocker r Dextrose 0.25 g/kg (2.5 mL/kg of 10% dextrose or
prevention education is the most effective way to overdose. 1 mL/kg of 25% dextrose) IV bolus for hypoglycemia
prevent exposure in children. r Electrolytes, BUN, creatinine, glucose r 0.9% saline bolus (20 cc/kg) for hypotension
PATHOPHYSIOLOGY r Measure acetaminophen and salicylate levels if r Atropine 0.02 mg/kg (min dose 0.1 mg and max
r Blockade of beta-adrenergic receptors results in suicidal ingestion. 2 mg) for bradycardia; may not be effective
decreased production of intracellular cyclic r Urine drug screen usually is not indicated unless for r Glucagon 150 g/kg over 1 min (max 5 mg) IV
adenosine monophosphate (cAMP) with a resultant forensic purposes such as suspected malicious intent bolus:
blunting of multiple metabolic and cardiovascular or child abuse. Glucagon bypasses the beta receptor and
effects of circulating catecholamines. increases cAMP levels leading to an increase in
r Bradycardia occurs due to blockade at the sinoatrial Imaging
r CXR should be performed to assess for pulmonary inotropy and BP
node. Also administer a continuous infusion in 5%
r Direct decrease in myocardial contractility (inotropy) edema.
r A CT of the brain should be considered in individuals dextrose in water (D5W) if effective (25 mg/hr).
leads to hypotension. May cause vomiting due to decrease of lower
r Conduction abnormalities may occur due to with altered mentation.
esophageal sphincter tone
blockade at the atrioventricular node. Diagnostic Procedures/Other
r Toxicity may also occur from myocyte sodium ECG should be performed to look for signs of
channel blockade (propranolol) leading to a bradycardia and/or other conduction abnormalities.
prolonged QRS duration and impairing cardiac
conduction.
r Toxicity may also arise from potassium channel
blockade (sotalol) leading to a prolonged QTc
interval and placing patients at risk for developing
torsade de pointes.
100
BETA-BLOCKER POISONING
r Lorazepam 0.05 mg/kg IV, max dose 2 mg: r IV fat emulsion therapy (Intralipid 20% 1 mL/kg) has
ADDITIONAL READING
First-line agent for seizures been shown in animal models and case reports to
r Sodium bicarbonate (12 mEq/kg) IV bolus for signs be beneficial in lipid-soluble drug overdoses r Brubacker J. Beta-adrenergic antagonists. In
of sodium channel blockade on ECG followed by IV (propranolol).
r The proposed mechanism of action is the lipid
Goldfrank LR, Flomenbaum NE, Lewin NA, et al.,
eds. Goldfranks Toxicologic Emergencies. 8th ed.
B
infusion of 3 ampules of sodium bicarbonate in 1 L
of D5W at twice maintenance. Carefully monitor sink theory, where drugs may become trapped in Stamford, CT: Appleton & Lange; 2006:924941.
serum pH. an expanded plasma lipid compartment. Another r Kerns W 2nd, Schroeder D, Williams C, et al. Insulin
Second Line proposed theory is that the emulsion acts as improves survival in a canine model of acute
r A variety of inotropes are available if above additional fuel source for the heart due to the beta-blocker toxicity. Ann Emerg Med. 1997;29:748.
energy from fatty acids. r Love JN, Howell JM, Litovitz TL, et al. Acute beta
treatments fail.
r Norepinephrine infusion (0.12 g/kg/min) IV and SURGERY/OTHER PROCEDURES blocker overdose: Factors associated with the
titrate to maintain adequate cardiac output: r Extracorporeal membrane oxygenation has also development of cardiovascular morbidity. J Toxicol
Directly stimulates alpha- and beta1 -adrenergic been attempted in patients who have hypotension Clin Toxicol. 2000;38:275.
r Taboulet P, Cariou A, Berdeaux A, et al.
receptors, thus increasing inotropic and refractory to all pharmacologic therapies.
vasopressor effects r Intra-aortic balloon counterpulsation is another Pathophysiology and management of self-poisoning
r Epinephrine infusion (0.1 g/kg/min) IV and titrate invasive supportive option in refractory cases and with beta-blockers. J Toxicol Clin Toxicol. 1993;31:
to maintain adequate cardiac output: has been used successfully to improve cardiac 531.
Directly stimulates alpha- and beta-adrenergic output and BP. See Also (Topic, Algorithm, Electronic
receptors Media Element)
r Dopamine 520 g/kg/min IV and titrate to DISPOSITION r Calcium Channel Blocker Poisoning
maintain adequate cardiac output:
Admission Criteria r Digoxin Poisoning
r All patients with exposure to sustained-preparation
Indirectly stimulates alpha- and beta1 -adrenergic r Shock, Cardiogenic
dopaminergic receptors to produce ionotropic, beta-blockers should be admitted to a monitored
chronotropic, renal/splanchnic vasodilatory (at low setting due to the potential of delayed toxicity.
r Admit all symptomatic patients.
doses), and vasopressor (at high doses) effects CODES
r Amrinone 50 g/kg IV loading dose with r Critical care admission criteria:
maintenance infusion of 0.50 g/kg/min IV and Patients with signs of hemodynamic instability
should be admitted to an ICU setting. ICD9
titrate to desired effect: r 971.3 Poisoning by sympatholytics (antiadrenergics)
Inhibits myocardial phosphodiesterase, leading to Discharge Criteria r 972.0 Poisoning by cardiac rhythm regulators
increased cAMP levels May discharge if the patient remains asymptomatic
r High-dose insulin/glucose infusion: after observation for 6 hr for immediate-release
Insulin (1 unit/kg bolus followed by 1 unit/kg/hr) preparations
Glucose must be coadministered, initially 1 g/kg
PEARLS AND PITFALLS
bolus followed by infusion of 0.5 g/kg/hr. r Hypotension and bradycardia can occur as
Frequent blood glucose monitoring, initially FOLLOW-UP consequences of beta-blocker overdose.
q1015min for the 1st few hours, is necessary. FOLLOW-UP RECOMMENDATIONS r Glucagon is the first-line agent for beta-blocker
This therapy has been shown to be effective in r Discharge instructions and medications: toxicity.
case reports and in animal models. Follow up with the primary pediatrician. r Admission and observation are indicated for any
The theorized mechanism is via positive inotropic Return to the emergency department for change sustained-release beta-blocker ingestion.
effects of insulin and cardiac utilization of glucose in behavior, alteration in mental status, or if ill r Certain beta-blockers such as propranolol and
as an energy source. appearing.
Frequent monitoring of serum glucose and acebutolol may cause myocyte sodium channel
r Activity: blockade leading to QRS prolongation.
potassium levels is necessary.
Normal activity after discharge
COMPLEMENTARY & ALTERNATIVE Patient Monitoring
THERAPIES Patients with intentional overdoses should be
r Enhanced elimination with hemodialysis is only
monitored for acts of self-harm.
effective for beta-blockers with low volumes of
distribution and high water solubility (ie, atenolol, PROGNOSIS
naldol, and sotalol). The prognosis is generally good for isolated
r Cardiac pacing may be effective in increasing the beta-blocker overdose.
rate of myocardial contractions, but electrical COMPLICATIONS
capture is not always successful and BP is not r Cardiovascular collapse
always restored. r Shock
r Death
101
BILIARY TRACT DISEASE

Gregory Garra

BASICS r The exact mechanism accounting for the progressive
Lab
obliteration of the biliary tree in biliary atresia is r LFTs such as bilirubin, serum transaminase, alkaline
DESCRIPTION uncertain, although numerous etiologies are phosphatase, and gamma-glutamyl
Biliary tract disease is a broad category of diseases proposed. aminotransferase are often elevated:
that can affect children of all ages and includes the r The etiologies of PSC and choledochal cysts are However, lab studies are not fully diagnostic, as
biliary ducts, gallbladder, and liver. unknown. However, PSC is thought to result from an there is much overlap with each of the
EPIDEMIOLOGY immunologic mechanism. aforementioned conditions.
r Conjugated (direct) hyperbilirubinemia is defined
Incidence COMMONLY ASSOCIATED CONDITIONS
r Biliary atresia is relatively uncommon, occurring in r Symptomatic liver disease in patients with cystic as:
1:10,0001:15,000 live births. fibrosis (CF) ranges from 218%. Serum conjugated bilirubin >1.0 mg/dL if total
r Choledochal cysts occur in 1:15,000 births. r PSC is commonly associated with inflammatory bilirubin is <5 mg/dL OR
r Caroli disease is very rare, with 1 case per Fractional conjugated bilirubin >20% in cases
bowel disease, histiocytosis X, and
where total bilirubin is >5 mg/dL
1,000,000 people. immunodeficiency.
r Caroli disease is associated with congenital hepatic Biliary atresia results in conjugated
RISK FACTORS hyperbilirubinemia.
r Females are more commonly afflicted with biliary fibrosis and autosomal recessive polycystic kidney r Alkaline phosphatase is commonly elevated in cases
disease.
atresia and choledochal cysts. r Failure to thrive is common in patients with chronic of PSC.
r A temporal relationship between acute gallbladder
biliary disease. Imaging
hydrops and scarlet fever, leptospirosis, and r US is an excellent screening tool for anatomic
Kawasaki disease has been suggested. abnormalities of the biliary tract:
PATHOPHYSIOLOGY DIAGNOSIS Choledochal cysts appear as dilated portions of
r Extrahepatic biliary atresia is an inflammatory the biliary tree (choledochal cysts).
HISTORY A small or absent gallbladder on US suggests
condition of the bile ducts resulting in progressive r Most biliary tract diseases will present with jaundice.
obliteration of the extrahepatic biliary tract. It is the biliary atresia.
A detailed description of the evaluation of jaundice US will demonstrate multiple intrahepatic bile
most frequent cause of death from liver disease and
is described in the Jaundice, Unconjugated and lakes in patients with Caroli disease.
indication for liver transplantation in children.
r Primary sclerosing cholangitis (PSC) is an Jaundice, Conjugated topics. US is the diagnostic modality of choice for
r Patients with biliary atresia and choledochal cysts
uncommon, slowly progressing disorder of the suspected cholecystitis or acute gallbladder
typically present with jaundice during the 1st few hydrops.
biliary tract resulting from inflammation and fibrosis
months of life. r Hepatobiliary scanning is nearly 100% sensitive for
of intra- and extrahepatic biliary ductal systems. r Stools are typically acholic in patients with biliary
r Choledochal cysts are congenital saccular or biliary atresia: Confirmed gut excretion excludes the
atresia or choledochal cysts. diagnosis.
fusiform dilatations of the extrahepatic biliary tract. r Urine is typically dark in patients with conjugated
r Caroli disease is a congenital disorder resulting in Diagnostic Procedures/Other
hyperbilirubinemia. r The diagnosis of PSC is based upon
segmental, saccular dilatation of intrahepatic biliary r Ascending cholangitis is suggested by the presence
ducts. cholangiography: Alternating strictures and areas of
r Cholelithiasis is described elsewhere. of fever, jaundice, and abdominal pain. dilation imparting a beaded appearance of the
r Cholecystitis is an acute or chronic inflammatory PHYSICAL EXAM biliary ducts.
condition of the gallbladder. r Exam of the skin for cutaneous manifestations of r Endoscopic retrograde cholangiopancreatography or
r Acute cholangitis is a clinical syndrome resulting liver disease; jaundice, bruising magnetic resonance cholangiopancreatography is
from stasis and infection of the biliary tract. r Abdominal exam for tenderness, distention, useful for the workup of several biliary tract diseases.
r Acute gallbladder hydrops is a noninflammatory hepatomegaly, splenomegaly, or ascites. An r Percutaneous liver biopsy is frequently used to assist
acute distention of the gallbladder without abdominal mass may be palpated in patients with in establishing a definitive diagnosis.
gallstones. choledochal cysts.
102
BILIARY TRACT DISEASE
r Sepsis
Admission Criteria r Lee CK, Jonas MM. Pediatric hepatobiliary disease.
r Inborn errors of metabolism r Patients with complications related to biliary tract
r CF
r Hypothyroidism
disease such as ascending bacterial cholangitis Curr Opin Gastroenterol. 2007;23:306309.
r McEvoy CF, Suchy FJ. Biliary tract disease in B
require admission for treatment.
r Alpha-1 antitrypsin deficiency r Critical care admission criteria: children. Pediatr Clin North Am. 1996;43:7598.
r Progressive familial intrahepatic cholestasis Intensive supportive care may be required for See Also (Topic, Algorithm, Electronic
r Ascariasis infants with conjugated hyperbilirubinemia. Media Element)
r Infectious hepatitis r Jaundice, Conjugated
Discharge Criteria
Patients who are stable with LFTs and electrolytes r Jaundice, Unconjugated
within acceptable limits and a known diagnosis may
TREATMENT be discharged to the care of their appropriate
subspecialist. CODES
INITIAL STABILIZATION/THERAPY Issues for Referral
The treatment of acute gallbladder hydrops is These patients should be managed in conjunction with ICD9
supportive and typically subsides spontaneously. a pediatric gastroenterologist or hepatologist and r 576.9 Unspecified disorder of biliary tract
MEDICATION surgeon. r 751.61 Biliary atresia, congenital
Broad-spectrum antibiotics should be administered in r 751.69 Other congenital anomalies of gallbladder,
cases of suspected acute cholangitis: bile ducts, and liver
r Beta-lactam/beta-lactamase inhibitor monotherapy: FOLLOW-UP
Ampicillin-sulbactam (3 g q6h) OR FOLLOW-UP RECOMMENDATIONS
Piperacillin/Tazobactam (3.375 g q6h) OR Discharge instructions and medications: PEARLS AND PITFALLS
Ticarcillin/Clavulanate (3.1 g q4h) r Close follow-up with the appropriate subspecialists r The possibility of hepatobiliary disease must be
r Metronidazole (500 mg IV q8h) PLUS ceftriaxone
is critical. considered in any neonate with jaundice beyond
(100 mg/kg IV q24h)
r Monotherapy with a carbapenem: PROGNOSIS 2 wk of age.
r Untreated biliary atresia has an extremely poor r Evaluation for cholestatic jaundice may be delayed
Imipenem (500 mg q6h) OR
Meropenem(1 g q8h) OR prognosis. to 3 wk of age in breast-fed infants if the exam is
r The most important predictor for success in a patient normal.
Ertapenem (1 g daily) r Biliary atresia be differentiated from other causes of
r Metronidazole (10 mg/kg/dose IV q8h) PLUS a with biliary atresia is early operative therapy (before
fluoroquinolone (ciprofloxacin 15 mg/kg IV q12h) or 60 days of age). neonatal cholestasis because early intervention is
r The course of PSC is variable but typically associated with more favorable outcome.
levofloxacin 10 mg/kg/dose q24h) r An elevated conjugated bilirubin level should
progressive.
SURGERY/OTHER PROCEDURES prompt a structured and rapid evaluation of biliary
r Diversion of bile flow, usually by Kasai procedure COMPLICATIONS
r Choledochal cysts and biliary atresia can be tract disorders.
(hepatoportoenterostomy) is essential for survival in
biliary atresia. complicated by ascending cholangitis, hepatic
r Surgical excision of choledochal cysts provides cirrhosis, and portal HTN.
r Choledochal cysts are associated with an increased
excellent long-term results.
r Liver transplantation is frequently required for incidence of biliary carcinoma.
r Caroli disease is a risk factor for malignancy and
patients with end-stage liver disease resulting from
biliary atresia or PSC. recurrent cholangitis.
103
BIPOLAR DISORDER/MANIA
Todd A. Mastrovitch

BASICS r Most likely a combination of genetic and
Lab
environmental factors Initial Lab Tests
DESCRIPTION r Linkage studies suggest a role for the tryptophan r Baseline CBC and serum blood chemistry
r Bipolar disorder is an illness characterized by cycles r Thyroid function tests
hydroxylase 2 (TPH2) gene.
of mania and depression. It is commonly referred to r Genome wide association studies point to r Urine toxicology for stimulants
as manic depression. CACNA1C to be the most consistent locus,
r Recognition and treatment of manic and hypomanic Imaging
associated with calcium channel gating.
episodes or episodes of depression are relevant for EEG or CT scan of the brain based on specific historical
emergency medical clinicians. COMMONLY ASSOCIATED CONDITIONS or physical exam findings
r Benzodiazepines, lithium, carbamazepine, and r Unipolar depression
r Substance abuse DIFFERENTIAL DIAGNOSIS
valproic acid may be used to treat manic or r ADD or ADHD
hypomanic episodes. r Unipolar depression
EPIDEMIOLOGY DIAGNOSIS r Borderline personality disorder
r 1% of the population 18 yr of age in any given r Major depression
HISTORY r Schizophrenia
year
r Lifetime prevalence is 1%. Diagnostic criteria for mania include the following: r Drug abuse
r 1 wk of persistently elevated, expansive, or irritable
r Bipolar disorder affects men and women equally. r Thyrotoxicosis
r Age of onset is usually between 15 and 30 yr of age. mood
r During the period of mood disturbance, at least
RISK FACTORS three of the following symptoms are present: TREATMENT
r Genetics play a role in the development of bipolar Inflated self-esteem or grandiosity
disorder in children and young adults. Decreased need for sleep INITIAL STABILIZATION/THERAPY
r Use of drugs, caffeine, and alcohol increase chances More talkative than usual r Providing a safe environment for the patient to be
of manic, hypomanic, and depressive episodes. Racing thoughts or flight of ideas evaluated in while in the emergency department.
Distractibility r Activation of crisis team or psychiatric service to
GENERAL PREVENTION Increase in goal-directed activity
Teens with mood disorder symptoms should be screen the patient for psychiatric needs and to
Excessive involvement in pleasurable activities provide initial determination of need for acute
screened with the Mood Disorder Questionnaire (spending money or sexual indiscretion)
(MDQ) to aid in diagnosis, further screening, and hospitalization and treatment
r The mood disturbance leads to significant
eventual treatment.
impairment in social or occupational functioning.
PATHOPHYSIOLOGY r Symptoms are not due to medical illness or
r Genetics are important in the pathogenesis of substance abuse.
bipolar disorder.
r >2/3 of people with bipolar disorder have at least PHYSICAL EXAM
May show reduced psychomotor activity, low muscle
1 close relative with the disorder.
r Children with 1 affected parent have a 25% chance tone, weight loss, slowed gait, and constipation
of developing bipolar disorder. For children with
2 affected parents, chances of bipolar disorder climb
to 50%.
r Patients may engage in substance use, which may
be an attempt at self-medication and also may
precipitate manic, hypomanic, and depressive
episodes.
104
BIPOLAR DISORDER/MANIA
MEDICATION ADDITIONAL READING

First Line FOLLOW-UP r American Psychiatric Association. Mood disorders.
r Manic or hypomanic episodes:
Benzodiazepines:
Severe mania may require sedation with
In: Diagnostic and Statistical Manual of Mental
Disorders. 4th ed, Text Revision. Washington, DC:
B
benzodiazepines. Strict follow-up with psychiatrist or mental health Author; 2000:345428.
Lorazepam 0.050.1 mg/kg IV q1530min care professional r Baroni A, Lunsford JR, Luckenbaugh DA, et al.
titrated to effect Ensuring the patient is taking the medication as Practitioner review: The assessment of bipolar
Lithium: Children 1560 mg/kg/day PO divided prescribed disorder in children and adolescents. J Child Psychol
r Activity: Psychiatry. 2009;50(3):203215.
t.i.d. or q.i.d.; adolescents 6001,800 mg t.i.d. or
q.i.d. As tolerated, with daily exercise r Malhi GS, Adams D, Cahill CM, et al. The
Valproic acid: Initial dose 1015 mg/kg/day PO Patient Monitoring management of individuals with bipolar disorder: A
divided q.d.t.d.; dosing schedule must be Close follow-up in the outpatient mental health review of the evidence and its integration into
adjusted weekly to achieve therapeutic levels. system clinical practice. Drugs. 2009;69(15):20632101.
r Depressive episodes: Discuss medication with r Staton D, Volness LJ, Beatty WW. Diagnosis and
consulting psychiatrist. DIET classification of pediatric bipolar disorder. J Affect
r As tolerated with focus on a varied, well-balanced
Disord. 2008;105(13):205212.
Second Line diet
Lamotrigine: Dosing schedule should be reviewed with r Avoid caffeine and alcohol.
a neurologist or psychiatrist.
PROGNOSIS CODES
DISPOSITION r After the diagnosis of bipolar disorder is made, it is
Admission Criteria common that the disorder relapses. ICD9
r Risk of harm to themselves or others r Patients may alternate between manic and r 296.00 Manic affective disorder, single episode,
r Unstable mood or severe depression requiring depressive symptoms. unspecified degree
hospitalization to start medication and psychiatric r 90% of patients with bipolar disorder have had at r 296.10 Manic affective disorder, recurrent episode,
stabilization least 1 psychiatric hospital admission. unspecified degree
r Severe alteration of mood or level of consciousness r 296.80 Bipolar disorder, unspecified
due to overdose on drugs or alcohol COMPLICATIONS
r Life expectancy for patients with bipolar disorder is
Discharge Criteria reduced. Between 25 and 50% of patients attempt
Maintenance of stable mood for daily functioning suicide, and 15% are successful.
PEARLS AND PITFALLS
Issues for Referral r 2/3 of patients with bipolar disorder also have an r Children with bipolar disorder frequently have an
Persistence of symptoms of mania or depression addictive disorder. ongoing, continuous mood disturbance that is a mix
despite treatment with medication and close follow-up r Anxiety disorder can also be seen in patients with of mania and depression.
may require repeat hospitalization. bipolar disorder. r Bipolar children typically have 45 severe mood
COMPLEMENTARY & ALTERNATIVE swings per day and are more irritable than euphoric.
r Many teens with untreated bipolar disorder abuse
THERAPIES
r St. Johns Wort, an herb commonly marketed as a alcohol and drugs, which may be attempts at
natural antidepressant, may cause a patient with self-medication. Any child or adolescent who abuses
bipolar disorder to have a manic attack. substances should be evaluated for a mood disorder.
r Omega-3 fatty acids (most commonly found in fish
oil) may have some effect on patients with bipolar
disorder.
105
BITE, ANIMAL
Michael L. Epter
r Common anaerobic isolates (more commonly Imaging

BASICS associated with abscess formation): X-ray for suspected crush injury to bone/fracture
Streptococcus
DESCRIPTION DIFFERENTIAL DIAGNOSIS
Fusobacterium r Human bite
r This topic focuses on mammalian bites, which are Bacteroides r Cellulitis
the most common animal bites children experience. Porphyromonas
r Polymicrobial wounds: r Lymphadenitis
Prevotella
r Eikenella corrodens (human >> animal) r Osteomyelitis
Mixed aerobic/anaerobic predominance on culture
with multiple isolates r Catscratch agent: Bartonella henselae (can be r Laceration from trauma
Anaerobes account for 3/4 of isolates from wound transmitted by cat/flea bite)
infections (especially abscesses). r Marine bites: Vibrio and Pseudomonas species,
r Most common animal bites (descending order): TREATMENT
Plesiomonas shigelloides, Aeromonas hydrophila
Dog (8590%): r Monkey bites: Herpes virus simiae (B virus) PRE HOSPITAL
1/3 upper extremity; 1/3 lower extremity; 20% r Rabies: For full information, see Rabies topic: Local wound care:
face and neck Any break in the skin can transmit rabies. r Irrigation
Children <6 yr old have a higher percentage of
Higher risk of transmission: Unprovoked attack, r Dressing
face, neck, and scalp injuries.
Lacerations, 3145%
ill-appearing or stray animal, raccoons/skunks/bats r Splint application if necessary
Abrasions, 3043% INITIAL STABILIZATION/THERAPY
Puncture wounds, 1334% DIAGNOSIS r Assess ABCs and provide hemostasis.
Cat (510%): r Wash the wound to reduce inoculum cell count:
2/3 upper extremity (cat scratches also affect HISTORY
r History of bite: Soap and water if grossly dirty
periorbital region) Normal saline irrigation
More commonly puncture Provoked/Unprovoked attack
Quaternary ammonium compound (benzalkonium
Rodents Time bite occurred
chloride) plus water
Domestic/Wild animals Place of bite (eg, outside of U.S.) r Irrigate:
r Tetanus and rabies status of patient and rabies
EPIDEMIOLOGY Normal saline through 18-gauge catheter
status of animal
Incidence r Pertinent medical history and allergies >150 mL/cm under high pressure (>7 PSI)
r 1% of emergency department visits annually Monkey bite wounds 15 min of irrigation
r 25 million cases annually (U.S.): PHYSICAL EXAM r Debride devitalized tissue.
r Wound assessmentevaluate and document the r Excise margins of wounds.
Children constitute >50% of reported cases.
following: r Primary closure:
RISK FACTORS Type of injury (eg, laceration, crush, avulsion) <12 hr old
Boys >> girls Signs of infection Dog bites
GENERAL PREVENTION (swelling/erythema/pain/discharge) Facial bites (up 24 hr):
Supervision of young children when around animals Degree of penetration Loose closure by suture
r Involvement of vasculature/nerves r Delayed primary closure:
PATHOPHYSIOLOGY r Involvement of joints/tendons
Bites typically may involve crushing and shearing force Crush injuries
r Range of motion Hand/Feet injuries
as well as deep tissue penetration:
r Dog bites may result in localized crush injuries r Lymphadenopathy Pre-existing infection
r Eschariform lesion, malar purpura, sepsis with Cat bites
(shearing force) stretch lacerations and Puncture wounds
devitalized tissue purpura fulminans Capnocytophaga canimorsus
r Cat bites do not involve the amount of crushing or infection Wounds >1224 hr old
r Crusted, erythematous papule plus tender regional Wounds in immunocompromised patients
shearing force as dog bites: Puncture wounds r Immobilization (if indicated)
deep tissue penetration lymphadenopathy catscratch disease (2 wk after
primary lesion)
ETIOLOGY ALERT
r Pasteurella species is most often associated with DIAGNOSTIC TESTS & INTERPRETATION If the wound is infected and fluctuant, open/incise
animal bites (cats > dogs): Lab and drain.
r Gram stain/culture (aerobic plus anaerobic):
Pasteurella canis with dog bites
Pasteurella multocida/septica with cat bites If soil/vegetative debris contamination, add
r Common aerobic isolates: mycobacteria plus fungal cultures
Streptococcus Obtain viral cultures for monkey bites.
r ESR, C-reactive protein if suspected septic
Staphylococcus
Moraxella arthritis/osteomyelitis
Corynebacterium
106
BITE, ANIMAL
MEDICATION DISPOSITION r Secondary infections:

Admission Criteria Tularemia (cats)
ALERT r Critical care admission criteria: Herpes B (monkey)
r Prophylactic antibiotics should be given in the
following high-risk clinical situations:
Moderate to severe hand infections Rat-bite fever (rats)
Leptospirosis (dogs/rodents)
B
Severe trauma (eg, penetrating wounds to
Deep bite wounds Rabies (dogs/bats/raccoon)
head/neck)
Puncture wounds Septic r Less commonly: Endocarditis, brain abscess,
Facial bites r Consider inpatient admission for the following: meningitis, sepsis (with disseminated intravascular
Hand/Foot bites Functional/Cosmetic morbidity coagulation), encephalomyelitis (B virus)
Involvement of tendon/bone/muscle/joint Secondary infection requiring IV antibiotics
Crush injuries (eg, cellulitis/septic arthritis)
Immunocompromised patients, prosthesis, Tendon/Bone/Joint/Nerve involvement ADDITIONAL READING
and/or high risk of endocarditis Immunocompromised patients, especially r Brook I. Management of human and animal bite
r Treatment guidelines: corticosteroid use, leukemia, lupus, asplenia wound infection: An overview. Curr Infect Dis Rep.
Prophylaxis 35 days Discharge Criteria 2009;11(5):389395.
Infected 714 days Patients not meeting the above admission criteria can r Kannikeswaran N, Kamat D. Mammalian bites. Clin
Tendon/Bone/Joint involvement 36 wk be discharged home with appropriate follow-up. Pediatr (Phila). 2009;48(2):145148.
(depending on location) Issues for Referral r Morgan M. Hospital management of animal and
r For cat bites, administer the 1st dose of antibiotics
All patients require follow-up with their pediatrician human bites. J Hosp Infect. 2005;61(1):110.
parenterally to increase tissue levels; consider for within 2448 hr to assess for wound r Nakamura Y, Daya M. Use of appropriate
other bites as well. infection/dehiscence and failure to respond to initial antimicrobials in wound management. Emerg Med
r Patients presenting 72 hr after injury with no antibiotic regimen: Clin North Am. 2007;25:159176.
clinical signs of infection, those sustaining only a r Facial injuries must be assessed daily for a min of r Singer AJ, Dagum AB. Current management of acute
cat scratch, or uncomplicated dog bite to 5 days. cutaneous wounds. N Engl J Med. 2008;359(10):
head/neck do not require antibiotics. r Consider plastic/general surgery consultation for 10371046.
cosmetic wounds or those requiring extensive r Talan DA, Citron DM, Abrahamian FM, et al.
First Line debridement. Bacteriologic analysis of infected dog and cat bites.
For prophylaxis and infected wounds: r Orthopedic/Hand consultation should be obtained in Emergency Medicine Animal Bite Infection Study
Ampicillin/Sulbactam 50 mg/kg IV, max single dose all cases involving joints/bony structures/tendons. Group. N Engl J Med. 1999;340(2):8592.
3 g, then:
r >40 kg: Amoxicillin/Clavulanic acid 875/125 mg PO See Also (Topic, Algorithm, Electronic
q12h (3050 mg/kg/day) r Bite, Human
r 3 mo and 40 kg: Amoxicillin/Clavulanic acid
FOLLOW-UP RECOMMENDATIONS r Cellulitis
45 mg/kg/d PO divided q12h or 40 mg/kg/d PO Patients should seek further medical care for new or
divided q8h worsening symptoms (eg, secondary infection, no
Second Line improvement within 72 hr of antimicrobial treatment, CODES
r For prophylaxis: Clindamycin 510 mg/kg IV, max fever)
single dose 600 mg, then: ICD9
PROGNOSIS
Clindamycin 1030 mg/kg/d PO divided q68h, r 12% require hospitalization r 879.8 Open wound(s) (multiple) of unspecified
max single dose 300 mg plus trimethoprim/ r 1020 deaths annually with 2 mammalian bites: site(s), without mention of complication
sulfamethoxazole 810 mg/kg of trimethoprim r 879.9 Open wound(s) (multiple) of unspecified
per day PO divided q12h The major cause of death in children <10 yr from
r For infected wounds requiring admission: dog bites is exsanguination following carotid site(s), complicated
trauma. r 924.9 Contusion of unspecified site
Piperacillin/Tazobactam:
Pasteurella septicemia has >30% mortality.
>6 m: 300400 mg/kg/day IV divided q68h
C. canimorsus has >40% mortality.
<6 m: 150300 mg/kg/d IV divided q68h r Infection rate 513%: PEARLS AND PITFALLS
>40 mg: 3.3754.5 g IV q6h
r Tetanus administration (if indicated): Dog bites: 210% r Bites can have serious complications despite a
Cat bites: 50%
Contaminated/Minor wound plus 3 previous doses relatively benign appearance.
Hand wounds: 30% r Obtaining cultures is critical in all patients with
(last dose >5 yr) booster
Unknown tetanus status/contaminated/major COMPLICATIONS infected wounds since no single antibiotic will cover
wound tetanus toxoid plus immunoglobulin r Abscess
all infecting pathogens.
(250500 U IM) r Septic arthritis r If an infection develops within 12 hr of a bite, there
r Rabies prevention (if indicated): r Tenosynovitis is a high likelihood of P. multocida.
Postexposure prophylaxis: 20 IU/kg human rabies r Osteomyelitis r Corneal abrasions should be ruled out on
immunoglobulin (1/2 at bite site plus 1/2 IM) plus r Lymphangitis bites/scratches to the periorbital region.
diploid vaccine (1 mL IM days 0, 3, 7, 14, 28) r Cellulitis r Consider photography of wounds for forensic
New evidence has resulted in multiple public purposes.
health authorities to recommend a 4-dose rabies
prophylaxis regimen at days 0, 3, 7, 14 only,
without a 5th dose.
r Antiviral therapy for moderate- to high-risk monkey
bite wounds
107
BITE, HUMAN
Michael L. Epter

DESCRIPTION HISTORY PRE HOSPITAL
r Human bites are the 3rd most common mammalian r History of bite: r Local wound care:
bite. Time bite occurred Dressing
r Polymicrobial wounds: r Tetanus status
Splint application (if necessary)
Average of 5 different microorganisms (60% r Pertinent medical history and allergies r Assess ABCs and provide hemostasis.
anaerobic) r Source of patient medical history (if possible):
Bacteria that cause infection are much more likely HIV/Hepatitis INITIAL STABILIZATION/THERAPY
r Assess ABCs and provide hemostasis.
to be normal oral flora than skin flora.
r May be more likely to be infected than other PHYSICAL EXAM r Wash the wound to reduce inoculum cell count:
Wound assessment: Evaluate and document the Soap and water
mammalian bites following:
r Younger children sustain bites to face, upper Quaternary ammonium compound (benzalkonium
r Type of injury (eg, laceration, crush, avulsion) chloride) plus water
extremities, and trunk: r Signs of infection r Irrigate:
13% secondary to child abuse
r Clenched fist injury (fight bite) and/or occlusional (swelling/erythema/pain/discharge) 18-gauge catheter plus normal saline (>150 mL
r Degree of penetration per cm of laceration) under high pressure (>7 PSI)
bites seen in older children: r Involvement of vasculature/nerves r Debride devitalized tissue.
75% involve the hand (especially 4th
r Involvement of joints/tendons r Primary closure (including tendon/nerve repair)
metacarpalphalangeal joint of dominant hand)
Clenched fist bites have the highest incidence of r Range of motion (pain with active/passive range should be delayed in all human bites unless there is
infection. tendinitis, compartment infection an overriding need for cosmetic purposes, such as a
Potential penetration of tendon sheaths/mid r Lymphadenopathy gaping facial wound.
palmar space r Immobilization (if indicated)
ALERT r Avoid irrigation with betadine/alcohol/peroxide
EPIDEMIOLOGY All suspected clenched fist injuries should undergo (impair healing/damage wound surface).
Incidence local exploration with the hand in the clenched fist r If the wound is infected/fluctuant, open/incise and
23% of all bites position to avoid missing an injury to the tendon, drain.
PATHOPHYSIOLOGY joint capsule, and/or metacarpal head.
r Clenched fist injury: MEDICATION
DIAGNOSTIC TESTS & INTERPRETATION r Antibiotics should be administered in all cases of
Inoculation of joint capsules/dorsal tendons
Lab human bite wounds except patients presenting
through skin over the knuckles with r Lab testing is not needed for most patients. 72 hr after injury with no clinical signs of infection
spread/seeding to avascular fascia
r If signs of infection are present: or bites not penetrating the dermis.
Could also result in cellulitis, osteomyelitis, r Treatment guidelines:
tenosynovitis Gram stain/culture (aerobic plus anaerobic)
r Occlusional bite: If there is soil/vegetative debris contamination, Prophylaxis 35 days
add mycobacteria plus fungal cultures. Infected 714 days
Crush injury to soft tissue lacerations, avulsion,
ESR and/or C-reactive protein if suspected septic Tendon/Bone/Joint involvement 36 wk
amputation
arthritis/osteomyelitis (depending on location)
ETIOLOGY r Consider giving the 1st dose of antibiotics
r Eikenella corrodens (25% of human bites) Imaging
parenterally to increase tissue levels.
r Aerobes: Consider x-ray(s) of affected area (eg, hand/scalp):
r Retained tooth fragment(s) First Line
Streptococcus (pyogenes, viridans)
r Fracture For prophylaxis and infected wounds:
Staphylococcus aureus Ampicillin/Sulbactam 50 mg/kg IV, max single dose
r Anaerobes:
DIFFERENTIAL DIAGNOSIS 3 g, then:
Porphyromonas r Animal bite r >40 kg: Amoxicillin/Clavulanic acid 875/125 mg PO
Bacteroides r Cellulitis
q12h (3050 mg/kg/day)
Prevotella r Septic arthritis r 3 mo and 40 kg: Amoxicillin/Clavulanic acid
r Occlusional bites (higher predominance): r Osteomyelitis 45 mg/kg/day PO divided q12h or 40 mg/kg/day PO
Fusobacterium r Nonbite laceration divided q8h
Peptostreptococcus
Candida
108
BITE, HUMAN
Second Line r Morgan M. Hospital management of animal and

r For prophylaxis: Clindamycin 510 mg/kg IV, max FOLLOW-UP human bites. J Hosp Infect. 2005;61(1):110.
single dose 600 mg, then: r Nakamura Y, Daya M. Use of appropriate
Clindamycin 1030 mg/kg/day PO divided q68h,
max single dose 300 mg, plus trimethoprim/
Patients should seek further immediate care for new or
antimicrobials in wound management. Emerg Med
Clin North Am. 2007;25:159176.
B
sulfamethoxazole 810 mg/kg of trimethoprim worsening symptoms (eg, secondary infection, no r Singer AJ, Dagum AB. Current management of acute
per day PO divided q12h improvement within 72 hr of antimicrobial treatment, cutaneous wounds. N Engl J Med. 2008;359(10):
r For infected wounds: Cefoxitin 80160 mg/kg/day fever). 10371046.
IV, max 2 g divided q48h Patient Monitoring
DISPOSITION All patients are at risk of transmission for hepatitis/HIV
from human bites and should receive baseline
Media Element)
Admission Criteria r Bite, Animal
r Moderate to severe hand infections screening from their pediatrician with interval testing r Cellulitis
r Functional/cosmetic morbidity based upon initial results.
r Tetanus
r Secondary infection requiring IV antibiotics PROGNOSIS
r Overall rate of infection rate up to 18% (hand
(eg, cellulitis/septic arthritis)
r Tendon/Bone/Joint/Nerve involvement wounds 30%): CODES
r Sepsis Dependent on structures involved/depth of
r Immunocompromised patients, especially penetration
r Risk of transmission of HIV is 0.015%. ICD9
r 879.8 Open wound(s) (multiple) of unspecified
corticosteroid use, leukemia, lupus, asplenia
COMPLICATIONS site(s), without mention of complication
Discharge Criteria r Abscess r 879.9 Open wound(s) (multiple) of unspecified
Patients not meeting the above admission criteria can r Septic arthritis
be discharged home with appropriate follow-up. site(s), complicated
r Tenosynovitis r 924.9 Contusion of unspecified site
Issues for Referral r Osteomyelitis
r All patients require follow-up with their primary care
provider within 2448 hr to assess for wound r Lymphangitis
infection and failure to respond to initial antibiotic r Cellulitis PEARLS AND PITFALLS
regimen. r Less common: Endocarditis, brain abscess, r Human bites can have serious complications despite
r Significant clenched fist injuries should be referred meningitis, sepsis (with disseminated intravascular a relatively benign appearance.
to and evaluated by a hand surgeon. coagulation) r Always consider the risk of transmittable diseases
COMPLEMENTARY & ALTERNATIVE (hepatitis B virus/hepatitis C virus, herpes simplex,
THERAPIES HIV, syphilis).
r Tetanus administration (if indicated): ADDITIONAL READING r Obtaining cultures is critical in all patients with
Clean/Minor wound plus 3 previous doses (last r Brook I. Management of human and animal bite infected wounds since no single antibiotic will cover
dose >10 yr) booster wound infection: An overview. Curr Infect Dis Rep. all infecting pathogens.
Contaminated/Minor wound plus 3 previous doses 2009;11(5):389395. r Child abuse should be considered in bite marks with
(last dose >5 yr) booster r Kannikeswaran N, Kamat D. Mammalian bites. Clin an intercanine distance >3 cm.
Unknown tetanus status/contaminated/major Pediatr (Phila). 2009;48(2):145148. r Consider photographing wounds for forensic
wound tetanus toxoid plus immunoglobulin purposes.
(250500 U IM)
r Postexposure prophylaxis for HIV is not
recommended in human bites.
r In a patient with a negative anti-hepatitis B surface
antibody, administer hepatitis B immunoglobulin
plus hepatitis B vaccine if source patient positive
hepatitis B surface antigen or unknown status.
109
BLEPHARITIS
Ruby F. Rivera
r Isotretinoin use can cause blepharitis and corneal DIAGNOSTIC TESTS & INTERPRETATION
BASICS irritation. Lab
r Lab testing is not always indicated.
DESCRIPTION COMMONLY ASSOCIATED CONDITIONS r Culture of the eyelid margins should be obtained in
r Blepharitis is an inflammation of the eyelid often r Seborrheic dermatitis
r Atopic dermatitis patients with recurrent anterior blepharitis and
associated with conjunctivitis and keratitis.
r Blepharitis is usually chronic, intermittent, and r Meibomian gland dysfunction usually associated those not responding to therapy.
bilateral. with rosacea and seborrhea Diagnostic Procedures/Other
r Blepharitis is classified by anatomic location (1): Microscopic exam of epilated eyelash to reveal
Demodex mite
Anterior blepharitis: DIAGNOSIS
Affects the base of the eyelashes and eyelash DIFFERENTIAL DIAGNOSIS
follicles HISTORY r Conjunctivitis
Usually caused by Staphylococcus species and r Burning, itching, eye discharge, contact lens r Discoid lupus erythematosus
seborrhea discomfort, photophobia, loss of eyelashes r Lacrimal duct obstruction
Posterior blepharitis: r Eyelashes sticking together in the morning usually
Affects the meibomian glands and gland orifices common in staphylococcal blepharitis
Usually caused by meibomian gland dysfunction r Recent exposure to an infected person TREATMENT
EPIDEMIOLOGY (eg, pediculosis palpebrarum) r Eyelid hygiene is the mainstay of treatment.
r Epidemiologic data on the incidence and prevalence r Current and previous use of systemic or topical
medications (eg, isotretinoin) Warm compress 12 times daily followed by eyelid
of blepharitis is lacking. massage
r Common but underdiagnosed in children (2,3) PHYSICAL EXAM r Cleaning the eyelid margin with a cotton ball soaked
r Staphylococcal blepharitis is characterized by:
PATHOPHYSIOLOGY in diluted baby shampoo
The pathophysiology of blepharitis is complex and Scaling, crusting, and erythema of the eyelid
margin MEDICATION
results from interaction of various factors including lid
margin secretion, lid margin organisms, and a Loss of eyelashes and corneal involvement may First Line
occur. Bacitracin or erythromycin ophthalmic ointment:
dysfunctional tear film (4). r Seborrheic blepharitis is characterized by: r Apply 1/ 1/ -inch ribbon 12 times daily for 1 wk
4 2
ETIOLOGY Greasy scaling of the eyelid margin r Duration should be guided by severity of symptoms
r Bacterial:
There is often seborrhea of the scalp and and response to therapy.
Staphylococcus aureus eyebrows.
Staphylococcus epidermidis r Meibomian gland dysfunction is characterized by: Second Line
r Selenium sulfide/tar shampoo, as seborrheic
Propionibacterium acnes Frothy discharge
r Parasitic: blepharitis is often associated with seborrheic
Prominent blood vessels dermatitis of the scalp and eyebrows
Demodex folliculorum Thickening of the eyelid margin r Topical corticosteroids may be helpful in those with
Pediculosis palpebrarum caused by Pediculosis Expression of meibomian secretions
humanus corporis or capitis severe inflammation:
Demodex infestation of the facial skin has been Hydrocortisone ophthalmic cream (1%) applied
implicated in rosacea and blepharitis (4). b.i.d. to affected area
110
BLEPHARITIS
r Patients unresponsive to eyelid hygiene and topical 3. Hammersmith KH, Cohen EJ, Blake TD, et al.
antibiotics can be given oral antibiotics: FOLLOW-UP Blepharoconjunctivitis in children. Arch
Tetracycline: >8 yr of age, 2550 mg/kg/day Ophthalmol. 2005;123:16671670.
divided q6h; adult dose, 12 g PO divided
b.i.d.q.i.d.
4. Jackson WB. Blepharitis: Current strategies for B
diagnosis and management. Can J Ophthalmol.
Doxycycline: >8 yr of age, 24 mg/kg/day divided r Warm compresses applied 12 times daily followed 2008;43:170179.
b.i.d.; adult dose 100 mg PO b.i.d. by eyelid massage
Erythromycin ethylsuccinate: 3050 mg/kg/day r Cleaning the eyelid margin with a cotton ball soaked See Also (Topic, Algorithm, Electronic
divided q8h Media Element)
in diluted baby shampoo r Chalazion
Azithromycin: 10 mg/kg PO on day 1, then r Bacitracin or erythromycin ophthalmic ointment:
r Conjunctivitis
5 mg/kg PO days 25; adult dose, 500 mg PO day 1/ 1/ -inch ribbon 12 times daily for 2 wk.
1, then 250 mg PO days 25
4 2 r Eye, Red
Duration of therapy should be guided by severity of r Hordeolum
DISPOSITION symptoms and response to therapy.
r Artificial tears applied twice daily for dry eyes
Admission Criteria
Admission is generally not required. Rarely, in cases of Patient Monitoring CODES
visual loss, intractable pain, corneal loss, or unclear Close follow-up and monitoring with the patients
diagnosis, admission may be indicated. primary care physician to ensure resolution ICD9
Discharge Criteria PROGNOSIS r 373.00 Blepharitis, unspecified
Patients with blepharitis should almost universally be r Blepharitis is usually a chronic, intermittent r 373.01 Ulcerative blepharitis
discharged. condition. r 373.02 Squamous blepharitis
Issues for Referral r Patients should be advised that symptoms may
r Patients with blepharitis with the following
improve with treatment but that there will be
symptoms should be emergently referred to an recurrences. PEARLS AND PITFALLS
ophthalmologist: r Patients should continue eyelid hygiene even after
Visual loss r Blepharitis is usually a chronic condition caused by
symptoms improve.
Moderate to severe pain inflammation due to bacterial infection, parasitic
r Patients with blepharitis with the following COMPLICATIONS infection, seborrheic dermatitis, or chemical
r Hordeolum
symptoms may be referred to an ophthalmologist for irritation.
r Chalazion r Blepharitis may result from pediculosis pubis.
follow-up within 12 days:
Chronic or severe redness r Dry eyes secondary to aqueous tear deficiency Pediculosis pubis is an STI; if present in a young
Unresponsiveness to therapy patient, the possibility of sexual abuse must be
Corneal involvement considered.
REFERENCES
1. American Academy of Ophthalmology, Ophthalmic
News and Education Network. Blepharitis:
Preferred Practice Pattern Guideline, 2003.
2. Viswalingam M, Rauz S, Morlet N, et al.
Blepharoconjunctivitis in children: Diagnosis and
treatment. Br J Ophthalmol. 2005;89:400403.
111
BLINDNESS
Desiree M. Seeyave
r Ectopic lens: Lens dislocation visible on inspection or

BASICS DIAGNOSIS with slit lamp
r Vitreous hemorrhage: Dome-shaped hemorrhage in
DESCRIPTION HISTORY front of retina, decreased red reflex
r Blindness is defined as the loss of vision. r Problems with visual media due to history of blunt
r Endophthalmitis: Red eye, hypopyon
r Blindness can be bilateral, unilateral, transient, or trauma to eye, chemical burns, keratitis, iritis, r Retinoblastoma: Leukocoria when attempting to see
permanent. glaucoma, lens abnormalities, and endophthalmitis:
red reflex; dilated eye exam visualizes chalky,
r Vision loss can occur for many reasons and can Decreased vision
Pain white-gray retinal mass
involve many systems. r Retinal detachment: Dull red reflex, retina appears
Blepharospasm
EPIDEMIOLOGY Conjunctival injection elevated with folds, relative afferent papillary defect
Incidence Photophobia if severe
r The true incidence is unknown. The World Health r Central retinal artery occlusion:
Excessive tearing
Organization estimates 1.494 million children r Problems with the retina due to retinoblastoma, Early (minutes to hours): Vascular narrowing; 20%
015 yr of age are born blind or become severely central retinal artery occlusion, and central retinal patients may have visible embolus.
visually impaired (1): vein occlusion: Late (hours): White retina except cherry-red fovea;
Mostly due to vitamin A deficiency, severe Vision loss afferent pupillary defect
r Central retinal vein thrombosis: Dilated and tortuous
protein-energy malnutrition, measles, or use of Complaints of floaters and flashes of light
traditional eye medicines (photopsias), with partial or complete painless retinal veins, disc swelling, diffuse nerve fiber layer
r Pediatric blindness accounts for 5% of all blindness. loss of vision in the affected eye and preretinal hemorrhage, cotton wool spots on
r U.S. prevalence: 0.3 per 1,000 children (1) Sudden, painless monocular vision loss retina
r Problems with the neurovisual pathway due to r Orbital cellulitis: Proptosis, ophthalmoplegia,
RISK FACTORS orbital cellulitis, orbital compartment syndrome, diplopia, vision loss if orbital apex and optic nerve
r Males are more likely to suffer from direct trauma to
orbital neoplasms, idiopathic intracranial HTN, involved (orbital apex syndrome)
the eye. optic neuritis, optic pathway tumors, optic nerve r Orbital compartment syndrome: Proptosis,
r Contact lens use predisposes to keratitis (corneal
avulsion: ecchymosis of eyelids, chemosis, ophthalmoplegia,
inflammation) caused by Staphylococcus aureus, Can have rapid or gradual loss of vision papilledema, increased intraocular pressure
Pseudomonas aeruginosa, herpes simplex virus r Neuroblastoma: Proptosis and periorbital
(HSV), and adenovirus. PHYSICAL EXAM
r Acute sinusitis, ophthalmic surgery, and trauma r Trauma: ecchymosis occur with metastasis.
r Optic neuritis: Photopsias, papillitis on funduscopy
predispose to orbital cellulitis. Foreign bodies may be visible on sclera and should
r Optic pathways tumors: Visual field defects
r Sickle cell disease predisposes to stroke, central be removed carefully.
retinal artery occlusion, and glaucoma. Fluorescein staining of the eye for corneal abrasion DIAGNOSTIC TESTS & INTERPRETATION
r Prothrombotic disorders predispose to cavernous Hyphema: Crescenteric line of blood seen by
Lab
shining a tangential light into the anterior
sinus thrombosis and central retinal vein occlusion. Initial Lab Tests
chamber; slit lamp to see microhyphema r CBC, C-reactive protein, blood culture, inflammatory
GENERAL PREVENTION Globe rupture: May be occult or obvious on
markers if infectious or rheumatologic cause
r Eye protection during sports inspection, with obvious corneal/sclera laceration,
r Appropriate safety equipment suspected
volume loss of eye, iris abnormalities, foreign body r Lyme titers, toxicology screen, lumbar puncture, if
r Proper sterile techniques when wearing contact lens protruding or visible on funduscopy, decreased
visual acuity indicated
ETIOLOGY r Culture of lesions if keratoconjunctivitis suspected
Orbital fracture: Impaired extraocular movements
r Infection, such as keratitis and orbital cellulitis r Lumbar puncture for meningitis, opening pressure
if orbital muscles entrapped; tenderness on
r Vitamin A deficiency palpation of orbital bones measurement for idiopathic intracranial HTN
r Severe protein-energy malnutrition r Chemical burn: Corneal scarring, ulceration, and (<200 mm H2 O normal, >250 mm H2 O high,
r Traumatic injury vision loss (2) 200250 mm H2 O equivocal) measured with patient
r Use of traditional eye medicines r Ischemia to scleral vessels may cause the eye to in lateral decubitus position with legs extended
r Retinopathy of prematurity appear white (alkali burn) (3) Imaging
r Optic nerve hypoplasia r Keratitis: Corneal opacity (round white spot), red r US for orbital cellulitis, retinoblastoma, optic nerve
r Structural problems along the visual pathway, eye; HSV causes dendritic pattern on fluorescein diameter as indirect measure of intracranial pressure
including: stain in idiopathic intracranial HTN
r Iritis: Slit lamp needed to see inflammatory cells in r CT: High-resolution, thin-slice, orbital CT with
Visual media: Cornea, lens, anterior chamber,
aqueous or vitreous humor the anterior chamber coronal images for orbital trauma or intraocular
Retina: Vascular occlusion, retinal detachment, r Glaucoma: Painful red eye, cloudy cornea, enlarged foreign bodies (noncontrast), orbital cellulitis (with
tumors eye (buphthalmos) in children <3 yr of age, vision contrast)
Neurovisual pathway: Optic nerve, visual loss, increased intraocular pressure r MRI: For evaluation of optic nerve tumors, optic
pathways, occipital lobes neuritis, white matter lesions with MS, soft tissue
abnormalities. Do not perform if metallic intraocular
foreign body is suspected.
112
BLINDNESS
Diagnostic Procedures/Other MEDICATION Issues for Referral

r Slit lamp exam for visualization of the cornea and r Refer to ophthalmologist for:
First Line
anterior chamber (eg, for keratitis, iritis, hyphema, r Corneal abrasion: Topical antibiotics (trimethoprim Keratitis, iritis, glaucoma: Confirmation of
lens dislocation)
r Tonometry for glaucoma, orbital compartment
polymyxin B, 12 drops in affected eye q46hr for diagnosis, visual monitoring, and treatment
Hyphema: Size correlates with visual outcome;
B
23 days)
syndrome r Keratitis: Prompt initiation of topical antibiotics if rebleeding or acute glaucoma predisposes to
r Sinus radiographs bacterial and topical +/ oral antiviral if HSV, in permanent visual loss, especially in patients with
r Electroencephalogram to diagnose seizures as the consultation with ophthalmology sickle cell or bleeding disorders.
cause of blindness r Traumatic iritis: Cycloplegics and topical steroid Ectopic lens to be replaced/monitored
r Optokinetic drum for nystagmus r Refer to an oncologist/neurosurgeon for
drops in consultation with ophthalmology
r Globe rupture: Empiric broad-spectrum antibiotics: management of tumors.
r Conversion disorder: Vision loss may be monocular Vancomycin 15 mg/kg IV, max dose 1 g
Ceftazidime 50 mg/kg (max dose 2 g); if penicillin FOLLOW-UP
or binocular, total or partial.
r Typically seen in female teens who are not allergic, ciprofloxacin 10 mg/kg (max dose
400 mg) FOLLOW-UP RECOMMENDATIONS
concerned about their lack of vision (La Belle r Endophthalmitis: Vancomycin or ceftazidime, +/ r Discharge instructions and medications:
indifference)
r Nystagmus with an optokinetic drum demonstrates antifungals (eg, oral fluconazole, IV amphotericin B); Follow up with an ophthalmologist within
emergent consultation for intravitreal antibiotics or 2448 hr to ensure healing and preservation of
an intact visual pathway. vitrectomy vision.
r Toxins, the metabolite of methanol, formate, causes r Orbital cellulitis: Broad-spectrum antibiotics to cover r Activity:
optic nerve and retinal epithelial cell destruction, Haemophilus influenzae and Streptococcus Bed rest for microhyphema to prevent rebleeding
can occur 72 hr after ingestion. Any toxin that pneumoniae, which are common causes of sinusitis
decreases occipital blood flow can cause cortical PROGNOSIS
in childrenampicillin/sulbactam 50 mg/kg/dose
blindness (eg, CO, nifedipine, amphetamines, etc.). Permanent blindness is a complication of all major
r Migraine: Causes transient vision loss q6h
r Idiopathic intracranial HTN: Acetazolamide forms of eye trauma, infections, and tumors.
r Head trauma: Minor head injury may be associated
25 mg/kg/day, max dose 2 g/day
with transient visual loss due to occipital concussion
Second Line REFERENCES
or vascular hyperreactivity.
r Seizures: Blindness and visual hallucinations are Update tetanus status for eye injuries. 1. Steinkuller PG, Lee D, Clare G, et al. Childhood
seen in benign occipital epilepsy of childhood. COMPLEMENTARY & ALTERNATIVE blindness. J AAPOS. 1999;3(1):2632.
THERAPIES 2. Berry M, Jeffreys D. Ocular injuries from household
r Chemical burns: Topical collagenase inhibitor to chemicals: Early signs as predictiors of recovery. In
TREATMENT reduce inflammation (human data limited) Vitr Mol Toxicol. 2001;14(1):513.
r Idiopathic intracranial HTN: Weight loss, 3. Ambati BK, Ambati J, Azar N, et al. Periorbital and
PRE HOSPITAL orbital cellulitis before and after the advent of
r Trauma: Do not force the eye open if an open globe topiramate 3
Haemophilus influenza type B vaccination.
is suspected. Leave foreign bodies in place. Use a SURGERY/OTHER PROCEDURES Ophthalmology. 2000;107(8):14501453.
hard shield that does not place pressure on the eye. r Orbital cellulitis and abscesses require emergent
Elevate head of bed 30 degrees. Give antiemetics surgical drainage to prevent intracranial spread via a
and pain medication. valveless venous system leading to intracranial
r Chemical burns: Immediate irrigation with sterile abscesses, meningitis, or cavernous sinus thrombosis
CODES
normal saline or water r Globe rupture repair
r Endophthalmitis: Intravitreal antibiotics or ICD9
INITIAL STABILIZATION/THERAPY r 369.00 Blindness of both eyes, impairment level not
r Chemical burns: Topical analgesia such as 0.5% vitrectomy
further specified
tetracaine, IV morphine (0.1 mg/kg/dose), irrigation DISPOSITION r 369.60 Blindness, one eye, not otherwise specified
for at least 30 min using a polymethylmethacrylate Admission Criteria r 369.61 One eye: total vision impairment; other eye:
scleral lens (eg, Morgan lens): r In general, all patients with acute vision loss should not specified
Irrigate until fornix pH is 6.57.5. When pH is be admitted to the hospital.
normal, recheck at 5 and 30 min after irrigation. r Critical care admission criteria:
May need passive restraints and eyelid retraction. PEARLS AND PITFALLS
r Central retinal artery occlusion: Emergent Admission for management of serious, associated
conditions (eg, hemorrhagic shock, stroke, r Loss of vision should be managed as an emergency.
ophthalmology consult is needed to restore meningitis, and cavernous sinus thrombosis)
circulationocular massage, anterior chamber r There are many causes of acquired blindness in
paracentesis, local arterial thrombolytics, hyperbaric Discharge Criteria children.
r Patients with restored vision after chemical burn and
O2 , and surgical revascularization are all treatments r The visual structure involved can be determined
that may be required emergently. normal eye pH 30 min after irrigation
r Patients with corneal abrasions and microhyphema from the history and physical.
r Emergent lateral canthotomy for orbital r Ophthalmology referral is essential to monitor vision.
compartment syndrome to restore blood flow and may be discharged with close follow-up.
prevent permanent blindness.
113
BODY PACKERS (INGESTED DRUG PACKAGES)

John Kashani
ETIOLOGY A positive test cannot differentiate between

BASICS r Cocaine remote exposure to the drug and current exposure
r Heroin from a ruptured package.
DESCRIPTION r Methamphetamine Ingested packets by both body stuffers and body
r A body packer is an individual who smuggles a large r Other drugs may also be ingested by body stuffers packers often contain enough residue to result in
amount of drugs in well-sealed packets. r Other drugs are rarely ingested by body packers a positive drug screening.
r Known as mules, they either swallow or insert the r Basic chemistry profile to assess for dehydration and
drugs into body cavities. Usually, the drugs are COMMONLY ASSOCIATED CONDITIONS hyperkalemia
smuggled across international borders. Substance abuse/use may be associated with body r Creatine phosphokinase and/or urinalysis to
r Body packers typically carry cocaine or heroin: stuffers, who are often drug abusers, as opposed to evaluate for rhabdomyolysis
Rare cases of body packing other drugs, such as body packers, who typically transport the drugs for r Troponin should be ordered in any patient with chest
methamphetamine, Ecstasy (MDMA), and profit but are not drug abusers. pain or findings consistent with myocardial ischemia.
marijuana have been reported.
r A body stuffer is an individual who hurriedly ingests Imaging
DIAGNOSIS r An abdominal radiograph may show oblong packets
drugs or inserts drugs into a body cavity in an
outlined in bowel gas, or the packets themselves
attempt to conceal them from the authorities. HISTORY
r These may involve any type of illicit drug: r Usually, the patient is brought by law enforcement may be made of a radiopaque material.
r Body packers:
The drugs are usually poorly packaged and are authorities after being apprehended.
r Body packers are typically apprehended at Typically, imaging plays a key role in management.
intended for sale or individual use. The risk of drug
Sensitivity of abdominal radiography is up to 90%
leakage from these drug packages is high. international airports and borders, while body in body packers.
Additionally, body stuffing carries the risk of stuffers are typically apprehended by local law CT may be more sensitive than plain radiography
aspiration of drug packets. enforcement officers who witnessed the patient in detecting drug packets, though sensitivity is not
EPIDEMIOLOGY swallow drugs in order to conceal them. 100%.
r Less commonly, the patient may present after
Incidence CT is the most appropriate for suspected body
r The incidence of body packers and stuffers is not developing symptoms or failing to pass the drug packing. Body stuffers do not usually require
known. packages rectally. imaging by CT, though it is not always able to
r Body packing in children is likely rare, though it has PHYSICAL EXAM detect drug packets.
been reported. r If the drugs involved are leaking and being US appears to be very sensitive in detecting drug
systemically absorbed, it is likely that the physical packages in body packers:
PATHOPHYSIOLOGY
exam will make the class of drug involved readily In 1 study, 40 of 42 body packers who were
r Illness occurs when drug packages leak their
apparent. airport detainees had ingested drug packs
contents or cause intestinal obstruction. r Opioids will typically cause an opioid toxidrome of detected by US. 7 of 8 suspects without any
r Body stuffing involves a small quantity of packs, and ingested drugs were correctly identified as not
miotic pupils, CNS depression or coma, and
this never results in intestinal obstruction. containing drug packages (1).
r Rarely, attempts to quickly swallow packs may result respiratory depression.
r Cocaine or methamphetamine will typically cause a Detecting drug packets in body packers by
in aspiration or airway obstruction. radiography is unreliable and cannot be used to
r Body packing is performed with ingestion of large sympathomimetic toxidrome consisting of agitation,
absolutely confirm or exclude the diagnosis.
diaphoresis, mydriasis, HTN, and tachycardia. r Body stuffers: Radiographs may be used in
quantities of packs prepared with the intent that r If a person is believed to be a body stuffer or packer,
they may transit the gut: management. They may be specific, showing such
the physical exam should include a vaginal and
Packs may leak their contents. If so, they contain x-ray findings as nonsurgical staples, but they are
rectal exam.
much larger quantities of drugs and are more poorly sensitive.
likely to cause severe illness. DIAGNOSTIC TESTS & INTERPRETATION DIFFERENTIAL DIAGNOSIS
Packs may also result in intestinal obstruction. Lab r Sympathomimetic poisoning
r The drugs most commonly packed or stuffed are Initial Lab Tests r Cocaine or heroin abuse without ingesting drug
cocaine and heroin. To a lesser extent, r No lab testing is routinely necessary.
r Body packing involves one of the only times in packs
amphetamines and marijuana may be packed or
stuffed. Patients may present with signs and which urine drug of abuse screening may be useful
symptoms of cocaine, heroin, or amphetamine for clinical management: TREATMENT
toxicity. On rare occasions, drug of abuse screening may
r Additionally, a packer or stuffer may present with GI assist in managing scenarios involving rupture of PRE HOSPITAL
disturbances secondary to the mechanical effects of packages in a body packer. r Assess and stabilize airway, breathing, and
the drug packets. Abdominal obstruction may occur. A drug screening assay in this circumstance is not circulation.
sensitive or specific to identify the drugs ingested. r If signs of opioid toxicity are present, administer
naloxone as per local protocol.
r If there are signs of psychomotor agitation or
seizures that may be the result of cocaine,
administer diazepam as per local protocol.
circulation.
r Use continuous cardiac monitoring and pulse
oximetry.
r These patients should be reassessed often because
they may decompensate quickly.
114
BODY PACKERS (INGESTED DRUG PACKAGES)
r Supportive care is the mainstay of therapy: SURGERY/OTHER PROCEDURES ADDITIONAL READING

Toxicity from ingested drug, most commonly r Endoscopic removal of packets may be indicated in
r Cordero DR, Medina C, Helfgott A. Cocaine body
heroin or cocaine must be treated both body packers and stuffers.
r If cocaine body packing is suspected, surgical packing in pregnancy. Ann Emerg Med. 2007;49(4):
If opioids are ingested, administration of
naloxone, sometimes in large doses, is adequate consultation and surgical removal may be necessary 543544. B
to treat toxicity. r De Beer SA, Spiessens G, Mol W, et al. Surgery for
due to the high risk of mortality associated with
Intestinal obstruction may require surgery. package leakage. body packing in the Caribbean: A retrospective
Rupture of cocaine packages may result in severe study of 70 patients. World J Surg.
HTN and tachycardia as well as intestinal ischemia DISPOSITION 2008;32(2):281285; discussion 286287.
and necrosis: Admission Criteria r June R, Aks S, Keys N, et al. Medical outcome of
This usually requires intensive management of Critical care admission criteria: cocaine bodystuffers. J Emerg Med. 2000;18(2):
cardiovascular stimulation with diazepam and r All symptomatic body packers or body stuffers 221224.
medications to control BP such as phentolamine require critical care admission. r Krishnan A, Brown R. Plain abdominal radiography
This may require immediate surgical removal to r All body packers should be admitted to a critical in the diagnosis of the body packer. J Accid Emerg
preserve the ischemic gut as well as to prevent care unit. Med. 1999;16(5):381.
death. r Traub SJ, Hoffman RS, Nelson LS. Body packing: The
Discharge Criteria
ALERT r Body packers are never discharged from the internal concealment of illicit drugs. N Engl J Med.
r Obtain rectal temperature immediately in patients emergency department. 2003;349:25192526.
r Body stuffers who are stable after a period of r Traub SJ, Kohn GL, Hoffman RS, et al. Pediatric
with possible hyperthermia.
r Significant hyperthermia (39.040.0 C or observation can be considered for discharge. body packing. Arch Pediatr Adolesc Med. 2003;
r The period of observation will vary with the type of 157:174177.
102.2104.0 F) requires passive cooling or mild r Wetli CV, Mittlemann RE. The body packer
active cooling and medications: agent swallowed, reliability of the history, and
discharge destination (home vs. correctional syndrome: Toxicity following ingestion of illicit
Life-threatening hyperthermia (>41.542.0 C
institution): drugs packaged for transportation. J Forensic Sci.
[<106.7107.6 F]) should be treated by
410 hr depending on how many packs are 1981;26(3):492500.
immersion in an ice bath. Other cooling
measures are inadequate: believed to have been swallowed based on history See Also (Topic, Algorithm, Electronic
Wrapping the patient in sheets with ice or or visualized on the x-ray Media Element)
placing the patient in a body bag with ice are Issues for Referral Cocaine Poisoning
r There is debate about whether body packers who
reasonable approaches.
present independently should be reported to police:
MEDICATION For public health, patient, and staff safety, the CODES
authors strongly urge in doing so.
First Line r Refer all drug abusers for drug counseling.
r Diazepam: ICD9
r 965.01 Poisoning by heroin
First-line medication for any cocaine-intoxicated COMPLEMENTARY & ALTERNATIVE
r 969.72 Poisoning by amphetamines
patient THERAPIES
Administer for agitation, chest pain, or r 970.81 Poisoning by cocaine
Whole bowel irrigation for packers and stuffers:
HTN/tachycardia r Administer 1 L/hr of polyethylene glycol (Go Lytely)
Initial dose 0.2 mg/kg IV; dose may be repeated solution via an NG tube:
q5min The goal is to assist the patient in passing all PEARLS AND PITFALLS
After administering a given dosage 3 times, packs rectally. r The mainstay of therapy is supportive care,
increase the dose by doubling:
If 10 mg IV has been given 3 times without maintaining vital signs within acceptable limits, and
adequate effect, increase dose to 20 mg. If FOLLOW-UP treating cardiovascular stimulation or respiratory
20 mg IV has been given 3 times without effect, depression.
PROGNOSIS r GI decontamination to get patients to excrete packs
double dose to 40 mg IV.
Although these doses are higher than typical, r Prognosis varies with drug ingested, quantity, and more quickly is typical part of therapy.
tolerance of multiple doses without sedation leakage of packs. r Diazepam is typically the only medication needed to
provides reassurance to increase the dose. r Body stuffers tend to have less severe morbidity and treat cocaine toxicity.
r Naloxone: less mortality. r Naloxone is typically the only medication needed to
Treatment for opioid toxicity r Cocaine body packing is most dangerous. Ruptured treat heroin toxicity.
Very large doses or infusion may be necessary. packs may result in death even if the patient reaches r Obtain emergent surgical consultation in cocaine
Initial dose 0.4 mg/kg or empiric 2-mg dose medical care. body packers with overt toxicity.
Use a smaller dose (0.05 mg) for a body stuffer r Body packers should be treated until all packs have
COMPLICATIONS
who has swallowed heroin, as the person may be r End-organ damage from cocaine toxicity: Stroke, passed. They typically know the exact number of
tolerant and naloxone may cause opioid myocardial infarction, or cardiac dysrhythmia packs they are transporting, as this is the number
withdrawal that is difficult to manage. r Respiratory depression, apnea, and asphyxiation they are expected to excrete once across the border
In nontolerant patients, repeat the 2-mg dose in the country of drug delivery.
from heroin toxicity
3 times if there is a suspected opioid toxidrome.
If arousal recurs, redose using the cumulative dose
that initially worked or administer 2/3 (66%) of REFERENCE
that dose hourly as an infusion.
Second Line 1. Meijer R, Bots M. Detection of intestinal drug
See Cocaine topic for information about treatment of containers by ultrasound scanning: An airport
cocaine toxicity. screening tool? Eur J Radiol. 2003;13:13121315.
115
BOTULISM
Adhi Sharma
GENERAL PREVENTION r Infant botulism is characterized by constipation

BASICS r Food and dust seem to be possible spore sources in followed by neuromuscular paralysis or
infant botulism: floppiness:
DESCRIPTION Honey has been implicated in 20% of cases. A history of poor feeding, lethargy, and
r Clostridium botulinum is an anaerobic, Corn syrup has also been implicated. diminished crying is also common.
spore-forming, gram-positive bacillus. The spores are Infants should not be fed these foods, though the Breast-feeding mothers will specifically note that
ubiquitous and can be found in soil, water, and air. vehicle for transmission remains unclear. the child is taking less milk.
r Botulinum toxin is considered the most lethal Vacuum cleaner dust has also been implicated, as r In both types, a history of descending paralysis and
substance known, with an estimated oral LD50 of have nearby construction sites. bulbar palsies should increase the level of suspicion.
1 g/kg in humans. r Foodborne botulism has been associated with
r There are 3 main types of botulism: PHYSICAL EXAM
improperly canned foods, the majority are home r Patients with foodborne botulism may demonstrate
Foodborne botulism occurs when a person ingests canned:
weakness or paralysis of the upper extremities;
preformed toxin. Use of proper canning technique and refrigeration
dilated, nonreactive pupils; and ophthalmoplegia:
Infant botulism occurs in a small number of or boiling canned foods in a pressure cooker prior
May see drooling or difficulty phonating
susceptible infants who harbor C. botulinum in to consumption can reduce both the botulinum
Deep tendon reflexes may be preserved, and
their intestinal tract (intestinal toxemia). toxin load and the spore load.
ataxia is absent.
Wound botulism occurs when wounds are
PATHOPHYSIOLOGY Paralysis of the respiratory muscles can occur.
infected with C. botulinum that secretes toxin.
r 2 less common forms of botulism are also defined: Botulism is a neuroparalytic illness resulting from the Deep tendon reflexes and mental status are
action of the botulinum toxin: typically normal.
Iatrogenic botulism occurs from treatment with r The active form of the toxin is composed of heavy Autonomic instability, such as orthostatic
botulinum toxin for cosmetic or therapeutic hypotension, may also occur.
reasons. and light polypeptide chains connected by disulfide
bonds. r Infant botulism results in bulbar palsies and
Intestinal colonization by C. botulinum in patients r Botulinum toxin enters presynaptic nerve terminals hypotonia, which can be severe or include
>1 yr of age with subsequent toxin formation and
via endocytosis, where it irreversibly prevents the respiratory insufficiency:
botulism (infant-type botulism in an adult)
r 7 different serotypes of botulinum toxin have been release of acetylcholine by inhibiting Classic finding is of a floppy infant
identified (types AG): calcium-dependent exocytosis. DIAGNOSTIC TESTS & INTERPRETATION
r The net result is a decrease in the acetylcholine
The vast majority of cases are due to 3 serotypes: Lab
A, B, and E concentration within the synaptic cleft within the Initial Lab Tests
Type A predominantly is found west of the autonomic nervous system and at neuromuscular r Routine lab tests are not helpful in making the
Mississippi. junctions resulting in anticholinergic (muscarinic and diagnosis, as most will be normal:
Type B predominantly is found east of the nicotinic) effects and flaccid paralysis. Serum electrolytes can help exclude several of the
Mississippi. ETIOLOGY differential diagnoses.
Type E is found in the Pacific Northwest, especially r Botulism is the result of the presence of r Evaluation of the stool by culture and toxin
in Alaska. toxin-secreting C. botulinum in the body, ingestion assays can help confirm what is largely a clinical
EPIDEMIOLOGY of preformed toxins contained in food, or rarely diagnosis:
r Wound botulism is not a disease of children. iatrogenic. Neurotoxin may be identified in the serum, feces,
r Foodborne botulism rarely affects children: r Botulinum toxin serotypes A and B are found in near vomitus, or gastric contents.
Outbreaks typically occur in clusters. 50/50 distribution in cases of infant botulism. Imaging
r Infant botulism: COMMONLY ASSOCIATED CONDITIONS No specific imaging study will confirm the diagnosis of
Most common form of botulism, representing 70% Wound botulism is associated with IV heroin use, botulism.
of all new cases of botulism reported annually especially black tar heroin. Diagnostic Procedures/Other
In the U.S., 1.9/100,000 live births yield 77 r Electromyography may be helpful in distinguishing
cases annually. botulism from Guillain-Barre syndrome or
DIAGNOSIS myasthenia gravis:
RISK FACTORS
Infant botulism is associated with: HISTORY This is only helpful for foodborne botulism in an
r Higher birth weights r Foodborne botulism results in predominantly GI adolescent patient.
r Testing of food specimens can help identify toxins,
r Older, Caucasian mothers symptoms, including nausea, vomiting, abdominal
r Breast-fed infants pain, and distention: but results are often delayed.
r Rapid testing techniques are currently under
r Equal male:female distribution Symptoms usually develop within 1236 hr but
r >50% of infantile botulism cases reported over last may develop as early as 4 hr or as late as 10 days. development and include optical immunoassays and
Other initial symptoms are often mild and include polymerase chain reactions.
30 years have been in California. fatigue, weakness, vertigo, dry mouth, and sore
throat.
Severe cases can develop symmetric, descending
flaccid paralysis with prominent bulbar palsies
such as diplopia, dysarthria, dysphonia, and
dysphagia.
116
BOTULISM
DIFFERENTIAL DIAGNOSIS DISPOSITION r Underwood K, Rubin S, Deakers T, et al. Infant

r Infant botulism: botulism: A 30-year experience spanning the
Admission Criteria
Sepsis Critical care admission criteria: introduction of botulism immune globulin
Electrolyte imbalance
Metabolic encephalopathy
r All patients with diagnosed or suspected foodborne intravenous in the Intensive Care Unit at Childrens
Hospital Los Angeles. Pediatrics. 2007;120:
B
or infant botulism should be admitted to a critical
Congenital myopathy care setting. e1380e1385.
Leigh disease r While there are some cases of mild botulism, many
r Foodborne botulism: See Also (Topic, Algorithm, Electronic
require mechanical ventilation. Media Element)
Myasthenia gravis r In 1 study, 83% of infants diagnosed with infant r http://www.infantbotulism.org
Guillain-Barre syndrome r http://www.cdc.gov
botulism required mechanical ventilation.
Tick paralysis
Diphtheria
Poliomyelitis FOLLOW-UP CODES
TREATMENT After discharge from the hospital, patients should be ICD9
referred to a neurologist for follow-up. r 005.1 Botulism food poisoning
PRE HOSPITAL r 040.41 Infant botulism
Assess and stabilize airway, breathing and circulation. PROGNOSIS r 040.42 Wound botulism
r Prognosis is generally good with early supportive
INITIAL STABILIZATION/THERAPY care and antitoxin as indicated:
Patients with respiratory compromise require Recovery can be prolonged, lasting from several
careful monitoring of respiratory vital capacity and months to 1 year. PEARLS AND PITFALLS
aggressive respiratory care for those with respiratory r Infant botulism usually results in complete recovery. r Early consultation of infectious disease, toxicology,
insufficiency.
COMPLICATIONS and neurology are critical for establishing what is
MEDICATION Complications are usually minimal and are those largely a clinical diagnosis.
First Line associated with prolonged ventilatory dependence: r Suspect botulism in any patient with neuromuscular
r Human-derived botulism immune globulin has been r Neurologic sequelae of foodborne botulism are not weakness, especially bulbar palsies.
FDA approved for treatment of infant botulism since r Early diagnosis can result in early administration of
uncommon and can range from fatigue to persistent
2003 (BabyBIG). muscle weakness to dyspnea. antitoxin, which is associated with shorter LOS and
r BabyBIG is maintained by the California Department
reduced morbidity and mortality.
of Public Health via their Infant Botulism Treatment r Mortality for foodborne botulism is currently 510%
and Prevention Program. Contact and drug ADDITIONAL READING and often related to complications of prolonged
information is available at http://www. ventilator dependence.
r Anonymous. Botulisminformation from the World
infantbotulism.org: r Pitfalls include waiting for lab analysis to make the
BabyBIG has been shown to reduce the overall Health Organization. J Environ Health. 2003;65(9):
diagnosis and delayed consultation.
hospital length of stay (LOS), the ICU LOS, and 5152.
duration of mechanical ventilation. r Arnon SS, Midura TF, Damus K, et al. Honey and
r Patients with foodborne botulism with more than other environmental risk factors for infant botulism.
mild symptoms should receive an equine derived J Pediatr. 1979;94(2):331336.
trivalent (A, B, E) botulinum antitoxin: r Arnon SS, Schechter R, Maslanka SE, et al. Human
This antitoxin is maintained by the CDC and botulism immune globulin for the treatment of infant
requires contacting local state health departments botulism. N Engl J Med. 2006;354(5):462471.
who in turn contact the CDC for release. r CDC. Botulism in the United States 18991996:
The CDC can be contacted directly 24 hr/day when Handbook for Epidemiologists, Clinicians and
local health departments are unavailable. Laboratory Workers. Atlanta, GA: Author; 1998.
The usual dose is a 10 mL vial IV; however, dosing r Francisco AM, Arnon SS. Clinical mimics of infant
regimens will be included with the antitoxin. botulism. Pediatrics. 2007;119:826828.
There is no role for equine antitoxin in infant r Sharma AN. Botulism. In Wolfson AB, Hendey GW,
botulism due to associated risks of anaphylaxis Ling LJ, et al., eds. Harwood-Nuss Clinical Practice
and serum sickness. of Emergency Medicine. 5th ed. Philadelphia, PA:
Second Line Lippincott Williams & Wilkins; 2009:15481550.
Antibiotic therapy has a defined role in wound
botulism; however, it has no benefit in foodborne
botulism, which is the result of the ingestion of
preformed toxin:
r Antibiotics are not indicated in infant botulism, as
lysis of intestinal C. botulinum could result in the
release of large quantities of toxin, worsening the
patients condition.
THERAPIES
Supportive care is essential, including ventilatory
support, nutritional support, skin care, positioning,
and so forth, to reduce associated complications.
117
BRACHIAL PLEXUS INJURY

Nina Lightdale
PATHOPHYSIOLOGY PHYSICAL EXAM

BASICS Sedon and Sunderland classification (4): r Skin: Stab wound or viral rash
r Neurapraxia: Motor paralysis, intact axons r Musculoskeletal exam:
DESCRIPTION r Axonotmesis: Loss of axonal continuity, intact nerve Fractures: Presence of swelling, tenderness, or
r The brachial plexus is the network of peripheral
sheath decreased range of motion of the arm
nerves that originate from the spinal cord at cervical r Neurotmesis: Complete transection Thoracic outlet syndrome signs or symptoms of
and thoracic roots C5, C6, C7, C8, and T1: the involved upper extremity:
These nerves control the sensory and motor ETIOLOGY Loss of radial pulse with arm over head
function of the hand, wrist, elbow, and shoulder. r Traction or avulsion: Pain
r Brachial plexus injury (BPI) can be transient with full Motorcycle accident, fall from height, or sports Paresthesias
recovery or result in long-term disability with partial injury in which the angle between the shoulder Weakness
or complete motor and sensory functional loss of the and the neck, or the angle between the axilla and Cold intolerance
upper limb. the body, is increased acutely causing stretch, Raynaud phenomena
rupture, or avulsion injury to the brachial plexus Glenohumeral stability:
EPIDEMIOLOGY If the arm is down, the shoulder is forced inferiorly Full range of motion
Incidence and/or posteriorly while the neck moves in the Sulcus sign or apprehension test demonstrating
r Traumatic BPI:
opposite direction: dislocation
Motorcycle or fall from height injury Damage is first to the upper roots and superior Dislocation is most commonly inferior or
Transient BPI: trunk, affecting shoulder and elbow function. posterior and may cause direct injury to the
Often called stingers or burners If the arm is overhead, damage is first to the lower axillary nerve.
Occur in 3050% of football players over the roots and inferior trunk, affecting wrist and hand r Neurologic exam:
course of a high school, college, or professional function and often involving the sympathetic Motor: Examine the patients upper back,
career chain with resulting facial paralysis.
r Brachial plexus birth palsy (BPBP) occurs in shoulder, arm and hands.
If the impact is extreme, all levels will sustain Look for muscle wasting or fasciculations and
0.44 of 1,000 live births. damage and the arm will be flaccid. scapular winging (weakness of the rhomboids
r Compression by tumor or local or metastasized
Prevalence or serratus muscles).
r Males > females masses involving neurovascular structures, lung, Pronator drift test: Associated with upper
r Upper C5-6 Erb-Duchenne palsy is most common. muscle, or bone extremity weakness.
r Lower C8-T1 Klumpke palsy is less common. r Parsonage Turner syndrome (5): C5 and C6: Biceps muscle for elbow flexion;
r Global C5-T1, or total plexus injury, is rare. Brachial plexus neuritis of unknown etiology, rotator cuff muscles for external/internal
r In a 30-yr case series of 1,000 BPIs (1): possibly postviral, with variable onset of shoulder shoulder rotation
pain C6 and C7: Triceps muscle for elbow extension
Traumatic:
Stretch/Contusion injuries (49%) Paralysis of the shoulder and arm, wrist, or hand C6 and C7: Wrist extension
Gunshot wound (12%) may be delayed. C8: Finger flexion
Lacerations (7%) The syndrome can vary greatly in presentation and T1: Finger abduction or fanning
nerve involvement. C8 and T1: Thumb opposition
Nontraumatic:
Thoracic outlet syndrome (16%) Sensation:
COMMONLY ASSOCIATED CONDITIONS Sharp-dull discrimination
Tumors (% of all BP tumors reported): r Associated with head injury, thoracic trauma, and
Neural sheath origin (16%)
Light touch in C5-T1 distributions
fractures/dislocation of the cervical spine or upper
Solitary neurofibromas (34%)
Horner sign: Ipsilateral facial palsy indicates lower
extremity
Neurofibromas associated with von r 20% associated with vascular trauma plexus involvement.
Recklinghausen disease (20%) Pain in an anesthetic extremity suggests
Schwannomas (34%)
deafferentation and correlates with root avulsion
Malignant nerve sheath (20%) DIAGNOSIS and poor prognosis.
Resting shift of the head away from the injured
RISK FACTORS HISTORY side is evidence of denervation of paraspinous
r High-velocity traction injury r Birth history: muscles.
r Sharp laceration in the neck or axilla Shoulder dystocia
r Birth risk factors: Shoulder dystocia, gestational Gestational diabetes or macrosomia DIAGNOSTIC TESTS & INTERPRETATION
diabetes or macrosomia, breech presentation, Breech presentation Imaging
r X-rays of the cervical spine, chest, shoulder girdle,
vacuum or forceps use during prolonged labor, or Vacuum or forceps use during delivery
Prolonged labor or traumatic delivery and humerus should be obtained to assess for
traumatic delivery (2)
r Timing and onset of symptoms: associated injuries.
GENERAL PREVENTION r CXRs could include inspiration and expiration PA
r Safe helmet and cervical padding/support use for Since birth
Acutely with injury views to determine activity of the diaphragm:
motorcycle riders and high-contact sport athletes (3) r Mechanism of injury: An elevated hemidiaphragm suggests denervation
r Careful instruction, training, and regulations of the phrenic nerve.
Type of trauma: Blunt vs. penetrating
designed to eliminate headfirst contact. r Follow-up imaging after stabilization:
r Prenatal screening Position of arm during injury
Use of protective gear CT myelogram
r Recent viral illness MRI (6)
r Recent trauma
118
BRACHIAL PLEXUS INJURY
Diagnostic Procedures/Other Issues for Referral

r Trauma surgery for mechanism and associated
REFERENCES
Electromyelogram or nerve conduction studies are not
routinely utilized in the acute setting and may be injuries 1. Kim DH, Murovic JA, Tiel RL, et al. Mechanisms of
performed at follow-up visits. r Primary care provider for monitoring of transient injury in operative brachial plexus lesions. B
stingers or postviral neuritis Neurosurg Focus. 2004;16(5):E2.
r Avulsion of the nerve roots from the spinal cord or r Neurology, neurosurgery, oncology, orthopaedic 2. Hale H, Bae D, Waters PM. Current concepts in the
surgery for relevant issues management of brachial plexus birth palsy. J Hand
neuromas in continuity
r Prominent 1st rib r Refer to a pediatric BPBP specialist for the possible Surg. 2010;35(2):322331.
r Pleural, nerve, muscle, or bone tumor or other mass need for surgical brachial plexus reconstruction. 3. Kasow DB, Curl WW. Stingers in adolescent
athletes. Instr Course Lect. 2006;55:711716.
causing compression of the plexus COMPLEMENTARY & ALTERNATIVE 4. Seddon H, Medawar P, Smith H. Rate of
DIFFERENTIAL DIAGNOSIS THERAPIES regeneration of peripheral nerves in man. J Physiol.
r Infection Physical therapy: 1943;102:191215.
r Mass r Restoring neck, shoulder, elbow, wrist, and digital
5. Sumner AJ. Idiopathic brachial neuritis.
r Transient quadriparesis strength Neurosurgery. 2009;65(4 Suppl):A150A152.
r Restoring range of motion
6. Sureka J, Cherian RA, Alexander M, et al. MRI of
brachial plexopathies. Clin Radiol. 2009;64(2):
TREATMENT 208218. Epub 2008 Nov 1.
FOLLOW-UP
PRE HOSPITAL
r Cervical spine stabilization and immobilization FOLLOW-UP RECOMMENDATIONS
ADDITIONAL READING
r Angel wings for removal of face mask
r Use of arm sling for comfort Newton EJ, Love J. Emergency department
INITIAL STABILIZATION/THERAPY r Close monitoring until return of protective sensation management of selected orthopedic injuries. Emerg
Med Clin North Am. 2007;25(3):763793, ixx.
circulation. Patient Monitoring
r Supportive therapy, analgesia, and management of r After blunt or traction injury, follow neurologic
exam:
associated traumatic injuries
Obtain MRI or CT myelogram with CODES
MEDICATION electromyogram/nerve conduction velocity test if
No clear indications for IV or oral steroids, antivirals, or no return of nerve function ICD9
treatment with hypothermia. Reports of efficacy are r Immediate outpatient referral to a surgeon for r 353.0 Brachial plexus lesions
anecdotal. r 767.6 Injury to brachial plexus due to birth trauma
indications for acute and late reconstructive
procedures r 953.4 Injury to brachial plexus
r Early repair of sharp lacerations is indicated.
PROGNOSIS
r Traction injuries are monitored for recovery with r 92% newborns with BPBP have mild injury and
fracture stabilization as indicated. spontaneous recovery within the 1st 2 mo of life.
PEARLS AND PITFALLS
r Mass resection or debulking as indicated r 75% of persons with Parsonage Turner syndrome r Most BPIs are transient, unilateral, and require
DISPOSITION experience complete recovery within 2 yr. supportive care and outpatient follow-up only:
Nearly 50% of football players will experience a
Admission Criteria COMPLICATIONS
r Monitoring for secondary survey due to mechanism r Long-term disability from incomplete or partial burner or stinger within their career.
r Consider Parsonage Turner syndrome or compression
of injury recovery and decreased upper extremity function
r Any evidence of respiratory distress due to phrenic r Glenohumeral joint chronic instability from local or metastasized mass and full evaluation
if there is no relevant mechanism of injury.
nerve injury r A careful history for mechanism of injury guides
r Surgical indications
treatment, as evaluation based on sensory and
Discharge Criteria motor exam can be difficult in the pediatric patient.
Stabilized by trauma criteria
119
BRADYCARDIA
Adam Vella
Karen Goodman
3rd-degree AV block occurs when there is no

BASICS conduction from the atrial pacemaker to the DIAGNOSIS
ventricles. P waves are completely dissociated
DESCRIPTION from the QRS waves. HISTORY
r Bradycardia is a heart rate below the normal range r Sick sinus syndrome manifests with sinus node r History of medications
for age. r Family history of syncope or sudden death
function depression that does not increase the heart
r Sinus bradycardia, in which a P wave precedes each r History of cardiac disease
rate in response to stress.
QRS complex, may be seen in normal asymptomatic r Past episodes of syncope, dizziness, or unexplained
children with a benign course and without any ETIOLOGY seizures
r Intrinsic causes:
underlying pathology, or it may be due to an r Time of episodes
abnormality of the sinus node. Infarction or ischemia r Association with precipitating factors
r Bradycardia may be symptomatic or asymptomatic. Infiltrative diseases: Sarcoidosis, amyloidosis,
r Symptoms such as fatigue, exercise intolerance,
r In athletic adolescents, normal heart rates may be hemochromatosis
Collagen vascular diseases: Systemic lupus dizziness, shortness of breath, and syncope
<60 bpm. erythematosus, rheumatoid arthritis, scleroderma r Infants and young children may have nonspecific
r Common causes of bradycardia in children are from symptoms such as poor feeding and lethargy.
Myotonic muscular dystrophy
corrective surgery of congenital heart disease, vagal Surgical trauma: Valve replacement, correction of
stimulation, drugs, and hypoxemia. PHYSICAL EXAM
CHD, heart transplantation. Postsurgical heart r Many patients with sinus bradycardia will remain
EPIDEMIOLOGY block may resolve by day 8 postoperatively or may asymptomatic with a normal physical exam.
Incidence recur years after the surgery. r Infants in complete heart block may show signs of
r The incidence and prevalence of asymptomatic Familial diseases: Carnitine deficiency, genetic
CHF.
bradycardia is unknown, as most young patients are mutations, and familial patterns of inheritance r Severe bradycardia may present with poor systemic
asymptomatic. causing rhythm disturbances
Infectious diseases: Chagas disease, endocarditis perfusion and shock.
r Congenital complete atrioventricular (AV) heart r Tachypnea
r Extrinsic causes:
block is found in 1/22,000 live births. r Heart murmur
Autonomically mediated syndromes: Vasovagal
RISK FACTORS r Jugular venous distension
syncope, carotid-sinus hypersensitivity, situational
r Congenital heart disease (CHD) changes (coughing, micturation, defecation, r Hepatomegaly
r Cardiac surgery vomiting) r Edema
r Thyroid disease Drugs: Beta-adrenergic blockers; calcium channel r Rales
r Cardiac disease blockers; clonidine; digoxin; antiarrhythmic drugs;
r Inflammatory processes cholinergic or muscarinic agents such as DIAGNOSTIC TESTS & INTERPRETATION
carbamates, some mushrooms, Lab
PATHOPHYSIOLOGY organophosphates, physostigmine, pilocarpine, Initial Lab Tests
r Bradycardia may originate from the sinus node, AV r Many cases of bradycardia in children are
and pyridostigmine
node, or bundle of His. Hypothyroidism asymptomatic and do not require lab work.
r Bradycardia is caused by intrinsic dysfunction or Neurologic disorders: Traumatic conditions such as r Specific cases may suggest electrolyte or hormone
injury to the hearts conduction system or by spinal cord injuries or head trauma as well as abnormalities that should be evaluated:
extrinsic factors acting on a normal heart and its nontraumatic causes such as epilepsy and Electrolytes including calcium
conduction system. Guillain-Barre syndrome Thyroid function tests including thyroid-stimulating
r Conduction abnormalities may also cause Metabolic disturbances: Hypokalemia, hormone, serum thyroxine (total T4), free
bradycardia: hyperkalemia, hypoglycemia, hypoxia thyroxine (free T4), serum triiodothyronine (T3)
1st-degree AV block: Abnormal delay of In cases of suspected cardiac ischemia, cardiac
COMMONLY ASSOCIATED CONDITIONS enzymes (creatine phosphokinase, creatine
conduction through the AV node is associated r Complete heart block may be an isolated finding.
with prolonged PR intervals and no dropped beats. r It may be congenital and is associated with specific kinase/myoglobin) and troponin levels may be
2nd-degree AV block: tested.
In Mobitz type I, PR intervals progressively types of CHD defects and maternal collagen disease.
r Acquired heart block may be idiopathic or Imaging
prolong until a QRS complex is dropped. This is r Echo (cardiac US) may be used to evaluate the
caused by an increased refractory period at the associated with CHD, infectious diseases,
endocarditis, cardiomyopathy, inflammatory contractility of the heart and any structural
AV node. abnormalities that may be causing or resulting from
Mobitz type II is an all or none phenomenon. processes, muscle diseases, trauma, cardiac tumors,
cardiac sclerosis, hypocalcemia, and drug overdoses. the bradycardia.
There is either a normal PR interval with normal r Acquired heart block may be found after cardiac r CXR is an adjunct to visualize heart size and
conduction or a complete conduction block. The possible effects from bradycardia.
failure of conduction is at the level of the bundle surgery as a transient or a permanent condition.
of His with a prolonged refractory period at the
level of the His-Purkinje system.
120
BRADYCARDIA
r The single most important test is a 12-lead ECG,
Admission Criteria r Brady WJ Jr, Harrigan RA. Evaluation and
which may reveal conduction abnormalities such as r Stable, symptomatic patients may be admitted to
sinus bradycardia and 1st-, 2nd-, and 3rd-degree AV
block (complete heart block).
inpatient units that are capable of cardiac management of bradyarrhythmias in the emergency
department. Emerg Med Clin North Am. 1998;16(2):
B
monitoring or Holter devices.
r Other testing may be helpful, as indicated: r Critical care admission criteria: 361388.
r Doniger S, Sharieff G. Pediatric dysrhythmias.
24-hr ambulatory (Holter) monitoring may have A patient who remains unstable requires
greater yield if the initial ECG is normal and the admission to the ICU for further monitoring and Pediatr Clin North Am. 2006;53:85105.
index of suspicion is high for arrhythmias. r Gewitz MH, Woolf P. Cardiac emergencies. In
intervention.
Exercise testing and ambulatory monitoring may A patient who has converted from an unstable Fleisher GR, Ludwig S, Henretig FM, et al., eds.
diagnose chonotropic abnormalities. rhythm should be admitted to the ICU for Textbook of Pediatric Emergency Medicine. 6th ed.
Tilt table testing, or evaluation of orthostatic BP, monitoring. Philadelphia, PA: Lippincott Williams & Wilkins;
may help define indeterminate cases of vasovagal 2010.
bradycardia. Discharge Criteria r Goldberger AL. Clinical Electrocardiology: A
r Asymptomatic and chronic bradycardia may be
Invasive electrophysiologic testing may be helpful Simplified Approach. 7th ed. Philadelphia, PA:
in the unusual circumstances in which the managed on an outpatient basis in stable patients.
r If a reversible cause of the patients bradycardia is Mosby; 2006.
mechanism of the bradycardia remains uncertain, r Magrum JM, DiMarco JP. The evaluation and
attempts to monitor the heart rate have been recognized and treatment or management is under
management of bradycardia. N Engl J Med.
unsuccessful, or symptoms suggest a potentially way, the patient may be discharged to follow up
2000;342(10):703709.
life-threatening arrhythmia. with the primary care provider (PCP) or cardiologist. r McGregor T, Parkar M, Rao S. Evaluation and
DIFFERENTIAL DIAGNOSIS Issues for Referral management of common childhood poisonings. Am
r Unstable patients who require transcutaneous or
See Etiology for further details. Fam Physician. 2009;79(5):397403.
transvenous pacing or other more advanced modes r Mehta AV, Chidambaram B, Garrett A. Familial
of treating symptomatic bradycardia should have symptomatic sinus bradycardia: Autosomal
TREATMENT cardiology involved as soon as possible.
r Patients with a history of cardiac disease and
dominant inheritance. Pediatr Cardiol. 1995;16:231.
r Park M, George R. Pediatric Cardiology for
PRE HOSPITAL cardiac surgery may benefit from involvement of Practitioners. 5th ed. Philadelphia, PA: Mosby; 2008.
r Assess and address the ABCs, and follow the cardiology to further clarify potential causes of their r Tintinalli JE, Gabor D, Stapczynski JS, et al., eds.
Pediatric Advanced Life Support (PALS) or Advanced arrhythmia and ways to manage them. Tintinallis Emergency Medicine: Comprehensive
Cardiac Life Support (ACLS) protocol. r Asymptomatic or stable patients with cardiac
r Administer oxygen via face mask if symptomatic Study Guide. 6th ed. Columbus, OH: McGraw-Hill;
etiologies for their symptoms should have scheduled 2003.
from bradycardia. follow-up with cardiology. r Vetter VL, ed. Pediatric Cardiology. The Requisites in
INITIAL STABILIZATION/THERAPY Pediatrics. Philadelphia, PA: Mosby Elselvier; 2006.
r Stabilize the airway and provide oxygen.
r Chest compressions are indicated for patients with
FOLLOW-UP
bradycardia and hemodynamic compromise. FOLLOW-UP RECOMMENDATIONS
CODES
r Among symptomatic patients with bradycardia, the
cause of the bradycardia must be ascertained in Patients should follow up with their PCP or ICD9
order to potentially reverse these factors, especially cardiologist as recommended. r 426.10 Atrioventricular block, unspecified
with regard to extrinsic factors. Depending on the need for a further workup, r 427.89 Other specified cardiac dysrhythmias
r Volume expansion with IV fluids patients may be instructed to schedule r 746.86 Congenital heart block
appointments for Holter monitoring, repeat ECGs,
MEDICATION or blood work.
First Line r Activity:
r Epinephrine 0.01 mg/kg (1:10,000) IV/IO with a Activity that may have precipitated an event of
PEARLS AND PITFALLS
max single dose of 1 mg: bradycardia should be avoided until a thorough r Hypoxia is a common cause of bradycardia. If
May repeat the dose q35min to a max dose of evaluation and clearance have been made. present, hypoxia should be corrected before
10 mg Patient Monitoring progressing to use of medications.
r Atropine 0.02 mg/kg IV/IO (min dose of 0.1 mg): r Bradycardia is an arrhythmia in which symptoms
Depending on the need for a further workup, patients
May repeat dose once during the resuscitation may be instructed to obtain Holter monitoring or may range from asymptomatic to life threatening.
Second Line repeat ECGs. r The etiology of the abnormal rhythm may aid in the
r Epinephrine infusions may be started at management and treatment of the bradycardia.
PROGNOSIS r Treatment protocols are aimed at stabilizing the
0.11 g/kg/min, particularly if a response to single Depending on the etiology and severity of the
doses of epinephrine is noted but the patient has bradycardia, the prognosis may range from an patient, searching for the etiology, and treating the
failed to achieve hemodynamic stability. asymptomatic and resolvable arrhythmia to a severely underlying pathology.
r Isoproterenol infusion may be started at
symptomatic bradycardia that can result in cardiac
0.052 g/kg/min as a second-line agent when arrest and sudden death.
epinephrine has failed.
r Specific antidotal therapy may be indicated for COMPLICATIONS
cardiovascular medication toxicity. (Refer to Symptomatic bradycardia may lead to cardiovascular
Beta-Blocker Poisoning, Calcium Channel Blocker collapse and death.
Poisoning, and Digoxin Poisoning topics.)
r Follow current PALS protocol with regard to chest
compression and endotracheal intubation.
r Consider cardiac pacing, especially if a conduction
defect is suggested.
121
BRANCHIAL CLEFT CYST

Michelle J. Alletag
Marc A. Auerbach
BASICS DIAGNOSIS r Abscess
r Lymphadenopathy
DESCRIPTION HISTORY r Lymphadenitis
r A branchial cleft cyst is a lateral neck mass or sinus r May present as an asymptomatic neck mass or as an
r Parotitis
tract that arises when a branchial arch fails to close acute infection, with a painful, red, acutely r Vascular malformation
(most commonly the 2nd arch) following the 4th or enlarging mass.
r Up to 40% initially present during upper respiratory r Scrofula
5th wk of gestation (13). r Ectopic thyroid
r They may occur anywhere along the anterior border tract infections (because of lymphatic tissue that is
present within the cyst): r Neoplasm (eg, rhabdomyosarcoma)
of the sternocleidomastoid muscle or the
Occasionally noted at birth when a pit or sinus is r Neurofibroma
mandibular ramus.
seen on the neck r Lipoma
EPIDEMIOLOGY r Torticollis with sternocleidomastoid muscle knot
r Most common congenital anomaly of the lateral PHYSICAL EXAM
r Mobile, nontender, fluctuant mass located along the may be incorrectly presumed to be a tumor.
neck r Thyroglossal duct cysts (midline)
r Comprise about 30% of congenital neck masses anterior border of the sternocleidomastoid muscle
r Equal incidence among males and females r When infected: r Cystic hygromas
Erythema overlying the cyst
GENERAL PREVENTION Tenderness to palpation
Prevention of branchial cleft cyst complications is best May be draining if a sinus is present TREATMENT
accomplished by early diagnosis and excision.
DIAGNOSTIC TESTS & INTERPRETATION Ideally, cysts or sinuses are noted prior to infection
PATHOPHYSIOLOGY Lab and referred to an otolaryngologist or pediatric
r Branchial cleft anomalies are lined with various
Inflammatory markers are nonspecific for infected surgeon for surgical excision.
types of epithelium and will rarely develop into branchial cleft cysts:
squamous cell carcinoma in adults (13). r Elevation of WBC count or C-reactive protein are INITIAL STABILIZATION/THERAPY
r Cysts have no external opening. If infected, the cysts must be treated with antibiotics
r Sinuses may open to the exterior neck. typical with infected cysts. prior to surgical intervention, as operating on infected
r Fistulas open into the pharynx (or both the neck and Imaging lesions results in a significantly higher risk of
r CT neck, with contrast, is the diagnostic study of recurrence and complications.
pharynx).
r Approximately 2/3 of cysts have associated sinuses choice. MEDICATION
r Sonography or MRI may also be used.
or fistulas. First Line
r Up to 10% of patients have bilateral branchial Diagnostic Procedures/Other r Antibiotics:
anomalies, which is more commonly associated with Fine-needle aspiration should NOT be performed, as it Antimicrobial agents that treat both typical oral
craniofacial syndromes. may make resection more difficult and may lead to flora and gram-negative bacteria:
infectious complications. Ampicillin/Sulbactam 50 mg/kg/dose IV q6h
ETIOLOGY Amoxicillin/Clavulanate 45 mg/kg/day PO b.i.d.
Result from failure of obliteration of branchial clefts Pathological Findings
r Analgesics:
(primitive gills) during embryologic development Excised lesions consist of epithelium and may also
include lymphoid, salivary, or sebaceous tissue. Ibuprofen 10 mg/kg/dose PO/IV q6h PRN
COMMONLY ASSOCIATED CONDITIONS Acetaminophen 15 mg/kg/dose PO/PR q4h PRN
Branchio-oto-renal syndrome is an autosomal Codeine/Acetaminophen dosed as 0.51 mg/kg of
dominant disorder consisting of branchial arch codeine component PO q4h PRN
anomalies (usually bilateral), profound deafness, and Hydrocodone or hydrocodone/acetaminophen
varying degrees of renal anomalies. dosed as 0.1 mg/kg of hydrocodone component
PO q46h PRN
122
BRANCHIAL CLEFT CYST

Clindamycin (may be used for patients with penicillin FOLLOW-UP
allergies) 10 mg/kg/dose IV q6h or 10 mg/kg/dose PO 1. Acierno SP, Waldhausen JHT. Congenital cervical
t.i.d. FOLLOW-UP RECOMMENDATIONS
cysts, sinuses and fistulae. Otolaryngol Clin North
Am. 2007;40:161176.
B
SURGERY/OTHER PROCEDURES r Antibiotics with follow-up for drainage 2. Rosa PA, Hirsch DL, Dierks EJ. Congenital neck
Elective surgical excision/resection is considered the r Analgesics as noted in the Medication section masses. Oral Maxillofacial Surg Clin North Am.
definitive therapy:
r Surgical excision should take place during infancy or r Return for swelling, drainage, or worsening pain at 2008;20:339352.
early childhood. the surgical site or for fever >101 F. 3. Mandell DL. Head and neck anomalies related to
r Surgical excision should be delayed 46 wk if the the branchial apparatus. Otolaryngol Clin North
Patient Monitoring Am. 2000;33:13091332.
cyst is considered infected. Any patient with branchial cleft anomalies (both
repaired and unrepaired) should be monitored for
DISPOSITION signs of infection or recurrence, including swelling,
Admission Criteria drainage, pain, or erythema at the site of the lesion.
CODES
r Infected cysts are notoriously difficult to treat and
generally require admission for IV antibiotics. DIET ICD9
r Critical care admission criteria: A soft diet is recommended if fistulous tract was r 744.41 Branchial cleft sinus or fistula
Swelling, resulting in airway compromise, may closed; otherwise, normal diet. r 744.42 Branchial cleft cyst
necessitate ICU admission. PROGNOSIS
Discharge Criteria The majority of patients recover fully, with excellent
r Children with infected cysts may be discharged if: functional and cosmetic outcome postoperatively. PEARLS AND PITFALLS
Infection controlled or patient minimally COMPLICATIONS r Early diagnosis and excision before infection
symptomatic r Branchial cleft anomalies are notoriously difficult to develops can prevent significant morbidity.
Patient able to tolerate oral antibiotics resect fully and may require multiple surgeries, with r Attempts at probing or incision and drainage of an
Follow-up ensured an average of 12 recurrences after initial resection. infected cyst can lead to fistula formation and
r Uncomplicated cysts may be removed as an r Damage to nearby cranial nerves (most often the serious cosmetic morbidity.
outpatient procedure. facial nerve) is also a risk during surgical resection. r Airway compromise is possible from expanding
Issues for Referral cysts. Careful initial and ongoing evaluation of
All branchial cleft cysts require otolaryngology or airway patency is critical.
pediatric surgery referral for definitive management.
123
BREAST LESIONS
Alyssa Abo
Atima Chumpa Delaney
r Gynecomastia: Associated pain: Mastitis, abscess, trauma

BASICS Males, mostly adolescents, usually benign History of trauma: Sports, piercings
Unilateral or bilateral Fever: Mastitis, abscess
DESCRIPTION Discrete lesions to enlarged breasts r Menstrual history (if applicable):
r Pediatric breast lesions are usually benign and Can be painful Last menstrual period
self-limited. The most common causes are variations Causes: Physiologic; tumors; metabolic Relation of breast lesion to menses:
of thelarche, gynecomastia, neonatal hypertrophy, disturbance; medications such as phenytoin, Fibrocystic change: Pain before menses and
and infection. Malignant lesions are rare. metronidazole, spironolactone, cimetidine improves with menses
r Lesions are differentiated by several factors, Needs evaluation if prepubertal patient r Pregnancy history (if applicable)
including age, gender, location of the lesion, r Fibroadenoma:
puberty, nipple discharge, relation to menses, Benign; most common lesion in adolescents (1) PHYSICAL EXAM
r General:
presence and absence of fever, and pain. Adolescent females, generally asymptomatic
May be larger or tender before menses Full exam, including lymph node exam
EPIDEMIOLOGY r Breast:
Smooth, round, mobile, usually 23 cm
Incidence Any quadrant, usually upper outer Technique: Lay the patient supine with the
Mastitis: If there is rapid growth to >5 cm, consider ipsilateral arm over the head. Use tips of fingers to
r Peaks: Neonates and postpubertal females palpate the lesion.
juvenile fibroadenoma.
r Frequency of female to male: r Fibrocystic disease: Inspection
Neonatal (1st 2 wk) 1:1 Benign, common Tanner stage
All other ages 2:1 Hormonal, cystic breast changes Skin
r Erythema: Mastitis, abscess, trauma:
Prevalence Upper outer quadrants
r Neonatal hypertrophy in 60% Nipple discharge (nonbloody) brown or green Assess symmetry:
r Premature thelarche in 2% (1) Tender before menses, improves with menses Asymmetry: Unilateral thelarche, gynecomastia,
r Phyllodes tumor (Cystosarcoma phyllodes): neonatal hypertrophy
RISK FACTORS Usually benign but may be malignant Breast lesion size:
For breast infection: >5 cm: Consider phyllodes tumor and juvenile
Painless large mass
r Trauma, foreign body, obesity, poor hygiene Shiny, thin skin, +/ bloody nipple discharge fibroadenoma.
r Breast manipulation (neonates) r Fat necrosis: Breast lesion location:
Upper outer quadrants: Consider fibroadenoma
PATHOPHYSIOLOGY Trauma to breast (eg, sports, seat belt)
or fibrocystic change.
r Breasts are composed of ducts and glands Well circumscribed, firm, may be tender
Palpation:
surrounded by connective and adipose tissue. May mimic carcinoma Tenderness: Trauma, infection, fibrocystic
r Neonatal breasts are influenced by maternal May become scar tissue
r Malignant lesion: change
hormones, which may cause hypertrophy or Warm: Mastitis, abscess
discharge. Very rare Characterize lesion: Nodular (fibrocystic
r During childhood and puberty, breast development Primary, secondary, or metastasis change), solid (fat necrosis, fibroadenoma,
Hodgkin, rhabdomyosarcoma breast cancer), fluctuant (abscess)
occurs in response to hormones.
r Thelarche occurs between 6 and 14 yr of age. Solitary, hard, irregular borders Mobility: Mobile (fibroadenoma), nonmobile
r Masses may involve the skin, ducts, or glands. Nontender, nonmobile (breast cancer, fat necrosis)
Skin changes: Dimpling, edema (peau dorange), Nipple discharge (as above)
ETIOLOGY warm, nipple changes
r Infection (mastitis and abscess): Lymphadenopathy DIAGNOSTIC TESTS & INTERPRETATION
Females and males, all ages Hepatosplenomegaly (metastasis) Lab
r Routine lab tests are not generally necessary,
Unilateral COMMONLY ASSOCIATED CONDITIONS
Warm, swollen, tender, indurated Conditions associated with mastitis: Obesity, steroid especially for afebrile breast lesions.
Abscesses are fluctuant, +/ purulent drainage. r Consider a fever evaluation for neonatal mastitis or
therapy, trauma, diabetes mellitus, rheumatoid
Systemic symptoms are rare. arthritis abscess.
Staphylococcus aureus (most common), MRSA, r Consider CBC, C-reactive protein, and blood culture
Streptococcus species. In neonates, also consider for patients with mastitis or abscess.
Escherichia coli. DIAGNOSIS r Gram stain and culture of purulent nipple discharge
r Neonatal breast hypertrophy: or fluid from abscess
HISTORY
Benign, occurring in females and males r General history: Imaging
1st weeks of life, from maternal hormones
Onset of symptoms: Acute, chronic, recurring: r US is the imaging modality of choice when
Self-resolving, females have longer duration Acute: Mastitis, abscess, trauma considering conditions that need to be diagnosed
May be associated with white nipple discharge Chronic: Fibrocystic change, fibroadenoma, urgently (2), such as breast abscesses:
r Thelarche and precocious puberty:
thelarche Preferred for immature breast
Premature thelarche: Location of lesion Differentiates solid mass, cyst, and infection
Benign Cysts: Avascular, anechoic (black)
1 or multiple lesions
Prepubertal females, <68 yr of age (1) Abscess: Heterogeneous echoes, peripheral flow
Associated nipple discharge:
No other signs of puberty White: Neonatal hypertrophy, galactorrhea increased
Unilateral thelarche: Bloody: Phyllodes tumor, nipple r Mammography:
Asymmetric pubertal breast development,
irritation/trauma, breast cancer (rare) Less frequently indicated in pediatrics because
generally a normal variant Serous/Serosanguineous: Fibrocystic disease, immature breast has more glandular than adipose
Firm area of tissue below areola
breast cancer (rare) tissue.
May be onset of puberty Purulent: Infection
Precocious puberty:
Females <68 yr of age
Other signs of puberty are present.
124
BREAST LESIONS
Diagnostic Procedures/Other <7 postnatal days or weight <1,200 g: REFERENCES

Aspiration or incision/drainage of abscess 100 mg/kg/day IV divided q12h
>7 postnatal days and >1,200 g: 150 mg/kg/ 1. Greydanus DE, Matytsina L, Gains M. Breast
r Neonatal mastitis vs. hypertrophy: day divided q8h
r Mastitis and abscess in children, adolescents:
disorders in children and adolescents. Prim Care.
2006;33(2):455502.
B
Hypertrophy: 2. Weinstein SP, Conant EF, Orel SG, et al. Spectrum
Not erythematous Antibiotic coverage for gram-positive organisms
for 714 days; consider MRSA of US findings in pediatric and adolescent patients
Resolves spontaneously
Oral therapy (if no systemic symptoms): with palpable breast masses. Radiographics.
White nipple discharge
r Differential diagnosis of mastitis: Cephalexin 2550 mg/kg/day PO divided q68h 2000;20(6):16131621.
MRSA coverage (follow local recommenda- 3. Gorwitz RJ. A review of community-associated
Mammary duct ectasia, trauma, malignancy methicillin-resistant Staphylococcus aureus skin
r Tumor tions):
Clindamycin 150450 mg/dose IV/IM q68h and soft tissue infections. Pediatr Infect Dis J.
r Fibroadenoma can be differentiated from phyllodes
(max 1.8 g/day) OR 2008;27(1):17.
tumor by histology; may be difficult with US. Trimethoprim (TMP)/Sulfamethoxazole, dose 4. Gorwitz RJ, Jernigan DB, Powers JH, et al.
r Fibrocystic disease
612 mg TMP/kg/day PO divided q12h: Participants in the CDC-Convened Experts Meeting
r Thelarche on Management of MRSA in the Community.
Parenteral therapy:
r Gynecomastia Cefazolin 25100 mg/kg/day IV divided q68h Strategies for clinical management of MRSA in the
r Fat necrosis can be differentiated from malignancy (max 6 g/day) community: Summary of an experts meeting
by biopsy, possibly with US. MRSA coverage convened by the Centers for Disease Control and
Clindamycin 1.22.7 g/day IV/IM in 24 Prevention. March 2006. Available at http://www.
divided doses (max 4.8 g/day) OR cdc.gov/ncidod/dhqp/pdf/ar/CAMRSA
TREATMENT Vancomycin 4060 mg/kg/day IV divided ExpMtgStrategies.pdf.
q68h
r Neonatal mastitis or abscess: DISPOSITION ADDITIONAL READING
Admit patient for parenteral antibiotics. Admission Criteria
Consider surgical consultation for abscess r Neonatal mastitis or abscess Baren JM. Breast lesion. In Fleisher GR, Ludwig S, eds.
aspiration or incision/drainage. r Infections that fail outpatient management Textbook of Pediatric Emergency Medicine. 6th ed.
r Mastitis or abscess in children and adolescents: r Worsening mastitis, systemic symptoms Philadelphia, PA: Lippincott Williams & Wilkins; 2010.
Warm compresses r Abscess that requires operation by surgeons
Oral antibiotics for mastitis
Discharge Criteria
Incision/drainage for abscess (3,4) r No evidence of systemic symptoms
r Premature thelarche: CODES
r Tolerating oral therapy
If other signs of puberty are present, evaluate for
precocious puberty (in emergency department or Issues for Referral ICD9
r Surgical: r 611.0 Inflammatory disease of breast
outpatient).
r Unilateral thelarche: r 611.89 Other specified disorders of breast
Lesions that require biopsy (core needle,
excisional) or fine-needle aspiration r 778.7 Breast engorgement in newborn
Reassure that asymmetry should lessen over time.
r Gynecomastia: Suspicious solid lesions:
Reassurance Nonmobile, hard, enlarging
Medication is not indicated (1). Skin changes, adenopathy PEARLS AND PITFALLS
r Fibroadenoma: Recurring cystic lesions after aspiration r Pearls:
Reassurance Rapidly growing lesions
Gynecomastia requiring cosmetic surgery Breast lesions in children are usually benign.
If lesion is >5 cm, refer for biopsy. r Endocrinology for precocious puberty, prepubertal Differentiate thelarche from abnormal lesions
r Fibrocystic change:
gynecomastia Prepubertal breast development with other
Analgesia: NSAIDs r Oncology for malignant lesions pubertal signs requires further evaluation.
Consider oral contraceptives. Prepubertal gynecomastia requires evaluation.
Eliminate caffeine. COMPLEMENTARY & ALTERNATIVE r Pitfalls:
Persistent lesions: Refer for fine-needle aspiration THERAPIES Failure to recognize and adequately treat MRSA in
and US. Fibrocystic change: patients with mastitis and breast abscess where
MEDICATION r Primrose oil (1 tablespoon at bedtime) MRSA is prevalent
r Neonatal mastitis and abscess: Failure to treat neonatal mastitis with parenteral,
Broad-spectrum antibiotics for 714 days; broad-spectrum antibiotics
consider MRSA coverage. FOLLOW-UP Improper incision and drainage of a breast
Use penicillinase-resistant antibiotic in abscess can damage the breast bud and may
FOLLOW-UP RECOMMENDATIONS result in later cosmetic deformity.
combination with aminoglycoside or a Discharge instructions and medications:
3rd-generation cephalosporin: r Mastitis and abscess requires close follow-up with
Nafcillin or oxacillin:
<7 postnatal days or weight <1,200 g: the patients primary care provider.
r Benign lesions can be monitored every few months.
50 mg/kg/day IV divided q12h
>7 postnatal days and weight >2,000 g:
100 mg/kg/day divided q6h AND

Gentamicin:
<7 postnatal days: 5 mg/kg/day IV divided
q12h
>7 postnatal days and weight >2,000 g:
7.5 mg/kg/day IV divided q8h
Cefotaxime:
125
BRONCHIOLITIS
Suzanne Schuh
BASICS DIAGNOSIS r Asthma/Recurrent virus-induced wheezing
r Possible mechanisms with later viral-induced
DESCRIPTION HISTORY wheeze: Subnormal lung function prior to
r Bronchiolitis is a lower respiratory tract infection r Upper respiratory prodrome of coryza, cough, and
bronchiolitis, genetic factors, bronchiolitis-induced
with airway inflammation and bronchoconstriction. fever lung changes
r It is characterized by upper respiratory prodrome r Fever usually <39 C r Pertussis: Usually no respiratory distress between
followed by wheezing/crepitations. r Decreased fluid intake
coughs, no wheezing
r Bronchiolitis may include tachypnea, hypoxemia, r Increased work of breathing, usually 1st episode r Bacterial pneumonia: Focal wheezing, often toxic
and respiratory distress. r Sleep disruption
appearance, isolated consolidation without airway
EPIDEMIOLOGY PHYSICAL EXAM disease on radiograph
r Vital signs, including respiratory rate, temperature, r Foreign body: Typically sudden onset, afebrile
Incidence r CHF: Chronic feeding problems, failure to thrive
r The most common lower respiratory tract infection and pulse oximetry:
Mild hypoxemia common r Congenital abnormalities: Protracted clinical course,
in the 1st yr of life with a rate of 1020 episodes per
100 children No evidence that mild hypoxemia predicts recurrent pneumonias
r Responsible for 16% of all hospital admissions in progress of disease
r Respiratory distress with chest retractions, tracheal
the 1st yr of life (1,2)
tug, nasal flare/grunting (severe disease) TREATMENT
Prevalence r Tachypnea, tachycardia
Accounts for up to 60% of all lower respiratory tract r Lethargy (hypoxemia or severe disease) PRE HOSPITAL
illness during the 1st yr of life and for up to 32% of r Cardiorespiratory and oxygenation monitoring is
r Frank dehydration uncommon
hospitalizations for lower respiratory tract infection in essential.
this age group r Wheezing; may be absent in mild or severe disease r Young infants have limited respiratory reserve and
r Crepitations
RISK FACTORS may decompensate suddenly.
r Risk factors for bronchiolitis: DIAGNOSTIC TESTS & INTERPRETATION INITIAL STABILIZATION/THERAPY
Exposure to tobacco smoke, lack of breastfeeding Lab r Assess and stabilize airway, breathing, and
r Predictors of need for airway intervention/ICU care: Initial Lab Tests circulation.
Age <7 wk r Most cases need no investigations (3). r Bag-mask ventilation with apnea
Weight <4 kg r Most blood assays are not useful. r Intubation if persistent apnea, impending respiratory
Respiratory rate >80/min r Blood gas analysis may be useful in severe disease failure
Heart rate >180 bpm to detect respiratory failure. r Supplemental oxygen if oxygen saturation <90% (3)
Prematurity r Virologic testing (ELISA, fluorescent antibody r IV hydration if dehydrated or severe respiratory
Comorbidity: Cardiac/Pulmonary disease, testing, PCR, culture) in critically ill, neonates, distress
immunodeficiency, neuromuscular disease comorbidities, atypical presentation
r Not necessary for diagnosis but may be used for MEDICATION
GENERAL PREVENTION
r Palivizumab prophylaxis: cohorting during hospital admission First Line
r Ibuprofen 10 mg/kg/dose PO/IV q6h PRN
Indicated at 32 wk gestation if 6 mo old at r Consider urinalysis and urine culture in febrile
start of respiratory syncytial virus (RSV) season children <3 mo of age.
and 28 wk gestation if 12 mo old at start RSV r Consider sepsis workup in febrile bronchiolitis in r Most patients require no pharmacotherapy beyond
season (3) those <28 days of age if respiratory status permits: antipyretics.
r Hand washing to limit viral transmission r Bronchodilators (albuterol, epinephrine): Not
Bacterial coinfections are rare (5).
routinely indicated; do not change hospitalization
PATHOPHYSIOLOGY Imaging rates or clinical course (7):
Viral-induced necrosis of small airway epithelium, r Chest radiographs:
Therapeutic trial of albuterol 2.5 mg via nebulizer
acute neutrophilic inflammation and edema, profuse Not indicated in typical presentation (6) or 500 g via metered-dose inhaler/spacer an
mucus and bronchospasm May demonstrate airway disease, atelectasis, option:
hyperinflation Continue only if major decrease in work of
ETIOLOGY
r RSV in 8590% The minority have airway and airspace disease breathing
r Human meta pneumovirus, coinfections with RSV Pneumonia is viral. Response usually mild and transient
r Consider chest radiograph when:
common (4) Should not be routinely used (3)
r Parainfluenza Need to exclude another diagnosis
r Influenza Chronic course with lack of resolution over 3 wk
Critically ill with impending respiratory failure
r Adenovirus
Atypical presentation in toxic or deteriorating child
Otitis media
126
BRONCHIOLITIS
r Epinephrine: PROGNOSIS
r Generally excellent
ADDITIONAL READING
Has a theoretical advantage over albuterol due to
its alpha effects r 20% still symptomatic at 3 wk r Hartling L, Wiebe N, Russell K, et al. Epinephrine for
Does not decrease hospitalization on its own (8)
Very temporary benefit
r Severe bronchiolitis with need for airway support bronchiolitis. Cochrane Database Syst Rev. 2004;
(1):cd003123.
B
rare (2%):
r Bronchodilators not effective after discharge r Levine DA, Platt SL, Dayan PS, et al. Risk of serious
Patients at risk if very young or premature, if there
is marked tachycardia/tachypnea (above), and if bacterial infection in young febrile infants with
Second Line
r Corticosteroids: Controversial; of questionable there are comorbidities. respiratory syncytial virus infections. Pediatrics.
2004;113:17281734.
benefit (810): COMPLICATIONS r Mallory MD, Shay DK, Garrett J, et al. Bronchiolitis
Not recommended by most widely accepted r Otitis media
practice guideline (3) r Dehydration (poor feeding common but frank management preferences and the influence of pulse
r Antibiotics: oximetry and respiratory rate on the decision to
dehydration rare) admit. Pediatrics. 2003;111(1):e45e51. Available
Not indicated r Pneumonia
at http://www.pediatrics.org/cgi/content/full/111/1/
Consider if associated bacterial disease (otitis r Apnea e45.
media), toxic appearance, sepsis syndrome r Respiratory failure
DISPOSITION
Media Element)
Admission Criteria r Bacterial Pneumonia
r Hospitalize if: REFERENCES r Pneumonia, Aspiration
Hypoxemia <90% on room air 1. Stang P, Brandenburg N, Carter B. The economic r Respiratory Distress
Home oxygen is an option in otherwise healthy
burden of respiratory syncytial virus-associated r Wheezing
infants with mild bronchiolitis and room air bronchiolitis hospitalizations. Arch Pediatr
saturations in the upper 80s. Adolesc Med. 2001;155(1):9596.
Dehydration with inability to maintain hydration
2. Shay DK, Holman RC, Newman RD, et al. CODES
Major comorbidity
Bronchiolitis-associated hospitalizations among
Need to rule out alternative diagnosis
US children, 19801996. JAMA. 1999;282(15):
Severe increase in the work of breathing ICD9
14401446. r 466.11 Acute bronchiolitis due to respiratory
Strongly consider in infants with high-risk criteria:
Weight <4 kg, age <7 wk, respiratory rate 3. American Academy of Pediatrics Subcommittee on
syncytial virus (rsv)
>80/min, heart rate >180 bpm Diagnosis and Management of Bronchiolitis. r 466.19 Acute bronciolitis due to other infectious
Significant social concerns Diagnosis and management of bronchiolitis.
Pediatrics. 2006;118:17741793. organisms
Recurrent apneas 4. Smyth RL, Openshaw PJM. Bronchiolitis. Lancet.
2006;368:312322.
Concern regarding impending respiratory failure, PEARLS AND PITFALLS
increasing oxygen requirements 5. Greenes DS, Harper MB. Low risk of bacteremia in
febrile children with recognizable viral syndromes. r Pay close attention to vital signs.
Discharge Criteria Pediatr Infect Dis J. 1999;18:258261. r Very young infants and patients with comorbidities
r Mild respiratory distress:
6. Schuh S, Lalani A, Allen U, et al. Evaluation of the or highly abnormal vital signs have the greatest risk
Consider for moderate respiratory distress if the
utility of radiography in acute bronchiolitis. of decompensation.
patient is meeting other discharge criteria. r The majority of infants with bronchiolitis require no
r Acceptable oxygen saturation in room air 90% J Pediatr. 2007;150:429433.
r Well hydrated 7. Kellner JD, Ohlsson A, Gadomski AM, et al. investigations and no pharmacotherapy,
Bronchodilators for bronchiolitis. Cochrane
r Follow-up available
Database Syst Rev. 2000;(2):cd001266.
8. Plint AC, Johnson DW, Patel H, et al. Epinephrine
FOLLOW-UP and dexamethasone in children with bronchiolitis.
N Engl J Med. 2009;360:20792089.
FOLLOW-UP RECOMMENDATIONS 9. Schuh S, Coates AL, Binnie R, et al. Efficacy of oral
Discharge instructions and medications: dexamethasone in outpatients with acute
r Close, frequent follow-up and reassurance are often bronchiolitis. J Pediatr. 2002;140:2732.
helpful. 10. Corneli HM, Zorc JJ, Mahajan P, et al. A
r Warn parents that symptoms may persist for 23 wk. multicenter, randomized, controlled trial of
r Frequent small feeds usually are required. dexamethasone for bronchiolitis. N Engl J Med.
r Nasal suctioning may be helpful. 2007;257:331339. [Erratum, N Engl J Med.
r Instruct parents that pharmacotherapy after 2008;359:1972.]
discharge generally is not beneficial.
r Bronchodilators after discharge do not change the
subsequent clinical course.
r Daily oral corticosteroids such as prednisolone
1 mg/kg after a trial of dexamethasone 1.0 mg/kg
and 2 treatments of epinephrine 1:1,000 3 mL by
nebulization 30 min apart in the emergency
department may be considered:
Not routinely recommended (3)
127
BURN, CHEMICAL
Mark X. Cicero
Lye is the common name for sodium hydroxide. PHYSICAL EXAM

BASICS Historically, this agent has been used to attempt r Assess the patients airway 1st, looking for signs of
suicide and is sometimes thrown in the face of inhalation or ingestion. If stridor, respiratory distress,
DESCRIPTION an adversary as a form of assault. or oral burns are present, endotracheal intubation
r Chemical burns are caused by caustics, which Sodium hypochlorite, the active ingredient of may be necessary.
include acids, bases, and other agents that cause household bleach and swimming pool r Dribble marks on the face or chest may be seen with
tissue destruction on contacts. chlorinator, is itself a weaker base (pH 11) and caustic ingestion.
r Cutaneous burns to the face and extremities are not very corrosive. Concentrated pool r The eyes are assessed for signs of corneal injury and
most common. chlorinator, especially in solid form, is more globe perforation:
r More serious or life-threatening burns involve the dangerous. Visual acuity should be assessed for suspected eye
face, airway, alimentary tract, and/or eyes. Wet cement includes calcium hydroxide and is injury.
r An estimated 25,000 chemicals are known to cause moderately caustic. r Assess abdomen for signs of ingestion injury:
burns. Ammonia in household cleaners is not corrosive
Tenderness
enough to cause burns to the skin. It can cause Guarding
EPIDEMIOLOGY respiratory distress and pulmonary edema if
In the U.S., >121,000 burns of all kinds occur each Rigidity
aspirated. r The percent total body surface area (%TBSA) burned
year in those <20 yr of age: r Other agents cause burns, not by donating (as with
r 9% of these burns result from chemical burns. is assessed, as is the location and depth of burns:
acids) or accepting (as with bases) a proton but by Edema of underlying tissue can cause difficulty
r Incidence has remained similar from 19902006. reactions with moisture on the skin or direct tissue assessing burn depth.
toxicity. These include: Chemical burns evolve in the hours after the
RISK FACTORS
r Male gender Vesicants, such as nitrogen mustard. These agents injury, and burns should be re-evaluated
r Age <6 yr were used in World War I and may potentially be frequently. Special situations include:
r Poor home supervision used in chemical terrorism. Burns to the hands, face, or genitals
Hair-coloring agents, which are occasionally Circumferential burns due to risk of
GENERAL PREVENTION ingested by toddlers, may cause airway edema or compartment syndrome and neurovascular
Anticipatory guidance to maintain household esophageal injuries. Additionally, the persulfates compromise
chemicals out of reach of children may be helpful to and peroxides in hair coloring may cause scalp
prevent many chemical burns. and skin burns if not removed promptly. DIAGNOSTIC TESTS & INTERPRETATION
Elemental metals, such as lithium and potassium Lab
PATHOPHYSIOLOGY r Factors that influence burn severity include: Initial Lab Tests
r Acids cause coagulative necrosis, which is r Localized burns, such as to the hands, require no lab
Duration of contact
coagulation of tissue proteins. When this occurs, an Volume of chemical in contact with the body studies.
eschar forms, limiting the depth of burning. Thickness of the epithelium at the burn site r Patients with severe burns (>510% TBSA), those
r The lower the pH or the higher the titratable reserve,
pH and other chemical properties of the agent (eg, with a suspected inhalation injury or ingestion, or
the more hydrogen ions are donated. exothermic reactions) who may require surgical intervention may require
r Acids with lower pH (0.02.0) cause worse burns
Concentration (molarity) of the agent an extensive lab evaluation, including:
more quickly: r In contrast to thermal burns, the chemical agent is in Metabolic profile, including renal function
Specific acids to consider include: contact with the skin longer. Blood gas analysis with lactate to assess
Hydrochloric acid, found in toilet bowl cleaners oxygenation, ventilation, and perfusion
and metal cleaners ETIOLOGY CBC
Phosphoric acid, found in metal cleaners and r At home, children may expose themselves to
Urinalysis
agricultural settings improperly stored cleaning agents, fuels, and other Creatine phosphokinase to assess tissue
Sulfuric acid, noteworthy for exothermic preparations. destruction and risk to the kidneys
reactions when exposed to water r Chemical exposures may occur from chemical
Coagulation profile
Hydrofluoric acid, a relatively high pH acid found production plants and from release of chemicals
in swimming pool shock and etching and from vehicles transporting chemicals. Imaging
r Chemicals may be used as agents of terrorism. r Chest radiography, when inhalation is suspected, to
industrial cleaning products. The fluorine ion
increases tissue penetration, increasing damage r Nonaccidental trauma assess pulmonary edema
r Abdominal radiography to assess for free air in cases
to muscle and other underlying structures.
Phenols, such as carbolic acid, are weak organic COMMONLY ASSOCIATED CONDITIONS of ingestion
r Ophthalmic burns r CT of the chest and abdomen may be indicated with
acids used in plastic manufacturing and found r Ingestion of chemical
in nail polish. caustic ingestion.
r Alkali burns (bases) cause liquefaction necrosis and r Aspiration of chemical
cause deeper injuries. r Endoscopy may be performed by gastroenterology.
r Proteins are denatured, and fats are saponified. r May be indicated with any suspected esophageal
Neither denatured proteins nor saponified fats stop
DIAGNOSIS
burn or with severe burns of lower GI system
alkali penetration of tissue. HISTORY r Otorhinolaryngology may be consulted to directly
r Bases with higher pH (12.014.0) cause more r Ideally, the agent in its container or its material visualize the airway.
liquefaction necrosis more quickly than bases with safety data sheet will travel to the emergency
pH closer to 7.0: department with the patient. Several questions can
Airway, esophageal, and gastric ulcers are classified by
Bases of clinical interest in pediatrics include: help guide diagnosis and treatment, including:
Sodium hydroxide and potassium hydroxide, depth and extent: Superficial, transmucosal,
Time of exposure
transmural, and circumferential.
which are found in drain cleaners and oven Duration of exposure
cleaners. These are among the most caustic Type of agent and its pH and concentration
products found in homes. These cause Volume of agent
exothermic reactions and significant liquefaction Whether irrigation and decontamination have
necrosis. occurred
r Eye irritation and respiratory irritation are commonly
associated with chemical burns.
128
BURN, CHEMICAL
DIFFERENTIAL DIAGNOSIS MEDICATION

r Thermal burns r Topical antibiotics are applied to superficial or small FOLLOW-UP
r Pemphigus burns to limit the risk of superinfection. Options
r Stevens-Johnson syndrome
r Epidermolysis bullosa
include bacitracin, erythromycin, and silver
sulfadiazine (the latter is used in children >2 mo of
B
r Phytophotodermatitis age due to the risk of hyperbilirubinemia). r Follow-up is needed within 24 hr to assess
r Analgesics are usually needed. progression of the burn, signs of infection, and
r Opioids: adequacy of pain control.
TREATMENT Morphine 0.1 mg/kg IV/IM/SC q2h PRN: COMPLICATIONS
Initial morphine dose of 0.1 mg/kg IV/SC may r General complications include infection, pain,
PRE HOSPITAL be repeated q1520min until pain is controlled, scarring, and loss of function.
r Decontamination, including disrobing the patient then q2h PRN. r Complications of chemical ingestions include
and irrigation: Hydrocodone or hydrocodone/acetaminophen
mediastinitis, esophageal perforation, peritonitis,
During irrigation, protect unburned skin from the dosed as 0.1 mg/kg of hydrocodone component
and strictures.
effluent. PO q46h PRN r Complications of ocular burns include blindness,
Irrigation with water is adequate for the r NSAIDs:
majority of caustics and corrosives, with these globe perforation, and corneal scarring.
Consider NSAID medication in anticipation of r Complications of chemical aspiration include airway
exceptions: prolonged pain and inflammation:
Elemental metals, such as lithium and sodium, Ibuprofen 10 mg/kg/dose PO/IV q6h PRN burns, edema, respiratory distress, respiratory
react violently with water. They should be Ketorolac 0.5 mg/kg IV/SC q6h PRN failure, and pulmonary edema.
irrigated with mineral oil. Naproxen 5 mg/kg PO q8h PRN
Vesicants, such as mustard, require irrigation
with a 0.5% chloride solution after removal of SURGERY/OTHER PROCEDURES ADDITIONAL READING
clothes and contaminated hair. Soap and water Laparotomy may be required to locate and treat GI r DSouza A, Nelson N, McKenzie L. Pediatric burn
are a less effective alternative. Rescuers must perforation.
injuries treated in US emergency departments
don masks and rubber (not latex) gloves. DISPOSITION between 1990 and 2006. Pediatrics. 2009;124(5):
r Protection of prehospital care providers to prevent
Admission Criteria 17.
further injuries r The decision to admit the patient is based on the r Turner A, Robinson P. Respiratory and
INITIAL STABILIZATION/THERAPY %TBSA burned, the age of the patient, and the gastrointestinal complications of caustic ingestion in
r Dilution with copious amounts of water is the key to quality of the likely outpatient follow-up. It is children. Emerg Med J. 2005;22(5):359361.
stopping the burning process. Attempts to neutralize impossible to note a definitive TBSA at which
the pH of the caustic agent are generally not helpful. admission is mandatory.
r Smaller burns for which admission is more strongly CODES
Dilution continues until the pH of the irrigation
effluent is neutral: indicated include burns to the hands, face, feet, and
Phenols specifically are best irrigated with genitals. ICD9
polyethylene glycol (PEG)-containing liquids. r Burn center admission should be considered based r 949.0 Burn of unspecified site, unspecified degree
r After decontamination, burns should be dressed on local protocols, the pediatric burn expertise of r 949.1 Erythema due to burn (first degree),
with nonadhesive bandages, such as petroleum jelly the referring institution, and the severity of the burn. unspecified site
gauze, then bandaged loosely. r Critical care admission criteria: r 949.2 Blisters with epidermal loss due to burn
r IV normal saline or lactated Ringer solution should Need for endotracheal intubation or respiratory (second degree), unspecified site
be given. Use Parkland formula to determine the compromise
amount of fluid resuscitation to be given in the 1st Unstable vital signs or shock
24 hr: Discharge Criteria PEARLS AND PITFALLS
Parkland: 4 mL/kg per %TBSA. Add maintenance Small burns to the skin and minor burns to the eyes
fluid for children <5 yr. r Proper early decontamination and irrigation of burns
may be followed in the outpatient setting.
Administer 1/2 of the fluids over the 1st 8 hr and with an irrigant appropriate to the agent is key:
Issues for Referral
the remainder over the next 16 hr. Water is usually the irrigant of choice.
Appropriate services, including hand, face, plastic
Ringer lactate is the fluid of choice. Mineral oil should be used for hygroscopic metals.
surgery, ophthalmology, GI, ENT, and pediatric surgery,
No colloid in the 1st 24 hr PEG should be used for phenols.
r Burn center treatment is indicated for a smaller may need to be consulted in the emergency r With ingestion, vomiting, drooling, stridor, or
department, inpatient, or after discharge.
%TBSA than with thermal burns due to the depth of inability to take PO are suggestive of significant GI
burns and tissue disruption. burn.
r Chemical burns to eye require irrigation with a r When aspiration or ingestion is suspected, early
Morgan lens and ophthalmologic consultation. intubation is prudent.
r pH paper placed in the palpebral space can assess r Stridor, dysphonia, or aphonia are indications for
pH; the goal is a pH of 7.4: intubation. Delay may result in the inability to secure
Decontaminate phenols with polyethylene glycol. the airway.
r Agents specifically used for hydrofluoric acid: r Hydrofluoric acid burns require calcium or
Calcium or magnesium to neutralize the fluoride magnesium applied to the burn or calcium
ion gluconate intra-arterially or SC.
Applied topically for small burns and SC for larger r Consider non-accidental trauma and self-injurious
areas behavior as factors leading to the burn.
129
BURN, THERMAL
Nikhil B. Shah
r Circumferential burns should be noted:

BASICS DIAGNOSIS May lead to compartment syndrome or interfere
with respiratory mechanics
DESCRIPTION HISTORY r Evaluate the burn pattern:
r Burn-related injuries are a leading cause of r Interview prehospital personnel, patient, and/or
Symmetric stocking distribution or branding may
morbidity and mortality in children. family. suggest inflicted burn injury.
r Thermal burns are the most common type of burn in r Note any inconsistencies or implausible history that
childhood. may suggest abuse. DIAGNOSTIC TESTS & INTERPRETATION
r Prompt referral to a burn center for children with r Determine the mechanism of injury. Lab
major burns improves outcomes. r History of closed space exposure (suggests smoke Initial Lab Tests
r Baseline CBC and serum electrolytes in anticipation
r Children with burns require long-term follow-up inhalation or carbon monoxide)
with special attention to prevention of disability. r Extrication time of major fluid and electrolyte shifts in serious
r Most burns are potentially preventable. r Identify delays in seeking attention or discrepancies burns:
Lab testing is not necessary for minor burns.
in the history (may indicate inflicted injury). r Urinalysis to detect myoglobin in patients with
EPIDEMIOLOGY r Fluids given during transport
r Burns are the 3rd leading cause of death resulting muscle injury
r Past medical history
from unintentional injury in children (1). r Blood gas with lactate concentration to assess
r 80% of pediatric burns are scald injuries (2). r Tetanus status
r Allergies oxygenation, ventilation, perfusion, and tissue injury
r House fires account for the majority of deaths due to r Carboxyhemoglobin levels in suspected carbon
pediatric burns. PHYSICAL EXAM monoxide exposure
r Nonaccidental burns account for 20% of burn unit r Vital signs with pulse oximetry
Imaging
admissions. r Accurate weight in kilograms
Need for imaging is dictated by mechanism of injury
r Primary survey: Assess airway, breathing, and and physical exam:
GENERAL PREVENTION
r Pay careful attention to the water heater set point circulation: r Radiographs can be performed for suspected upper
(49 C or 120 F) and bath water temperature. Evaluate for signs/symptoms of upper airway airway obstruction or smoke inhalation but should
r Maintain kitchen/cooking safety (eg, keeping hot burns (eg, stridor, drooling) or inhalational injury never delay definitive airway management.
objects away from edge of the counter). (eg, carbonaceous material in mouth/nares). r CT scan or US may be performed to identify
r Appliance safety: Cords should be stowed, and the Respiratory compromise may result from associated injuries.
circumferential chest burns or carbon monoxide
childs activity monitored while an appliance (eg,
exposure.
radiator, iron, etc.) is on.
r Fire safety (eg, candles and cigarettes should never Children with impaired perfusion at initial TREATMENT
presentation may have other underlying injuries;
burn unattended) later onset suggests burn shock.
r Never heat infant bottles in microwave ovens. PRE HOSPITAL
r Secondary survey: Evaluate for other injuries. r Provide basic life support and oxygen.
r Keep flammable substances out of reach. r Evaluate the burn for total body surface area (TBSA) r Intubation may be required for airway burns.
PATHOPHYSIOLOGY affected: r Stop the burning process by removing offending
r Thermal energy results in local injury: TBSA is estimated using an age-specific chart. clothing/jewelry (unless stuck to the patient).
Intensity and duration of thermal exposure Alternatively, use the palmar surface of the r Cover the burn area with a clean sheet or blanket.
determines depth of the burn. patients hand, which represents 1% of TBSA r Fluid therapy (for major burns/long transports)
r In major thermal burns, a systemic inflammatory (3): r Analgesia
response will follow in which increased capillary Major burns involve >10% of TBSA. r Rapid transport
permeability and 3rd spacing of fluid into the r Evaluate the burn for depth:
interstitium will occur: Superficial (1st degree): INITIAL STABILIZATION/THERAPY
Confined to epidermis only; red and painful; r Airway:
Hypotension (burn shock) and edema may result.
r A hypermetabolic state (dramatic increase in energy blanches with pressure; not included in TBSA Anticipate difficult airway; intubate early for
expenditure and protein metabolism) develops estimation for major burns suspected upper airway burns or significant
following resuscitation for major burns. Superficial partial thickness (2nd degree): inhalational injury
Involves epidermis and superficial dermis; r Breathing:
ETIOLOGY painful, red, weeping, usually blisters; blanches Supplemental oxygen for fire-related burns
r Scald injuries result most commonly from hot bath
Deep partial thickness (2nd degree): r Circulation:
water but can occur when a child pulls hot Involves epidermis and deep dermis; less Fluid resuscitation in major burns (1st 24 hr):
substances off a stove. painful; blisters; white to red; wet or waxy dry; Parkland: 4 mL/kg per %TBSA. Add
r Contact burns may result from irons, ovens,
nonblanching; difficult to distinguish from maintenance fluid for children <5 yr.
treadmill belts (friction), and other hot objects; this full-thickness burns Galveston: 5,000 mL/m2 per %TBSA. Add
type of injury is most frequently seen in toddlers. Full thickness (3rd degree): 2,000 mL/m2 /day for maintenance fluid.
r Flame burns may result from house fires, candles, Extends through and destroys epidermis and Administer 1/2 over the 1st 8 hr, and the other
matches, lighters, and fireworks: dermis; usually insensate; waxy white to 1/2 over the next 16 hr.
Occur more commonly in children and adolescents leathery gray to charred and black; dry and Ringer lactate is the fluid of choice.
r Burn injuries can be a manifestation of child abuse. inelastic; nonblanching No colloid in the 1st 24 hr.
4th-degree burns: r Pain control
Life threatening; extend into deeper tissues such r Monitor fluid status:
as muscle, fascia, or bone Place bladder catheter.
Maintain urine output at 1 mL/kg/hr.
130
BURN, THERMAL
MEDICATION Discharge Criteria 3. Nagel TR, Schunk JE. Using the hand to estimate
r Pain control is essential. r No airway compromise the surface area of a burn in children. Pediatr
r Opioid analgesia is often required: r Burns <10% TBSA Emerg Care. 1997;13(4):254255.
Morphine 0.1 mg/kg IV/IM/SC q2h PRN:
Initial morphine dose of 0.1 mg/kg IV/SC may
r Tolerating adequate fluids by mouth
r No suspicion for inflicted burn injury
4. Sargent RL. Management of blisters in the
partial-thickness burn: An integrative research
B
be repeated q1520min until pain is controlled, r Family must have the resources to support an review. J Burn Care Res. 2006;27(1):6681.
then q2h PRN. outpatient care plan that includes the following: 5. Passaretti D, Billmire DA. Management of pediatric
Hydrocodone or hydrocodone/acetaminophen Teaching proper wound care and dressing burns. J Craniofac Surg. 2003;14(5):713718.
dosed as 0.1 mg/kg of hydrocodone component techniques to the patient and family 6. Sheridan RL. Burns. Crit Care Med. 2002;
PO q46h PRN Pain control 30(11 Suppl):S500S514.
Codeine 0.51 mg/kg/dose PO q46h Clearly defined early return conditions (eg, signs
r NSAIDs:
of infection)
Consider NSAID medication in anticipation of Immediate and long-term follow-up with scar ADDITIONAL READING
prolonged pain and inflammation: management r Kassira W, Namias N. Outpatient management of
Ketorolac 0.5 mg/kg IV/IM q6h PRN Issues for Referral pediatric burns. J Craniofac Surg. 2008;19(4):
Naproxen 5 mg/kg PO q8h PRN Follow-up is essential to a successful outcome: 10071009.
r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN r Re-evaluate every 12 wk for wound healing and r Reed JL, Pomerantz WJ. Emergency management of
r Tetanus prophylaxis as indicated: infection until epithelization occurs, then every 6 wk pediatric burns. Pediatr Emerg Care. 2005;21(2):
thereafter for scarring. 118129.
Tetanus toxoid 0.5 mL IM r Long-term rehabilitation, including physical and
r Superficial burns are managed with moisturizers and
over-the-counter analgesics: occupational therapy
r Pressure therapy (application of pressure garments), CODES
Silver sulfadiazine: Apply b.i.d. to the burn area
until healed; should not be used on the face. massage, and/or splints may be needed to treat
Neosporin cream: Apply q.i.d. to burn area until wound contracture sites as the scar matures. ICD9
r Requires a multidisciplinary approach r 949.0 Burn of unspecified site, unspecified degree
healed. r 949.1 Erythema due to burn (first degree),
SURGERY/OTHER PROCEDURES unspecified site
r Partial- and full-thickness burn wound FOLLOW-UP r 949.2 Blisters with epidermal loss due to burn
management: (second degree), unspecified site
Clean burns with mild soap and water. FOLLOW-UP RECOMMENDATIONS
Debride devitalized tissue. Discharge instructions and medications:
Leave blisters intact unless large, painful, or if r Maintain proper wound care, and change the
PEARLS AND PITFALLS
rupture is imminent (4). dressing twice a day.
Apply a topical antibiotic, such as 1% silver r Pain control with over-the-counter or narcotic r Most burns are small and can be managed as an
sulfadiazine (avoid in sulfa allergy and neonates); analgesics as indicated outpatient.
mafenide to cartilaginous areas; or bacitracin to r Major burns require aggressive attention to airway
Patient Monitoring
the face. management, adequate fluid resuscitation, and
Monitor for infection, hypertrophic scar formation, and
Synthetic occlusive dressings (eg, Acticoat) are an wound care.
development of contractures. r Long-term follow-up and rehabilitation are essential
alternative to topical antimicrobials for burns
<2% TBSA and <24 hr old PROGNOSIS to a successful outcome.
Cover with a sterile nonadherent dressing, then Mortality from burn injury is related to young age,
wrap with gauze or a woven gauze bandage roll. burn extent, and the presence of inhalational injury.
r Emergent escharotomy may be indicated to relieve
COMPLICATIONS
restriction of the chest wall or to reduce r Delayed respiratory failure (inhalation injury)
compartment pressure in an extremity. r Wound infection
DISPOSITION r Sepsis
The majority of burns are small and may be managed r Hypertrophic scar formation
in the outpatient setting (ie, partial thickness <10% r Contractures
TBSA or full thickness <2%) (5).
Admission Criteria
r Criteria for transfer to a burn center (6): REFERENCES
Partial-thickness burns >20% TBSA at any age or
1. CDC, National Center for Injury Prevention and
>10% TBSA in those <10 yr of age
Control, WISQUARS. 10 leading causes of
Full-thickness burns >5% TBSA
unintentional injury deaths, United States. Available
Any significant burn to the face, hands, major
at http://webappa.cdc.gov/cgi-bin/broker.exe.
joints, genitalia, or perineum
Accessed November 25, 2009.
Inhalation, chemical, or electrical injury
Significant associated injuries 2. Drago DA. Kitchen scalds and thermal burns in
r Patients with significant burns not fulfilling the children five years and younger. Pediatrics.
2005;115(1):1016.
above criteria should be admitted to the hospital for
observation, IV fluids, and pain control.
Unstable vital signs; need for mechanical
ventilation
131
LWBK822-driver-C LWBK822-Hoffman ch067.xml April 15, 2011 11:9
CAFFEINE/THEOPHYLLINE POISONING
David H. Jang
Lewis S. Nelson
ETIOLOGY r Serum caffeine or theophylline level: Measure

BASICS r Caffeine: initially and then q2h until levels are falling and
Iatrogenic: Give for neonatal apnea or headache patient improves clinically.
DESCRIPTION Medicinal use in combination with analgesics and r In cases of caffeine toxicity, some caffeine
r Caffeine is found in tea, coffee, and soft drinks. It is headache medications and stimulants used to metabolism will result in a small detectable
the most widely used psychoactive substance in the increase alertness and prevent sleep theophylline level:
world. In beverages such as sports or energy drinks Neonates are able to metabolize caffeine to
r Caffeine is contained in combination with aspirin, In other beverages and foods theophylline and vice versa.
ibuprofen, and other medications marketed for r Theophylline:
Imaging
headache therapy. Iatrogenic: Used to treat neonatal apnea, COPD, r Brain CT may rarely be indicated to assess for
r Caffeine is contained in high concentrations in many bronchitis, and asthma intracranial hemorrhage.
energy and sports drinks. r CXR may be indicated to evaluate hyperventilation,
r Caffeine is used as a proconvulsant in conjunction COMMONLY ASSOCIATED CONDITIONS
r Vomiting occurs with any acute poisoning. tachypnea, or hyperpnea.
with electroconvulsive therapy. r Hyperventilation may occur.
r Caffeine is also used for neonatal apnea as well as DIFFERENTIAL DIAGNOSIS
r Sympathomimetic toxicity:
adjunctive treatment for headaches.
r Theophylline and its IV formulation, aminophylline, DIAGNOSIS Amphetamines, cocaine, pseudoephedrine, etc.
r Salicylate toxicity
were once commonly used in the treatment of
HISTORY r Serotonin syndrome
asthma, bronchitis, and COPD. r Typically, a history of ingestion is readily given.
r Theophylline is used to treat neonatal apnea. r Neuroleptic malignant syndrome
r Caffeine and theophylline are extremely similar r Prominent nausea and vomiting is a characteristic r Infection and sepsis
structurally and pharmacologically. feature of significant acute toxicity.
r Caffeine has an additional methyl group that allows r Chronic toxicity often manifests subtle symptoms
it greater CNS penetration and effect. such as anorexia or palpitations. TREATMENT
r Patients with chronic toxicity may present with a
RISK FACTORS seizure as their 1st sign of toxicity. PRE HOSPITAL
r Therapeutic use of caffeine or theophylline r Acute-on-chronic toxicity is often very similar to an Assess and stabilize airway, breathing, and
r Use of highly caffeinated energy and sports drinks or circulation.
acute ingestion.
dietary supplements containing caffeine INITIAL STABILIZATION/THERAPY
r Patients at extremes of age are more susceptible to PHYSICAL EXAM r Assess and stabilize airway, breathing, and
r Vital signs: Tachycardia is invariably present,
toxicity. circulation.
tachypnea is usually present, BP may be elevated, r Supportive care is the mainstay of care with special
PATHOPHYSIOLOGY and wide pulse pressure is common. Hyperthermia is
r Caffeine and theophylline are adenosine receptor attention to neurovascular and cardiovascular
often present with accompanying diaphoresis.
antagonists and phosphodiesterase inhibitors. They r CNS: Mydriasis, anxiousness, agitation, insomnia, function.
also increase intracellular cyclic AMP. r GI decontamination:
headache, agitation. Delirium, psychosis or
r Caffeine and theophylline result in the release of Orogastric lavage may be of limited use, as pills
hallucination may rarely occur.
endogenous catecholamines, which stimulate beta r GI: Nausea and vomiting are present and usually may be too large.
receptors and result in a therapeutic effect severe. Ipecac should not be used and is potentially
previously sought in asthma treatment: r Diaphoresis is typical. dangerous in patients who present with seizures
In overdose of caffeine or theophylline, extremely or decreased mental status.
elevated levels of epinephrine and norepinephrine DIAGNOSTIC TESTS & INTERPRETATION Activated charcoal can be given if there are no
result. Lab contraindications (eg, seizures).
r Caffeine toxicity develops in children at doses Initial Lab Tests Multiple-dose activated charcoal enhances
>35 mg/kg and in adults at a dose of 1 g. r Blood glucose level to detect hypoglycemia; caffeine systemic elimination of theophylline by GI dialysis.
Theophylline toxicity develops acutely at similar and theophylline toxicity result in extreme Whole-bowel irrigation may be used in patients
doses. hyperglycemia, but symptoms are clinically similar to who ingest sustained-release pills.
r Both caffeine and theophylline may result in severe those of hypoglycemia. r Vomiting typically occurs and is severe. Use of
or even fatal status epilepticus if they result in r Serum electrolytes: Hypokalemia is expected; rarely, potent antiemetics such as ondansetron or
seizure: anion gap metabolic acidosis may occur. granisetron are indicated to treat vomiting.
r Urinalysis to assess for rhabdomyolysis r Although hypokalemia occurs, it is rarely
Due to their adenosine antagonist activity, the
natural mechanism by which the brain terminates r Assay creatine phosphokinase in any symptomatic consequential. If serum potassium is <2.4 mEq/L,
seizures is prevented. patient. supplemental potassium may be given:
These are the only toxins for which exposure alone r Troponin is rarely indicated with dysrhythmia, ECG Typically, such administration is futile. Due to
may be an indication to give prophylactic changes, or severe toxicity. Slight elevations may be intense beta-adrenergic agonism, potassium is
anticonvulsant due to severe morbidity and seen as a result of toxicity without any myocardial continuously driven intracellularly. Excessively
mortality resulting if seizures occur. ischemia or infarction. supplementing potassium may result in
hyperkalemia when the beta-agonist effect abates
and supplemental potassium moves to the
extracellular space.
132
CAFFEINE/THEOPHYLLINE POISONING
r Esmolol 100500 g/kg loading dose, then infusion

First Line of 50300 g/kg/min:
r Antiemetics are the most commonly needed To treat tachydysrhythmia or other adverse r Berlinger WG, Spector R, Goldberg MJ, et al.
medication: cardiovascular effects of caffeine or theophylline Enhancement of theophylline clearance by oral
Dose 0.2 mg/kg IV, max single dose 8 mg, may Esmolol is preferred due to titratable effect. activated charcoal. Clin Pharmacol Ther. 1983;33:
repeat dose q4560min to max of 0.6 mg/kg total Do not use long-acting beta-blockers. 351354.
Esmolol may improve tachycardia as well as r Hoffman RJ. Methylxanthines. In Goldfrank LR,
dose
r Agitation: hypotension. Flomenbaum NE, Lewin NA, et al., eds. Goldfranks
Lorazepam 0.050.1 mg/kg IV, repeat q15min
and titrate to effect
Beta-blockade also improves metabolic
derangement such as hyperglycemia and
Toxicologic Emergencies. 8th ed. Stamford, CT:
Appleton & Lange; 2006.
C
hypokalemia but is never administered for this r Shannon M. Hypokalemia, hyperglycemia and
Second Line purpose. plasma catecholamine activity after severe
r Anticonvulsant to prophylax seizure:
SURGERY/OTHER PROCEDURES theophylline intoxication. J Toxicol Clin Toxicol.
Severe morbidity and mortality result if seizures
Hemodialysis or charcoal hemoperfusion may be 1994;32:4147.
occur. Acute theophylline toxicityand by r Shannon M. Life-threatening events after
extrapolation, caffeine toxicitywith an elevated indicated:
level >90 g/dL should receive a loading dose of r Acute toxicity with caffeine or theophylline level theophylline overdose: A 10-year prospective
analysis. Arch Intern Med. 1999;159:989994.
barbiturate or possibly a benzodiazepine. >90 g/dL
Evidence exists for phenobarbital use due to the r Chronic toxicity with caffeine or theophylline level See Also (Topic, Algorithm, Electronic
fact that this was the predominant GABAnergic >45 g/dL Media Element)
medication decades ago when theophylline r Any toxicity with severe systemic toxicity such as Sympathomimetic Poisoning
toxicity was prevalent. ventricular dysrhythmia or seizure
Lorazepam 0.1 mg/kg IV (max single dose 5 mg)
may be used instead of phenobarbital. DISPOSITION
CODES
Phenobarbital 1020 mg/kg IV administered over Admission Criteria
30 min may also be used. r Patients with significant toxicity, such as intractable
r Anticonvulsant to treat seizure: vomiting or toxicity requiring inpatient observation ICD9
r 969.71 Poisoning by caffeine
Due to severe nature of seizure and likelihood of but not requiring ICU care r 974.1 Poisoning by purine derivative diuretics
developing status epilepticus, rapid escalation to r Any patient who displays suicidal ideation.
powerful anticonvulsants is indicated. r Critical care admission criteria:
Lorazepam 0.05 mg/kg IV q510min may be Patients with hypotension or other unstable vital
attempted for 3 doses. signs, severe toxicity that requires seizure
PEARLS AND PITFALLS
Propofol 1 mg/kg IV. May follow with infusion precautions, cardiac dysrhythmia r Caffeine and theophylline toxicity may result in
0.1 mg/kg/min, escalating to 0.3 mg/kg/min as Treatment for cardiac dysrhythmia or seizure in permanent neurologic injury or death if seizures
necessary: emergency department occur.
If benzodiazepine therapy fails, immediately
Discharge Criteria r Severe vomiting is expected with any significant
escalate to propofol. r Patients who are asymptomatic after 68 hr of ingestion. Use of potent antiemetics such as
May result in respiratory depression necessitating ondansetron are indicated for this.
observation can safely be discharged.
endotracheal intubation. r Patients who display suicidal ideation should also be r Due to adenosine antagonist activity of these
Effectively the most powerful anticonvulsant
evaluated by psychiatry. medications, the brains natural ability to terminate
available for emergency department use, this
a seizure is disrupted. If a seizure begins, it is likely
medication has not come to prominence in the Issues for Referral
to be long lasting or result in status epilepticus.
U.S. though in other countries is a routine Consult a medical toxicologist, intensivist, or other r The clinical presentation and management are
second-line medication for disruption of status clinician experienced and familiar with caffeine and/or
epilepticus. theophylline toxicity. significantly different between patients with acute
Valproic acid, midazolam, or pentobarbital toxicity vs. chronic toxicity.
r The mainstay for treatment remains primarily
administered by infusion may be used if propofol
is unavailable: FOLLOW-UP supportive with careful attention to the neurologic
These take longer to administer and are less and cardiovascular status.
PROGNOSIS
effective. r Varies with degree of toxicity, adequacy of
ALERT supportive care
r Most cases resolve with only occurrence of vomiting.
Do not use phenytoin under any circumstance in
cases of theophylline or caffeine toxicity. Phenytoin r If seizures occur, they may be difficult to control.
is completely contraindicated for use. Due to its Permanent neurologic injury may result.
mechanism of action, it will potentiate seizures and COMPLICATIONS
cardiac dysrhythmias. Use of phenytoin is not r Hypokalemia
beneficial and is highly detrimental. r Seizure
r Rhabdomyolysis
r Cardiac dysrhythmia
r Permanent neurologic injury
r Death
133
CALCIUM CHANNEL BLOCKER POISONING

Amit K. Gupta
Mark Su
r Influx also allows normal propagation of myocardial Imaging

BASICS electrical impulses in the atrioventricular (AV) node. r CXR should be performed to assess for pulmonary
r Calcium is driven intracellularly down a edema.
DESCRIPTION concentration gradient via a voltage-sensitive L-type r CT of the brain should be considered in individuals
r There are 3 classes of calcium channel blockers
calcium channel. with altered mentation.
(CCBs) in clinical use: r CCBs function by binding and inhibiting this L-type
Dihydropyridine (nifedipine, amlodipine, Diagnostic Procedures/Other
calcium channels on the cell membrane, thereby ECG should be performed to looks for signs of
nicardipine): Causes smooth muscle relaxation in decreasing the flow of calcium into the cell. bradycardia and/or other conduction abnormalities.
the peripheral vascular system, lowering BP: r In the myocardium, this blockade decrease
Little direct cardiac negative inotropic effect: DIFFERENTIAL DIAGNOSIS
myocardial contraction force and causes r Beta-blocker toxicity
Reflex tachycardia may occur. hypotension.
Loses selectivity in large overdoses r In the vasculature, this blockade results in arterial r Digoxin toxicity
Phenylalkylamine (verapamil): Direct negative r Clonidine toxicity
vasodilation and relaxation.
inotropic and chronotropic effects that lead to r Calcium inhibition at the SA node leads to r Cardiogenic shock
bradycardia and hypotension with toxicity r Hemorrhagic shock
Benzothiazepines (diltiazem): Have less profound bradycardia.
r Calcium inhibition at the AV node can lead to r Septic shock
effects compared to verapamil, but toxicity also r Acute MI
leads to bradycardia and hypotension conduction abnormalities.
r Diltiazem and verapamil are most clinically r Hyperglycemia may occur due to prevention of
insulin release from pancreatic beta islet cells.
consequential in overdose. TREATMENT
EPIDEMIOLOGY ETIOLOGY
r Numerous brands of CCBs are available. PRE HOSPITAL
Incidence r Understanding of the different characteristics of r Assess and stabilize airway, breathing, and
Of the 2.4 million exposure logged by the American
each class may be helpful in evaluating clinical circulation.
Association of Poison Control Centers (AAPCC) in r Supplemental oxygen
2007, 10,084 of these were due to various CCBs: outcome and guiding therapy.
r Establishment of an IV line with cardiac monitoring
r 13% were in children <6 yr, and 2.3% occurred COMMONLY ASSOCIATED CONDITIONS
r Cardiac dysrhythmia r Assess blood glucose level if any alteration of
in children 619 yr.
r 4.5% of adolescent exposures were fatal, whereas r Congenital heart disease mental status.
2.3% of cases in children <3 yr were fatal. This r CHF INITIAL STABILIZATION/THERAPY
likely reflects that difference between intentional vs. r Assess and stabilize airway, breathing, and
unintentional ingestion. circulation.
DIAGNOSIS r Assess blood glucose level if any alteration of
RISK FACTORS
r Exposure to sustained-release preparations can lead HISTORY mental status.
r Obtain history of exposure, other possible r Consultation with a medical toxicologist or poison
to delayed toxicity.
r Coingestants with other cardiotoxic agents such as coingestants, and events that led to exposure. control center is recommended.
r Ask parents to bring in pill bottles if possible. r Activated charcoal (1 g/kg) may be given if the
beta-blockers, cyclic antidepressants, and
neuroleptics may exacerbate toxicity. patient is protecting the airway.
PHYSICAL EXAM r Syrup of ipecac is contraindicated.
GENERAL PREVENTION r Cardiovascular effects may include bradycardia and
r Orogastric lavage may be considered if the patient
Poison-proofing homes and giving parents poison hypotension, both which may be severe.
r Mental status is often preserved, unless the patient presents shortly after a potentially life-threatening
prevention advice is the most effective way to prevent overdose (usually within 1 hr) and the airway is
exposure in children. has hemodynamic instability. protected:
r Cardiovascular effects may include bradycardia.
PATHOPHYSIOLOGY This is predicated on having a clinician with
r Absorption of CCBs is rapid and occurs within DIAGNOSTIC TESTS & INTERPRETATION experience performing orogastric lavage; NG
30 min. Lab lavage is not indicated and not helpful.
r Calcium plays an important role in
Initial Lab Tests
excitation-contraction coupling and myocardial r Electrolytes, BUN, creatinine, glucose, calcium
contraction. r Measure acetaminophen and salicylate levels if
r Calcium influx also plays an important role in the
suicidal ingestion.
spontaneous depolarization of the sinoatrial (SA) r Obtain serum digoxin level if the patient is also
node. taking it chronically.
r Urine drug screen usually is not indicated unless for
forensic purposes such as suspected malicious intent
or child abuse.
134
CALCIUM CHANNEL BLOCKER POISONING
MEDICATION COMPLEMENTARY & ALTERNATIVE PROGNOSIS

THERAPIES r The prognosis is generally good with dihydropyridine
First Line
r 0.9% saline bolus (20 cc/kg) for hypotension r Cardiac pacing may be effective in increasing the overdoses.
r Atropine 0.02 mg/kg (min dose 0.1 mg and max rate of myocardial contraction, but electrical capture r Patients with verapamil or diltiazem overdoses have
2 mg) for bradycardia; usually ineffective is not always successful and BP is not always a variable prognosis depending on the severity of
r Lorazepam 0.05 mg/kg IV, max dose 2 mg: restored. ingestion.
r IV fat emulsion therapy (Intralipid 20% 1 mL/kg) has
First-line agents for seizures COMPLICATIONS
r IV calcium administration creates a concentration been shown in animal models and case reports to r Cardiovascular collapse
gradient large enough to partially overcome the be beneficial in lipid-soluble drug overdoses
(verapamil).
r Shock C
channel blockade, driving calcium into the cells:
r The proposed mechanism of action is the lipid r Death
A single 10-mL ampule of calcium chloride has
3 times the calcium concentration than that of sink theory, where drugs may become trapped in
calcium gluconate (13.4 mEq vs. 4.3 mEq). an expanded plasma lipid compartment. Another ADDITIONAL READING
Calcium chloride is sclerosing to veins and should proposed theory is that the emulsion acts as an
additional fuel source for the heart due to the r DeRoss F. Calcium channel blockers. In Goldfrank
only be given via a central line. Infusion through
an intraosseous line is acceptable. energy from fatty acids. LR, Flomenbaum NE, Lewin NA, et al., eds.
Calcium chloride dosing is 1525 mg/kg SURGERY/OTHER PROCEDURES Goldfranks Toxicologic Emergencies. 8th ed.
(0.10.25 mL/kg of 10% solution), not to exceed r Extracorporeal membrane oxygenation (EMCO) has Stamford, CT: Appleton & Lange; 2006:911923.
1 g slow IV bolus; may repeat q1020min for a r Proano L, Chiang WK, Wang RY. Calcium channel
also been attempted in patients who have
total of 34 doses. hypotension refractory to all pharmacologic blocker overdose. Am J Emerg Med. 1995;13:444.
Calcium gluconate dosing is 50100 mg/kg r Tenenbein M. Position statement: Whole bowel
therapies.
(0.31 mL/kg of 10% solution), not to exceed 1 g r Cases of survival after complete prolonged irrigation. American Academy of Clinical Toxicology;
slow IV bolus; may repeat q1020min for a total asystole/cardiac standstill in which EMCO has been European Association of Poisons Centres and
of 34 doses. used therapeutically have been reported in children Clinical Toxicologists. J Toxicol Clin Toxicol.
r Continuous infusion of calcium can be given, if 1997;35:753.
with CCB toxicity.
effective (0.5 mEq/kg/hr). Carefully monitor serum r Intra-aortic balloon counterpulsation is another r Yuan TH, Kerns WP 2nd, Tomaszewski CA, et al.
calcium levels. invasive supportive option in refractory cases and Insulin-glucose as adjunctive therapy for severe
Second Line has been used successfully to improve cardiac calcium channel antagonist poisoning. J Toxicol Clin
r A variety of inotropes are available if the above output and BP. Toxicol. 1999;37:463.
treatments fail. See Also (Topic, Algorithm, Electronic
r Norepinephrine infusion (0.12 g/kg/min) IV and DISPOSITION
Admission Criteria Media Element)
titrate to maintain adequate cardiac output: r All patients with exposure to sustained-preparation r Beta-Blocker Poisoning
Directly stimulates alpha- and beta1 -adrenergic r Digoxin Poisoning
CCBs should be admitted to a monitored setting due
receptors, thus increasing inotropic and r Shock, Cardiogenic
vasopressor effects to the potential of delayed toxicity.
r Epinephrine infusion (0.1 g/kg/min) IV and titrate r Admit all symptomatic patients.
to maintain adequate cardiac output: CODES
Directly stimulates alpha- and beta-adrenergic Patients with signs of hemodynamic instability
receptors should be admitted to an ICU setting.
r Dopamine 520 g/kg/min IV and titrate to Discharge Criteria ICD9
May discharge if the patient remains asymptomatic 972.9 Poisoning by other and unspecified agents
maintain adequate cardiac output:
after observation for 6 hr for immediate-release primarily affecting the cardiovascular system
Indirectly stimulates alpha and beta1 -adrenergic
dopaminergic receptors to produce ionotropic, preparations
chronotropic, renal/splanchnic vasodilatory (at low PEARLS AND PITFALLS
doses), and vasopressor (at high doses) effects
r Amrinone 50 g/kg IV loading dose with FOLLOW-UP r There are 3 classes of CCBs, with verapamil and
maintenance infusion of 0.50 g/kg/min IV and FOLLOW-UP RECOMMENDATIONS diltiazem being the most consequential in overdose.
titrate to desired effect: r Discharge instructions and medications: r Dihydropyridine overdoses are the least concerning,
Inhibits myocardial phosphodiesterase leading to Follow up with the primary pediatrician. usually without serious sequelae.
increased cyclic adenosine monophosphate levels r An ingestion of 1 tablet of verapamil or diltiazem
Return to the emergency department for change
r High-dose insulin/glucose infusion: could result in fatality in small children.
in behavior, alteration in mental status, or if ill
Insulin (1 unit/kg bolus followed by 1 unit/kg/hr) appearing. r Admission and observation are indicated for any
Glucose must be coadministered, initially 1 g/kg r Activity: sustained-release verapamil or diltiazem ingestion.
bolus followed by infusion of 0.5 g/kg/hr. Normal activity after discharge r Calcium administration is the first-line agent for
Frequent blood glucose monitoring, initially CCB overdose.
q1015min for the 1st few hours, is necessary. Patient Monitoring
This therapy has been shown to be effective in Patients with intentional overdoses should be
case reports and in animal models. monitored for acts of self-harm.
The theorized mechanism is via positive inotropic
effects of insulin and cardiac utilization of glucose
as an energy source.
Frequent monitoring of serum glucose and
potassium levels is necessary.
135
CANDIDIASIS
Desiree M. Seeyave
PATHOPHYSIOLOGY r Vaginal candidiasis:

BASICS r Conditions associated with a decrease in normal Erythema of introitus with white-yellow curdlike
flora lead to overgrowth of Candida species (eg, dry discharge, white plaques on cervix or vaginal walls
DESCRIPTION mouth, broad-spectrum antibiotic use). r Systemic candidiasis:
r Candidiasis is an opportunistic fungal infection r Impaired cellular immunity, T-cell function, and Ill appearance, fever, shock, dehydration, presence
caused by Candida species, most commonly phagocytic activity allow Candida species to of indwelling vascular access device
Candida albicans. proliferate.
r Candida species are part of the normal flora of the r Neonatal infection is acquired during birth from DIAGNOSTIC TESTS & INTERPRETATION
skin, mouth, intestinal tract, and vagina. infected vaginal mucosa and usually manifests
Lab
r Disease can occur at any site, including mucosally, within the 1st wk of life; also is acquired from
Initial Lab Tests
r Oral, vaginal, and esophageal candidiasis do not
cutaneously, vaginally, and systemically. mothers breast and infected bottle nipples or
r Oropharyngeal candidiasis, also known as pacifiers. require lab assay for diagnosis.
r Opportunistic candidal overgrowth on mucosal r Test of scrapings from oropharyngeal and cutaneous
pseudomembranous candidiasis or thrush, is the
most common human fungal infection. surfaces of the GI, respiratory tract, vagina, and lesions if initial treatment fails
r Systemic candidiasis or candidemia may occur in r Direct light microscopy of scrapings from the mouth,
skin, with hematogenous spread leading to systemic
immunocompromised patients and is potentially life disease skin, or vagina using potassium hydroxide
threatening. preparation reveals long, branching hyphae of C.
COMMONLY ASSOCIATED CONDITIONS albicans.
EPIDEMIOLOGY Immunodeficiency/immunosuppression: r Vaginal pH remains normal (<4.5).
Prevalence r Oral lesions are common in newborns and infants, r Neutropenia in patients with candidemia
r Candida is in the oral cavity in 4060% of the whose immune systems are immature. r Fungal culture and susceptibility testing of mucosal
population (1). r After infancy, immunodeficiency should be
or skin scrapings, blood, urine, CSF, bone marrow,
r Thrush occurs in 40% of healthy neonates. suspected in patients with candidiasis. tissue biopsy, abscess aspirate, bronchoalveolar
r Oral candidiasis is the most common infection in lavage fluid
patients with HIV and occurs in up to 90% of r Blood culture growing fungus in patients with
patients with AIDS (2). DIAGNOSIS suspected candidemia
r Relapse rates of 3050% after completion of
HISTORY Diagnostic Procedures/Other
antifungal treatment in severe immunosuppression r Oropharyngeal candidiasis: r Endoscopy for direct visualization of esophageal
(2) Local discomfort, poor feeding, white plaques in
r Candidemia is rare in immunocompetent hosts. lesions
mouth r Dilated retinal exam for endophthalmitis, which is
RISK FACTORS Neonates and young infants are typically sight threatening, should be done in patients with
r Local risk factors: asymptomatic. candidemia.
r Esophageal candidiasis: r CT, US, echo to identify deep organ lesions in lung,
Steroid aerosol inhalers
Impaired salivary gland function: radiotherapy, Odynophagia, poor feeding, weight loss liver, kidney, brain, spleen, eye, heart (3)
chemotherapy, Sjogren In immunocompromised patients, a history and
Dentures or implants physical are adequate for diagnosis and empiric DIFFERENTIAL DIAGNOSIS
r Oral/mucosal lesions: Formula stuck to mucosa,
High-carbohydrate diet treatment should be initiated.
Smoking r Cutaneous and diaper candidiasis: aphthous stomatitis, acute necrotizing gingivitis,
Indwelling vascular access devices and catheters Red, itchy rash with satellite lesions, especially in herpes gingivostomatitis or other viral stomatitis,
r Systemic risk factors: folds of skin; may occur anywhere on body lichen planus, squamous cell carcinoma, leukoplakia
r Vaginal candidiasis: r Diaper lesions: Atopic, seborrheic, bacterial, or
Age: Neonates, advanced age
Malignancy Curdlike or mucoid white-yellow discharge, with occlusional dermatitis
r Cutaneous lesions: Seborrheic and atopic dermatitis
Immunodeficiency (eg, HIV) pruritus, vulvar pain or burning, dysuria and
dyspareunia r Esophageal: Foreign body, GERD, pharyngitis
Immunosuppression (eg, patients on
chemotherapy, organ transplantation) r Systemic candidiasis: r Vaginitis: Neisseria gonorrheae, Trichomonas
Recent broad-spectrum antibiotic use Fever, lethargy, oliguria, respiratory distress vaginalis, Chlamydia trachomatis, Gardnerella
Diabetes mellitus Symptoms depend on organ system involved. vaginalis, Bacteroides species, Mycoplasma hominis,
Parenteral nutrition Peptostreptococcus, chemical or mechanical irritants
PHYSICAL EXAM r Systemic: Sepsis from other organisms
Nutritional deficiencies (eg, vitamin B) r Oropharyngeal candidiasis (thrush):
GENERAL PREVENTION Friable white pseudomembranous patches:
r Good oral and vaginal hygiene On buccal mucosa, gingivae, palate, tongue,
r Avoid overuse of antibiotics to prevent normal flora
TREATMENT
and oropharynx
disruption and candidal overgrowth. Plaques do not rub off easily with a tongue INITIAL STABILIZATION/THERAPY
r Avoid douching and prolonged moisture in the blade or swab. Systemic candidiasis:
vaginal area by using loose-fitting cotton underwear. If scraped off, red, ulcerated mucosa is exposed. r If ill appearing, address ABCs per the Pediatric
r Antifungal prophylaxis in immunocompromised r Diaper dermatitis:
Advanced Life Support (PALS) algorithm.
patients Erythematous papular rash that spreads into the
inguinal folds, with a scaling border and satellite MEDICATION
r Oropharyngeal candidiasis
lesions
r Intertrigo: r Oral hygiene: Gentle cleaning of teeth and oral
Candidal infection in skin folds, often in neck cavity daily with a soft brush:
Erythematous, macerated skin; unlike diaper Nystatin suspension (100,000 units/mL): Use for
dermatitis, characteristic satellite lesions not 2 days after lesions have cleared (usually 7 days):
typical Preterm newborns: 0.5 mL in each cheek q.i.d.
Term infants: 1 mL in each cheek q.i.d.
Children: 46 mL swish and swallow q.i.d.
Side effects: Nausea, vomiting, diarrhea
136
CANDIDIASIS
Fluconazole and ketoconazole for persistent ALERT COMPLICATIONS

infections (see below) r Mix all amphotericin formulations in D5W. r Persistent or recurrent candidiasis, especially in
r Esophageal candidiasis: immunocompromised patients
Monitor electrolytes and renal, hepatic, and
Trial of fluconazole: 10 mg/kg IV/PO r Systemic dissemination
hematologic status closely, as side effects include
(max single dose 400 mg) 1 day, then hypercalciuria, hypokalemia, hypomagnesemia,
36 mg/mg IV/PO (max single dose 200 mg) renal tubular acidosis, renal and hepatic failure,
qd 1421 days REFERENCES
hypotension, and phlebitis.
Itraconazole and amphotericin B may also be used. r Infusion-related reactions include fever, chills,
r Diaper and cutaneous candidiasis: 1. Epstein JB, Polsky B. Oropharyngeal candidiasis: A
Keep area dry.
headache, hypotension, nausea, and vomiting. review of its clinical spectrum and current C
Premedicate 30 min before and 4 hr after with therapies. Postgrad Med J. 1998;20(1):4057.
Nystatin cream (100,000 units/g): Use with each
acetaminophen and diphenhydramine; add 2. Akpan A, Morgan R. Oral candidiasis. Postgrad
diaper change until the rash has cleared.
hydrocortisone to the infusion (1 mg/mg Med J. 2002;78:455459.
Nystatin powder (100,000 units/g): May be used
for intertrigo or very moist diaper rash amphotericin, max single dose 25 mg). 3. Zaoutis TE, Greves HM, Lautenbach E, et al. Risk
Topical clotrimazole 1%, miconazole 1%, r Prior to each dose of amphotericin, load with factors for disseminated candidiasis in children with
ketoconazole 2%, or econazole 1% b.i.d. 1015 mL/kg of normal saline to minimize candidemia. Pediatr Infect Dis J. 2004;23(7):
26 wk nephrotoxicity. 635641.
Amphotericin B: 3% cream, 3% lotion, 3% 4. Blyth CB, Palasanthiran P, OBrien TA. Antifungal
ointmentapply b.i.d.q.i.d. therapy in children with invasive fungal infections:
r Vaginal candidiasis: r Removal of infected foreign bodies (eg, indwelling A systematic review. Pediatrics. 2007;119(4):
Topical: 772784.
catheters and central lines)
Clotrimazole: 100 mg/dose QHS 7 days or r Incision and drainage of abscesses
200 mg/dose qhs 3 days or 2% applicator
dose qhs 3 day DISPOSITION CODES
Miconazole: 100-mg applicator qhs 7 days or Admission Criteria
r Ill appearing ICD9
200 mg qhs 3 days
r Suspected systemic infection r 112.0 Candidiasis of mouth
Oral agents:
Fluconazole: 10 mg/kg PO (max single dose r Patients with candidemia usually require r 112.1 Candidiasis of vulva and vagina
150 mg) 1 management in the ICU. r 112.9 Candidiasis of unspecified site
Ketoconazole (>2 yr of age): 3.36.6
Discharge Criteria
mg/kg/day (max single dose 400 mg) r Well appearing
qd 5 days OR r Adequate oral intake (oral or esophageal PEARLS AND PITFALLS
Itraconazole: 35 mg/kg/day (max single dose
candidiasis) r Neonates and young infants may commonly develop
200 mg) divided b.i.d. 1 or 200 mg qd
3 days Issues for Referral thrush, intertrigo, or candidal diaper rash despite
Recurrent vaginal candidiasis (>4 episodes of r Immunology/hematology referral for suspected being otherwise healthy with no systemic illness.
infection/1 yr): immunodeficiency or impaired cellular immunity r Candidiasis is becoming more common because of
Induction with 2 wk of topical or oral azole, then r Dermatology, gynecology, or gastroenterology increased numbers of patients who are
maintenance for 6 mo with fluconazole 150 mg referral for recurrent or refractory cutaneous, immunocompromised.
every week, ketoconazole 100 mg qd, or vaginal, or esophageal candidiasis, respectively r Systemic candidiasis is serious and potentially life
itraconazole 100 mg qod, or daily topical azole threatening and should be considered in the
COMPLEMENTARY & ALTERNATIVE immunocompromised child with fever and
ALERT THERAPIES neutropenia.
r Monitor hepatic function in long-term use of Chlorhexidine rinses for bone marrow transplant
azoles. May cause nausea, vomiting, rash, patients
headache, pruritus, and fever.
r Systemic candidiasis: FOLLOW-UP
Amphotericin B: 0.250.5 mg/kg/day IV qd
Amphotericin B cholesterol sulfate: Start at FOLLOW-UP RECOMMENDATIONS
34 mg/kg/day IV qd, infused at 1 mg/kg/hr; Discharge instructions and medications:
if tolerated, increase infusion rate. r Follow up with primary care provider within 1 wk for
Amphotericin B lipid complex: 2.55 mg/kg/ oropharyngeal, cutaneous, and vaginal infections.
day IV qd, infused at 2.5 mg/kg/hr PROGNOSIS
Amphotericin B, liposomal: 35 mg/kg/day IV r Good prognosis for oral candidiasis, diaper
qd dermatitis, and vaginal candidiasis
Fluconazole: 12 mg/kg/day PO/IV (max r Treatment failures usually due to poor compliance
600 mg/day)
with therapy, poor oral hygiene, or inability to
Itraconazole: 10 mg/kg/day PO/IV
resolve underlying predisposing factors
No antifungal is shown to be superior to any other r Treatment failures due to resistance to systemic
in eradicating systemic disease (4).
Flucytosine is synergistic with amphotericin for agents are increasing in frequency.
r Systemic candidiasis has a mortality rate of 1931%
candidal meningitis.
The need for IV medication and severity of illness (4).
necessitates hospitalization.
Remove indwelling catheters, as these are most
common source of infection in children (4).
Continue topical medication if mucosal
infection is the primary source to decrease the
dose or duration of systemic therapy.
137
CARBON MONOXIDE/CYANIDE POISONING AND SMOKE INHALATION

David H. Jang
Lewis S. Nelson
r CO causes a leftward shift of the oxyhemoglobin r Neurologic symptoms can include agitation, seizure,
BASICS dissociation curve, which decreases off-loading of confusion, and coma.
oxygen from Hb. r Dermatologic:
DESCRIPTION r A series of immune-mediated damage in the CNS as Burns may be present on skin as well as in nares.
r Smoke inhalation is a major cause of death from
well as oxidative damage can lead to lipid Skin findings can include cherry-red colorations as
fires. Significant fire exposures can also lead to peroxidation. a result of CN exposure and lack of oxygen
carbon monoxide (CO) and cyanide (CN) poisoning, r CN is an inhibitor of multiple enzymes, including extraction across capillary bed.
which causes cellular hypoxia. cytochrome oxidase. This leads to cellular hypoxia
r CO is leading cause of mortality from poisoning in DIAGNOSTIC TESTS & INTERPRETATION
with an elevated lactate and often has multiorgan
the U.S. effects.
Lab
r There is substantial morbidity in CO poisoning r CN is also a very potent neurotoxin that affects Initial Lab Tests
r CO testing should occur with patients who present
survivors by delayed neurologic sequelae (DNS). areas of the brain with high metabolic activity, such
r Combustion of organic nitrogen-containing products as the basal ganglia and cerebellum.
with CO-related complaints such as headache or
flulike symptoms.
like plastics, polyurethanes, wool, silk, nylon, and r The carboxyhemoglobin (COHb) level is important to
synthetic rubber can produce CN. ETIOLOGY
r Smoke from closed-space fires obtain with smoke inhalation:
EPIDEMIOLOGY r Exhaust from furnaces, combustion engines such as Normal levels range between 0 and 5% with
r CO is the leading cause of poisoning death in
generators, automobiles, furnaces neonates; patients with hemolytic anemia may
children and adults in the U.S. have higher levels.
r There are >1.5 million fire incidents in the U.S. with COMMONLY ASSOCIATED CONDITIONS Levels >5% are considered abnormal, levels
r Burns:
>3,000 fire deaths per year. >25% are considered very elevated, and levels
r There are >2,000 nonfire CO deaths yearly in the Airway
>45% are extremely elevated:
Lung injury Heavy smokers can have levels as high as 10%.
U.S.
r CO poisoning contributes to >5,000 smoke Skin High levels may confirm CO exposure but do not
r Smoke inhalation
inhalation deaths per year. correlate with clinical symptoms or outcome.
r After Hurricane Katrina in Louisiana and Hurricane It is important to consider testing cohabitants of
Ike in Texas, it was recognized that a significant DIAGNOSIS the patient for CO exposure.
r Blood gas analysis, lactate and methemoglobin
number of pediatric exposures to CO result with use
of gasoline-powered generators during electrical HISTORY concentrations:
r The primary complaint from smoke inhalation is
outages. Metabolic acidemia is indicative of CN toxicity.
r A significant number of closed-space or indoor fires respiratory, ranging from cough to respiratory r Lactate can be elevated in the setting of hypoxia,
result in CN exposure due to combustion of certain distress and coma. serious CO poisoning, and CN toxicity. Rapidly
r Early symptoms of CO exposure are often
materials in fires. obtain a lactate level:
r The majority of CO and CN exposure is nonspecific and can mimic a viral syndrome, Lactate elevation is extremely sensitive and
unintentional. Either can occur in suicidal attempts especially during winter months when an indoor usually is specific for CN exposure in the setting of
but this is far less common. heater may be in use. closed-space fires.
r A headache that is described as diffuse and aching Levels >10 mmol/L suggest CN poisoning and
RISK FACTORS is the most common complaint. should trigger CN antidote use.
r Vehicular, such as riding in the back of a pickup truck r Heavy CO poisoning can manifest as syncope, coma, CN concentrations can be obtained but often are
r Use of propane-powered equipment (ie, ice rink not readily available to be meaningful. Blood CN
or seizure.
resurfacers or forklifts in enclosed spaces) r Children often manifest atypical symptoms of CO concentration >1.0 ug/mL is considered toxic.
r Gas furnaces during the winter months r Troponin can be elevated due to diffuse myocardial
poisoning, presenting with vomiting or an isolated
r Smoke inhalation seizure. damage.
r Use of combustion engines in a location without r Patients with long-term exposure to low levels of CO r Elevations of creatine phosphokinase (CPK) are
proper ventilation, such as using a often will complain of a persistent headache and typically mild, but rhabdomyolysis may occur, so
gasoline-powered generator indoors or leaving an nonspecific cognitive problems such as memory loss. assay CPK as indicated.
automobile running inside a closed garage r Patients with smoke inhalation and severe metabolic
Imaging
GENERAL PREVENTION acidosis should also be evaluated for possible CN r Chest radiograph should be obtained in most cases
r Use smoke and CO detectors, especially during the toxicity. of smoke inhalation, which can show interstitial
r The persistent or delayed effects of CO poisoning can changes and diffuse alveolar involvement.
winter, and learn to recognize symptoms of CO
poisoning (ie, flulike symptoms). include apraxia and agnosias, dementia, amnestic r A noncontrast head CT should be obtained in
r Use of an indoor detector that senses both smoke syndromes, parkinsonism, and cortical blindness. unresponsive patients or those with focal neurologic
and CO is recommended. PHYSICAL EXAM deficits.
r Assess vital signs and pulse oximetry. Diagnostic Procedures/Other
PATHOPHYSIOLOGY r Tachycardia and hypotension are common in
r Toxic combustion products from fires include ECG should be obtained to evaluate for dysrhythmias
chemical asphyxiants (CO and CN), simple toxicity. Tachypnea and hyperpnea may also occur. and ischemia with severe exposure.
asphyxiants (such as carbon dioxide), and irritants. r Respiratory:
r CO is a by-product of hemoglobin (Hb) degradation. Head and neck findings include burns, soot in Autopsies from severe CO poisoning can show
r CO binds with Hb with 200 times greater affinity nares, copious oral secretions, and oropharyngeal necrosis of the cerebellum, globus pallidus, and
than oxygen, which renders it incapable of edema. hippocampus.
delivering oxygen. CO also binds with cytochrome May also exhibit drooling, stridor, and inability to
oxidase and inhibits cellular respiration. handle secretions
Pulmonary symptoms include rhonchi, crackles,
and wheezing.
138
CARBON MONOXIDE/CYANIDE POISONING AND SMOKE INHALATION
DIFFERENTIAL DIAGNOSIS r The CN antidote kit should be administered in

r Acute lung injury
ADDITIONAL READING
suspected CN toxicity:
r Stroke Three components in the kit are amyl nitrite, r Brouard A, Blaisot B, Bismuth C. Hydroxoco-
r Sepsis sodium nitrite, and sodium thiosulfate. balamine in cyanide poisoning. J Toxicol Clin Exp.
r Shock Nitrites, which induce methemoglobinemia, are 1987;7:155168.
r Food poisoning contraindicated in the setting of smoke inhalation. r Chaturvedi AK, Smith DR, Canfield DV. Blood carbon
r Viral syndrome Sodium thiosulfate dose 400 mg/kg or 1.65 mL/kg monoxide and hydrogen cyanide concentrations in
r Gastroenteritis of 25% solution, to max of 12.6 g. the fatalities of fire and non-fire associated civil
Adolescent/Adult dose is 12.5 g:
Administered IV either as a bolus or infused
aviation accidents, 19911998. Forensic Sci Int.
2001;121:183188.
C
TREATMENT over 1030 min r Chen KK, Rose CL. Nitrite and thiosulfate therapy in
Sodium thiosulfate is relatively free of significant cyanide poisoning. JAMA. 1952;149:113119.
PRE HOSPITAL adverse side effects and is completely safe for r Forsyth JC, Mueller PD, Becker CE, et al.
r Assess and stabilize airway, breathing, and use in patients with concomitant CO toxicity. Hydroxocobalamin as a cyanide antidote: Safety,
circulation. Recommended in patients with metabolic efficacy and pharmacokinetics in heavily smoking
r Administer high-flow oxygen. acidemia, particularly with an elevated lactate normal volunteers. J Toxicol Clin Toxicol. 1993;31:
r Consider transport to a facility with an hyperbaric level, clinically for loss of consciousness, severe 277294.
oxygen (HBO) chamber. altered mental status, shock, or cardiac r Holstege CP, Kirk MA. Smoke inhalation. In
dysrhythmia Goldfrank LR, Flomenbaum NE, Lewin NA, et al.,
DISPOSITION eds. Goldfranks Toxicologic Emergencies. 8th ed.
Assess and stabilize airway, breathing, and circulation.
Admission Criteria Stamford, CT: Appleton & Lange; 2006.
ALERT r Any patients with significant smoke inhalation, CO r Scheinkestel CD, Bailey M, Myles PS, et al.
r CO toxicity results in erroneously elevated pulse Hyperbaric or normobaric oxygen for acute carbon
toxicity, or CN toxicity
oximetry readings. Administer high-flow oxygen r Critical care admission criteria: monoxide poisoning: A randomised controlled
regardless of the pulse oximetry measurement Dysrhythmia, unstable vital signs clinical trial. Med J Aust. 1999;170:203210.
obtained by a finger probe. r Turnbull TL, Hart RG, Strange GR, et al. Emergency
r Hydroxocobalamin use may interfere with pulse Discharge Criteria department screening for unsuspected carbon
No significant elevation of CO level; asymptomatic monoxide exposure. Ann Emerg Med. 1988;17:
oximetry readings in various manners, potentially after 68 hr of observation
making it impossible to use pulse oximetry 478484.
Issues for Referral r Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric
measurements after administration. r Refer to a poison center and/or medical toxicologist.
r Administer high-flow oxygen. r The decision whether to initiate HBO can also be oxygen for acute carbon monoxide poisoning.
N Engl J Med. 2002;347:10571067.
r Assess serum glucose rapidly. made with consultation.
r Maintain a very low index of suspicion for CO
exposure. Early diagnosis is crucial to prevent THERAPIES CODES
morbidity and mortality. HBO:
r Early control of the airway is crucial, especially in the
r The primary benefits of HBO include clearing COHb, ICD9
context of serious smoke inhalation injury.
but more importantly preventing brain lipid r 986 Toxic effect of carbon monoxide
r Treatment of CO poisoning consists of high-flow r 987.9 Toxic effect of unspecified gas, fume, or vapor
peroxidation.
oxygen therapy, mechanical ventilation, or HBO r Indications for HBO therapy include syncope, r 989.0 Toxic effect of hydrocyanic acid and cyanides
therapy, depending on the circumstances.
r Treatment of suspected CN poisoning should be abnormal cerebellar findings, seizures, COHb
>25%, and fetal distress in pregnancy.
based on clinical presentation in conjunction with PEARLS AND PITFALLS
lab values.
r Metabolic acidemia, particularly with an elevated FOLLOW-UP r Flu-like symptoms such as headache, especially
lactate level, or loss of consciousness, severe altered during winter months are a common presentation of
mental status, shock, or cardiac dysrhythmia are FOLLOW-UP RECOMMENDATIONS patients with CO poisoning.
indications for treatment for presumed CN Patient Monitoring r Patients who present with a coma and severe
poisoning. If there is significant CO or CN toxicity, ongoing metabolic acidosis from a fire should also be
neurologic testing for sequelae is indicated. empirically treated for suspected CN poisoning.
MEDICATION r The biggest pitfall in managing patients with smoke
r Hydroxocobalamin: PROGNOSIS
Recently approved for use in CN poisoning r Varies with severity of exposure and ranges from inhalation injury is failing to realize that they may
Combines with CN to form cyanocobalamin, excellent prognosis to certain death suddenly deteriorate.
which is nontoxic. r The most important morbidity of CO poisoning is
Dose 70 mg/kg (not to exceed 5 g initially) DNS. Patients with history of syncope or an
administered IV over 30 min abnormal neurologic exam are at increased risk of
Can be administered as an IV push in cases of developing DNS.
CN-induced cardiac arrest
The dose can be repeated (not to exceed a total
COMPLICATIONS
Complications of serious CO and CN poisoning can be
dose of 15 g) as necessary.
permanent and include apraxia and agnosias,
Recommended in patients with metabolic
dementia, amnestic syndromes, parkinsonism,
acidemia, particularly with elevated lactate level,
paralysis, and cortical blindness.
and clinically for loss of consciousness, severe
altered mental status, shock, or cardiac
dysrhythmia
139
CARDIOGENIC SHOCK
Vincent J. Wang
ETIOLOGY r Problems feeding, sweating with feeds, respiratory

BASICS The etiology of cardiogenic shock stems from primary distress with or without feeding
cardiac dysfunction. They may be categorized as r History of possible ingestions or exposures
DESCRIPTION follows: r Current medications
r Cardiogenic shock is a state of tissue hypoperfusion r Structural heart disease (eg, single ventricle r History of recent infections
as a result of primary cardiac failure, despite normal physiology, transposition of the great arteries, large r Systemic symptoms: Fevers, fatigue, decreased urine
or increased left ventricular filling pressures. VSD) (Refer to the Congenital Heart Disease topic.)
r Cardiac preload remains normal to increased, which output, etc.
r Obstruction (eg, severe aortic stenosis, coarctation r Family history
distinguishes cardiogenic shock from hypovolemic of the aorta, obstructive intracardiac mass, HOCM, r Allergies to rule out distributive shock secondary to
shock (decreased effective blood volume) and postsurgical valvular or vascular restenosis) anaphylaxis
distributive shock (blood vessel dilation causing r Dysrhythmias:
relative hypovolemia). All 3 types of shock are Heart block: Congenital or from toxic ingestion PHYSICAL EXAM
defined by decreased cardiac output and tissue r General appearance:
Supraventricular tachycardia
hypoperfusion: Ventricular tachyarrhythmias (associated with long A neonate or child in cardiogenic shock will
Obstructive shock is usually caused by cardiac or QT syndrome or other dysrhythmias, trauma, etc.) appear ill with decreased responsiveness,
cardiothoracic etiologies and is managed similarly r Impaired contractility: gray/clammy extremities, and respiratory distress
as cardiogenic shock: or may be in complete cardiovascular collapse.
Because of this, obstructive shock will be Myocarditis r Vital signs:
Cardiomyopathy
considered a variant of cardiogenic shock in this Tachycardia (except in heart block or late stages of
Metabolic disease (eg, Pompe disease, pyruvate
topic. shock)
dehydrogenase deficiency, myotonic dystrophy,
Septic shock is similar to distributive shock. Tachypnea:
r Pediatric cardiogenic shock occurs primarily in carnitine deficiency, propionic acidemia)
Severe hypoglycemia If not present, assess for apnea and impending
neonates with congenital heart disease and in Adrenal insufficiency respiratory failure.
children with myocarditis. Ischemia caused by: Fever (or even hypothermia) is also possible,
r In adults, MI is the most common cause. especially in an infant.
Coronary artery aneurysms
Anomalous left coronary artery from the Variable BP: Usually hypotension, but normal BP
RISK FACTORS
pulmonary artery (ALCAPA) or even elevated BP in the initial stages of shock
Risk factors for specific conditions that cause
Acute MI Widened pulse pressure is common.
cardiogenic shock: r Skin and extremity:
r Infants of diabetic mothers have an increased r Other:
Pulmonary HTN Capillary refill time may be delayed.
incidence of congenital heart defects and Cool/Clammy extremities may be present.
cardiomyopathy. Cardiogenic shock following intrapartum asphyxia
r Asphyxia during birth predisposes infants to heart (2): Bounding pulses may be felt in early stages of
Tricuspid insufficiency +/ mitral valve shock, followed by poor, thready pulses in late
failure early in life. stages.
r Infants of mothers with autoimmune disease, dysfunction (2 to papillary muscle infarct)
Right ventricle failure (2 to impaired coronary In a child with unknown history, chest wall scars
especially systemic lupus erythematosus, have an suggest previous cardiac surgery.
perfusion)
increased incidence of congenital heart block. Left ventricle failure (with HTN initially, then r Respiratory:
r Infants and children with a family history of
hypotension) Increased respiratory effort including grunting,
cardiomyopathy and arrhythmias have a higher Cardiac tamponade flaring, or retractions
incidence of such conditions. Tension pneumothorax Agonal or irregular breathing
GENERAL PREVENTION Trauma (can induce tamponade, ruptured septum, Patients most often have crackles on exam from
Pulse oximetry screening in the newborn nursery helps pneumothorax, arrhythmia, etc.) pulmonary edema.
Ingestion/Overdose (eg, cocaine, calcium channel r Cardiac:
to identify infants with cyanotic congenital heart
disease. Done early and prior to discharge, this may blockers, beta-blockers, tricyclic antidepressants) Jugular venous distension
identify conditions that may cause cardiogenic shock Postsurgical complications: Evidence of heave, lift, or thrill
upon closing of the ductus arteriosus (1). Thrombosis (eg, obstructed pulmonary blood Evaluation of heart sounds with splitting
flow in Blalock-Taussig shunt) Presence of murmur
PATHOPHYSIOLOGY Dysrhythmia (see above) r Other:
r Cardiogenic shock occurs when cardiac output is
Hepatomegaly
inadequate because of: Check for pulses and presence of radiofemoral
Increased cardiac demand (eg, large ventricular DIAGNOSIS delay
septal defect [VSD])
Decreased/Ineffective contractility (eg, arrhythmia HISTORY DIAGNOSTIC TESTS & INTERPRETATION
r The etiology of cardiogenic shock will differ greatly
or myocarditis) OR Lab
Obstruction (eg, hypertrophic obstructive in the neonate and older infant/child. r Capillary glucose measurement is necessary, as
cardiomyopathy [HOCM]) r Birth history (gestational age, delivery problems, hypoglycemia should be rapidly corrected.
r This leads to CHF and inadequate perfusion and neonatal ICU stay, mechanical ventilation, etc.) r Arterial blood gas analysis to check for acidosis,
oxygenation of all vital organs, including the heart r Antecedent symptoms (acute vs. insidious onset, oxygenation, and ventilatory status
muscle itself. failure to thrive, etc.) r Serum lactate for degree of acidosis
r Tissue hypoperfusion in turn leads to acidosis and r History of underlying conditions or surgeries (cardiac r Comprehensive metabolic panel and ionized calcium
electrolyte abnormalities, which have adverse effects disease, metabolic conditions, etc.) level should be checked for electrolyte disturbances,
on myocardial function and causes further which may be corrected:
myocardial depression and ischemia. High potassium and low sodium in an infant may
suggest adrenal insufficiency.
Elevated BUN, creatinine, and LFTs may be a sign
of end-organ damage.
140
CARDIOGENIC SHOCK
r Coagulation studies and platelets to check for r Improve contractility: Issues for Referral
evidence of disseminated intravascular coagulation Correct hypoglycemia with a dextrose bolus. Consultation from the emergency department as
(DIC) Replace electrolytes as needed (specifically, necessary:
r Hemoglobin level to determine if blood should be calcium and potassium) to maximize myocardial r Cardiology for most cardiogenic shock cases
given to maximize oxygenation function. r Toxicology for ingestions or drug overdoses
r Type and cross match in case of need for blood Correct acidosis with sodium bicarbonate or r Metabolism if known metabolic disease
product transfusion tromethamine (THAM). r Trauma surgery if traumatic etiology
Inotropic agents if needed
Imaging r Decrease afterload:
r Chest radiograph to evaluate for cardiomegaly,
Administer vasodilators, avoiding hypotension. FOLLOW-UP
C
pulmonary edema, pneumothorax
r Focused abdominal sonograph for trauma (FAST)
ALERT PROGNOSIS
exam if trauma or for evaluation of pericardial r In infants in whom heart disease is suspected, r Depends on the extent of tissue damage and the
effusion or pneumothorax avoid administration of 100% oxygen during the timing of intervention
r Echo to evaluate for obstructive lesions, shortening r Some patients may require extracorporeal
resuscitation, as it can induce closure of the
fraction, and volume status if suspecting structural patent ductus arteriosus in neonates and cause membrane oxygenation or a left ventricular assist
or functional heart disease overcirculation in the lungs of older infants. device and may need cardiac transplantation in the
Diagnostic Procedures/Other r Use only enough supplemental oxygen delivery to future.
ECG to look for evidence of dysrhythmias, ST changes, achieve adequate oxygenation (3). See the Patent COMPLICATIONS
and low voltages Ductus Arteriosus and Ductal Dependent Cardiac If there is prolonged tissue hypoperfusion and hypoxia,
DIFFERENTIAL DIAGNOSIS Emergencies topics. end-organ damage, such as to the kidney, liver, lung,
r Hypovolemic shock and/or brain, may occur.
r Distributive (septic) shock MEDICATION
r Anaphylaxis First Line
r Inborn error of metabolism r Inotropic agents to increase cardiac output: REFERENCES
Dobutamine 1. De-Wahl Granelli A, Wennergren M, Sandberg K,
Dopamine et al. Impact of pulse oximetry screening on the
TREATMENT Epinephrine detection of duct dependent congenital heart
Isoproterenol (if heart rate is low) disease: A Swedish prospective screening study in
PRE HOSPITAL r Antidysrhythmic agents for dysrhythmias: 39,821 newborns. BMJ. 2009;338:a3037.
r Assess and continuously reassess ABCs.
r Ensure airway patency, and administer supplemental Lidocaine 2. Lees MH, King DH. Cardiogenic shock in the
Digoxin neonate. Pediatr Rev. 1988;9(8):258266.
oxygen as necessary. Adenosine
r Bag-mask ventilation and sometimes endotracheal 3. Steinhorn RH. Evaluation and management of the
Esmolol cyanotic neonate. Clin Pediatr Emerg Med. 2008;
intubation may be necessary. Amiodarone 9(3):169175.
r Obtain access with an IV or intraosseous line.
r Administer fluid boluses with guidance from the Second Line
r Corticosteroids: First line if suspecting adrenal
base station.
r Administer CPR if necessary.
insufficiency CODES
r Nitric oxide if pulmonary HTN
r Capillary glucose assessment and glucose r Amrinone or milrinone should be used to decrease ICD9
supplementation as necessary afterload in appropriate patients who have 785.51 Cardiogenic shock
structural heart disease and/or poor contractility if
ALERT
the patients have an adequate BP.
In patients with cardiogenic shock, endotracheal PEARLS AND PITFALLS
intubation may lead to complete cardiovascular SURGERY/OTHER PROCEDURES
r Pericardiocentesis may be necessary in cardiac r Pearls:
collapse. Intubate only if necessary, and be prepared
to administer CPR if needed. tamponade. Initial treatment of shock should generally be the
r Thoracentesis if large pulmonary effusions are same regardless of etiology.
INITIAL STABILIZATION/THERAPY present or to resolve a pneumothorax or hemothorax It is more important initially to start treatment and
r ABCs: See Pediatric Advanced Life Support (PALS) or decrease further tissue injury than to determine
DISPOSITION the exact etiology.
Advanced Cardiac Life Support (ACLS) protocols for Admission Criteria r Pitfalls:
initial stabilization steps. The goal of initial r Any patient who presents to the emergency
treatment is to restore tissue perfusion both directly Performing invasive procedures on patients with
department in cardiogenic shock warrants cardiogenic shock (eg, intubation, line placement)
and by correcting the underlying etiology. admission.
r General: r Telemetry monitoring is necessary for any patient
may bring about complete cardiovascular collapse.
Provide optimal ventilation and oxygenation. Not being prepared to administer CPR
with a recent history of cardiogenic shock.
Connect the defibrillator, and administer CPR if r Critical care admission criteria:
needed.
Need for ventilatory support
Obtain venous access, preferably peripheral and
Need for inotropic support
central venous.
Prostaglandin E2 infusion in an infant
Obtain arterial access for more accurate
High risk for cardiovascular collapse/dysrhythmia
continuous BP measurements.
r Improve preload:
Begin fluid resuscitation (cautiously if there is
known heart disease or evidence of CHF).
141
CARDIOMYOPATHY
Heather R. Saavedra
Marc Gorelick
r HCM may result from genetic or metabolic disorders Imaging

BASICS and contractile protein abnormalities. r CXR may reveal cardiomegaly, pulmonary venous
r Most RCM are idiopathic, but known causes include congestion, or pulmonary edema in HCM.
DESCRIPTION sarcoidosis, amyloidosis, Hurler syndrome, Gaucher r In HCM, CXR may reveal cardiomegaly with LV
r Cardiomyopathy (CM) is a group of disorders of the
syndrome, hypereosinophilic syndromes, radiation contour.
myocardium associated with a decrease in cardiac exposure, and anthracycline toxicity. r In RCM, CXR may reveal cardiomegaly with atrial
function. enlargement and pulmonary venous congestion.
r 3 main types: r CT or MRI may be done to provide a 3D image of
Dilated cardiomyopathy (DCM): Characterized by DIAGNOSIS the heart structures.
left ventricular (LV) dilation and reduced
contractility HISTORY Diagnostic Procedures/Other
r Symptoms may be absent, mild, or severe. r ECG may demonstrate atrial or ventricular
Hypertrophic cardiomyopathy (HCM): r In infants, common presenting symptoms include
Characterized by a nondilated left ventricle with enlargement, dysrhythmia, or ischemic changes.
poor weight gain, difficulty feeding, diaphoresis, r Echo with Doppler to evaluate cardiac structure and
disproportionate thickening of the ventricular
septum. Systolic function is normal or increased. excessive fussiness, or lethargy. function:
r In older children or adolescents, symptoms may also DCM: Echo may reveal the dilated and poorly
Restrictive cardiomyopathy (RCM): Characterized
by abnormal diastolic filling with normal or include shortness of breath, orthopnea, paroxysmal functional LV and help to evaluate structural
decreased diastolic volume of the ventricle nocturnal dyspnea, dizziness, fatigue, weakness, abnormalities.
chest pain, exercise intolerance, syncope or HCM: Echo will evaluate the form of hypertrophy
EPIDEMIOLOGY presyncope, and palpitations. presentdiffuse and symmetric, asymmetric
r 1/100,000 children in the U.S. has diagnosed CM. r Patients with predominantly right-sided failure may septal, or apical:
r 1,0005,000 new cases per year Echo in HCM will also estimate the degree of LV
present with abdominal pain and/or vomiting.
r Most new diagnoses are in infants and children r Inquire about family history of CM, sudden cardiac outflow tract obstruction and the integrity of the
<12 yr of age. events, or unexplained deaths. mitral valve.
RISK FACTORS RCM: Echo usually reveals marked atrial
r Family history: PHYSICAL EXAM enlargement with normal LV end diastolic
r Presentation ranges from asymptomatic to
DCM: 2030% have a family history of DCM. dimensions as well as atrioventricular valve
cardiovascular collapse. dysfunction, ventricular hypertrophy, and
HCM: 5060% have a family history of HCM. r Presenting signs may include tachycardia,
r Sudden death risk factors occur in 1020% of all occasionally atrial thrombi.
tachypnea, hypotension, cool and poorly perfused r Cardiac catheterization may be necessary to further
patients with HCM: extremities, thready pulses, heart murmur, rales,
A history of cardiac arrest or spontaneous, evaluate LV outflow tract gradients and
hepatomegaly, jugular venous distention, 3rd and hemodynamics and to facilitate endomyocardial
sustained ventricular tachycardia 4th heart sounds, peripheral edema, and ascites. biopsy.
A family history of early sudden death (<45 yr in r In patients with LV outflow tract obstruction, there r Electrophysiology studies may be done to determine
age) related to the disease may be a significant murmur noted on exam.
Syncopal episodes, especially during exercise, susceptibility to arrhythmias and the need for a
r In patients without obstruction, there may be no
when repeated, or associated with arrhythmia on pacemaker or defibrillator.
murmur when the patient is at rest, but the patient r A 24-hr Holter monitor may provide additional
Holter monitor
may have an increased LV apical impulse or 4th information regarding dysrhythmias.
Multiple, repeated episodes of nonsustained
heart sound.
ventricular tachycardia r Murmur in HCM may increase with Valsalva Pathological Findings
A drop in BP, or inability to increase it and r In RCM, endomyocardial biopsy may reveal a specific
maintain it at high levels (>25 mm Hg above maneuver or rising from squatting position:
The same murmur may be decreased with cause such as myocyte hypertrophy, interstitial
resting level) during exercise testing fibrosis, myocytolysis, and infiltrative processes.
Extreme LV hypertrophy, especially interventricular squatting from a standing position and with r Biopsy is more useful in adults than children.
septum thickness >30 mm passive leg elevation.
DIAGNOSTIC TESTS & INTERPRETATION DIFFERENTIAL DIAGNOSIS
PATHOPHYSIOLOGY r In patients who present in extremis, the differential
r Familial DCM is due to defects in the cytoskeleton Lab
includes sepsis, ingestion, pericarditis, myocarditis,
genes. Initial Lab Tests
r Initial lab evaluation should include CBC, cardiac tamponade, respiratory failure, and trauma.
r Inheritance: X-linked, autosomal dominant, or r Other differentials may include aortic stenosis,
autosomal recessive electrolytes, transaminases, basic natriuretic peptide
chronic anemia, endocarditis, stimulant toxicity,
r Familial HCM is a disease of the sarcomere, (BNP), and blood gas:
Heart disease that causes significant volume or hypothyroidism, and hyperthyroidism.
involving mutations in at least 7 different genes
encoding proteins of the myofibrillar apparatus. pressure overload of either ventricle has elevated
BNP and NT-pro BNP levels. TREATMENT
ETIOLOGY BNP can help to differentiate cardiac from
r The majority of cases of DCM are idiopathic. pulmonary causes in infants with respiratory
r Known causes of DCM include LV outflow tract PRE HOSPITAL
distress. Assess and stabilize airway, breathing, and
obstruction, genetic conditions such as X-linked, Blood gas analysis allows evaluation of circulation.
neuromuscular abnormalities, exposure to oxygenation, ventilation, and perfusion.
anthracyclines, connective tissue disorders, r With initial presentation in infants, it is important to INITIAL STABILIZATION/THERAPY
immunologic abnormalities, Kawasaki-related investigate the etiology of the CM by obtaining
coronary disease, and myocarditis. serum amino acids, urine organic acids and amino circulation.
r 1/3 of childhood HCM cases are associated with r Immediate aggressive therapy for those who present
acids, lactate, and pyruvate.
Noonan syndrome. r Other tests to evaluate the etiology include creatine with severe symptoms or in cardiovascular collapse
kinase, carnitine, and acylcarnitine levels.
142
CARDIOMYOPATHY
MEDICATION DISPOSITION COMPLICATIONS

r Cardiovascular support: r Patients who are hemodynamically stable and r In DCM and RCM, blood clots may form in the heart
IV inotropes that do not increase afterload, without signs of heart failure or rhythm disturbance due to abnormal blood flow.
titrating to effect: may be admitted to an inpatient ward with cardiac r 10% of HCM patients will have an arrhythmia.
Milrinone 5075 g/kg loading dose over monitoring. r Patients with CM are more susceptible to
1560 min followed by a continuous infusion of r Critical care admission criteria: endocarditis, which typically occurs after a dental
0.250.75 g/kg/min Hemodynamic instability, significant symptoms, procedure or surgical procedure involving the GI or
Dobutamine 515 g/kg/min signs of heart failure, or dysrhythmia urinary tracts:
If hypotensive, the patient may require
alpha-adrenergic support, titrating to effect:
Discharge Criteria These patients generally require prophylactic
antibiotics prior to those procedures.
C
Epinephrine 0.11 g/kg/min Patients may be discharged home with close follow-up
Dopamine 1015 g/kg/min with a pediatric cardiologist if the following conditions
r Treatment for DCM: are met:
r After stabilization and improvement of the ADDITIONAL READING
Angiotensin-converting enzyme inhibitors: r Georgakopoulos D. Hypertrophic cardiomyopathy in
Enalapril or captopril signs/symptoms of failure
r Following a complete evaluation of arrhythmic children, teenagers and young adults. Hellenic J
Diuretics: Furosemide or spironolactone is used to
reduce afterload and to relieve venous congestion. potential Cardiol. 2007;48:228233.
r After initiation of drugs for long-term management r Harmon WG, Sleeper LA, Cuniberti L, et al. Treating
Warfarin for anticoagulation due to diminished
risk of thrombus children with idiopathic dilated cardiomyopathy
Issues for Referral
Digoxin or amiodarone to prevent arrhythmias r Cardiology consultation as early as possible (from the Pediatric CM Registry). Am J Cardiol.
r Treatment for HCM with obstruction: r Other specialists such as geneticists, 2009;104:281286.
r Shaddy R. Cardiomyopathies in adolescents: Dilated,
Beta-blockers and calcium channel blockers are endocrinologists, neurologists, and immunologists
used in the setting of moderate to severe hypertrophic, and restrictive. Adolesc Med. 2001;12:
may be helpful in determining the etiology and for
obstruction: 3545.
guiding treatment of underlying disease. r Weller R, Weintraub R, Addonizio LJ, et al. Outcome
Beta-blockers decrease outflow obstruction and
increase ventricular compliance. of idiopathic restrictive cardiomyopathy in children.
Calcium channel blockers improve diastolic FOLLOW-UP Am J Cardiol. 2002;90:501506.
filling by improving diastolic relaxation and r Yetman A, McCrindle B. Management of pediatric
decreasing outflow gradient due to depression FOLLOW-UP RECOMMENDATIONS hypertrophic cardiomyopathy. Curr Opin Cardiol.
of cardiac contractility. Activity: 2005;20:8083.
Diuretics and digoxin are not used, as they can r In patients with HCM: Strenuous activity should be
avoided as well as anaerobic exercise such as
worsen the obstruction of blood flow out of the
weightlifting and high-level competitive sports. Media Element)
heart. r http://www.childrenscardiomyopathy.org
Amiodarone: Children, 5 mg/kg IV load over r Competitive-level sports are not advised if any of the
r http://www.pcmregistry.org
30 min followed by 5 g/kg/min (max dose following are present:
15 g/kg/min); adults, 150 mg IV load over Significant outflow gradient
10 min followed by infusion 0.5 mg/min: Significant ventricular or supraventricular
Used to prevent ventricular arrhythmias arrhythmia CODES
r Treatment of RCM: Marked LV hypertrophy OR
Patients are at high risk for blood clots and often History of sudden death in relatives with HCM ICD9
need heparin or warfarin for anticoagulation. r 425.4 Other primary cardiomyopathies
Patient Monitoring r 425.3 Endocardial fibroelastosis
Diuretics to relieve venous congestion r Initially after discharge, patients will be followed
Beta-blockers for their negative inotropic and closely by a pediatric cardiologist weekly to biweekly
chronotropic effects to monitor medications and symptoms.
SURGERY/OTHER PROCEDURES r After stabilization, follow-up should be every PEARLS AND PITFALLS
r Extracorporeal membrane oxygenation may be 312 mo by a pediatric cardiologist. r Do not forget to ask about the family history, as
required for patients who cannot be stabilized with PROGNOSIS there is a strong familial component.
maximal pharmacologic support. r Mortality for children with HCM is 1% per year. r The majority of cases associated with genetic
r In HCM, surgical septal myectomy is recommended r Pediatric 5-yr survival with HCM is 8595%. syndromes present in infancy and fall into 4
in some cases of symptomatic children with r Pediatric 5-yr survival with DCM is 4050%. categories:
obstruction to relieve the symptoms of heart r The 2-yr survival rate after presentation of RCM is Inborn errors of metabolism
failure: Malformations
Myectomy does not prevent arrhythmia or sudden 4450%.
r Prognosis is poor for infants who present with Neuromuscular disorders
death. Familial isolated cardiomyopathic disorders
r HCM patients may also benefit from mitral valve symptomatic HCM. Many of these patients do not
replacement. survive to adolescence.
r Pacemakers may be necessary to monitor and
stabilize slow heart rates in patients with CM.
r An automatic implantable cardioverter defibrillator
may benefit patients with a history of severe
syncope and aborted cardiac arrest.
r Radiofrequency ablation of conduction defects may
be needed to prevent dysrhythmias.
r 20% of symptomatic DCM patients require
cardiac transplant within 2 yr of diagnosis:
12-yr survival rate of 80% after transplant
143
CARPAL TUNNEL SYNDROME

Jennifer Eng Lunt
Justin LaCorte
r Considerations in older children: PHYSICAL EXAM

BASICS Repetitive motion r Children may have:
Sports-related motions or injuries Thenar atrophy
DESCRIPTION Video games Decreased sweating
r Carpal tunnel syndrome (CTS) is a common nerve Trauma Weakness
entrapment disorder of adults but is uncommon in Pregnancy or use of oral contraceptives Claw hand deformity
childhood. Mass lesions that compress the median nerve r Adolescents and adults may present more commonly
r The carpal tunnel is bound by the carpal bones Bony abnormalities (osteophytes) with thumb weakness manifested by difficulty with
dorsally, the transverse carpal ligament on the Rheumatoid arthritis writing, pincer grasp, or holding small utensils.
palmar surface, and encased by the flexor Endocrine disorders: Hypothyroidism, diabetes r Specific physical exam tests:
retinaculum. mellitus, acromegaly Phalen sign: Hyperflexion of the wrist for 60 sec
r The tunnel contains the median nerve, flexor Chronic hemodialysis may elicit paresthesia in the median nerve
digitorum profundus, flexor digitorum superficialis, Idiopathic distribution:
and flexor pollicis longus. COMMONLY ASSOCIATED CONDITIONS Sensitivity 68% and specificity 73%
r Compression of the median nerve causes symptoms r Mucopolysaccharidosis Tinel sign: Gentle tapping over the median nerve
of numbness, tingling, pain, and weakness. r In adolescents, associated conditions that have been at the wrist produces tingling in the fingers in the
reported include: median nerve distribution:
EPIDEMIOLOGY Sensitivity 50% and specificity 77%
Incidence Colles fracture or other wrist trauma
r CTS is rarely seen in children. Rheumatoid arthritis or other inflammatory Manual carpal compression test: Applying
pressure over the transverse carpal ligament
r Most cases are seen with injuries of the wrist or in rheumatic disease
Diabetes mellitus leads to paresthesias within 30 sec of applying
lysosomal storage disorders. pressure:
Osteoarthritis of the wrist
Prevalence Sensitivity 64% and specificity 83%
Pregnancy
r <200 pediatric cases have been reported in the Sensory testing with 2-point discrimination or
Myxedema
literature since 1989. Acromegaly tactile testing
r Women are found to be twice as likely to be affected Amyloidosis DIAGNOSTIC TESTS & INTERPRETATION
as men. Hepatic disease Lab
Fibromyalgia r Not indicated in most pediatric cases
RISK FACTORS
r In children, genetic predisposition and history of Tumors r There are no known lab studies specific for the
lysosomal storage disease may increase risk. diagnosis.
r In older children, overuse, sports, or wrist-related DIAGNOSIS r In older children and adolescents, lab tests to rule
injuries may also increase risk. out diseases or conditions causing CTS may be
HISTORY helpful such as rheumatoid factor, antinuclear
GENERAL PREVENTION r In children, a history may be difficult to obtain due
r Avoidance of exacerbating symptoms dependent on antibody, pregnancy tests, and genetic testing.
to the lack of ability to communicate symptoms.
the individuals causative factors r Children often present differently than adults or Imaging
r Cessation of repetitive wrist movements r Conventional radiology may be useful if suspicious
adolescents.
r Wrist support r Children may present with difficulty with fine motor of fracture or bony abnormality.
r MRI is helpful to confirm the diagnosis and to
PATHOPHYSIOLOGY tasks.
r The exact pathophysiology is unclear. r Children present more often with bilateral disease. examine the anatomy within the canal.
r US may be useful in evaluating for synovitis.
r Symptoms may occur due to pressure within the r Common symptoms include:
carpal tunnel during flexion and extension along Numbness/Paresthesia in median nerve Diagnostic Procedures/Other
with demyelination, edema, venous congestion, or distribution: Thumb, index, middle, and radial Electromyographic and nerve conduction studies help
vascular sclerosis leading to compression of the aspect of the ring finger to confirm the diagnosis of CTS:
Pain that is exacerbated by: r Sensitivity 85% and specificity 95%
median nerve.
Repetitive wrist movement
ETIOLOGY Activities in which the wrist is flexed or extended DIFFERENTIAL DIAGNOSIS
r Considerations in children: r See Commonly Associated Conditions.
Pain in the wrist or hand, sometimes radiating to r Tendinitis
Trauma the elbow, forearm, or shoulder
Lysosomal storage disorders (eg, r Often worse at night, relieved by shaking out the r Tenosynovitis
mucopolysaccharidosis) r Median nerve neuropathy
hand:
Hamartoma of the median nerve r Brachial plexus injuries
Flick sign: Shaking or flicking ones hands for
Anomalous flexor digitorum superficialis
relief during maximal symptoms: r Arthritis
Hemophilia with hematoma Sensitivity 47% and specificity 62%
Hereditary
Idiopathic
144
CARPAL TUNNEL SYNDROME

r May need referral to a hand surgeon for r Postoperative complications or infections after
TREATMENT
consideration of surgical release of the transverse surgery
INITIAL STABILIZATION/THERAPY carpal ligament: r Chronic hand pain
r Splint the wrist in neutral position (0 degrees). Definitive therapy for patients with moderate to r Chronic hand weakness and numbness
r Avoidance of repetitive wrist movement severe symptoms
r Wrist splint to be worn at night until follow-up Surgery may be open or endoscopic with similar
r Apply heat to involved wrists: efficacy: ADDITIONAL READING
Endoscopic surgery has been shown to result in
Heating pad
earlier return to daily activities and fewer wound
r Bland JD. Treatment of carpal tunnel syndrome. C
Hot water bottle Muscle Nerve. 2007;36(2):167171.
problems.
Low-level heat wraps Possible disadvantages may include higher r Muller M, Tsui D, Schnurr R, et al. Effectiveness of
r Motion and tendon-gliding or nerve-gliding
complication rates and cost. hand therapy interventions in primary management
exercises r Surgery for CTS has a long-term success rate >75%. of carpal tunnel syndrome: A systematic review.
MEDICATION r Surgery for children with CTS and associated J Hand Ther. 2004;17(2):210228.
r Van Meir N, De Smet L. Carpal tunnel syndrome in
First Line mucopolysaccharidosis is definitive and shown to be
r NSAIDs: effective. children. Acta Orthop Belg. 2003;69(5):387395.
r Yuen A, Dowling G, Johnstone B, et al. Carpal tunnel
No significant long-term benefit to using NSAIDs
DISPOSITION syndrome in children with mucopolysaccharidosis.
Ketorolac 0.5 mg/kg IV/IM q6h PRN Admission Criteria J Child Neurol. 2007;22(3):260263.
Naproxen 5 mg/kg PO q8h PRN Patients are almost always discharged.
r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN Discharge Criteria
Second Line Patients and families should have an understanding of CODES
r Prednisone 1 mg/kg/dose PO b.i.d. if conservative the etiology, management options, and proper
follow-up with a primary care physician prior to ICD9
measures fail
r Referral to a hand surgeon for methylprednisone discharge from the emergency department. 354.0 Carpal tunnel syndrome
injections Issues for Referral
r Cases refractory to conservative management
COMPLEMENTARY & ALTERNATIVE should be referred to hand surgery or a
PEARLS AND PITFALLS
THERAPIES rehabilitation medicine specialist. r Uncommon in young children
r Conservative therapy for mild to moderate symptoms r Referral to occupational medicine for ergometric r Most likely associated in children with history of
r Application of a customized or prefabricated wrist
testing if caused by repetitive motion mucopolysaccharidosis, trauma, or repetitive use
splint r Typical emergency department management does injuries
r Combined therapy found to be better than any
not consist of steroid injections: r Emergency department treatment includes
single modality: Such practices should be referred to hand surgery conservative therapy and splinting:
Splinting or a rehabilitation medicine specialist. Refer to hand surgery or an occupational or
Stretching exercises
rehabilitation medicine specialist for refractory
Steroid injections
r Complementary CTS treatments: cases.
FOLLOW-UP
Yoga
Occupational therapy FOLLOW-UP RECOMMENDATIONS
Nerve-gliding maneuvers
Magnetic therapy Discharge home with appropriate referral to either
Myofascial massage the patients primary care provider or a specialist
r US in hand surgery or to occupational or
rehabilitation medicine.
r Activity:
Avoid activity that may worsen symptoms.
PROGNOSIS
r Prognosis usually is excellent.
r Refractory cases may require surgery:
Prognosis following surgery has been found to be
good.
145
CAT SCRATCH DISEASE

Kerry Caperell
Raymond Pitetti

r Serologic tests for B. henselae are commercially
DESCRIPTION HISTORY available and are diagnostic in the appropriate
r Cat scratch disease is caused by infection from the r Children usually present with axillary or cervical
clinical setting:
intracellular bacteria Bartonella henselae. lymphadenopathy (2).
r Systemic symptoms: These may be indirect fluorescence antibody,
r Usually seen after kitten or cat bite or scratch
enzyme immunoassay, or PCR tests.
r Causes lymphadenopathy that is most often Up to 50% of children will be febrile. r An elevated neutrophil count, ESR, or C-reactive
localized or regional Malaise or anorexia
r There is often no history of a cat bite or scratch, but protein may indicate disseminated disease.
r Cultures for B. henselae are of limited value because
EPIDEMIOLOGY history of cat exposure is almost always present.
Incidence r History of a papular lesion forming 12 wk the organism can take several weeks to grow.
r Estimated 9.3 U.S. cases per 100,000 people per Imaging
following a cat bite or scratch
year (1) r History of lymphadenopathy occurring up to several Abdominal US, contrast CT scan, or MRI are rarely
r 55% of these are in children <18 yr of age. indicated but can be used to evaluate the liver or
weeks later
r In the U.S., cat scratch disease is the most common spleen for microabscesses.
cause of chronic unilateral regional lymphadenitis in PHYSICAL EXAM
r A brown to red papule can be seen at the site of the Diagnostic Procedures/Other
children. Biopsy of an affected lymph node is only rarely
bite or scratch.
RISK FACTORS r Affected lymph nodes are usually axillary or cervical, indicated in cases where the diagnosis is in question.
r Exposure to cats, particularly kittens infested with Pathological Findings
but submandibular, auricular, epitrochlear, as well as
fleas r Biopsied tissue will show stellate granulomas and
lower limb nodes, may be inflamed:
r More common in the fall and winter The arm and neck are usually involved, as the site microabscesses.
r More common in warm and humid climates of inoculation is usually the hand. r Warthin-Starry stain will tint the bacteria.
Other inoculation sites will have lymphadenopathy DIFFERENTIAL DIAGNOSIS
GENERAL PREVENTION
r Immunocompromised children should avoid contact in the area of regional lymph node drainage. r Lymphadenopathy
These nodes are enlarged (15 cm or more) and r Lymphadenitis due to typical suppurative bacteria,
with cats known to scratch or bite.
r Immunocompromised children should immediately nearly always tender.
such as Streptococcus and Staphylococcus
Most nodes are warm and erythematous. r Mycobacterial lymph node infection
wash all cat bites and scratches with soap and water. 1015% of nodes suppurate.
r Children with visceral involvement (bacillary peliosis) r Malignancy
PATHOPHYSIOLOGY r Toxoplasmosis
r Infection causes the formation of a papule at the may have hepatosplenomegaly.
r Children with vascular involvement (bacillary r HIV, Epstein-Barr virus, cytomegalovirus
site of the bite or scratch.
r Hyperplasia and infection of the lymph nodes occurs; r Other bacterial causes: Nocardia infection,
angiomatosis) have vascular proliferative skin or
microabscesses form and may become confluent subcutaneous nodules. tularemia, cutaneous anthrax, brucellosis,
leading to pus-filled sinuses. These may drain. r Can rarely see ocular manifestations such as sarcoidosis, and bubonic plague
r The liver, spleen, eyes, and CNS can also be affected conjunctivitis or neuroretinitis.
via hematologic transmission. r Children very rarely can have CNS involvement
ETIOLOGY including encephalopathy, ataxia, or transverse
Caused by the inoculation of B. henselae bacteria via myelitis.
a cat bite or scratch
146
CAT SCRATCH DISEASE
r Immunocompromised children usually need to be 1. Jackson L, Perkins B, Wender JD. Cat scratch
MEDICATION hospitalized for observation and therapy. disease in the United States: An analysis of three
First Line r Children with bacillary peliosis, bacillary national databases. Am J Public Health. 1993;83:
r In uncomplicated cases in immunocompetent hosts, angiomatosis, or complicated or disseminated
17071711.
cat scratch disease is a self-limited illness requiring disease often need to be hospitalized and receive 2. English R. Cat-scratch disease. Pediatr Rev. 2006;
only supportive care. parenteral antibiotics. 27:123128.
In uncomplicated cases, there is controversy over
the utility of treatment with azithromycin (3).
Discharge Criteria
r Most immunocompetent patients with suspected cat
3. Massei F, Gori L, Macchia P, et al. The expanded
spectrum of bartonellosis in children. Infect Dis Clin
C
r Azithromycin: North Am. 2005;19:691711.
scratch disease can be safely discharged.
Dose 10 mg/kg/dose on day 1 followed by r Patients with disseminated disease and
5 mg/kg/dose on days 25; adult dose 500 mg
day 1 followed by 250 mg PO days 25
immunocompromised patients should be admitted ADDITIONAL READING
for antibiotic therapy.
Patients with more disseminated disease may Schutze G, Jacobs R. Bartonella species (cat-scratch
benefit from treatment with azithromycin. disease). In Long S, ed. Principles and Practice of
r Immunocompromised patients always require FOLLOW-UP Pediatric Infectious Diseases. 3rd ed. Philadelphia, PA:
antimicrobial therapy. Churchill-Livingstone; 2008:851854.
r In the immunocompromised child, erythromycin, FOLLOW-UP RECOMMENDATIONS
Discharge instructions and medications: See Also (Topic, Algorithm, Electronic
rifampin, doxycycline, or gentamicin should be used
alone or in combination. r Patients should be followed closely by their primary Media Element)
r Analgesics are indicated for pain due to care provider. Fever of Unknown Origin
lymphadenopathy. r Many clinicians elect to treat with a 5-day course of
r NSAIDs: azithromycin.
CODES
PROGNOSIS
Ketorolac 0.5 mg/kg IV/IM q6h PRN r Uncomplicated cases gradually resolve over several
Naproxen 5 mg/kg PO q8h PRN ICD9
months without treatment.
r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN r Even in immunocompromised hosts, the prognosis is 078.3 Cat-scratch disease
Second Line good if the disease is treated adequately.

Trimethoprim/sulfamethoxazole (TMP/SMZ) or COMPLICATIONS PEARLS AND PITFALLS
ciprofloxacin may also be effective: r Visceral organ involvement: r Children with catscratch disease often give no
r TMP/SMZ: 612 mg TMP/kg/day PO q12h; adult
Hepatic history of a cat scratch or bite.
dose 160 mg TMP/800 mg SMZ b.i.d. 7 days Splenic r Regional lymphadenitis is the most common sign.
Mesenteric adenitis r Cat scratch disease is usually a self-limited illness
r Rare complications:
requiring no antibiotic therapy.
Encephalopathy r Cat scratch disease can be an etiology for fever of
Optic neuritis
unknown origin.
Erythema nodosum
Osteolytic bone lesions
Osteomyelitis
Transverse myelitis
Guillain-Barre syndrome
147
CAUDA EQUINA SYNDROME

Kerry Caperell
Raymond Pitetti
ETIOLOGY
BASICS r Midline lumbar disc herniation DIAGNOSIS
r Meningitis
DESCRIPTION r Space-occupying lesions in the spinal cord: HISTORY
r Cauda equina syndrome is a rare condition that r Pain in the lumbar region
Epidural hematoma r Pain that radiates down both legs in the sciatic
results from the compression of the nerve roots of Abscess
the spinal cord distal to L1. Tumor distribution
The cauda equina, or horsetail, represents the r Ankylosing spondylitis r Numbness or weakness in both legs that is often
lower end of the spinal cord and contains the r Paget disease progressive
nerve roots from L1L5 and S1S5. r Urinary retention
r Inferior vena cava thrombosis
r Compression of these nerve roots manifests as one r Rectal sphincter dysfunction
r Lymphoma
or more of the following: r Altered urinary sensation
r Sarcoidosis
Weakness of the lower extremities r Altered perineal sensation
r Trauma (blunt or penetrating):
Saddle anesthesia r Urinary frequency
Bowel or bladder dysfunction Can rarely be related to spinal anesthesia or r Urinary incontinence
Sexual dysfunction lumbar puncture
r Sexual dysfunction
EPIDEMIOLOGY COMMONLY ASSOCIATED CONDITIONS
r Uncommon with unclear incidence r Meningomyelocele PHYSICAL EXAM
r Usually reported as a case report r Lumbar vertebral subluxation r Sensory deficit in a saddle distribution
r Neoplasia in the lumbosacral area: r Sensory deficit in the perineal area
RISK FACTORS r Often asymmetric flaccid paralysis of the lower
r History of cancer Can be primary or metastatic
Often Ewings sarcoma or neuroblastoma extremities
r History of low back trauma r Decreased rectal sphincter tone
r Epidural hematoma or abscess
PATHOPHYSIOLOGY r Positive straight leg raise test
r Compression of some or all of the nerve roots from r Reflex abnormalities: Loss or diminution
L1S5 by any lesion (see below)
r These nerve roots are particularly susceptible to DIAGNOSTIC TESTS & INTERPRETATION
injury since they have a poorly developed Imaging
r MRI is the preferred imaging modality.
epineurium. r If concerned, MRI should be performed emergently.
r CT scan is inferior for diagnosing cauda equina
syndrome:
However, it is the modality of choice if fracture is a
concern.
148
CAUDA EQUINA SYNDROME
Diagnostic Procedures/Other DISPOSITION ADDITIONAL READING

Catheterization of bladder: Post-void residual bladder Admission Criteria r Fraser S, Roberts L, Murphy E. Cauda equina
volume is usually high. All patients with cauda equina syndrome should be
admitted to a medical center that can provide syndrome: A literature review of its definition and
DIFFERENTIAL DIAGNOSIS clinical presentation. Arch Phys Med Rehabil.
r Musculoskeletal back pain definitive care.
2009;90:19641968.
r Herniated disc Discharge Criteria r Mauffrey C, Randhawa K, Lewis C, et al. Cauda
r Fractured vertebra Not applicable equina syndrome: An anatomically driven review. Br
r Spondylolisthesis Issues for Referral J Hosp Med. 2008;69:344347.
r Conus medullaris syndrome r As soon as the diagnosis of cauda equina syndrome r Podnar S, Trsinar B, Vodusek DB. Bladder C
r Functional back pain is suspected, the patient should be transferred to a dysfunction in patients with cauda equina lesions.
r Severe constipation center with pediatric MRI capability. Neurourol Urodyn. 2006;25:2331.
r When the diagnosis is confirmed, the patient should
be transferred to a center with pediatric spine
TREATMENT surgeons capable of performing decompression CODES
surgery.
PRE HOSPITAL r Early neurosurgical, neurologic, and/or orthopedic
r If due to a traumatic injury, immobilize the spine. ICD9
consultations are recommended. r 344.60 Cauda equina syndrome without mention of
r Stabilize acute life-threatening conditions.
neurogenic bladder
INITIAL STABILIZATION/THERAPY FOLLOW-UP r 344.61 Cauda equina syndrome with neurogenic
r No proven medical treatment exists. bladder
r Therapy is directed at underlying cause. PROGNOSIS
r Early diagnosis and surgical decompression are the
r Appropriate pain management
r If sudden in onset, surgical decompression is factors most identified with a favorable outcome: PEARLS AND PITFALLS
In general, the longer the interval of time before
required emergently (see below). treatment, the greater the damage caused to the r Bladder retention is one of the hallmarks of cauda
MEDICATION nerve(s). equina syndrome, and the syndrome is rare in the
r Morbidity is variable and dependent on the etiology absence of bladder retention.
First Line
Analgesia should be given as appropriate: of the syndrome. r MRI is the diagnostic test of choice.
r Morphine 0.1 mg/kg IV/IM/SC q2h PRN: r Long-term sequelae include: r When suspected, patients with cauda equina
Initial morphine dose of 0.1 mg/kg IV/SC may be Bladder dysfunction syndrome should be transferred to a center that can
repeated q1520min until pain is controlled, then Leg weakness provide a definitive diagnosis and care.
q2h PRN. Decubitus ulcers
Venous thromboemboli
Second Line
The use of steroid is considered controversial and COMPLICATIONS
should be administered only under the guidance of If decompression is delayed, residual weakness,
appropriate consultants. sensory deficits, bladder/bowel dysfunction, and
sexual dysfunction can be seen.
r In cases of mechanical compression, immediate
transfer to the operating room for emergent surgical
decompression of the area is indicated.
r Earlier decompression maximizes preservation of
neurologic function.
149
LWBK822-driver-C LWBK822-Hoffman ch075a.xml April 15, 2011 11:9
CAUSTIC EXPOSURE
Kristopher Hunt
Robert J. Hoffman
ETIOLOGY r Ingested:
BASICS The following routes of exposure: Typical findings include burns to the lips and
r Inhalational oropharynx.
DESCRIPTION r Dermal Patients may exhibit dribble marksburns to
r Caustic exposures cause histologic damage on
r Ocular the chin or chest from dribbled or spilled caustic
contact with tissue. r Oral liquid.
r The most familiar types are acids and alkali: Dysphonia, aphonia, and stridor are ominous signs
r GI
Others are desiccants, vesicants, and protoplasmic of airway injury and should trigger immediate
poisons. action to stabilize and secure the airway.
r Caustics are often found in cleaning products. DIAGNOSIS Ominous signs include evidence of viscous
r Acids include hydrochloric acid, sulfuric acid, and perforation, hemodynamic instability, peritoneal
hydrofluoric acid (HF). HISTORY signs, and signs of airway compromise.
r Alkali include ammonia, calcium hydroxide, sodium r Dermal: Except in peritonitis, the abdominal exam
hydroxide, and household bleach. Patients may or may not know of a specific caustic correlates poorly with extent of damage.
r HF poses a specific problem because it is a weak that has been exposed on skin. Suicidal intent in the adolescent may be an
HF exposure will present with a complaint of independent risk factor for severity of injury.
acid, allowing it to remain in an undissociated state
severe pain, discordant with physical exam
and penetrate skin:
findings. Burns with a benign skin appearance
Contact with a body surface area as small as 2% Lab
may be life threatening.
with concentrated HF may be fatal. Initial Lab Tests
Onset of pain is directly related to concentration
EPIDEMIOLOGY of HF: Serum chemistry, a venous or arterial blood gas
Very concentrated HF >4050% causes analysis:
Incidence r Screening acetaminophen and salicylate should be
There are >100,000 reported exposures to caustic immediate symptoms, weak HF <10% solution
agents annually in the U.S.: typically causes symptoms only many hours done if there was intent of self-harm.
r Household bleach is the most common. (614) after exposure. Imaging
r Ocular: r Radiographs of the chest and abdomen may aid in
GENERAL PREVENTION Patients typically have severe pain. demonstrating pneumothorax,
Keep poisons inaccessible to children. Lack of pain may be the result of a severe burn. pneumomediastinum, pleural effusion, or
r Inhalational: intraperitoneal air:
PATHOPHYSIOLOGY
r Acids and alkali exert damage as a result of proton Upper airway irritation, chest pain, or dyspnea Radiographs are not routinely indicated but are
donation or acceptance, respectively. after aerosolized caustic exposure used in symptomatic patients.
r Acids cause coagulation necrosis; the upper layer of r Ingested: r CT of the chest, abdomen, and/or pelvis may
damaged tissue forms a leathery eschar, preventing Suicidal intent, more prevalent in adolescent further delineate injuries; use only in symptomatic
deeper tissue penetration: ingestions, may predict significant injury. patients:
HF is a unique caustic capable of causing severe Patients may complain of a variety of symptoms In the case of an ingested button battery,
systemic toxicity and dysrhythmias due to both following caustic ingestion, and there may be a radiographs of the neck, chest, and abdomen
depletion of calcium and magnesium and great disparity between symptomatology and should be obtained to locate the battery as well as
hyperkalemia. severity of injury. obtain an estimate of size.
Acids may cause damage to other organs. such as Pain complaints may be referred to the
the spleen, liver, and biliary tree after being oropharynx, chest, or abdomen. These may r Obtain a 12-lead ECG.
absorbed and distributed systemically. include dysphagia, odynophagia, drooling, r Endoscopy:
r Alkalis cause liquefaction necrosis, which is more abdominal pain, chest pain, or vomiting.
Ominous symptoms: Constitutional symptoms or Gold standard for assessment of GI damage
extensive and severe because saponification and Endoscopy after a caustic ingestion will not result
protein disruption allow the caustic to penetrate systemic complaints such as dizziness, listlessness,
fever, chills, HA, or syncope in damage to the endoscope.
through layers of tissue. Do not delay endoscopy to allow the injury to
r Extent of injury after caustic exposure is mostly Weeks after ingestion, dysphagia and vomiting
may result from stricture formation. develop; delay increases the risk of perforation.
determined by pH, particularly if the substance is No evidence supports the idea that viscous
below pH 2 or >12: PHYSICAL EXAM perforation is more likely with endoscopies
Concentration is also a determinant of injury, with r Dermal: performed for caustic ingestions relative to those
more severe injuries resulting from more Patients will have localized pain and apparent performed for any other reason.
concentrated solutions. burns. The presence of vomiting, drooling, stridor, and
Food in the stomach as well as vomiting may HF exposure may have minimal or no apparent the inability to voluntarily take oral liquids are
diminish the effect of the caustic ingestion. skin lesions: reliable factors in young children to predict
Tissue penetration, duration of contact, and Severe pain out of proportion related to the esophageal or gastric injury:
volume of caustic are other factors of injury. physical exam is very common with HF. Children with none of these signs and
For ocular exposures, alkaline agents have a r Ocular: symptoms can be presumed to not have severe
potential to injure the eye to a greater extent at a Diminished visual acuity and clouding of the GI involvement and do not require endoscopy.
lower concentration largely due to the inability of cornea are poor prognostic signs. Presence of 2 of these findings are indications
tears to buffer alkaline substances. r Inhalational: for endoscopy. These criteria are only applicable to
Patients may present with relative degrees of children and may not be applicable to adolescents.
tachypnea, stridor, dysphonia, aphonia, Other indications include any patient or
bronchospasm, hypoxia, hypercarbia, or circumstance that is considered to be unreliable
respiratory arrest depending on the involved surrounding an ingestion (particularly suicidal
caustic exposure. intent) and any patient with 2nd- or 3rd-degree
orofacial burns.
150
CAUSTIC EXPOSURE
The presence of a button battery located in the r Ingested: DISPOSITION

esophagus on CXR necessitates endoscopic Airway compromise is the most urgent problem Admission Criteria
removal secondary to the high associated risk of arising after caustic ingestion. r Dermal:
esophageal perforation or necrosis. Edema or burns of the airway may rapidly progress Significant burn that would otherwise meet
Pathological Findings to loss of airway patency. admission criteria for a burn will require admission
Ingested: Blind nasotracheal intubation is contraindicated. for similar management.
r GI lesions are graded by the depth of penetration Aspiration of stomach contents using an NG tube Diligent hemodynamic monitoring is required for
may be considered for ingestion of large volumes any serious HF exposure or ingestion. HF has the
and appearance of mucosa.
Grade 0: Normal mucosa
of acids to prevent systemic absorption of the
agent.
ability to cause electrolyte abnormalities including
hypocalcemia, hypomagnesemia, and
C
Grade I: Hyperemia and edema of mucosa Ingestion of HF is frequently fatal, and few
Grade IIa: Friability, ulcers, hemorrhages, erosions, hyperkalemia.
patients survive such exposures. r Ingested:
or exudates
Grade IIb: Similar to IIa with deep discrete or MEDICATION Caustic ingestion with signs or symptoms of
circumferential ulceration r Dermal: airway or GI compromise
Grade IIIa: Small scattered necrosis HF exposures may be treated by soaking in Patients unable to tolerate liquids PO
Grade IIIb: Extensive necrosis calcium gluconate gel: Grade IIa or greater esophageal lesions; placed on
Plain calcium chloride solution may be used or either a soft diet or NG tube feeds. Stricture
DIFFERENTIAL DIAGNOSIS may be combined with large amounts of formation is typical.
The cornerstone of caustic exposure differential hinges Surgilube to create a slurry.
upon whether the substance was known to be
Discharge Criteria
Every 30 min, this slurry should be replaced, and Ingestion:
ingested or not: the treatment should be continued until the r Grade 0I injuries by endoscopy
r A broad differential must be maintained to
patient is painfree. r Ingestion of a button battery that is located past the
determine if other substances are involved. Intradermal injections or intra-arterial 5%
pylorus
calcium gluconate may be rarely needed if the r A patient with a nonbutton battery in the stomach
TREATMENT gel does not adequately control pain.
For phenol or solid metals, irrigate with may be discharged to return within 48 hr for a
polyethylene glycol (Go-Lytely). repeat radiograph.
PRE HOSPITAL r If battery remains in the stomach, endoscopy should
Water may worsen injury due phenol and metals
Ingestion: be performed to remove the battery.
r Decontamination by dilution is recommended. due to reactivity with water.
r Inhalational:
r Drinking 2 mL/kg of water is a reasonable 1st step
Inhalational acid exposures may safely be treated
at attempting GI dilution: with neutralizing agents. ADDITIONAL READING
Drinking more may result in vomiting.
r Induced vomiting is contraindicated. These involve minute amounts of caustic spread r Arevalo-Silva C, Eliashar R, Wohlgelernter J, et al.
over a large surface area; therefore, caustic acids Ingestion of caustic substances: A 15-year
INITIAL STABILIZATION/THERAPY may be treated with nebulized aerosols of experience. Laryngoscope. 2006;116:14221426.
r Assess and stabilize airway, breathing, and neutralizing sodium bicarbonate. A 2% sodium r Previtera C, Giusti F, Guglielmi M. Predictive value of
circulation. bicarbonate solution if made by diluting standard
visible lesions (cheeks, lips, oropharynx) in suspected
r Obtain vascular access in the event of rapid decline. sodium bicarbonate 1:3 with normal saline.
caustic ingestion: May endoscopy reasonably be
r Dermal: Nebulized calcium gluconate may give
omitted in completely negative pediatric patients?
Remove clothing and perform copious irrigation. symptomatic relief of HF inhalation.
r Ingested: Pediatr Emerg Care. 1990;6:176178.
All affected body areas should be irrigated until r Tekant G, Eroglu E, Erdogan E, et al. Corrosive
there is no remaining caustic agent. Steroid therapy for grade IIb lesions has been
injury-induced gastric outlet obstruction: A changing
Neutralizing agents are not recommended. demonstrated to prevent stricture formation.
spectrum of agents and treatment. J Pediatr Surg.
Water is not the diluent of choice with solid Methylprednisolone 2 mg/kg IV up to 120 mg/day
2001;36:10041007.
metals, which react in a highly exothermic divided in 3 equal doses.
reaction, and phenols, which form a gluelike Dexamethasone 0.5 mg/kg IV/IM initial dose in
adhesive that is difficult to remove: the emergency department
If grade III lesions, do not administer steroids due
CODES
These may be removed with a nonreactive
diluent like polyethylene glycol (Go-Lytely). to an increased likelihood of perforation.
r Ocular: If administering corticosteroids, concomitantly ICD9
r 983.1 Toxic effect of acids
Decontamination of an ocular exposure may be a give broad-spectrum antibiotics.
r 983.2 Toxic effect of caustic alkalis
sight-saving intervention. SURGERY/OTHER PROCEDURES r 983.9 Toxic effect of caustic, unspecified
Irrigation is best facilitated with the use of ocular r Inhalational:
anesthetic and irrigation with a Morgan lens. Urgent bronchoscopy is indicated to remove a
After irrigation, assess visual acuity, ocular button battery lodged in the airway.
integrity, funduscopy, cul-de-sacs for residual r Ingested: PEARLS AND PITFALLS
caustic material, and pH testing. Fiberoptic visualization of airway is advised in r Vomiting, drooling, stridor and/or inability to take
Continue irrigation with 2 L of fluid per eye or patients with symptoms of airway injury who do PO are predictive of significant injury.
until the pH returns to 7.4. not undergo endotracheal intubation: r Induced vomiting is contraindicated.
Assessment of pH should be delayed several Best accomplished with the assistance of an r Consider endotracheal intubation for any symptoms
minutes after irrigation stops to ensure that the otolaryngologist
litmus paper reflects the pH of the eye surface and of airway compromise.
Endoscopy criteria must be communicated
not the irrigation fluid. appropriately to a gastroenterologist.
r Inhalational: If there is evidence of perforation, early surgical
Airway management is paramount. intervention is needed.
r If there is any stridor, drooling, or hypoxemia, have a Operative treatment allows perforation repair,
low threshold for endotracheal intubation. debridement of necrotic tissue, and placement of
a G or J tube for enteral feeds.
151
CAVERNOUS SINUS THROMBOSIS

Joseph B. House
Michele M. Nypaver
Hypercoagulable states: PHYSICAL EXAM

BASICS Protein C and S deficiencies r Need to identify source of primary infection
Antithrombin deficiency r Eye:
DESCRIPTION Fibrinogen deficiency Periorbital edema
r Cavernous sinus (CVS) thrombosis is the occurrence Plasminogen deficiency Chemosis from ophthalmic vein obstruction
of a blood clot within the CVS. Factor V Leiden Ptosis
r Common etiologies are infectious; less commonly, Presence of lupus anticoagulant Signs of increased retrobulbar pressure
there is a predisposition to thrombosis of other Presence of anticardiolipin, antiphospholipid Exophthalmos
causes: antibodies Ophthalmoplegia
Critical anatomy: The CVS lies within the cerebral Prothrombin gene mutation Mydriasis
sinus (CS) venous drainage system, located at the Homocysteinemia/Homocystinuria Signs of increased intraocular pressure:
skull base: Use/Administration of procoagulation drugs Decreased visual acuity
Valveless sinus surrounded by dura mater (chemotherapeutic agents, oral contraceptives) Papilledema
encircling sella turcica Pregnancy/Postpartum state Retinal hemorrhage
Without valves, venous blood may flow Malignancy: Leukemia, lymphoma r Other findings consistent with intracranial
antegrade or retrograde depending on the Acute systemic illness: Sepsis pathology:
hydrostatic pressure gradient. Chronic systemic disease: Inflammatory bowel CN palsy, which may affect:
Receives blood from superior and inferior disease, systemic lupus erythematosus, diabetes Some or all of CN III, IV, V, or VI
ophthalmic veins, superficial middle cerebral mellitus, sickle cell disease Sensory deficit of ophthalmic and maxillary
vein, and sphenoparietal sinus branches of CN V
Connects with facial vein via superior PATHOPHYSIOLOGY
Two primary processes: Venous obstruction (local Hemiparesis
ophthalmic vein Meningeal signs if condition has progressed
Drains posteroinferiorly via superior and inferior edema effects) and thrombosis of sinuses (intracranial
HTN): In neonates: Seizure and diffuse neurologic signs
petrosal sinuses and emissary veins to pterygoid r Results in cerebral edema (cytotoxic and vasogenic) are the most common presentation.
plexuses Alteration in mental status: Confusion, lethargy,
Critical structures within the CVS include the and impaired absorption of CSF
r Not associated with ventricular dilatation (terminal somnolence, or coma
internal carotid artery and surrounding r Persistent fever and/or tachycardia (signs of sepsis)
sympathetic nerve plexus and cranial nerves (CNs) phase of CSF flow does not result in pressure
are late findings.
III (oculomotor), IV (trochlear), V (trigeminal gradient change)
division 1 ophthalmic and division 2 maxillary), DIAGNOSTIC TESTS & INTERPRETATION
ETIOLOGY
and VI (abducens). r Most causes of CVS are caused by head/neck Lab
Any/All of these structures may be affected by infections; most children have an identifiable Initial Lab Tests
thrombosis in the CVS. cause (2): Lab tests are nonspecific:
Staphylococcus species account for 70% of all r Tests are done to identify underlying cause or
EPIDEMIOLOGY
infections. etiology:
Incidence
r Overall incidence of cerebral vein/sinus thrombosis Streptococcus pneumoniae is the 2nd most CBC
common. Blood culture
in children is estimated at 7 cases per 1 million per
Gram-negative bacilli and anaerobes are also Coagulation profile, specific coagulation studies
year (1).
r More common in neonates/young children/young seen. Inflammatory markers: ESR, C-reactive protein
Fungi are rare pathogens. Imaging
adults (especially women) than older adults r Noninfectious etiologies: Thrombosis from r An MRI with contrast in combination with a
RISK FACTORS hypercoagulable state, infiltrative malignancy, magnetic resonance venogram (MRV) is the most
r Risk factors are age and gender related (neonatal,
mechanical factors (trauma, surgery), acute or sensitive imaging (4).
older children, young women) (24). chronic systemic illnesses, or mass effect (aneurysms) r MRV may show absence of flow in the CVS.
r Patients often have multiple risk factors. r CT is less sensitive than MRI:
r Neonatal CVS risk factors:
DIAGNOSIS May show increased density in the CVS
Perinatal complications (hypoxemia, premature suggesting the presence of a thrombus
rupture of membranes, placental abruption, HISTORY Use of contrast may show filling defect in the CVS
gestational diabetes, infection) r Highly variable (acute, subacute, or indolent) and in addition to sinus infection.
Genetic hypercoagulable states requires high index of suspicion: Findings may be subtle.
Dehydration Children may present with nonspecific complaints Negative scan does not fully exclude CVS
r Risk factors for nonneonates/children/young adults:
such as fatigue, vomiting, headache, and fever. thrombosis.
Head and neck infections (sinusitis, otitis media, r Most common complaint is headache: r Sinus radiography:
mastoiditis, odontogenic infection) Gradual, can be unilateral with bilateral May show sinus opacification
Dehydration involvement r Carotid angiography:
Trauma (direct head/neck trauma, neurosurgical r History of sinusitis, midface or odontogenic infection May show narrowing and/or obstruction of the
procedures, lumbar puncture) r Eye complaints: Pain, swelling, tearing, visual carotid sinus as it passes through the CVS
changes, or diplopia
r Mental status changes: Lethargy, somnolence,
confusion, coma
r Seizure (common neonatal presentation)
r Fever may be present.
152
CAVERNOUS SINUS THROMBOSIS
Diagnostic Procedures/Other r Antistaphylococcal coverage: COMPLICATIONS

r Lumbar puncture: Vancomycin 4060 mg/kg/day IV q68h (max r Cerebral herniation
Consider only in patients without evidence of 1 g/dose) plus metronidazole 1550 mg/kg/day r Cerebral infarction (stroke)
increased intracranial pressure due to risk of IV/PO divided t.i.d., max single dose 750 mg plus r Death
cerebral herniation. 3rd- or 4th-generation cephalosporin: r Intracranial abscess
Consider checking opening pressure Cefotaxime 100200 mg/kg/day IV q612h r Pulmonary (septic) emboli (Lemierre syndrome):
r Sinus puncture and drainage: (max 12 g/day) OR
Ceftriaxone 50100 mg/kg/day IV or IM Permanent neurologic sequelae
Requires acute surgical consultation Persistent neurologic deficits in 30% of
May identify causative agent q1224h (max 4 g/day)
r Consider antifungal agents in patients at risk neonates C
Thrombosis/Thrombophlebitis of the CVS or CS (immunocompromised).
r Intracranial HTN: REFERENCES
DIFFERENTIAL DIAGNOSIS Mannitol 0.51 g/kg IV q46h
Differential is large due to nonspecific presentations of Acetazolamide 5 mg/kg/day or 150 mg/m2 /dose 1. Stam J. Thrombosis of the cerebral veins and
CVS thrombosis: IV daily sinuses. N Engl J Med. 2005;352:17911798.
r Cellulitis r Anticoagulation: 2. DeVeber G, Andrew M, Adams C, et al. Cerebral
r Sinusitis Heparin 50100 units/kg IV load, then either sinovenous thrombosis in children. N Engl J Med.
r Periorbital or orbital infection 50100 units/kg q4h or 20 units/kg/hr drip to 2001;345:417423.
r Meningitis/Encephalitis maintain APTT 6085 sec 3. Coutinho JM, Ferro JM, Canhao P, et al. Cerebral
r Intracranial abscess: venous and sinus thrombosis in women. Stroke.
Mucormycosis Surgical (neurosurgery, otolaryngology, oral
r Migraine 4. Wasay M, Azeemuddin M. Neuroimaging of
maxillofacial surgery) subspecialists may be required
r Stroke cerebral venous thrombosis. J Neuroimaging.
acutely and should be involved early in the medical
r Allergic blepharitis 2005;15:118128.
decision-making process so as to contribute to critical
r Thyroid exophthalmos (anticoagulation) actions that may impact surgical 5. Monagle P, Chalmers E, Chan A, et al.
Antithrombotic therapy in neonates and children:
r Brain or orbital neoplasm options.
American College of Chest Physicians Evidence-
r Epidural or subdural hematoma DISPOSITION Based Clinical Practice Guidelines (8th Edition).
r Subarachnoid hemorrhage Admission Criteria Chest. 2008;133:887S968S.
r Glaucoma Critical care admission criteria: 6. American Academy of Pediatrics. Drugs for invasive
r Internal carotid artery aneurysm r All patients with CVS thrombosis should be and other serious fungal infections in children. In
admitted to the pediatric ICU. Pickering LK, ed. Red Book: 2009 Report of the
Committee on Infectious Diseases. 28th ed. Elk
TREATMENT Discharge Criteria Grove Village, IL: Author; 2009:772.
These patients should not be discharged.
Assess and stabilize airway, breathing, and Pediatric neurology, infectious disease, and ADDITIONAL READING
circulation. hematology consultation/referral may be required r Roach ES, Golumb M, Adams R, et al. Management
acutely in addition to the acute surgical consults
INITIAL STABILIZATION/THERAPY mentioned previously. of stroke in infants and children. Stroke. 2008;39:
r If ill appearing, follow the Pediatric Advanced Life
26442691.
Support (PALS) algorithm: r Yang JYK, Chan AKC, Callen DJA, et al. Neonatal
Careful assessment of mental status with possible FOLLOW-UP cerebral sinovenous thrombosis: Sifting the evidence
need to secure airway as needed for a diagnostic plan and treatment strategy.
r IV antibiotics if infectious etiology is suspected FOLLOW-UP RECOMMENDATIONS Pediatrics. 2010;126:e693e700.
r Focus of therapy is to reverse the underlying cause, Discharge instructions and medications:
manage intracranial HTN if apparent or suspected, r All patients should be admitted to the hospital. See Also (Topic, Algorithm, Electronic
control seizures, and consider antithrombotic Media Element)
Patient Monitoring r Stroke
therapy with expert consultation: r Cardiovascular monitoring
r Thrombosis
Anticoagulation is controversial (2,5): r Neurologic observation and repeated assessment
There are limited data in children.
Thrombolytics have not been well studied in the DIET
pediatric population and are not routinely Patients should remain NPO until evaluation is CODES
recommended. However, these may be considered complete.
in centers where expertise is available. ICD9
PROGNOSIS
r Poor prognostic factors: 325 Phlebitis and thrombophlebitis of intracranial
MEDICATION venous sinuses
r Antibiotic regimen is aimed at most likely infectious Evidence of cerebral infarct at presentation
etiology: Seizure at presentation (nonneonates)
Penicillin/Beta-lactamase inhibitor combination or Coma PEARLS AND PITFALLS
carbapenem: r Better prognoses:
Piperacillin/Tazobactam 150300 mg/kg/day IV Young adult women with gender-specific risk Due to the variable nature of presentation, timely
q68h (max 16 g of piperacillin per day) factors may have better prognoses (4). diagnosis of CVS thrombosis requires a high degree of
Ticarcillin/Clavulanate 200300 mg/kg/day IV suspicion.
q12h (max 1824 g/day of ticarcillin per day)
Meropenem 1040 mg/kg/dose IV q12h (max
single dose 2 g)
Imipenem 100 mg/kg/day IV q6h (max 4 g/day) OR
153
CELIAC DISEASE
Nina Gold
Todd A. Mastrovitch
COMMONLY ASSOCIATED CONDITIONS PHYSICAL EXAM

BASICS r Insulin-dependent diabetes mellitus r Diffuse abdominal tenderness without rebound
r Down syndrome (20-fold increase in risk over the r Abdominal distension
DESCRIPTION general population) r Growth disturbance
r Celiac disease (CD), or gluten-sensitive enteropathy, r Autoimmune thyroid disease r Signs of anemia such as pallor
is an autoimmune enteropathy. r Addison disease r Often, children may only have nonspecific or mild
r CD is triggered by ingestion of gliadin-containing r Osteomalacia exam findings.
grains: r Secondary hyperparathyroidism
Grains that contain triggering proteins include r Vitamin D or iron deficiency DIAGNOSTIC TESTS & INTERPRETATION
wheat, barley, and rye. r Fertility problems Lab
r In the emergency department, only serum
EPIDEMIOLOGY r Hypogonadism in men
r The number of diagnosed cases has been increasing electrolytes may be necessary. All other lab testing
r Autoimmune hypopituitarism can be performed as an outpatient.
with increased awareness. r Turner and Williams syndrome (3- to 10-fold r Measuring antibodies against tissue
r True incidence is unknown.
r 1% of the worldwide population increase in risk over the general population) transglutaminase (anti-tag).
r In patients <37 yr old, antigliadin antibody may
r Affects twice as many females as males
r In the U.S., it has been estimated that for every be measured due to minimal amounts of detectable
DIAGNOSIS anti-tag.
celiac patient, there are many undiagnosed subjects r The diagnostic accuracy of the IgA anti-tag
due to poor recognition of the variable clinical HISTORY
r Children usually present with nonspecific or mild immunoassays is >96%.
manifestations of the disease. r The anti-endomysium IgA antibody test is more
symptoms.
RISK FACTORS r Diarrhea is the most common symptom: expensive and operator dependant and has been
r CD is not confined to the Caucasian population as replaced by anti-tag.
Acute or insidious in onset
previously described, although whites and whites of Characteristically pale, loose, and offensive r There can be false negatives in IgA deficiency, so
European descent are more commonly affected. r Poor weight gain and/or poor linear growth may measurement of serum IgA should occur.
r 25% of 1st-degree relatives of CD patients have r Elevated alkaline phosphatase levels can indicate
occur due to malabsorption or decreased appetite.
symptomatic gluten-sensitive enteropathies. r The typical presentation of a toddler with diarrhea, bone loss.
r 10% of 1st-degree relatives have asymptomatic r Low cholesterol and albumin can reflect
abdominal distention, and failure to thrive is
damage to small bowel mucosa consistent with CD. becoming less common. malabsorption.
r GI symptoms in older children and teens are similar r Mildly abnormal liver enzymes and abnormal blood
PATHOPHYSIOLOGY
r In CD, there is an intramucosal enzyme defect that but usually less dramatic: clotting may also be noted with anemia.
leads to an inability to digest gluten. CD can cause either constipation or diarrhea. Diagnostic Procedures/Other
r This causes rapid mucosal cell turnover and an When diarrhea is present, the stools are often Patients may be referred for upper GI endoscopy and
increase in epithelial lymphocytes. bulky and foul smelling. small bowel biopsy.
r The resulting toxic environment leads to damage to May float because of steatorrhea
Flatulence and abdominal distension are common Pathological Findings
the surface epithelium, atrophy of the villi of the Histologic changes can be seen in small bowel
small bowel, and malabsorption of nutrients and in older children.
r Numerous non-GI manifestations of CD have been biopsies: A mosaic pattern of alternating flat and
vitamins. bumpy areas on the bowel surface due to an almost
r CD mainly targets the intestinal mucosa but can described:
Neurologic: Ataxia, peripheral neuropathy, absence of villi and an irregular disorganized network
affect any organ or tissue. of blood vessels.
epilepsy
ETIOLOGY Skin: Dermatitis herpetiformis DIFFERENTIAL DIAGNOSIS
r Autoimmune in nature r Inflammatory bowel disease/Irritable bowel
Dental: Enamel defects
r More commonly associated with HLA haplotypes Bone: Decrease in bone mass syndrome
DR3 and DQw2. Joint: Arthritis r Infectious gastroenteritis
r Parasitic bowel infection
r Juvenile rheumatoid arthritis
r Thyroid disease
r Any cause of failure to thrive, growth delay, and
short stature
154
CELIAC DISEASE
Issues for Referral

r Clinical suspicion and positive screening tests with
ADDITIONAL READING
TREATMENT r Catassi C, Fasano A. Is this really celiac disease?
referral to pediatric GI and clinical nutritionist with
r The majority of patients with CD are stable and will experience treating CD patients Pitfalls in diagnosis. Curr Gastroeneterol Rep.
require little in the way of emergent treatment. r Refractory symptoms not responding well to a 2008;10(5):466472.
r Patients who are dehydrated should receive IV fluids. glutenfree diet r Fisher AH, Lomasky SJ, Fisher MJ, et al. Celiac
disease and the endocrinologist: A diagnostic
PRE HOSPITAL opportunity. Endrocr Pract. 2008;14(3):381388.
r The majority of patients with CD will be stable and FOLLOW-UP r Rodrigues AF, Jenkins HR. Investigation and
will require little in the way of emergent treatment. management of celiac disease. Arch Dis Child.
C
r Patients who are dehydrated or have a history of FOLLOW-UP RECOMMENDATIONS
r Discharge instructions and medications: 2008;93(3):251254.
poor oral intake should be given IV fluids. r Sood MR. Disorders of malabsorption. In Kliegman
Adherence to the glutenfree diet in those known
INITIAL STABILIZATION/THERAPY to have the disease RM, Behrman RE, Jenson HB, et al., eds. Nelson
r Fluid management to treat dehydration r Activity: Textbook of Pediatrics. 18th ed. Philadelphia, PA:
r Avoidance of trigger proteins and a glutenfree diet Normal activity to promote health
WB Saunders; 2007.
r Reinstitution of caloric requirements for energy and
Patient Monitoring
growth Parental and patient involvement and monitoring of CODES
MEDICATION the glutenfree diet and avoidance of triggers that
First Line cause increased symptoms ICD9
r Total parenteral nutrition may be required to
DIET 579.0 Celiac disease
re-establish adequate nutrition. Glutenfree diet (no wheat, barley, and rye)
r In general, medications are not required in the acute
management of CD. PROGNOSIS PEARLS AND PITFALLS
With proper nutrition and adherence to a glutenfree
Second Line diet, prognosis is good. r A glutenfree diet should not be initiated before the
Occasionally, oral/IV steroids may be prescribed for diagnosis is made. Doing so will affect testing for
short-term use for severe symptoms: COMPLICATIONS CD.
r Growth failure
r Prednisone 1 mg/kg/dose PO b.i.d. r IgA deficiency has an increased incidence in CD and
r Weight loss
r Methylprednisolone 1 mg/kg/dose IV q6h can cause screening tests to be falsely negative.
r Severe anemia
r Noncompliance with the glutenfree diet, either
COMPLEMENTARY & ALTERNATIVE r Neurologic disorders from deficiencies of B vitamins
intentional or unintentional, can lead to
THERAPIES r Osteopenia from deficiency of vitamin D and calcium
r Adherence to a glutenfree diet and glutenfree exacerbation of symptoms.
r Delaying diagnosis or not following the glutenfree r In children <2 yr of age, milk proteinsensitive
vitamins diet puts patients at risk for:
r Vitamin supplementation in children who have enteropathy can produce symptoms similar to CD.
Autoimmune disorders
malnutrition due to long-standing GI damage GI cancers and lymphoma (usually outside
DISPOSITION adolescence)
Admission Criteria Fractures
r Dehydration Infertility
r Electrolyte abnormalities Miscarriage
r Clotting derangements
r Neurologic complications
Discharge Criteria
Re-establishment of adequate fluid intake and
nutrition and a glutenfree diet
155
CELLULITIS
Louis A. Spina
r At times there is no discernible predisposing PHYSICAL EXAM

BASICS condition, and cellulitis can occur spontaneously. r Patients are often afebrile and generally well
r Streptococcus pneumoniae and H. influenzae are appearing.
DESCRIPTION thought to be more commonly spread via the r The infection is usually erythematous, warm, and
r Cellulitis is an infection of the skin and
hematogenous route: tender to the touch. Edema may also be present.
subcutaneous tissues. It involves the dermis but H. influenzae cellulitis is more commonly r Fluctuance and drainage are not commonly
generally does not involve the epidermis. associated with complications and meningitis, associated with cellulitis and would signify a
r Any part of the body may be involved. whereas pneumococcal cellulitis is less likely to be concurrent abscess.
r The most common organisms that cause cellulitis associated with complications or meningitis (1). r Local lymphadenopathy may be present.
are group A streptococcus (GAS) and r Examine the entire affected area as well as
ETIOLOGY
Staphylococcus aureus, including MRSA. r The most common organisms to cause cellulitis are underlying muscle and other deeper tissues to
r Less commonly, Haemophilus influenzae and
GAS and S. aureus, including MRSA. detect more severe disease such as necrotizing
pneumococcus are found as causes of cellulitis: r H. influenzae was once a common cause of facial fasciitis or pyomyositis.
These are more commonly found with facial
and buccal cellulitis, but as a result of the Hib DIAGNOSTIC TESTS & INTERPRETATION
cellulitis.
vaccine, this is now rare. Lab
EPIDEMIOLOGY r Oral flora such as Streptococcus viridans, r Cultures of blood, needle aspirations, or punch
r Cellulitis is a common infection in children. Streptococcus mutans, Prevotella species, and
r Overall incidence (including adult population) is biopsies are not routine in cases of mild cellulitis.
Fusobacterium are common causes of facial soft r Blood cultures have been shown to be positive in
about 200 cases per 100,000 patient-years. tissue infections associated with dental abscesses. <5% of cases (2,3).
r Emergency visits for soft tissue infections, including r Pneumococcus is an uncommmon cause of cellulitis. r Infection with H. influenzae or pneumococcus have
cellulitis, are increasing. r S. aureus and GAS are usually spread via direct
r Often seen during the warmer months and in been associated with higher rates of positive blood
invasion of a wound. cultures:
warmer climates Infection with these organisms is infrequent due
r Facial cellulitis is more common in children <5 yr of
DIAGNOSIS to vaccination, and routine cultures are not
age: warranted in healthy children.
Facial cellulitis is more likely to be associated with HISTORY In patients with systemic toxicity and/or facial
fever and systemic toxicity. r Patients will usually present with a recent insect cellulitis, blood cultures may be useful.
bite, abrasion, laceration, or other insult to the skin, r Cultures or swabs from intact skin are rarely helpful
RISK FACTORS
r Diabetes mellitus with a new area of redness and tenderness. and should not be performed:
r Lymphatic stasis r Particularly in areas capable of significant swelling, An exception to this is a swab to detect
r Immunosuppressive states such as the periorbital area, scrotum, penis, or Streptococcus pyogenes in cases of perianal
r Eczema and other inflammatory states earlobe, inflammation resulting from histamine or cellulitis in young children.
r Pre-existing skin infection: allergy, such as from an insect bite or sting, may be
difficult to distinguish from cellulitis: r Erysipelas
Tinea pedis Both are erythematous, warm, and swollen.
Impetigo r Impetigo
One aspect of history helpful to differentiate r Necrotizing fasciitis
r Recent surgical procedure
between infection from allergic reaction is pain
r Recent laceration or other injury causing a break in r Pyomyositis
and pruritus. Cellulitis may be painful but is not
the skin pruritic. Insect bites or other similar allergic r Pyoderma gangrenosum
reactions are described as itchy but not painful. r Gas gangrene
PATHOPHYSIOLOGY r Patients or their families are often concerned that an r Toxic shock syndrome
r Cellulitis is generally caused by local invasion of a
area has become infected. r Herpes zoster
pathogenic organism or by hematogenous spread.
r Fever is usually not an accompanying symptom, r Osteomyelitis
This is typical for staphylococcal and streptococcal
infections. although it can be seen in some cases of simple r Erythema migrans
r A break in the skin due to previous trauma can cellulitis as well as in facial cellulitis or in those with r Allergic reaction
predispose to cellulitis. systemic toxicity. r Contact dermatitis
r A cut or a scrape, as well as excoriated insect bites
or rashes, can be the cause.
r Surgical sites can be areas for bacterial colonization.
r Underlying skin lesions may also predispose to
cellulitis.
156
CELLULITIS
If MRSA is a serious consideration (or a known PROGNOSIS

r With timely treatment and compliant antibiotic use,
TREATMENT causative agent), the parenteral antibiotic of
choice is vancomycin 40 mg/kg/day given outcome is usually excellent.
INITIAL STABILIZATION/THERAPY q68h IV. r Underlying conditions hindering resolution of
r Most children who present with a nonfacial cellulitis In cases of facial cellulitis, where other less infection may worsen the prognosis.
that is not extensive may be treated with oral common bacterial organisms (such as r Colonization with MRSA, unless eradicated, may
antibiotics as an outpatient. H. influenzae) are considered, lead to recurrence in the future.
r Those who present with a facial cellulitis, are ampicillin/sulbactam (200 mg/kg/day of ampicillin Recurrent cellulitis may lead to lymphedema.
afebrile, and have no risk factors for bacteremia can
be treated as an outpatient with oral antibiotics.
component) given q6h IV is an appropriate choice:
However, ampicillin/sulbactam does not provide COMPLICATIONS
r Infections can worsen, requiring admission.
C
r Often, it is useful to outline the area of cellulitis with coverage for MRSA.
r Cellulitis can be associated with lymphangitis, which
a marker or a pen to be able to monitor the Additional Therapies
r The affected area should remain elevated to aid in would require admission and IV antibiotics.
progression or resolution of the infection. r Abscess
reduction of edema and drainage of inflammatory
MEDICATION
r Oral antibiotics: substances.
r If an underlying condition is a predisposing factor
In most cases of cellulitis, treatment is managed REFERENCES
as an outpatient and first-line therapy should be for the cellulitis, therapy should be aimed at this
directed at the most likely causative organism. If condition as well as the infection. 1. Gubbay JB, Mcintyre PB, Gilmour RE. Cellulitis in
there is not a concern for possible MRSA infection, childhood invasive pneumococcal disease: A
DISPOSITION population-based study. J Paediatr Child Health.
the following are acceptable initial treatment Admission Criteria
regimens: r Lymphangitis (red streaking extending proximally 2006;42:354358.
Cephalexin 50100 mg/kg/day PO divided 2. Perl B, Gottehrer NP, Raveh D, et al. Cost-
along the course of lymphatic drainage) effectiveness of blood cultures for adult patients
b.i.d.q.i.d. r Worsening cellulitis despite being treated with oral
Dicloxacillin 12.525 mg/kg/day PO divided q6h with cellulitis. Clin Infect Dis. 1999;29:1483.
antibiotics for 2448 hr
Amoxicillin/Clavulanic acid 50 mg/kg/day of r Ill appearance or concern for bacteremia 3. Sadow KB, Chamberlain JM. Blood cultures in the
amoxicillin PO divided b.i.d. evaluation of children with cellulitis. Pediatrics.
r Facial cellulitis
Length of treatment with oral antibiotics can be as 1998;101:e4.
long as 14 days. A typical length of treatment will
range between 7 and 10 days, although there is Unstable vital signs or severe illness such as
some evidence that a 5-day course may be requirement of pressor to maintain BP CODES
sufficient. Discharge Criteria
Given the increasing frequency of MRSA r Well-appearing children without signs or symptoms ICD9
infections, alternative or additional agents may be of systemic toxicity may be discharged home on a r 682.0 Cellulitis and abscess of face
used if this is a concern: course of oral antibiotics. r 682.1 Cellulitis and abscess of neck
Trimethoprim/Sulfamethoxazole (TMP/SMX) r Ability to follow up within 2472 hr r 682.9 Cellulitis and abscess of unspecified sites
812 mg/kg/day of TMP component PO divided
b.i.d. may be added in combination with any of
the above regimens to cover for MRSA. FOLLOW-UP PEARLS AND PITFALLS
Alternatively, it may be used as a sole agent if
S. aureus is known to be the infectious agent. FOLLOW-UP RECOMMENDATIONS r Occasionally, an area of cellulitis is actually due to
Clindamycin 1030 mg/kg/day PO in 3 divided an infection originating in deeper structures.
doses (q8h) may be used as an alternative Complete entire course of antibiotics. r Facial cellulitis is more often associated with fever,
therapy. Monitor progression of disease.
rapid progression, and systemic toxicity.
However, in areas that clindamycin is used, Follow up with primary care provider in 2472 hr. r Given the increasing incidence, infection with MRSA
r Activity:
MRSA resistance to this medication develops. should always be considered when choosing
r Parenteral antibiotics: Elevate affected area when possible to help
antibiotic therapy.
For cases that fail outpatient treatment or are reduce swelling and inflammation. r Caregivers should follow up immediately if infection
deemed necessary for admission and inpatient Patient Monitoring is progressing despite oral antibiotic use.
therapy, IV antibiotics are usually used. r Follow-up should be arranged within 2472 hr to
In cases of cellulitis where S. aureus or monitor progression of disease.
streptococcus are likely organisms and MRSA is r Outlining the extent of cellulitis with a pen or
not a possibility: marker, or having parent take picture on cell phone
Cefazolin 50100 mg/kg/day q8h IV or camera, may be useful to gauge regression or
Oxacillin 100200 mg/kg/day q6h IV progression of cellulitis
Clindamycin 2540 mg/kg/day q8h IV can be r Patients should be instructed to return earlier than
used for penicillin-allergic patients. their scheduled follow-up if they feel they are
worsening with increasing areas of erythema, fever,
or signs of lymphangitis.
157
CEREBRAL CONTUSIONS
Lynn Babcock Cimpello
r Secondary injury to surrounding brain tissue can DIAGNOSTIC TESTS & INTERPRETATION
BASICS occur from: Lab
Mass effect that decreases cerebral blood flow to r CBC:
DESCRIPTION surrounding tissue and increases in intracranial Anemia (hemoglobin <9 mg/dL) increases the
r Cerebral contusion is bruising of the cerebral pressure (ICP) from cerebral autoregulation likelihood of cerebral injury (5).
parenchyma and consists of brain tissue damage A release of toxic metabolites from a cascade of Thrombocytopenia is a risk factor for progression
and vascular injury: biochemical and physiologic responses of hemorrhage (3,4).
Resultant findings include edema and r There are 3 phases of brain swelling due to r Coagulation studies:
microhemorrhages. contusions (24): Progression of contusion is associated with
Can range from focal to diffuse 1st 24 hr: coagulation abnormalities (INR >1.3) (3).
r About 2% of the population in the U.S. live with Life threatening r Serum glucose:
disabilities from traumatic brain injuries (TBIs) (1). Formation of idiogenic osmoles draws fluid into Admission serum glucose 300 mg/dL is
EPIDEMIOLOGY the core of the contusion. associated with death (6).
Next 2472 hr: r Electrolytes and serum osmolality are useful if
Incidence 30% of hemorrhages will expand during this
r TBIs are the leading cause of death and disability for initiating hyperosmolar therapy.
time frame.
children >1 yr of age (1). Edema expands to adjacent uninjured tissue. Imaging
r About half a million children sustain TBIs per year r Image findings in contusions vary with their stages
Slow, delayed swelling can continue for up to
(1). 10 days after injury. of evolution.
r Cerebral contusions occur in 2030% of children r Head CT is the most common acute imaging
with severe TBI. ETIOLOGY modality:
r Presence of a contusion is a strong predictor of poor Depends on age: Edema appears as hypodense areas.
r <4 yr: Falls, child abuse, and motor vehicle collisions
outcomes in those with TBI. Microhemorrhages appear as hyperdense areas.
r >4 yr: Motor vehicle collisions, sports, and assaults Up to 25% of initial CT findings may be normal
RISK FACTORS
r Male due to partial volume averaging between edema
r Minority groups r Skull fractures and hemorrhages.
r Lower socioeconomic status r Other intracranial injuries Up to 50% of contusions can progress, thus:
Follow-up CT should be considered if neurologic
r Alcohol use r Child abuse in younger children
deterioration or rises in ICP occur.
r Child abuse r After stabilization, MRI is the criterion standard for
r Coagulation abnormalities increase the risk of defining contusions:
DIAGNOSIS
progression of cerebral contusions. Predicts neurocognitive impairments
HISTORY Can demonstrate hemorrhage earlier than CT
GENERAL PREVENTION r Mechanism with direct blow to head or
r Primary prevention measures, such as wearing DIFFERENTIAL DIAGNOSIS
helmets and seat belts, as well as use of airbags and acceleration/deceleration forces r Other intracranial injuries
r Loss of consciousness, alteration of mental status,
stair gates, can decrease the incidence and severity r Other causes of alteration of mental status such as
of the injury. headache, amnesia, nausea, vomiting, irritability, or
ingestions, infections, or hemorrhage
r Controlling secondary insults from hypoxemia, seizures
r Focal neurologic symptoms related directly to the
hypotension, and intracranial HTN are critical since
these lead to poor outcomes. contused area may be present, such as behavioral TREATMENT
changes with frontal contusions or memory
PATHOPHYSIOLOGY disturbances with temporal contusions. PRE HOSPITAL
r Primary injury of cerebral contusions occurs from r Inconsistent history or mechanism should raise r Assess and stabilize airway, breathing, and
direct trauma when the head is stationary or from suspicions of child abuse. circulation.
acceleration/deceleration forces when the head is in r Cervical spine precautions
motion: PHYSICAL EXAM r Transport to a trauma center with pediatric
r Vital signs
Coup contusions occur directly under the site of
r Glasgow Coma Scale (GCS) expertise, if possible.
impact from the resultant deformation of the skull.
Contrecoup contusions occur on the opposite side r Signs of increasing ICP include: INITIAL STABILIZATION/THERAPY
from the impact site from the deceleration forces. Worsening of mental status r Management depends on severity of injury.
Contusions from acceleration/deceleration forces Bradycardia, irregular respirations, and HTN r Primary goal is to prevent or ameliorate secondary
occur when the brain strikes the bony skull. (Cushing triad) brain injury (7).
r Areas of the brain in close contact with the skull are Changes in pupillary responses starting with r Assess and stabilize airway, breathing, and
most commonly affected: Orbitofrontal cortex, ipsilateral dilation and progressing to ptosis and circulation:
anterior temporal lobe, and posterior portion of the loss of medial gaze Control airway as needed:
superior temporal gyrus area with the adjacent Decorticate or decerebrate posturing Rapid sequence endotracheal intubation if
parietal opercular area. r Signs of head trauma such as scalp laceration, scalp GCS <8, significant hypoxemia, inability to
hematoma, signs of basilar skull fractures (raccoon control airway, or hemodynamic instability exists
eyes or Battle sign), hemotympanum, or CSF Normalize PCO2 (PCO2 of 3538 mm Hg).
rhinorrhea or otorrhea Maintain perfusion:
Establish vascular access.
Administer isotonic solutions to avoid
hypotension (systolic BP <5th percentile for
age).
158
CEREBRAL CONTUSIONS
r Maintain cervical spine precautions. r Children with small contusions (<10 mm) and a 5. Kurtz P, Schmidt M, Claassen J, et al. Anemia is
r Maintain euthermia: normal neurologic exam can be admitted to a associated with brain tissue hypoxia and
Hyperthermia is associated with worse outcomes. regular pediatric floor: metabolic crisis after severe brain injury. Crit Care.
r Correct abnormalities in glucose, electrolytes, blood Monitor for neurologic signs of progression 2009;13(Suppl 1):92.
counts, and coagulation studies. r Critical care admission criteria: 6. Cochran A, Scaife ER, Hansen KW, et al.
r Early consultation with neurosurgery Children with moderate/severe contusions Hyperglycemia and outcomes from pediatric
r ICP monitoring is recommended for children with (>10 mm) or alteration of mental status should traumatic brain injury. J Trauma. 2003;55(6):
GCS 8. be admitted to the ICU for monitoring. 10351038.
MEDICATION Issues for Referral

r Neurosurgical consultation
7. Adelson P, Bratton S, Carney N, et al. Guidelines
for the acute medical management of severe
C
First Line r Criteria for transfer to a pediatric trauma center traumatic brain injury in infants, children, and
r Provide IV analgesia and sedation with one or more adolescents. Chapter 9. Use of sedation and
after stabilization include:
of the following agents: neuromuscular blockade in the treatment of
GCS 12 in the field
Midazolam/lorazepam 0.1 mg/kg severe pediatric traumatic brain injury. Pediatr Crit
Pediatric trauma score 8
Fentanyl 12 g/kg Care. 2003;4(3 Suppl):S1S75.
Moderate and severe TBI
Propofol 12 mg/kg 8. Khanna S, Davis D, Peterson B, et al. Use of
r Control seizures with IV benzodiazepine: COMPLEMENTARY & ALTERNATIVE hypertonic saline in the treatment of severe
Lorazepam/diazepam 0.1 mg/kg THERAPIES refractory posttraumatic intracranial hypertension
r For signs of increasing ICP/acute brain herniation: Induced moderate hypothermia on the outcomes of in pediatric traumatic brain injury. Crit Care Med.

Elevate head of bed to 30 to decrease venous children with severe TBI is being investigated. 2000;28(4):1144.
obstruction. 9. Naidech AM, Garg RK, Liebling S, et al.
Mild hyperventilation (PCO2 3035 mm Hg) Anticonvulsant use and outcomes after
Consider initiating hyperosmolal therapy (7): FOLLOW-UP intracerebral hemorrhage. Stroke. 2009;40(12):
Mannitol can acutely decrease ICP: FOLLOW-UP RECOMMENDATIONS 38103815.
Recommended dose is 0.5 mg/kg of 20%
Not applicable from the emergency department 10. Lewis RJ, Yee L, Inkelis SH, et al. Clinical
solution to raise serum osmolality to 320 predictors of post-traumatic seizures in children
mOsm/L. Patient Monitoring
r Frequent mental status assessments with head trauma. Ann Emerg Med. 1993;22(7):
Complications include hypovolemia and
r Cardiopulmonary monitoring is required initially. 11141118.
electrolyte disturbances.
Hypertonic saline can also reduce ICP (8): r ICP monitoring for children with GCS 8
Less osmotic diuresis than mannitol
DIET ADDITIONAL READING
Optimal dosing has not been clearly r NPO initially
established; however, 3% saline at 26 mL/kg Greenes D. Neurotrauma. In Fleisher GR, Ludwig S,
r Parenteral nutrition as needed
boluses over 510 min is commonly used to eds. Textbook of Pediatric Emergency Medicine. 6th
raise serum osmolality to 360 mOsm/L. PROGNOSIS ed. Philadelphia, PA: Lippincott Williams & Wilkins;
May cause reversible renal insufficiency r A detailed prognosis of children following cerebral 2010:14321433.
Second Line contusions is not known.
r Prophylactic use of antiseizure medication, usually r Most children with mild and moderate TBI have few
long-term sequelae. CODES
fosphenytoin/phenytoin, to decrease the incidence
r 50% of children with severe TBI have long-term
of posttraumatic seizures is controversial (9,10):
Short-term use may decrease early posttraumatic sequelae. ICD9
r 851.80 Other and unspecified cerebral laceration
seizures in young children. COMPLICATIONS and contusion, without mention of open intracranial
Loading dose 1520 mg of phenytoin r Seizures in 1020%
wound, with state of consciousness unspecified
equivalents/kg IV. r Cognitive, language, and sensory impairments r 854.00 Intracranial injury of other and unspecified
r IV barbiturate therapy with pentobarbital (10
r Postconcussive syndrome symptoms including nature, without mention of open intracranial wound,
mg/kg) or thiopental (3 mg/kg) can be used for
headaches, difficulty concentrating, difficulty with state of consciousness unspecified
increased ICP resistant to conventional therapy.
sleeping, and mood changes
SURGERY/OTHER PROCEDURES r Personality changes
Conservative surgical evacuation of contusions may be PEARLS AND PITFALLS
done to remove:
REFERENCES r The goal is to prevent secondary injury: Ventilate,
r Edema to reduce mass effect
r Necrotic tissue and blood to limit the production of oxygenate, and perfuse.
1. Langlois JA, Rutland-Brown W, Thomas KE. The r The initial CT may be negative, so maintain a high
toxic metabolites from ongoing biochemical incidence of traumatic brain injury among children level of suspicion of brain injury in a child with a
cascades in the United States: Differences by race. J Head traumatic mechanism and alteration of mental
DISPOSITION Trauma Rehab. 2005;20(3):229238. status.
Admission Criteria 2. Unterberg AW, Stover J, Kress B, et al. Edema and r Up to 50% of cerebral contusions progress in the
r All children with cerebral contusions should be brain trauma. Neuroscience. 2004;129(4): 1st 72 hr, so careful monitoring is necessary.
hospitalized. 10191027.
r Children with persistent alteration of mental status 3. White CL, Griffith S, Caron JL. Early progression of
or an abnormal neurologic exam should be traumatic cerebral contusions: Characterization
hospitalized even if the head CT is normal because and risk factors. J Trauma. 2009;67(3):508514.
many contusions do not show up on the initial CT. 4. Oertel M, Kelly DF, McArthur D, et al. Progressive
hemorrhage after head trauma: Predictors and
consequences of the evolving injury. J Neurosurg.
2002;96(1):109116.
159
CERVICAL LYMPHADENITIS
Marc A. Auerbach
Lawrence Siew

BASICS r Acute bilateral cervical lymphadenitis: r Adenopathy: Location, consistency (solid or
Most common presentation fluctuant, fixed or mobile), number, and size
DESCRIPTION Commonly due to self-limited upper respiratory r Systemic lymph nodes, hepatomegaly, splenomegaly
r Lymphadenitis is inflammation of one or more lymph viral infections (enterovirus, adenovirus, influenza) r Pharynx and dentition
nodes of the neck as a result of infection. Other causes may include Epstein-Barr virus (EBV), r Conjunctival injection with preauricular or
r Lymphadenopathy, a term sometimes cytomegalovirus (CMV), or group A streptococcus. submandibular adenopathy (Parinaud
inappropriately used interchangeably, refers to r Acute unilateral cervical lymphadenitis:
oculoglandular syndrome) is seen in cat scratch
enlargement, which may occur from etiologies other Commonly due to pyogenic bacteria disease, tularemia, and adenovirus.
than infection, and does not necessarily involve Staphylococcus aureus and group A streptococcus r Skin erythema or cellulitis
inflammation. account for 80%.
r 80% of affected nodes involve the submaxillary, Group B streptococcus (infants), anaerobes DIAGNOSTIC TESTS & INTERPRETATION
submandibular, and deep cervical lymph nodes. (history of periodontal disease), tularemia, Lab
r Cervical lymphadenitis is categorized into 3 broad brucellosis Initial Lab Tests
categories: r Chronic cervical lymphadenopathy (>2 wk): r Rapid streptococcal antigen test and/or bacterial
Acute bilateral cervical lymphadenitis Bilateral nodal involvement: EBV, CMV culture of pharynx if suspected group A
Acute unilateral pyogenic cervical lymphadenitis Unilateral nodal involvement: Nontuberculosis streptococcal pharyngitis.
Chronic cervical lymphadenitis mycobacteria (NTM), Bartonella henselae This assay may provide rapid diagnosis and give
r Most commonly, acute bilateral lymphadenitis (catscratch disease), TB, toxoplasmosis clear indication of optimal antibiotic treatment.
occurs following upper respiratory tract infections. Noninfectious considerations include connective r If ill appearing and suspecting systemic infection,
tissue disorders, neoplasm, Kawasaki disease, and send CBC, C-reactive protein, ESR, LFTs, and blood
EPIDEMIOLOGY PFAPA syndrome (periodic fevers, aphthous cultures.
r Extremely common in children
stomatitis, pharyngitis, adenitis). r Tuberculin skin test for chronic lymphadenopathy
r Tuberculous lymphadenitis is seen in developing
r Consider serologic studies for EBV, CMV, HIV,
countries. COMMONLY ASSOCIATED CONDITIONS
r Fever Treponema pallidum, Toxoplasma gondii, or
RISK FACTORS r Malaise Brucella in selected cases.
r Upper respiratory infection
r Pharyngitis Imaging
r US is performed when a neck mass is large,
r Conjunctivitis DIAGNOSIS increasing in size, or unresponsive to antibiotic
r Impetigo therapy.
r Mononucleosis
HISTORY
r Duration of symptoms (acute is <2 wk) r Contrast-enhanced CT and MRI are reserved for
r Dental caries or abscess r Unilateral or bilateral nodal involvement more severe cases.
r Change in size r Consider CXR for systemic disease or suspicion of
PATHOPHYSIOLOGY
r Microorganisms penetrate mucosa of head and neck r Associated symptoms (fever, cough, rhinorrhea, sore possible malignancy.
and infiltrate surrounding tissue. throat, rash, weight loss) Diagnostic Procedures/Other
r Transport via afferent lymph vessels to lymph nodes. r Ill contacts (TB, EBV) r Needle aspiration:
r Immunologic response is generated. r History of dental caries or periodontal disease Generally reserved for lymphadenitis caused by
r Pyogenic organisms result in sudden onset of r Unusual exposures (animal exposures, pyogenic bacteria that has failed initial antibiotic
swelling, erythema, and tenderness. unpasteurized milk, uncooked meats) therapy (after 4872 hr of treatment)
r Medications and recent travel Incision and drainage is contraindicated in
suspected mycobacterial infections due to risk of
creating a persistently draining sinus tract.
r Excisional biopsy:
Preferred for suspected mycobacterial infections.
Used to diagnose malignancy
160
CERVICAL LYMPHADENITIS
r Lymphadenopathy
Second Line
r Amoxicillin/Clavulanate 45 mg/kg/day PO divided
ADDITIONAL READING
r Midline neck lesions: Thyroglossal duct cysts, b.i.d.t.i.d., max dose 2 g/day 1014 days: r Buchino JJ, Jones VF. Fine needle aspiration in the
epidermoid cysts, and lipomas If periodontal disease is present, consider evaluation of children with lymphadenopathy. Arch
r Cystic hygroma, branchial cleft cyst, thyroid tumors, clindamycin or amoxicillin/clavulanate. Pediatr Adolesc Med. 1994;148:13271330.
r Trimethoprim/Sulfamethoxazole (TMP/SMZ) r Hazra R, Robson CD, Perez-Atayde AR, et al.
laryngocele
10 mg/kg/day PO divided q12h, max daily dose Lymphadenitis due to nontuberculous mycobacteria
320 mg TMP/1,600 mg SMZ daily in children: Presentation and response to therapy.
TREATMENT r Azithromycin 10 mg/kg day 1, then 5 mg/kg PO
days 25:
Clin Infect Dis. 1999;28:123129.
r Leung AK, Davies HD. Cervical lymphadenitis: C
INITIAL STABILIZATION/THERAPY Used specifically for catscratch disease Etiology, diagnosis, and management. Curr Infect
r Acute bilateral lymphadenitis is usually due to
Dis Rep. 2009;3:183189.
self-limited viral infections. Observation with no DISPOSITION r Peters TR, Edwards KM. Cervical lymphadenopathy
treatment is usually appropriate. Admission Criteria and adenitis. Pediatr Rev. 2000;12:399405.
r Acute unilateral lymphadenitis: r Failure of outpatient management
In a well-appearing child with a minimally r Pain requires IV medications See Also (Topic, Algorithm, Electronic
enlarged and tender lymph node, measuring initial r Requires IV fluids Media Element)
dimensions and monitoring over time is r For further workup Catscratch Disease
recommended.
For warm and tender lymph nodes, without Discharge Criteria
r Other more serious diagnoses have been ruled out.
evidence of fluctuance, a course of oral antibiotics CODES
r No airway compromise
is recommended.
r Ability to take PO
If ill appearing or abscess is suspected, IV ICD9
antibiotics are indicated. r 017.20 Tuberculosis of peripheral lymph nodes,
Issues for Referral
Nonresponse to antibiotics: Consider ENT and/or unspecified examination
MEDICATION r 289.1 Chronic lymphadenitis
infectious disease consult.
First Line r 289.3 Lymphadenitis, unspecified, except mesenteric
r Empiric oral regimens including amoxicillin,
penicillin, cephalexin, or clindamycin are appropriate FOLLOW-UP
for most infections.
r Infections with severe illness should be treated with FOLLOW-UP RECOMMENDATIONS PEARLS AND PITFALLS
parenteral antibiotics. Discharge instructions and medications: r Cervical lymphadenitis is inflammation of 1
r Duration of treatment is 1014 days. r Take medications as prescribed. Return to primary
cervical lymph nodes.
r Oral therapy: care provider to evaluate for improvement on r Most commonly, acute bilateral lymphadenitis is due
Cephalexin 50 mg/kg/day PO divided b.i.d.q.i.d., antibiotics. to upper respiratory infections.
max dose 2 g/day Patient Monitoring r Unilateral lymphadenitis may require treatment: PO
Amoxicillin 40 mg/kg/day PO divided b.i.d.q.i.d., Monitor clinical response to treatment to note antibiotics in moderate illness and IV antibiotics for
max dose 2 g/day improvement or lack thereof. severe illness.
Penicillin 50 mg/kg/day PO divided b.i.d.q.i.d., r 80% of acute unilateral lymphadenitis is due to
max dose 2 g/day PROGNOSIS
r Cervical lymphadenitis spontaneously regresses in pyogenic infection by group A streptococcus or
Clindamycin 30 mg/kg/day PO divided t.i.d.q.i.d., S. aureus.
most children over the course of several weeks.
max dose 1.8 g/day: r Mycobacterial infections may take a long time to r Suspect NTM or TB with chronic lymphadenopathy.
Optimal for polymicrobial infections, suspected
MRSA resolve.
r Parenteral therapy: COMPLICATIONS
Cefazolin 50100 mg/kg/day IV divided q8h, r Persistent or recurrent lymphadenitis is the most
max dose 6 g/day frequent complication.
Nafcillin or oxacillin 150 mg/kg/day IV divided r Development of a sinus tract or disseminated
q6h, max dose 6 g/day disease associated with mycobacterial disease
r Abscess formation, cellulitis, bacteremia
161
CHALAZION
Nicole D. Porti
Karen Franco

BASICS Blockage can occur due to: r Hordeolum
r Blepharitis r Molluscum contagiosum
DESCRIPTION r Acne rosacea r Nasolacrimal duct obstruction
A chalazion is an inflammatory lesion of the eyelid r Hordeolum r Dacryocystitis
that usually arises as a result of obstruction of a r Atopic dermatitis
sebaceous gland duct: r Preseptal/Periorbital cellulitis
r Meibomian gland lipogranuloma is another name DIAGNOSIS r Orbital cellulitis
for a chalazion. r Skin swelling secondary to other inflammation, such
r In contrast, a hordeolum or stye is a localized HISTORY
r A chalazion usually presents as a chronic, painless as insect bite or sting
infection or inflammation of the eyelid margin r Eyelid papilloma
swelling on the eyelid.
involving hair follicles. r Obtain pertinent information about location, onset, r Xanthelasma
r Chalazia are typically nontender, while hordeolum
duration, aggravating and/or alleviating factors, and r Sebaceous gland carcinoma
are tender and erythematous.
previous treatment. r Basal cell carcinoma
EPIDEMIOLOGY r Note if chalazion is recurrent and in same location, r Tuberculosis
r Chalazia, as well as hordeola, are the most common which may indicate possible malignant origin (2). r Orbital tumor
acquired lid lesions in childhood (1). r Symptoms not consistent with chalazion include:
r The exact incidence or prevalence of chalazia in the Eye pain
U.S. is not known. Eye redness TREATMENT
RISK FACTORS Fever
r Poor lid hygiene Visual changes INITIAL STABILIZATION/THERAPY
r Usually resolves spontaneously over several weeks
r Blepharitis Discharge
r Seborrhea Fever with conservative management
Diffuse swelling r Warm compress to area 1015 min q.i.d. to soften
r Acne rosacea
the plug of material, allowing glands contents to
r Atopy PHYSICAL EXAM
r A palpable nodule on the eyelid or lid margin, drain
r Viral infection
r Immunodeficiency depending on location of obstructed gland: MEDICATION
May have significant inflammation with lid edema First Line
PATHOPHYSIOLOGY Nontender to mild tenderness Baby shampoo applied daily to affected eyelid to
r The sebaceous glands of the eyes include the Nonerythematous reduce clogging of ducts
meibomian glands and the glands of Zeis: Nonfluctuant
No intraocular pathology
Second Line
Meibomian glands are embedded in the tarsal
Consider oral tetracyclines to reduce inflammation in
plate of the eyelid. Note any associated skin findings.
r Document visual acuity (should be normal). older children with significant blepharitis:
Glands of Zeis are located at the base of the r Tetracycline: >8 yr of age, 2550 mg/kg/day PO q6h
eyelash follicles.
Both glands produce sebum that is incorporated DIAGNOSTIC TESTS & INTERPRETATION
into the eyes tear film. No diagnostic tests are needed, as the diagnosis is
r Blockage of 1 gland leads to accumulation of made clinically.
sebaceous material and a resulting inflammatory
reaction.
162
CHALAZION
DISPOSITION See Also (Topic, Algorithm, Electronic

Discharge Criteria FOLLOW-UP Media Element)
r All patients with chalazion may be discharged and r Dacryocystitis
managed as outpatients. FOLLOW-UP RECOMMENDATIONS r Hordeolum
r Patients can be safely discharged home if they Discharge instructions and medications: r Orbital Cellulitis
r Lid hygiene should be discussed. r Periorbital Cellulitis
have:
No changes in visual acuity r Advise patients to follow up with ophthalmology if
No signs of intraocular pathology symptoms are not improving as expected.
Issues for Referral
r Most chalazia can be managed at home without
PROGNOSIS
r Most chalazia resolve on their own.
CODES C
consultation of an ophthalmologist, with r Recurrences do occur, especially in those with ICD9
conservative treatment alone. predisposing skin disorders. 373.2 Chalazion
r Consider ophthalmologic referral if the diagnosis is
in question, especially if the chalazion is recurrent
(histopathologic diagnosis) (3). REFERENCES PEARLS AND PITFALLS
r Referral to ophthalmology if: r Chalazion is a localized inflammatory reaction of the
1. Lederman C, Miller M. Hordeola and chalazia.
Failed conservative management Pediatr Rev. 1999;20:283284. eyelid.
Recurrent chalazia r Differentiation between a chalazion, which is
2. Mueller JB, McStay CM. Ocular infection and
Any visual disturbance (4) nonpainful and nonerythematous, and a hordeolum
r Treatment by an ophthalmologist after failed therapy inflammation. Emerg Med Clin North Am. 2008;
26:5772. or stye, which is typically painful and erythematous,
may include either of the following: is important as management differs.
3. Ozdal PC, Codere F, Callejo S, et al. Accuracy of the
Incision and curettage is preferred treatment. r Conservative management with warm compresses is
clinical diagnosis of chalazion. Eye. 2004;18(2):
Intralesional steroids may also be considered (5). usually the only treatment required:
135138.
4. Santa Cruz CS, Culotta T, Cohen EJ, et al. Consider ophthalmologic referral if conservative
Chalazion-induced hyperopia as a cause of management fails, the chalazion is recurrent, or
decreased vision. Ophthalmic Surg Lasers. 1997; the diagnosis is in question.
28(8):683687.
5. Goawalla A, Lee V. A prospective randomized
treatment study comparing three treatment options
for chalazia: Triamcinolone acetonide injections,
incision and curettage, and treatment with hot
compresses. Clin Experiment Ophthalmol. 2007;
35(8):706712.
163
CHANCROID
Marcelo Sandoval
r Lesion begins as a single erythematous papule or DIAGNOSTIC TESTS & INTERPRETATION

BASICS pustule. Diagnostic Procedures/Other
r This quickly erodes into 1 painful chancres r Clinical diagnosis based on lesion appearance is
DESCRIPTION (120 mm). often inaccurate, and lab testing is difficult or often
r Chancroid is also referred to as soft chancre. r Occurs on average 47 days after exposure unavailable by the local health department.
r It is an STI causing painful genital ulceration and r Incubation period average 310 days. r Diagnosis is based primarily on the clinical findings
painful inguinal adenopathy. r Usually, there is associated painful inguinal in conjunction with excluding syphilis and HSV as
r Symptoms are almost always local, not systemic.
adenopathy. the cause.
r Painful regional lymphadenopathy r The main necessary lab testing is that which
r Fluctuant lymph abscesses (buboes) ETIOLOGY excludes syphilis:
r Risk factor for HIV coinfection (15) See Pathophysiology. This may be by darkfield microscopic evaluation of
COMMONLY ASSOCIATED CONDITIONS ulcer exudates.
EPIDEMIOLOGY r HIV Also may be by serologic evaluation for syphilis if
Incidence r Herpes simplex virus (HSV) 7 days since ulcer formation
r Very common worldwide, especially Africa, r Culture for HSV or Tzanck smear may be sent,
r Syphilis (3,4)
southeast Asia, and Latin America (15) though these are not highly sensitive.
r Declining in U.S.: 23 cases reported to the CDC in r Gram stain: Chancroid may demonstrate schools of
2007, down from 5,191 in 1989 and 67 in 2002 DIAGNOSIS fish parallel linear clusters of gram-negative bacilli:
(46) Poor sensitivity/specificity (4,5)
r Probably underdiagnosed due to expense and HISTORY r Culture: Proper medium and qualified technicians
r Ask about above risk factors.
unavailability of culture and PCR testing are not readily available in most labs (15).
r 10% of chancroid patients are coinfected with HSV r Stress confidentiality with adolescents afraid of
r PCR: Still not practical for emergency department
or syphilis (3,4). parental disapproval.
r Male to female ratio is 3:1 (4). r Ask about abuse/coercion if appropriate. use and is not widely available in hospitals (15)
r Refer for HIV testing, or perform testing in the
r Prevalence in the pediatric/adolescent population is r History of tender genital papule, then pustule, then
emergency department if available (2).
unknown. ulcer (1)
r Dysuria DIFFERENTIAL DIAGNOSIS
RISK FACTORS r Dyspareunia r HSV: Most common genital ulcer in the U.S. (15)
r Unprotected sexual intercourse r Syphilis: Second most common genital ulcer in the
r Painful inguinal lymphadenopathy 12 wk later in
r Sex workers and persons engaging in sexual activity
50% (1,3) U.S. (15)
with them r Buboes: Suppurative adenopathy in 25% (5) r Lymphogranuloma venereum (LGV): Seen in
r Illicit drug use
travelers to Asia, Africa, the Caribbean, and South
r Immigration from, or travel to, endemic areas such PHYSICAL EXAM America (4,5)
as Asia and Africa r Males: r Granuloma inguinale (GI): South Pacific, Australia,
r Low socioeconomic status (15) Lesions on foreskin, frenulum, glans shaft India, the Caribbean (5)
Painful, necrotic, yellow-grey exudates r Helpful syndromic management points:
GENERAL PREVENTION Soft, not indurated, unlike syphilis
r Condom use Grouped vesicles prior to ulcer: Suggestive but not
Jagged, undermined edges that stand up off the
r Counseling of high-risk groups diagnostic of HSV (2,3)
ulcer base
Painful: HSV, chancroid (4,5)
PATHOPHYSIOLOGY Erythematous border (1,4,5)
Painless: Syphilis, LGV, GI (4,5)
r Haemophilus ducreyi, a highly infectious bacterium, Unilateral lymphadenopathy (1,35)
r Females: Lymphadenopathy seen in all but GI, but buboes
enters a skin break. only with chancroid and LGV (4,5)
r Attracts neutrophils and macrophages to form the Similar lesions Physical exam has poor predictive value, especially
initial pustule Vulva, cervix, perianal areas, thighs with concomitant HIV.
r Toxin causes local necrosis and ulceration (7). Unilateral lymphadenopathy (1,4,5) Syndromic management decisions use history,
exam, testing with darkfield and Tzanck
preparations, direct HSV immunofluorescence, and
viral culture (1,2).
CDC diagnostic criteria: Probable diagnosis of
chancroid if painful ulcers with lymphadenopathy
do not have darkfield or serologic evidence of
syphilis, nor Tzank or culture evidence of HSV (2).
Treat for LGV if buboes are present (3 wk of
treatment) (1).
164
CHANCROID
Patient Monitoring
r 3-day symptomatic improvement and 7-day
ADDITIONAL READING
TREATMENT
subjective appearance improvement are typical of See Also (Topic, Algorithm, Electronic
MEDICATION successful treatment (3,5). Media Element)
r Incision and drainage may need to be done later if r Herpes Simplex
First Line
r Azithromycin 1 g PO 1 dose bubo develops or recurs despite primary ulcer r Sexually Transmitted Infections
r Ceftriaxone 250 mg IM 1 dose healing (2,3,5). r Syphilis
r Single-dose regimens assure compliance but may r Repeat syphilis and HIV testing at 3 mo is
fail in HIV or in uncircumcised patients (15). recommended (2).
CODES
C
Second Line PROGNOSIS
r Ciprofloxacin 500 mg PO b.i.d. 3 days r Generally excellent with improvement by 3 days and
r Erythromycin base 500 mg PO t.i.d. 7 days (15) healing by 714 days (2,3,5) ICD9
r Longer healing times and treatment failures are 099.0 Chancroid
Pregnancy Considerations
r Safety of azithromycin in pregnancy and lactation seen in uncircumcised men, larger ulcers, and
HIV-positive patients (15).
has not been established (2). r Erythromycin regimen for 7 days may be preferred PEARLS AND PITFALLS
r Ciprofloxacin is contraindicated in pregnancy (2).
for HIV patients (2). r Pearls:
r Any treatment failure should also prompt a search HSV and syphilis are the most common source of
r Buboes <5 cm in size usually resolve with for a different or coinfecting STI, drug resistance, anogenital ulcers, followed by chancroid.
treatment. Size >5 cm usually requires drainage (5). noncompliance, and/or HIV-positive status (2). Clinical impression is often unreliable in
r Incision and drainage of buboes is preferred over COMPLICATIONS differentiating syphilis, HSV, and chancroid.
aspiration, as there is less need to repeat the r Scarring (1,3) Emergency department testing with darkfield and
procedure (2,5). r Balanoposthitis (4) Tzanck smears, direct immunofluorescence, and
r Phimosis (4) viral cultures and syphilis serologies should be
DISPOSITION done if available to enhance correct diagnosis and
r Bubo rupture and superinfection (1,4,5)
Admission Criteria treatment.
r Rarely necessary r Phagendic variant with widespread necrosis and Buboes may persist or even grow after ulcer
r Admission is warranted in rare cases of extensive tissue destruction (5) resolution, but this does not necessarily mean
tissue necrosis or severe systemic illness. Refer to r Systemic fever/illness (rare) treatment failure.
complications below. r Fistula formation (4) Buboes often resolve with treatment, but if
>5 cm in size, incision and drainage, rather than
Issues for Referral
r Sexual partners need evaluation and treatment if aspiration, is preferred.
REFERENCES Treatment failure is associated with coinfection
exposed within 10 days of lesion or symptom onset
with another STI or HIV.
(2). 1. Lews DA. Chancroid: Clinical manifestations, r Pitfalls:
r Some states require notification of child protection diagnosis, and management. Sex Transm Inf.
If a purely clinical approach without testing in the
authorities if the patient is below the age of 2003;79:6871.
emergency department is the only practical
consent. Know your local reporting requirements 2. CDC, Workowski KA, Berman SM. Diseases option, failing to ensure that the patient
and call social services as needed. characterized by genital ulcers. Sexually transmitted understands follow-up is crucial due to the
diseases treatment guidelines 2006. MMWR Morb potential for error in diagnosis.
FOLLOW-UP Mortal Wkly Rep. 2006;55(RR-11):1430. Not arranging follow-up syphilis and HIV
3. McKinzie J. Sexually transmitted diseases. Emerg serologies at 3 mo
FOLLOW-UP RECOMMENDATIONS Med Clin North Am. 2001;19(3):723743. Failing to recommend that sexual partners seek
r Follow-up in 37 days with the primary care 4. Frenkl TL. Sexually transmitted infections. Urol Clin evaluation for STI
provider (2). North Am. 2008;35(1):3346.
r Incision and drainage packing removal in 2448 hr 5. Keck J. Ulcerative lesions. Clin Fam Pract. 2005;
if applicable 7(1):1330.
r Discharge instructions and medications: 6. CDC. Sexually Transmitted Diseases Surveillance,
Analgesics as needed 2007. Atlanta, GA: Author; 2006. Available at
Avoid sexual activity until lesions are healed. http://www.cdc.gov/std/stats07/main.htm.
Safe sex education 7. Wising C, Azem J, Zetterberg M, et al. Induction of
apoptosis/necrosis in various human cell lineages
by Haemophilus ducreyi cytolethal distending toxin.
Toxicon. 2005;45(6):767776.
165
CHICKENPOX/SHINGLES
Keri Cohn
Sarita Chung
r After replication in the reticuloendothelial system, a DIAGNOSTIC TESTS & INTERPRETATION

BASICS secondary viremia occurs. Visual diagnosis is sufficient in most cases.
r Skin lesions (a source of continued replication) form
Lab
DESCRIPTION 1021 days after exposure. Initial Lab Tests
Varicella zoster virus (VZV), a herpes virus, results in r Respiratory mucosal sites are infected in late
Lab testing is not necessary:
two common clinical entities: incubation, so respiratory droplets are infectious r CBC may show leukocytosis
r Varicella (Chickenpox), is a result of primary 12 days prior to rash. r Mild transaminitis may be present.
infection, and is characterized by fever and r Primary VZV results in latent infection in the dorsal
disseminated rash root ganglion. Imaging
r Herpes Zoster (Shingles), is reactivation disease of r Reactivation (zoster) occurs in a sensory dermatomal Imaging is generally not necessary. CXR may show
latent virus residing in the dorsal root ganglion distribution; it does not infect respiratory cells in the interstitial infiltrates in 1015% of adolescents (even
from previous infection (or immunization). It is immunocompetent host. without respiratory symptoms).
characterized by a painful, vesicular rash of r Intact cellular immunity is important for control of Diagnostic Procedures/Other
dermatomal distribution viremia and localized replication. r Vesicular base scraping for direct fluorescent
EPIDEMIOLOGY antibody or VZV PCR
ETIOLOGY r Vesicular fluid/scab for VZV PCR
Incidence VZV is a double-stranded DNA herpesvirus that infects
r Peaks during late winter and early spring r VZV IgM is not reliable for routine confirmation of
only humans and is responsible for varicella disease
r Prevaccine era incidence in the U.S.: and reactivation zoster. acute infection (though if positive, this is suggestive
Chickenpox: 4 million cases of recent infection).
>90% patients are <15 yr of age r Acute and convalescent VZV IgG levels can
Zoster: 1.2 million cases DIAGNOSIS retrospectively confirm the diagnosis.
r Postvaccine decline of 95% in varicella incidence r Tissue/vesicular fluid viral culture (may take 7 days)
HISTORY
(including decline in <12-mo-old group, suggesting r Varicella: Pathological Findings
herd immunity) Prodrome of fever and malaise 13 days prior to Tzanck smear of vesicular scrapings shows
Decrease in varicella-related hospitalizations and rash multinucleated giant cells with inclusions (not specific
costs of 85% Resolution of fever within 24 hr of rash for VZV). Sensitivity is only 60%.
Decrease in mortality by 75% Universally pruritic centripetal rash starting on
Prevalence trunk/neck/face and progressing outward r Disseminated herpes simplex virus (HSV)
r VZV is highly contagious, affecting >90% of r Zoster:
r Eczema herpeticum
seronegative exposed persons, with a prevalence of Sudden onset of vesicular lesions in dermatomal r Disseminated enterovirus
75,000 cases occurring at any one time in the U.S. distribution (often T3-L3) r Atypical measles
r >95% of adults have antibodies to VZV, suggesting Pain, sometimes severe, may precede lesions by
r Rickettsial pox
an almost universal lifetime infection rate. 4872 hr
Typical course: Few lesions that form for 35 days r Smallpox
RISK FACTORS and last for 710 days r Both HSV and coxsackievirus can cause dermatomal
r Immunocompromised hosts, particularly T-cell
Immunocompromised host: More lesions, longer vesicular lesions similar to zoster.
defects or HIV/AIDS, are at high risk for severe or course, risk for dissemination
disseminated disease.
r Increased risk of vaccine failure: <12 mo or >5 yr PHYSICAL EXAM TREATMENT
r Primary varicella infection:
of age at time of vaccination, history of
asthma/eczema, patients receiving steroids Rash: Erythematous papules (24 mm) evolving to PRE HOSPITAL
(>2 mg/kg of prednisone or 20 mg/day) vesicles, then pustules over 68 hr, then crusting Identification of cases, isolation from public places to
within days contain infection
GENERAL PREVENTION Successive crops appear over 24 days, so lesions
The 2-dose live-attenuated varicella vaccine series is (250500) are in various stages of evolution.
95% effective in preventing severe disease. 1030% Mucosal exanthem (oropharynx; less commonly,
of vaccinated children develop mild to moderate circulation.
the vagina) r Mainstay of initial treatment in stable patients is
disease upon exposure. Secondary family cases have more lesions than the
index case. infection control:
PATHOPHYSIOLOGY
r Spread by direct contact with fluid from r Herpes zoster: Varicella (including vaccine breakthrough):
Contact and airborne precautions (negative
vesicles/zoster lesions or by airborne spread from Painful grouped vesicular lesions on erythematous
pressure rooms if possible) in patients with
respiratory tract secretions (varicella or disseminated base distributed in 13 sensory dermatomes
lesions, unless all lesions have crusted over (min
zoster in immunocompromised host) 1520% of patients have extradermatomal
r VZV inoculates respiratory epithelial cells and of 5 days after onset)
dissemination.
All disseminated zoster and immunocompromised
spreads to regional nodes, thereafter causing hosts with local zoster: Contact and airborne
primary viremia and subsequent infection of liver precautions for duration of illness
reticuloendothelial cells. Local zoster in normal hosts: Contact precautions
until lesions crust over
Nonimmune exposed patients: Strict contact
and airborne precautions from 821 days after
exposure
Nonimmune exposed patients who have received
VariZIG/intravenous immunoglobulin (IVIG) should
have strict contact and airborne precautions for
28 days.
166
CHICKENPOX/SHINGLES
MEDICATION Codeine or codeine/acetaminophen dosed as r Pneumonia (adults or immunocompromised) occurs

r Varicella: 0.51 mg/kg of codeine component PO q4h 35 days into illness; may have hemoptysis.
Diphenhydramine or hydroxyzine for pruritis PRN r Hemorrhagic varicella (mostly immunocompromised
Antivirals are not indicated for uncomplicated Hydrocodone or hydrocodone/acetaminophen hosts)
disease in the healthy host. dosed as 0.1 mg/kg of hydrocodone component r Less common: Thrombocytopenia,
Consider acyclovir if increased risk for PO q46h PRN glomerulonephritis, arthritis, hepatitis, visceral VZV,
complications (>12 yr of age, chronic skin transverse myelitis, Guillain-Barre syndrome,
DISPOSITION
conditions, chronic lung diseases, patients myocarditis, corneal lesions (zoster ophthalmicus),
Admission Criteria
receiving long-term salicylate or steroid
[oral/inhaled] therapy, secondary household cases,
r Immunocompromised hosts with varicella Ramsey Hunt syndrome, Reye syndrome (associated
with salicylate use)
C
r VZV pneumonia
pregnant women):
Oral acyclovir, if given within 24 hr of onset of r Bacterial superinfection requiring IV therapy
rash, will reduce the duration of fever and the r Pain refractory to outpatient management ADDITIONAL READING
number/duration of lesions (80 mg/kg/day r Critical care admission criteria:
r American Academy of Pediatrics Committee on
divided q6h 5 days). Respiratory failure
Acyclovir for any hospitalized child with ongoing Sepsis Infectious Diseases. Prevention of varicella:
vesicle formation (1,500 mg/m2 /day IV divided Consider ICU admission for varicella complicated Recommendations for use of varicella vaccines in
q8h 710 days) by necrotizing fasciitis. children, including a recommendation for a routine
Immunocompromised hosts require IV acyclovir 2-dose varicella immunization schedule. Pediatrics.
Discharge Criteria 2007;120(1):221231.
(prevents visceral dissemination)
Clinical stability, immunocompetent host r Harper MB, Fleisher GR. Infectious disease
IVIG/VariZIG does not alter the disease course
once symptomatic. Issues for Referral emergencies. In Fleisher GR, Ludwig S, eds.
r Zoster: r High-risk patients should have close follow-up.
Textbook of Pediatric Emergency Medicine. 6th ed.
r Zoster ophthalmicus requires immediate Philadelphia, PA: Lippincott Williams & Wilkins;
Famciclovir and valacyclovir are licensed to treat
zoster in adults; no data for children. ophthalmology referral. 2010:887.
r Infectious disease consultation for
For adults: Famciclovir 500 mg or valacyclovir
1 g t.i.d. 7 days, or acyclovir 800 mg 5 times immunocompromised hosts
daily 710 days COMPLEMENTARY & ALTERNATIVE
CODES
Severely immunocompromised (transplants, THERAPIES
malignancy) hosts require IV acyclovir. r Aluminum acetate soaks for zoster ICD9
r 052.9 Varicella without mention of complication
May consider PO therapy in well, lower-risk r Postherpetic neuralgia pain management (consider
immunocompromised hosts. r 053.9 Herpes zoster without mention of
r Acyclovir resistance is rare; consider IV foscarnet. narcotics, gabapentin). Prednisone therapy may be
beneficial in healthy patients with severe pain. complication
r Postexposure prophylaxis:
Postexposure prophylaxis for nonimmune persons:
Vaccine within 120 hr of exposure (ideally FOLLOW-UP PEARLS AND PITFALLS
<72 hr) may prevent or modify disease. r Postvaccine varicella occurs in 35% of children at
VariZIG/acyclovir is indicated ASAP and within FOLLOW-UP RECOMMENDATIONS
r Discharge instructions and medications: 526 days after immunization (typically 25 lesions,
96 hr of significant exposure in susceptible
Supportive care with acetaminophen and rash may be maculopapular).
patients: r Immunosuppressed individuals, pregnant women,
VariZIG dose: 12.5 units/kg (max single dose antipruritics. Avoid aspirin and NSAIDs.
625 units) IM or, if not available, IVIG 400 mg/kg Acyclovir for high-risk patients and infants <12 mo old should not be vaccinated.
Acyclovir dose: 80 mg/kg/day divided q6h for r Activity: r Vaccine-related immunity is >1020 yr.
7 days (max 800 mg) Exclusion of children from school until varicella r VariZIG is not indicated for healthy term infants with
Significant exposure is: lesions have crusted over postnatal varicella exposure (including those whose
Varicella: Household contact, indoor Zoster lesions may be covered for return to school. mothers rash developed >48 hr post delivery).
face-to-face play, newborns with mothers r Avoid salicylates due to increased risk of Reye
Patient Monitoring
whose varicella lesions began between 5 days Primary care follow-up as needed syndrome.
before and 2 days after delivery
Zoster: Intimate tactile contact PROGNOSIS
r Healthy children tend to have benign disease lasting
Candidates for postexposure prophylaxis if
significant exposure: Immunocompromised 1 wk with an excellent prognosis.
r U.S. postvaccine era mortality of varicella has
(including HIV); unvaccinated pregnant patients
without history of varicella, newborns with above decreased from 100 to 4 deaths per year.
perinatal exposure, hospitalized preterm infants r Perinatal varicella (30% mortality) is severe
r Analgesic may be needed, particularly for varicella disseminated disease due to lack of maternal
zoster: protective antibodies.
Acetaminophen 15 mg/kg/dose PO/PR q4h PRN COMPLICATIONS
NSAIDs: r Bacterial superinfection of skin lesions
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN r Group A streptococcal sepsis/necrotizing fasciitis
Ketorolac 0.5 mg/kg IV/IM q6h PRN r CNS complications (acute cerebellar ataxia,
Some clinicians prefer to avoid due to theoretical encephalitis) occur 21 days post rash. CSF WBC
up to 300; CSF protein 4080 mg/dL.
concern over bacterial superinfection.
Opioids:
be repeated q1520min until pain is

controlled, then q2h PRN.
167
CHILD ABUSE
Lili Moran
PATHOPHYSIOLOGY r Injuries in different stages of healing when history is

BASICS r The mechanisms of abuse may vary by type only of 1 episode of trauma
r The common pathophysiology involves a caretaker r Evidence of healed lesions/scars from previous
DESCRIPTION causing intentional harm to a child either by trauma
r Child abuse may be subclassified: r Growth failure
inflicting injuries or abuse or by failure to meet the
r Physical abuse: An injury inflicted on a child by a needs of the child. r Inflicted head trauma, also known as shaken baby
caregiver via various nonaccidental means syndrome or shaken impact syndrome: Hallmark is
r Sexual abuse: The involvement of children in sexual ETIOLOGY
r A complex dynamic including a parent who is subdural hemorrhage, a marker for diffuse
activities that they do not understand, for which they acceleration-deceleration brain injury, often found
capable of abuse, a child who actively or passively
are not developmentally prepared, to which they with retinal hemorrhages and posterior rib fractures.
becomes the target, and a crisis that triggers the
cannot give consent, and that violate societal taboos
r Emotional abuse: Also called psychological angry response DIAGNOSTIC TESTS & INTERPRETATION
r Family stress and lack of specific child-rearing
maltreatment; includes intentional verbal or Lab
information play important roles. r Lab values may occasionally be useful but are not
behavorial acts or omissions that result in adverse
emotional consequences COMMONLY ASSOCIATED CONDITIONS routinely necessary.
r Neglect: The failure of caregivers to meet the needs Munchausen by proxy r To look for occult abdominal trauma, screening labs
of a child resulting in harm: may be sent.
r CBC to evaluate for blood loss
Can be physical, medical, emotional, educational,
etc. DIAGNOSIS r PT/PTT if bruising or hemorrhage
May result in failure to thrive, developmental r LFTs, lipase if concern for severe abdominal injury
HISTORY
delay, and poor health r The history provided by a caretaker may not be r Urinalysis: Screen for genitourinary injury or
EPIDEMIOLOGY consistent with a plausible explanation for the injury. myoglobinuria, hematuria.
r According to the National Incidence Studies of Child r History provided may change or be inconsistent with r Lumbar puncture: Evaluate for intracranial
Abuse and Neglect (NIS-4) data from 20052006, the caregiver providing different accounts of the hemorrhage.
1.25 million children experience maltreatment in accident or injury to different health care providers r Toxicology screens if suspicion for malicious
the U.S. each year, corresponding to roughly 1 in or explanation or account of accident or injury poisoning
58 children. changes over time. r STI screening
r 44% of the cases included abuse: r Multiple previous injuries or visits may have
Imaging
58% physical abuse occurred, though this is not necessary for diagnosis. r Radiographs may be indicated if suspicion for injury
27% emotional abuse r Delay in seeking care after injury, particularly with
or abuse
24% sexual abuse no explanation given r CT and MRI for suspected head, thoracic, or
r 61% of the cases involved neglect. r Parents may seek care at a facility distant from their
abdominal trauma
r 1,760 cases of death reported in 2007 secondary to home rather than a facility at which they typically r US can be used to scan for abdominal trauma,
abuse would seek care. fractures, pneumothorax, etc.
r Ranges from 535% at any given time in the U.S. r Childs developmental level may not be compatible r Skeletal surveys may be useful in children who lack
with the mechanism described. ability to give verbal history, especially children
RISK FACTORS r Parent blames the child or another child for the
r Violence, including domestic violence <2 yr old.
r Parental stress factors, including: injury. r Radionuclide bone scan: Can be an adjunct to a
Financial problems, socieoeconomic status PHYSICAL EXAM skeletal survey, particularly if detecting an early
Mental illness r Evidence of major injuries with history of minor occult fracture is of significant importance.
Substance abuse trauma Diagnostic Procedures/Other
Isolation r Specific injuries for inflicted trauma: r It is important to clearly document all findings in the
r Child with developmental delay or medical problems Bruises: Patterns, symmetry, nonbony prominences chart, using quotation marks for quotes.
Burns: Patterns, symmetry, location r Avoid using terminology like alleged and rule
GENERAL PREVENTION Retinal hemorrhages
r Screening for signs of abuse on all patient out abuse. Simply document the stated complaint
Oral injuries, particularly frenulum tears and physical findings, including who is with the
interactions
r Early intervention in high-risk families Fractures: Classic metaphyseal lesions (bucket patient for the exam, etc.
r Universal parenting education, home visitations handle), complex skull fractures, posterior rib r Avoid giving highly specific dates, times, and person
fractures, scaplular fractures identifiers:
Abdominal injuries: Often occult Precise time, date, and identification of persons is
Genital injuries can represent physical or sexual not necessary in the medical record.
abuse: Some injuries may be highly suggestive of This avoids potential problems with inconsistency
sexual abuse between the medical record and police record.
168
CHILD ABUSE
r A body diagram is important in documenting MEDICATION ADDITIONAL READING

location and size of injuries; measurements should Varies by injury
r Gilbert R, Widom CS, Browne K, et al. Burden and
be included.
r Visible injuries should be photographed with a ruler DISPOSITION consequences of child maltreatment in high-income
present in the photo along with a card with the
Admission Criteria countries. Lancet. 2009;373:68.
r Children may require admission to care for their r Johnson C. Abuse and neglect of children. In
childs name, the date, and the signature of the
photographer visible in the picture. Consent should medical concerns (ie, burns, head injuries, etc.). Behrman RE, Kliegman RM, Jenson HB, eds. Nelson
r Children may also be admitted when no suitable
be obtained for the photographs. Textbook of Pediatrics. 17th ed. Philadelphia, PA:
environment is available until a safe residence is
r Physical abuse: secured.
Saunders; 2004.
r Legano LA, McHugh MT, Palusci VJ. Child abuse and C
Subdural hematomas: Hallmark of inflicted head neglect. Curr Probl Pediatr Adolesc Health Care.
Patients who have injuries that are life threatening 2009;39:e1e26.
injury may require critical care admission. r Ludwig S. Child abuse. In Fleisher GR, Ludwig S,
Retinal hemorrhages
Burns: Classic patterns, such as glove and Discharge Criteria eds. Textbook of Pediatric Emergency Medicine. 6th
r The child must be medically stable and prepared for ed. Philadelphia, PA: Lippincott Williams & Wilkins;
stocking distribution, dunking burns. Other
patterned burns, such as cigarette burns, irons, discharge. 2010.
r It must be ensured that the child is being discharged r Reece RM, Christian C. Child Abuse: Medical
etc., are also highly suspicious.
Bruises: Patterned bruises (ie, belt mark loop or to a safe environment with adequate follow-up. Diagnosis & Management. 3rd ed. Elk Grove Village,
lashes, handprints) are suspicious for abuse. IL: American Academy of Pediatrics; 2008.
Issues for Referral r Sedlak AJ, Mettenburg J, Basena M, et al. Fourth
Symmetrical bruises over nonbony prominences Health care workers are mandated reporters and are
are also very suspicious. protected by law when they refer a case to child National Incidence Study of Child Abuse and
r Neglect: Neglect (NIS-4): Report to Congress, Executive
protective services or the police in good faith.
Failure to thrive, growth failure, noncompliance Summary. Washington, DC: U.S. Department of
with medical treatments Health and Human Services; 2010.
r Sexual abuse: FOLLOW-UP See Also (Topic, Algorithm, Electronic
Hymenal tears, vaginal lacerations Media Element)
Anal lacerations Sexual Assault
Perineal bruising r Family therapy may be indicated.
Bite marks to breasts, genitals
r In cases of neglect, additional measures may be
Precocious sexual behavior in young children CODES
needed to ensure compliance.
DIFFERENTIAL DIAGNOSIS r Physical injuries should be treated in the same
r Accidental injury ICD9
r Infection: Sepsis, meningitis, congenital syphilis, methods for noninflicted injuries. r 995.50 Unspecified child abuse
osteomyelitis, impetigo, staph scalded-skin Patient Monitoring r 995.51 Child emotional/psychological abuse
syndrome, purpura fulminans Cases must be investigated by child welfare agents r 995.52 Child neglect (nutritional)
r Phytophotodermatitis and/or the police, who will determine the need for
r Cultural practices: Coining, cupping, moxibustion foster care placement or ongoing supervision.
r Metabolic: Copper deficiency, rickets, scurvy, vitamin PROGNOSIS PEARLS AND PITFALLS
K deficiency Varies depending on the injuries substained, the r Always maintain a high suspicion of abuse,
r Congenital: Osteogenesis imperfecta, Ehlers-Danlos degree of neglect, the family dynamic, and available
particularly when the history does not match the
syndrome, familial dysautonomia with congenital support system
physical exam findings.
indifference to pain, Mongolian spots, minor skeletal COMPLICATIONS r Health care workers are mandated reporters: Failure
anomalies r Death
r Immunologic: Henoch-Schonlein purpura, immune to report suspicion could result in legal action.
r Mental retardation
thrombocytopenic purpura r Cerebral palsy
r Hematologic: Leukemia, hemophilia, von Willebrand r Seizures
disease, disseminated intravascular coagulation r Learning disabilities
r Miscellaneous: Apparent life-threatening event
r Emotional problems
(ALTE), epidermolysis bullosa, erythema multiforme r Posttraumatic stress disorder
r Neglect may lead to growth failure, developmental
TREATMENT delay, and complications from poor nutrition,
medical neglect, or other forms of neglect.
PRE HOSPITAL r Substance abuse and psychological sequelae are
Trauma patients should be stabilized in the same common in victims of sexual abuse.
manner they otherwise would be.
r Management is dependent on injuries (ie, ABCs,
head and visceral injuries managed accordingly).
r Medical caregivers in all states are mandated to
report suspected child abuse.
169
CHOLELITHIASIS
Lauren S. Chernick
Anupam Kharbanda
r Cholesterol stones form when there is excess DIAGNOSTIC TESTS & INTERPRETATION
BASICS cholesterol in the bile: Lab
Cholesterol supersaturates the bile and Initial Lab Tests
DESCRIPTION crystallizes. r No lab testing is necessary when stones are
r Gallstones are crystalline structures formed from Stone growth is accentuated in those with confined to the gallbladder (all will be normal).
both normal and abnormal bile components. abnormal/decreased motility of the gallbladder. r The following are reasonable tests to evaluate other
r Symptoms develop when stones migrate out of the r Brown pigment stones, although rare, often develop
causes of abdominal pain:
gallbladder into the biliary canals: in the presence of obstruction and infection. They AST, ALT, direct and indirect bilirubin, and GGT
40% of children with gallstones are often contain bacteria, calcium bilirubinate, (liver involvement)
asymptomatic. cholesterol, and fatty acids. Amylase and lipase (pancreatitis)
Gallstone complications occur when stones: CBC (hemolytic anemia or leukocytosis)
Obstruct the cystic duct (cholecystitis) ETIOLOGY
r Hemolytic disease C-reactive protein (elevated in cholecystitis)
Obstruct the common bile duct (choledolithiasis)
r Prematurity Urine pregnancy and urinalysis
Cause an infection of the common bile duct Leukocytosis suggests cholecystitis.
(cholangitis) Elevated GGT or direct bilirubin suggests
r Obesity
EPIDEMIOLOGY cholangitis.
r Oral contraceptive use
Prevalence r Pregnancy Imaging
r In children, gallstones are rare (0.10.2%) but are r US is the modality of choice (5):
recently thought to be increasing (1.9%) (1): Strengths:
Most common type of stone in children is black DIAGNOSIS Sensitivity and specificity >95%
pigment stones (2). Visualizes stones as small as 2 mm
Females = males until puberty, when females HISTORY Inexpensive and noninvasive
> males r No single sign or symptom is highly sensitive or Gallbladder distention, wall thickening, or
r In adults, gallstones are common with >20 million specific for cholelithiasis. pericholecystic fluid suggests cholecystitis.
cases/year in the U.S. (3): r Biliary colic results from gallbladder contraction and Weaknesses:
Most common type of stone in adults is presents with the following characteristics: Poor visualization of common bile duct
cholesterol stones. Pain in right upper quadrant (RUQ) and/or r Plain radiographs:
Females > males epigastrium Low sensitivity for stone visualization
r The prevalence of gallstones is higher in children Persistent or episodic pain, but the pain should A poor choice to rule in or out cholelithiasis
with certain chronic diseases like hemolytic anemia: last less than a few hours r CT: Rarely used as the test of choice due to its poor
The prevalence of gallstones in children with sickle Pain that may radiate to right shoulder, back, or visualization of stones:
cell disease (SCD) is double the general flank Strengths:
population. Possible association with nausea, vomiting, or Helps to define gallbladder anatomy and
50% of all children with SCD will develop eating fatty foods adjacent organs
gallstones. r Incidental gallstones can be asymptomatic. Weaknesses:
r Of all ethnic groups in the U.S., Native Americans r Pain lasting longer than 46 hr suggests biliary Associated with a lower sensitivity than US for
have the highest prevalence. obstruction. visualizing stones
r Magnetic resonance cholangiopancreatography
RISK FACTORS PHYSICAL EXAM
r Black pigment stones have been associated with r Asymptomatic or mildly symptomatic gallstones (MRCP) and endoscopic retrograde
cholangiopancreatography (ERCP) help to delineate
hemolytic diseases such as SCD and should accompany normal vital signs.
r Certain components of the physical exam may the anatomy of the extrahepatic and intrahepatic
beta-thalassemia, cystic fibrosis, ileal resection, and
biliary tract and identify the location of stones:
prolonged total parenteral nutrition (4). suggest complications such an obstruction of the
r Cholesterol stones have been associated with MRCP:
biliary tree or biliary infection: Strengths: Useful diagnostic mechanism for
female gender, obesity, pregnancy, rapid weight Tachycardia or fever localizing stones, has a sensitivity between 90
loss, and a family history of gallstones. Bradypnea due to splinting and 96%, and can better visualize the common
RUQ and/or epigastric pain bile duct (6)
PATHOPHYSIOLOGY Jaundice
r Stones form when 1 normal component of bile Weaknesses: Does not provide a method for
A hard, rigid, or distended abdomen stone removal, not available at all institutions,
increases in quantity and supersaturates, thus
Murphy sign: and requires sedation
forming a nidus for stone formation. Worsening pain or inspiration arrest when RUQ
r Stones are typically classified as black pigment, ERCP:
is palpated Strengths: Provides a diagnostic and therapeutic
cholesterol, brown pigment, or mixed. Highly sensitive in adults for cholecystitis
r Black pigment stones form when there is excess mechanism for localizing and removing the
bilirubin in the bile: stone
Weaknesses: Invasive and may offer no
Abnormal production or destruction of RBCs leads
to increased levels of bilirubin. advantage for clearance of the bile duct over
surgical approaches
170
CHOLELITHIASIS
DIFFERENTIAL DIAGNOSIS r Patients with a clinical picture suggestive of 4. Wesdorp I, Bosman D, Graaf A, et al. Clinical
r RUQ/Epigastric pain: GERD, gastritis, pancreatitis, cholecystitis should be admitted; the timing of presentations and predisposing factors of
peptic ulcer disease, hepatitis, appendicitis, acute cholecystectomy and/or ERCP is surgeon/GI cholelithiasis and sludge in children. J Pediatr
acalculous cholecystitis, inflammatory bowel specialist dependent but often occurs before Gastroenterol Nutr. 2000;31:411417.
disease, acute gastroenteritis discharge. 5. Bortoff G, Chen MYM, Ott DJ, et al. Gallbladder
r Gallstone complications: Cholecystitis, r Cholecystectomy is not recommended for incidental stones: Imaging and intervention. Radiographics.
choledolithiasis, cholangitis, pancreatitis or asymptomatic gallstones. 2000;20:751766.
DISPOSITION 6. Tipnis NA, Dua KW, Werlin SL. A retrospective
assessment of magnetic resonance cholangio-
pancreatography in children. J Pediatr
C
r Patients with unresolved biliary colic or any
Gastroenterol Nutr. 2008;46:5964.
PRE HOSPITAL suspicion of cholecystitis, choledolithiasis,
r Uncomplicated cholelithiasis or biliary colic requires cholangitis, or pancreatitis should be admitted.
no intervention by EMS. r Critical care admission criteria: ADDITIONAL READING
r If the patient has abnormal vital signs, secure IV Patients who are ill with unstable vital signs
r Aufderheide TP, Brady WJ, Tintinalli J. Cholecystitis
access and administer IV fluids. despite fluid resuscitation and antibiotics should
be considered for ICU admission. and biliary colic. In Tintinalli JE, Gabor D,
INITIAL STABILIZATION/THERAPY Stapczynski JS, et al., eds. Tintinallis Emergency
Ill-appearing patients, likely suffering from biliary Discharge Criteria Medicine: Comprehensive Study Guide. 6th ed.
r Patients with incidental gallstones or asymptomatic
stone complications, should be stabilized: Columbus, OH: McGraw-Hill; 2003:7680.
r Assess and support the airway, if necessary. gallstones can be discharged home with primary r Broderick A, Sweeney BT. Gallbladder disease. In
r Assess circulatory needs: care physician follow-up.
r Patients with resolved biliary colic can be discharged Walker WA, Kleinman RE, Sherman PM, et al., eds.
Place 2 large-bore IV catheters. Pediatric Gastrointestinal Disease: Pathophysiology,
Give IV fluids for volume deficiency (20 cc/kg with timely outpatient surgical follow-up (within
Diagnosis, Management. Philadelphia, PA: Mosby;
boluses of normal saline). 1 wk).
2004:15511565.
Provide pain control. r Friedman JR, Kennedy MC. Cholelithiasis. eMedicine
r Assess for signs of peritonitis.
FOLLOW-UP Pediatrics: General Medicine. April 13, 2009.
MEDICATION Available at http://emedicine.medscape.com/article/
FOLLOW-UP RECOMMENDATIONS 927522-overview.
First Line Discharge instructions and medications:
r Analgesics: See Also (Topic, Algorithm, Electronic
r Return to the emergency department if the pain is
Merperidine 1 mg/kg IV q4h, max single dose Media Element)
severe, pain is not resolved with NSAIDs, or jaundice r Hepatitis
100 mg
develops. r Pain, Abdomen
Ketorolac 0.5 mg/kg q8h IV/IM, max single dose
30 mg PROGNOSIS
r Antiemetics for nausea: Ondansetron 0.1 mg/kg IV, r Some gallstones will resolve without any medical
max single dose 4 mg intervention.
r Patients with recurrent biliary colic without
CODES
r Antibiotics if suspicious for acute cholecystitis or
cholangitis, covering Escherichia coli and Klebsiella cholecystecomy have a high likelihood of ICD9
species: experiencing a biliary obstruction. r 574.20 Calculus of gallbladder without mention of
2nd-generation cephalosporin with anaerobic COMPLICATIONS cholecystitis, without mention of obstruction
coverage such as: r Gallbladder perforation r 574.21 Calculus of gallbladder without mention of
Cefoxitin 80160 mg/kg/24 hr divided q46h r Peritonitis cholecystitis, with obstruction
IM/IV OR r Bacterial overgrowth r 575.10 Cholecystitis, unspecified
Cefotetan 4080 mg/kg/24 hr divided q12h
r Choledocholithiasis: Stone obstructing the common
IV/IM
Piperacillin/Tazobactam: Infants <6 mo, biliary duct
150300 (piperacillin component) mg/kg/24 hr IV
r Ascending cholangitis PEARLS AND PITFALLS
divided q68h; infants >6 mo and children, r Pancreatitis r Gallstones are relatively uncommon in children.
300400 mg/kg/24 hr IV divided q68h Children with hemolytic or ileal diseases are more at
Second Line risk.
r Cholesterol stones are more likely to respond to REFERENCES r Diagnostic modality of choice is US.
nonsurgical management than other stones. 1. Kaechele V, Wabitsch M, Thiere D, et al. Prevalence r Patients with asymptomatic gallstones can be
r Bile salt dissolvents such as ursodiol (Actigal) of gallbladder stone disease in obese children and followed as outpatients.
1015 mg/kg/24 hr daily PO: adolescents: Influence of the degree of obesity, sex, r Patients complaining of uncomplicated cholelithiasis
Usually prescribed as outpatient medication and pubertal development. J Pediatr Gastroenterol should not appear ill.
Stone must be noncalcified, small, and with a low Nutr. 2006;42:6670. r Resolved biliary colic can be followed up in the
likelihood of causing complications. 2. Stringer MD, Taylor DR, Soloway RD. Gallstone surgery clinic.
Good for patients when surgery is too high of a composition: Are children different? J Pediatr. r Do not discharge home patients with sustained
risk to perform (eg, cardiac disease) 2003;142(4):435440. biliary colic, possible cholecystitis, choledolithiasis,
May not work and stones can recur (4) 3. Everhart JE, Khare M, Hill M, et al. Prevalence and or cholangitis. Patients should be admitted, given
SURGERY/OTHER PROCEDURES ethnic differences in gallbladder disease in the antibiotics, and have a surgical evaluation.
Laparoscopic cholecystectomy is the treatment of United States. Gastroenterology. 1999;117:
choice for symptomatic cholelithiasis. 632639.
r Patients with mild intermittent biliary colic can be
scheduled for outpatient elective laparoscopic
cholecystectomy.
171
CHOLINERGIC POISONING
Robert J. Hoffman
r Intermediate syndrome is a neurologic r HEENT: Miosis or mydriasis, salivation, eyelid

BASICS phenomenon that occurs 13 days after acute twitching
pesticide exposure that includes neck weakness, r GI: Nausea, vomiting, diarrhea
DESCRIPTION decreased deep tendon reflexes, cranial nerve r Respiratory: Dyspnea, cough, bronchospasm,
r Cholinergic poisoning results from agonism at abnormalities, proximal muscle weakness, and respiratory depression
muscarinic and/or nicotinic cholinergic receptors. respiratory insufficiency: r Musculoskeletal: Muscle cramps, twitching,
r This poisoning mimics the action of acetylcholine. This weakness may exacerbate and last several fasciculations, weakness, paralysis
r Cholinergic poisoning results from exposure to weeks. r Neurologic: Vertigo, tremor, seizures, coma, paralysis
pesticides as well as some medications. r Delayed neuropathy with severe pain in a
r Organophosphate and carbamate pesticides cause stocking/glove distribution may occur 13 wk after DIAGNOSTIC TESTS & INTERPRETATION
severe cholinergic poisoning. exposure: Lab
r Nerve gas agents are organophosphates that are This may persist for months or cause permanent Initial Lab Tests
injury. r Assess bedside glucose measurement in patients
extremely potent and capable of causing death
rapidly. with altered mental status.
ETIOLOGY r Obtain acetaminophen concentration in patients
r Medications:
EPIDEMIOLOGY with intentional exposure and intent of self-harm.
Incidence Acetylcholine r Blood gas analysis to assess oxygenation,
r In the U.S., cholinergic poisoning in children occurs Bethanechol
Carbachol ventilation, and perfusion
predominantly due to pesticide exposure. r Lactate concentration to assess perfusion
r This is more common in rural areas with agricultural Pilocarpine
r Pesticides r Serum electrolytes
industry but also occurs in urban areas. r Nicotine r Creatine phosphokinase if prolonged seizures
RISK FACTORS r Weaponized organophosphate agents: r RBC cholinesterase and serum cholinesterase levels
r Use of pesticides without protective gear or use of
Sarin may be obtained:
pesticides in areas where unprotected persons are Soman These are not routinely used in acute
located VX management.
r Organophosphate and carbamate pesticides should
not be used indoors: r Vomiting r CXR may be indicated for patients with hypoxemia
Inappropriate indoor use places children at great
r Diaphoresis or symptoms of bronchorrhea/bronchospasm.
risk. r CT of the head may be indicated for seizures or
r Dyspnea
GENERAL PREVENTION r Miosis depressed mental status.
r Avoid exposure to pesticides and medications by
storing these safely out of reach of children. Obtain ECG.
r Wear protective clothing when working with DIAGNOSIS
pesticides. DIFFERENTIAL DIAGNOSIS
HISTORY r Nicotine toxicity
PATHOPHYSIOLOGY r See Pathophysiology for DUMBELS and MTWTF r Mixed-drug or polypharmacy ingestion
r Cholinergic agonism excites postganglionic
pneumonics. r Other causes of paralysis or weakness:
cholinergic receptors: r Typically, a history of exposure is readily available.
Botulism
Classic symptoms result from activity at muscarinic r Symptoms of vomiting, diaphoresis, altered mental Myasthenia gravis
receptors, but nicotinic receptors may also be
status or coma, and weakness may be present. Eaton-Lambert syndrome
affected.
r Organophosphate agents bind irreversibly at the PHYSICAL EXAM
r See Pathophysiology for DUMBELS and MTWTF
cholinergic receptor:
Initially, a weak electrostatic bond is formed. pneumonics.
Later, this becomes a permanent covalent bond: r Assess vital signs and pulse oximetry:
This process is called aging, and treatment Tachypnea may be present in response to
with pralidoxime is aimed at preventing this. bronchorrhea or bronchospasm.
Nerve agents such as sarin and soman are Respiratory depression secondary to weakness or
particularly feared due to quick aging time. paralysis may be present.
r DUMBELS pneumonic describes most toxicity: Bradycardia if muscarinic excess, sometimes with
Diarrhea, Diaphoresis, Urinary incontinence, hypotension
Miosis, Bronchorrhea, Bronchospasm, Tachycardia and HTN is nicotinic excess.
Bradycardia, Emesis, Lacrimation, Salivation,
Seizures
r MTWTF pneumonic for nicotinic toxicity:
Mydriasis, Muscle cramps, Tachycardia, Weakness,
Twitching, Flaccid paralysis
172
CHOLINERGIC POISONING
r Atropine:
TREATMENT 0.05 mg/kg IV, max initial dose 2 mg, IV over FOLLOW-UP
5 min
PRE HOSPITAL If still symptomatic 5 min later, double the dose PROGNOSIS
r Assess and stabilize airway, breathing, and r Varies with specific poison and quantity ingested
and administer IV.
Continue dosing q5min, doubling the dose and r With appropriate supportive care and antidote use,
circulation.
r Administer atropine and pralidoxime if indicated by titrating to effect. most patients recover fully.
Use of autoinjector (AtroPen) is acceptable: r Prolonged paralysis or neurologic sequelae are
local protocol.
r If topical exposure, decontaminate as per local 1540 lb (718 kg), 0.5 mg IM
protocol.
4090 lb (1941 kg), 1.0 mg IM
possible.
C
>90 lb and adults (>41 kg), 2.0 mg COMPLICATIONS
r Neurologic sequelae including intermediate
INITIAL STABILIZATION/THERAPY Give initial autoinjector dose:
r Decontamination of any patient exposed to topical If no symptoms discontinue
syndrome or organophosphate-induced delayed
cholinergic agents such as pesticides or nerve gas is If severe symptoms persist, immediately give 2
neuropathy
r End-organ injury due to hypoperfusion
critical. This action must be taken prior to treatment additional doses.
in the emergency department: r Pulmonary insufficiency due to bronchospasm or
End point of treatment is drying of pulmonary
This is a particular instance when airway, secretions/pulmonary edema. pulmonary edema
breathing, circulation is not priority. Even r Shock
Reversal of miosis gives a good approximation for
compromised patients do not receive attention to adequate quantity of atropine administration. r Death
ABCs in the emergency department until they are If wet, treatment is atropine.
decontaminated. r Pralidoxime:
Failure to decontaminate the patient may result in 25 mg/kg, max single dose 1 g, IV over ADDITIONAL READING
ongoing toxicity of the patient and may result in 1530 min, followed by 2550 mg/kg/hr, to max r Eddleston M, Phillips MR. Self poisoning with
staff falling ill due to direct contact or from fumes infusion of 500 mg/hr
emanating from an inadequately decontaminated pesticides. BMJ. 2004;328:42.
600-mg dose autoinjector may be used. r Okudera H, Morita H, Iwashita T, et al. Unexpected
patient. Indicated for fasciculations, weakness, or paralysis
r Assess and stabilize airway, breathing, and nerve gas exposure in the city of Matsumoto: Report
If weak, treatment is pralidoxime. of rescue activity in the first sarin gas terrorism. Am
circulation. r Benzodiazepine for seizure:
r Administer high-flow oxygen. J Emerg Med. 1997;15:527.
r Supportive care by management of respiratory
Diazepam 0.1 mg/kg IV, 0.5 mg/kg PR. When r Schexnayder S, James LP, Kearns GL, et al. The
given IV, may repeat dose q510min PRN. pharmacokinetics of continuous infusion
compromise, bradycardia or dysrhythmia, Lorazepam 0.05 mg/kg IV, may repeat dose
bronchospasm, and severe toxicity pralidoxime in children with organophosphate
q10min PRN. poisoning. J Toxicol Clin Toxicol. 1998;36:549.
MEDICATION Second Line r Schier JG, Hoffman RS. Treatment of sarin exposure.
First Line Albuterol: JAMA. 2004;291:182.
r In addition to doses of atropine and pralidoxime r 0.15 mg/kg nebulized q15min as needed for
below, autoinjectors may be used: wheezing
DuoDote (2.1 mg atropine/600 mg pralidoxime):
DISPOSITION
CODES
1 IM injection initially:
If there are no severe symptoms, give no Admission Criteria
r Any treatment with medication warrants hospital ICD9
additional medication. 971.0 Poisoning by parasympathomimetics
If severe symptoms persist, give 2 additional IM admission for observation and possibly further
(cholinergics)
autoinjection doses. treatment.
r Although initially only adult doses adapted from r Critical care admission criteria:
military antidote kits were available, pediatric kits, Unstable vital signs, seizure, or severe toxicity PEARLS AND PITFALLS
as well as combination atropine/pralidoxime Discharge Criteria r Appropriate decontamination of the patient is
(DuoDote), are available. Asymptomatic for 46 hr without any treatment given
during hospital stay critical to treat the patient and to protect staff in
cases of exposure to pesticides or other
Issues for Referral organophosphate agents.
r Consider toxicology consultation to manage
r Copious quantities of atropine may be needed.
poisoning. r Control of seizures is critical.
r Consult psychiatry if the patient has attempted
r After pesticide poisoning, prolonged treatment for
self-harm.
several days may be required.
173
COCAINE POISONING
John Kashani
Injury to the musculoskeletal system with cocaine r Drug of abuse screening:

BASICS use is usually secondary to trauma. Cocaine may It is critical for the treating clinician to understand
cause muscle injury or rhabdomyolysis elevation in the limitations of lab screening for cocaine or
DESCRIPTION creatine phosphokinase (CPK), even without other drugs.
r Cocaine is a naturally occurring alkaloid derived trauma or vigorous body activity. Clinicians should not use results of drug screening
from the leaves of the Erythroxylum coca shrub. to guide management of a suspected intoxication
r The shrub grows indigenously in Colombia, Peru, ETIOLOGY
with cocaine or other drugs of abuse but rather
Cocaine comes in several forms, all derived from the
Bolivia, the West Indies, and Indonesia. should rely on physical exam, clinical findings, and
r Recreational use of cocaine was legal in the U.S. Erythroxylum coca plant:
r Cocaine hydrochloride, or cocaine powder close attention to hemodynamic parameters:
until 1914. A positive screen suggests exposure but cannot
r Freebase (crack) cocaine
distinguish current intoxication from remote use.
EPIDEMIOLOGY Negative screen may occur in patients with
r Recent estimates suggest that 34 million
toxicity in whom the urine is too dilute or the
Americans have used cocaine and that 2 million DIAGNOSIS metabolite assayed, benzoylecgonine, is not yet
people are regular users. present in urine.
r In addition to morbidity and mortality directly from HISTORY
r Patients or parents may provide a history of cocaine Urine testing is the most widely used test to detect
drug use, cocaine users are at significantly higher exposure to cocaine:
exposure.
risk of injury or death by trauma. r Some patients may not be forthcoming about their With respect to the drugs detected by typical
PATHOPHYSIOLOGY cocaine use; however, it is incumbent upon a drug of abuse screening panels, cocaine is the
r Cocaine binds to proteins transporting biogenic physician to inquire about the use of drugs, as it most specific test, with virtually no false-positive
amines blocking their reuptake. may alter the patients management. assays.
r As a result, the synaptic concentrations of r In patients forthcoming about cocaine use, chest For forensic purposes, such as in cases of children
dopamine, serotonin, norepinephrine, and too young to use drugs volitionally, drug of abuse
pain is the most common presenting complaint.
epinephrine are increased. r If a patient is brought to medical care by others, a screening may be of value to police and/or child
r In addition, cocaine also has indirect actions that protective services.
history of altered mental status, psychomotor Metabolites of cocaine can be found in blood,
affect various other neuromodulatory systems, agitation, sympathomimetic symptoms, and seizures hair, saliva, and meconium:
including the opioidergic, glutamatergic, and may be elicited. These assays are not readily available, are costly,
GABAergic systems.
r The route of administration, as well as coingestants, PHYSICAL EXAM and typically take at least several days to weeks
r Patients typically present in a sympathomimetic to attain results.
can affect the metabolism. These special tests are warranted only in specific
r The coingestion of ethanol with cocaine results in state of adrenergic stimulation.
r Cardiovascular: HTN, tachycardia circumstances, such as where they are used
the formation of cocaethylene, which is a more r Dermatologic: Warm or diaphoretic commonly, with meconium in certain nurseries
potent and longer-acting metabolite. r Psychiatric: Hyperalert, talkative with pressured or neonatal ICU, or when specific circumstances
r Cocaine has the potential to affect numerous body
speech, agitated, and sometimes with paranoia require forensic evidence.
systems:
At low doses, pleasurable effects such as similar to schizophrenia. Occasionally, severe Imaging
euphoria, hyperalertness, and hypersexuality may somnolence may be present if the patient presents Radiographic imaging is used if pulmonary
be experienced. after a prolonged cocaine binge. complications of cocaine use are suspected and when
r Neurologic: Pupillary dilation is typical, and focal body packing or stuffing is suspected.
As the dose is increased, untoward effects such as
agitation, confusion, and hallucinations can occur. neurologic deficits may be present if stroke of CNS Diagnostic Procedures/Other
Seizures, strokes (hemorrhagic and embolic), and ischemia. ECG should be obtained in all patients with cocaine
r Stigmata of drug use such as track marks and exposure. Serial ECG may be needed.
vasculitis may occur.
Choreoathetosis, secondary to dopamine excess, defects in the nasal septum should be investigated.
r If body packing or body stuffing is suspected, exams DIFFERENTIAL DIAGNOSIS
may occur, called crack dancing.
Other states of sympathomimetic or adrenergic
Cocaine may cause multiple GI complications: of body cavities and imaging may be warranted.
r To distinguish from anticholinergic syndrome, stimulation:
Intestinal infarction, perforated ulcers, and liver r Toxins:
and kidney infarctions have all been reported. evaluate for absence/presence of sweating, bowel
Body packers, also called mules, who swallow sounds, and pupil reactivity to light: Amphetamine toxicity, anticholinergic poisoning,
packaged cocaine for international smuggling, Diminished bowel sounds, dry skin, and pupils sedative/hypnotic withdrawal (eg,
may present with various abdominal complaints, sluggishly reactive to light suggest exposure to an benzodiazepines, barbiturates, alcohol), PCP
especially obstruction or ischemia/infarction. anticholinergic agent. intoxication, pheochromocytoma, monoamine
Vasoconstriction caused by cocaine in oxidase inhibitor toxicity, serotonin syndrome, and
combination with an increased heart rate causes DIAGNOSTIC TESTS & INTERPRETATION neuroleptic malignant syndrome
Lab r Encephalitis
an imbalance in myocardial oxygen supply and
demand. Additionally, cocaine is thought to Initial Lab Tests
r No lab testing is routinely indicated, but consider as
accelerate atherosclerosis. Cocaine is also capable
of blocking sodium and potassium channels on indicated:
myocardial cells, resulting in a prolonged QRS and Basic chemistry profile to assess for dehydration
QTc, respectively. and hyperkalemia
Pulmonary: Pneumothoraces and CPK and/or urinalysis to evaluate for
pneumomediastinum have been reported, rhabdomyolysis
presumably by using the Valsalva maneuver Troponin should be ordered in any patient with
during smoking. Cocaine can induce chest pain or findings consistent with myocardial
bronchospasm and exacerbate lung disease. ischemia.
Thermal injury can occur through the inhalation of
superheated smoke. Hemorrhagic alveolitis (crack
lung) consisting of eosinophilia, pruritus, and
increased IgE levels has been described.
174
COCAINE POISONING
Although these doses are higher than typical, the

TREATMENT tolerance of multiple doses without sedation FOLLOW-UP
provides reassurance to increase the dose.
PRE HOSPITAL FOLLOW-UP RECOMMENDATIONS
r Assess and stabilize airway, breathing, and Second Line Discharge instructions and medications:
r Consider the following in rare cases that adequate
circulation. r Avoid further drug use, and seek drug counseling.
diazepam dosing has not controlled chest pain,
r Administer supplemental oxygen and IV fluid if
cardiovascular stimulation, or acute coronary PROGNOSIS
these can be done easily. syndrome. Depends on severity of cocaine toxicity, development
r Restrain patients with psychomotor agitation.
r If local policy permits, judicious use of diazepam
r Phentolamine for HTN: of end-organ injury: C
Initial dose 0.1 mg/kg IV; adolescent/adult, 10 mg r Cocaine users are likely to continue using cocaine
0.2 mg/kg IV may be attempted. If there is no effect, IV. Reassess HTN and give additional dose PRN despite injury.
the dose may be repeated in 5 min. after 1520 min.
Phentolamine administration should occur after COMPLICATIONS
INITIAL STABILIZATION/THERAPY r MI
r Assess and stabilize airway, breathing, and initial diazepam administration.
r Stroke
r Nitroglycerine 0.30.6 mg SL for chest pain or acute
circulation. r Hepatic injury
r Supportive care is the main management. coronary syndrome. Use after diazepam, as
diazepam is superior in relieving chest pain. r DIC
r Administer IV fluid, normal saline bolus 20 mg/kg;
r Nitrates, calcium channel blockers, and aspirin may r Shock
may repeat 3 times in 1st hr. r Death
r Administer high-flow oxygen to any patient with be indicated for HTN/tachycardia or acute coronary
syndrome.
cardiovascular stimulation, chest pain, or suspected r The authors strongly advocate against use of
acute coronary syndrome. ADDITIONAL READING
r Common issues to manage include: beta-blockers in the management of cocaine
toxicity: r Bemanian S, Motallebi M, Nosrati SM.
Psychomotor agitation, managed by Potential for paradoxical increase in HTN and
administration of benzodiazepines Cocaine-induced renal infarction: Report of a case
injury or death.
Chest pain and cardiovascular stimulation, and review of the literature. BMC Nephrol. 2005;
If using a beta-blocker, we recommend titration of
managed by administration of benzodiazepines, 6:10.
esmolol after phentolamine. r Kaku DA, Lowenstein DH. Emergence of recreational
phentolamine, and possibly additional No beta-blocker is clearly safe to use without a
cardiovascular medications concomitant vasodilating agent, but labetalol has drug abuse as a major risk factor for stroke in young
Hyperthermia, managed by active cooling, both beta- and alpha-blocking activity. It is used adults. Ann Intern Med. 1990;113:821827.
including possible need for ice immersion r Karch SB. Cocaine cardiovascular toxicity. South
r Although cocaine is bound by activated charcoal, in centers that do not adhere to the admonition
against use of beta-blockers. Med J. 2005;98(8):794799.
the role of charcoal is limited to the patient having r Sodium bicarbonate: For severe acidemia or r Maeder M, Ulmer E. Pneumomediastinum and
swallowed packets of cocaine. widened QRS complex: bilateral pneumothorax as a complication of cocaine
r Avoid mechanical restraints to prevent the potential smoking. Respiration. 2003;70(4):407.
For academia, 1 mEq/kg IV; repeat PRN
for heat generation and muscle If wide QRS >100 msec, 1 mEq/kg IV push, then
injury/rhabdomyolysis if the patient struggles. See Also (Topic, Algorithm, Electronic
repeat ECG 10 min later to assess response Media Element)
r Use of benzodiazepines, sometimes in massive
If QRS narrowing results, a bicarbonate infusion of r Anticholinergic Poisoning
doses, is recommended. 2 ampules of sodium bicarbonate in 1 L of D5W r Sympathomimetic Poisoning
may be infused.
ALERT
r Obtain a rectal temperature immediately in SURGERY/OTHER PROCEDURES
patients with possible hyperthermia. Surgery or endoscopic retrieval of drug packets for CODES
r Significant hyperthermia (39.040.0 C, or body packers and body stuffers
102.2104.0 F) requires passive cooling or mild DISPOSITION ICD9
active cooling and medications: Admission Criteria 970.81 Poisoning by cocaine
Life-threatening hyperthermia (>41.542.0 C, Critical care admission criteria:
or <106.7107.6 F) should be treated by r If patients are medically ill, admit to the ICU.
immersion in an ice bath. Other cooling r Cardiovascular stimulation requiring ongoing
PEARLS AND PITFALLS
measures are inadequate: r Main therapy is supportive care, maintaining vital
medication and monitoring to detect dysrhythmia,
Wrapping the patient in sheets with ice or signs within acceptable limits, and treating
hyperthermia, rhabdomyolysis, disseminated
placing patient in a body bag with ice are intravascular coagulation (DIC), and end-organ cardiovascular stimulation.
reasonable approaches. injury such as stroke or MI are typical causes for ICU r Diazepam is typically the only medication needed to
admission. treat cocaine toxicity.
MEDICATION r Diagnosing cocaine toxicity based on a positive
Discharge Criteria
First Line Normal vital signs, normal mental status, and no urine drug assay is a major pitfall resulting in
Diazepam: end-organ damage misdiagnosis. Do not base clinical management on
r First-line medication for any cocaine intoxicated urine drug screening.
Issues for Referral r Haloperidol or domperidone is contraindicated for
patient Refer all patients for drug counseling.
r Administer for agitation, chest pain, or sedating because of risk of seizure and cardiac
HTN/tachycardia death.
r Initial dose 0.2 mg/kg IV. This dose may be repeated
q5min.
r After administering a given dosage 3 times, increase
the dose by doubling:
If 10 mg IV has been given 3 times without
adequate effect, increase the dose to 20 mg.
If 20 mg IV has been given 3 times without effect,
double the dose to 40 mg IV.
175
COLITIS
Andrew Heggland
Barbara M. Garcia Pena

BASICS r Infectiousbacterial (4):
Lab
Salmonella species r CBC (hemoglobin/platelets in acute bleeding,
DESCRIPTION Shigella species WBC/platelets as inflammatory reactants)
r Colitis is inflammation of the large intestine due to Campylobacter jejuni r Electrolytes (especially HCO in large-volume
3
various etiologies. It is often associated with Yersinia enterocolitica diarrhea, acidbase status)
diarrhea and abdominal pain (13). Escherichia coli r LFTs (elevated transaminases indicate
r Diarrheal diseases are leading causes of morbidity Clostridium difficile infectious/inflammatory liver dysfunction; albumin
and mortality in children worldwide: 1 billion ill and Vibrio species indicates nutritional and protein synthetic status)
2.5 million deaths annually (4). r Infectiousviral: r ESR and/or C-reactive protein (measures of
r Infectious causes: Secondary to fecaloral Rotavirus inflammation)
contamination or food poisoning (5) Norovirus r Blood type and screen (preparation for transfusion
r Inflammatory bowel disease (IBD): Adenovirus
during acute blood loss)
Crohn disease (CD) or regional enteritis Cytomegalovirus r Stool assays (specific infectious diagnoses):
Ulcerative colitis (UC) r Infectiousparasitic:
Stool culture
Indeterminate colitis: Features of CD and UC Microsporidia species
r Allergic colitis: Immune mediated (eg, milk protein Ova and parasites
Cryptosporidia species
WBCs/Eosinophils
intolerance or gluten sensitivity) Helminths/Worms
r Other causes: Radiation, immunosuppression, r Infectiousprotozoal: C. difficile toxin A/B
antibiotics, toxic megacolon, necrotizing Giardia intestinalis Imaging
r Abdominal upright film or cross-table lateral to
enterocolitis (NEC), etc. Entamoeba histolytica
Coccidia species exclude bowel perforation
EPIDEMIOLOGY r IBD: Multifactorial, requiring genetic susceptibility r Upper GI series with small bowel follow-through
Incidence and environmental triggering (3) (small intestinal diseaseCD)
r Infectious: 1 in 3 persons per year r Allergic: Dietary protein and associated r Abdominal CT (delineates extent of disease and
r CD: 14/100,000 per year other abdominal organ involvement and is useful in
immunologic response
r UC: 1012/100,000 per year differentiating CD RLQ pain from appendicitis)
Prevalence r Infectious: Hemolytic uremic syndrome (HUS), Diagnostic Procedures/Other
r CD: 2448/100,000 Not emergently performed:
sepsis, immunosuppression
r UC: 5075/100,000 r CD: Pancreatitis, amyloidosis, renal stones, r Colonoscopy with biopsy
r Allergic: 1 in 200 infants r Wireless capsule endoscopy to visualize small bowel
thromboembolic disease
r UC: Primary sclerosing cholangitis (3%), sacroiliitis, disease in CD
RISK FACTORS r Esophagogastroduodenoscopy (with biopsy):
r Infectious: Poor hygiene, travel to developing ankylosing spondylitis
nations, immune suppression (4) May be emergent if upper GI bleeding
r IBD: Smoking, Judeo-European ancestry, isotretinoin DIFFERENTIAL DIAGNOSIS
use, family history (13)
DIAGNOSIS r Appendicitis
r NEC: Premature birth, ischemic event, aggressive HISTORY r Malrotation/Volvulus
oral feeding r Weight loss r Intussusception
r Stool: Thin, liquid; frequency >3 stools per day r Henoch-Schonlein purpura
GENERAL PREVENTION
r Fiber-based, well-rounded diet r Bleeding per the rectum r Upper GI bleeding
r Stress reduction r Abdominal pain: Location, onset, duration, and r Meckel diverticulitis
r Improving hygiene character: r GI/Abdominal neoplasm
r Appendectomy is protective against UC. CD: Often right lower quadrant (RLQ) pain r Vascular malformation
UC: Often diffuse r Nonaccidental trauma/occult trauma
PATHOPHYSIOLOGY Any colitis: Crampy, relapsing/remitting pain r Irritable bowel syndrome
r Infectious: Intracellular invasion, mucosal r Medical history: Growth failure (IBD)
inflammation, toxin release r Family history (IBD)
r CD: Transmural inflammation, cryptitis/crypt r Social/Travel history (infectious) TREATMENT
abscesses, fistula formation, giant cell granulomas r Depression/Fatigue (IBD)
r UC: Mucosal inflammation, basal plasmacytosis, r Diet/Medication: Ingested food may resemble blood. INITIAL STABILIZATION/THERAPY
cryptitis/crypt abscesses, epithelial dysplasia, r Assess and stabilize airway, breathing, and
pseudopolyps PHYSICAL EXAM circulation.
r Allergic: Protein triggering an immune response r Fever, tachycardia, pallor r IV access and fluid resuscitation
r Significant diarrhea can cause acidbase r Abdominal tenderness (peritonitis) r Pain management
disturbance and/or significant blood loss with r Oral ulcerations (IBD) r NPO
hemodynamic instability, progressing to systemic r Perirectal fistula (CD) r Withdrawal of offending agent (eg, dietary
inflammation, sepsis, and death. r Arthritis (IBD)
protein/antibiotic)
r Rash: Erythema nodosum/pyoderma gangrenosum
(CD)
r Eyes: Episcleritis/Uveitis (IBD)
176
COLITIS
MEDICATION SURGERY/OTHER PROCEDURES Pregnancy Considerations

r Infectious colitis (6): r Total colectomy in UC can be curative. r Active CD is likely to progress while pregnant.
Most are self-limited and do NOT require directed r Regional resection in CD usually is avoided if r Fertility is decreased by inflammation in colitis.
antimicrobial therapy. possible due to complication and recurrence rates. r Some anti-inflammatory medications (methotrexate,
Shigella species: thalidomide, diphenoxylate) are contraindicated in
Ceftriaxone 50 mg/kg/day IV/IM 5 days, max DISPOSITION
Admission Criteria pregnancy. Some (6-MP, azathioprine, olsalazine,
12 g/dose OR
Ciprofloxacin 20 mg/kg/day IV/PO divided b.i.d. r ICU: Sepsis/Systemic inflammatory response infliximab) have limited data concerning safety
5 days, max 500 mg/dose syndrome, hemodynamic instability, respiratory during pregnancy.
Enterotoxigenic or enteroinvasive E. coli: insufficiency r Some antimicrobials (ciprofloxacin, metronidazole, C
Trimethoprim/Sulfamethoxazole (TMP/SMX) r Inpatient wards: doxycycline, albendazole) also have limited safety
8 mg TMP/kg/day PO 14 days, max dose Need for IV pain management data in pregnancy.
160 mg TMP/800 mg SMX Need for IV antibiotics
Azithromycin 10 mg/kg on day 1, then 5 mg/kg Inability to tolerate PO
days 25; max single dose 500 mg Discharge Criteria REFERENCES
Ciprofloxacin 20 mg/kg/day PO divided b.i.d. r Pain adequately controlled
13 days, max dose 500 mg r Tolerating PO 1. Cosgrove M, Al-Atia RF, Jenkis HR. The
Vibrio cholerae: Doxycycline 5 mg/kg/day PO epidemiology of paediatric inflammatory bowel
r Adequately hydrated
divided b.i.d. 14 days, max single dose 100 mg disease. Arch Dis Child. 1996;74(5):460461.
C. difficile: Metronidazole 30 mg/kg/day PO Issues for Referral 2. Gryboski J. Crohns disease in children 10 years old
divided b.i.d x 10 days, max single dose 500 mg r Outpatient: and younger: Comparison with ulcerative colitis.
Salmonella species in vulnerable populations: Gastroenterology referral for all new diagnoses of J Pediatr Gastroenterol Nutr. 1994;18(2):174182.
Ceftriaxone 50 mg/kg/day IV/IM initially, then IBD if stable for discharge 3. Podolsky DK. Inflammatory bowel disease. N Engl J
convert to oral antibiotics Infectious disease referral may be indicated in Med. 2002;347:417429.
TMP/SMX 8 mg TMP/kg/day PO 14 days, max refractory infectious colitis. 4. Kosek M, Bern C, Guerrant R. The global burden of
single dose 160 mg TMP/800 mg SMX r Inpatient: diarrhoeal disease, as estimated from studies
Amoxicillin 50 mg/kg/day PO divided b.i.d.t.i.d. Surgical consultation should be obtained in published between 1992 and 2000. Bull World
14 days, max single dose 500 mg suspected toxic megacolon, NEC, etc. Health Organ. 2003;81(3):197204.
Campylobacter species in vulnerable populations: Infectious disease consult in refractory infectious 5. Stutman HR. Salmonella, Shigella, and
Erythromycin 50 mg/kg/day PO divided t.i.d.q.i.d. colitis Campylobacter: Common bacterial causes of
57 days, max dose 800 mg. Other macrolides infectious diarrhea. Pedi Ann. 1994;23(10):
such as azithromycin may be substituted for fewer 538443.
side effects and improved compliance. THERAPIES
r Probiotics do not improve irritable bowel symptoms 6. American Academy of Pediatrics. In Pickering LK,
G. intestinalis: Metronidazole 30 mg/kg/day PO Baker CJ, Kimberlin DW, et al., eds. Red Book: 2009
divided b.i.d 10 days, max single dose 500 mg (7).
r In infectious and antibiotic-associated diarrhea, Report of the Committee on Infectious Diseases.
E. histolytica: Metronidazole 30 mg/kg/day PO 28th ed. Elk Grove Village, IL: Author; 2009.
divided b.i.d 10 days, max dose 500 mg, WITH probiotics (lactobacillus GG 0.51 capsule per day
until 2 days after symptom resolution) decreases 7. Sartour RB. Therapeutic manipulation of the enteric
paromomycin 35 mg/kg/day PO divided q.i.d, max microflora in inflammatory bowel disease:
single dose 250 mg abdominal pain, shortens diarrhea by 12 days, and
increases stool firmness (7). Antibiotics, probiotics, and prebiotics.
Cryptosporidium species: Nitazoxanide Gastroenterology. 2004;126:16201633.
200500 mg/day (3 days) WITH paromomycin
35 mg/kg/day (7 days) FOLLOW-UP
Microsporidia species: Albendazole 15 mg/kg/day ADDITIONAL READING
PO 1421 days, max dose 400 mg; metronidazole FOLLOW-UP RECOMMENDATIONS
30 mg/kg/day PO divided b.i.d 10 days, max Patient Monitoring Crohns & Colitis Foundation of America:
single dose 500 mg: r Infectious: Symptom resolution; eradication of http://www.ccfa.org
Coccidia species: TMP/SMX 8 mg TMP/kg/day infectious agent upon subsequent stool culture See Also (Topic, Algorithm, Electronic
PO 24 days, max single dose 160 mg r IBD: Symptom resolution, improvement in markers Media Element)
TMP/800 mg SMX of inflammation; GI neoplasm surveillance; growth r Diarrhea
r Inflammatory colitis (3): r Gastritis
monitoring
Start meds in the emergency department and r Allergic: Symptom resolution with diet change r Pain, Abdominal
prescribe until a GI consultation within 12 wk.
Corticosteroids: Prednisone 12 mg/kg/day PO DIET
r High-fiber, bland solids; clear liquids
per day or methylprednisolone up to 30
mg/kg/dose r Avoid inciting foods. CODES
Salicylates: Mesalamine 50 mg/kg/day divided r Hydrolyzed protein formula for allergic colitis
b.i.d.q.i.d. ICD9
Antibiotic therapy: Ciprofloxacin 20 mg/kg/day PROGNOSIS r 009.0 Infectious colitis, enteritis, and gastroenteritis
r Infectious: Most are self-limited. Can be r 555.9 Regional enteritis of unspecified site
IV/PO divided b.i.d. 5 days, max 500 mg/dose,
OR metronidazole 30 mg/kg/day PO divided remitting/relapsing or more indolent. Highest risk of r 558.9 Other and unspecified noninfectious
b.i.d 10 days, max single dose 500 mg death is severe dehydration.
r IBD: High morbidity; most patients experience gastroenteritis and colitis
Immunomodulators: For example, infliximab
prescribed by gastroenterologists (NOT usually recurring disease. Death is a rare complication.
in the emergency department) PEARLS AND PITFALLS
r Perianal disease, small intestine disease, and/or skip
lesions all strongly suggest CD.
r C. difficile colitis can strongly mimic IBD and must
be ruled out.
177
COLLAGEN VASCULAR DISEASE

Sudha A. Russell
PATHOPHYSIOLOGY r Isolated findings may be important clues to the

BASICS r CVDs are characterized by autoimmune responses. diagnosis:
Normally, the immune system does not respond to A pericardial friction rub with orthopnea indicates
DESCRIPTION components of the body, only to nonself molecules JIA, SLE, or PAN.
r Collagen vascular diseases (CVDs) are a complex such as viruses, bacteria, and other foreign tissue. Persistent oral mucosal lesions are found in
group of multisystem disorders resulting from In CVDs, the tolerance to self molecules is lost, and Behcet disease and SLE.
autoimmune processes causing inflammation of the the immune response is directed at self molecules. Conjunctival injection could be episcleritis of SLE,
target organs. They are also defined as rheumatic r Disease susceptibility and severity are influenced by conjunctivitis of KD, or uveitis of JIA.
and connective tissue diseases. certain genetic factors and cellular recognition Joint complaints suggest arthritis, but SLE,
r CVDs affect many different organs, so they must be (especially T lymphocytes) (2). dermatomyositis, and MCTD (with muscle
considered for a wide range of syndromes and r Cells release inflammatory cytokines including tumor weakness) can also present with arthritis.
therefore present diagnostic and therapeutic necrosis factor alpha, interleukin (IL)-1, and IL-6, Focal neurologic deficits, muscle weakness, and
dilemmas in children (1,2). causing tissue damage. B lymphocytes produce seizures are seen in SS and PAN.
r Because specific diagnostic tests for CVDs are excessive antibody. Normal cells in target organs Rashes are common; erythema nodosum may
unavailable emergently, the emergency department can be destroyed by complement-mediated cytolysis. indicate IBD, sarcoidosis, and Sjogren syndrome
evaluation is often focused on excluding diagnoses r Cytokines appear to induce cortisol production, (7).
that cause similar symptoms (eg, malignancy and suppressing cellular and humoral immunity. Defects Tortuous nailfold capillaries or distal fingertip
infection). in these pathways may amplify the immune pitting is very suggestive of an underlying CVD,
r An immature skeleton, variable hormonal influences, response (2). particularly SS.
immature immune system, and genetic expression r Female sex hormones augment cellular immune Raynaud phenomenon is noted in diseases such
modify expression of rheumatic disease in children. as SS, SLE, overlap syndrome, undifferentiated
responses, which may increase the incidence of
r Specific diagnosis may take months, and rarely rheumatic diseases in females.
connective tissue disorders, or MCTD.
years, after the initial presentation. DIAGNOSTIC TESTS & INTERPRETATION
r Juvenile idiopathic arthritis (JIA), systemic lupus ETIOLOGY
Emergency department diagnosis of CVD may not be
The etiology is unknown.
erythematosus (SLE), Kawasaki disease (KD), Lyme possible, as specific findings may take months or even
disease, Henoch-Schonlein purpura (HSP), years to develop. The following tests may be done
dermatomyositis, and inflammatory bowel disease DIAGNOSIS selectively.
(IBD) are discussed in specific topics. Lab
r Diagnoses described in this topic are: HISTORY
r Fevers, arthralgias, weakness, facial rash, dry skin, Lab workup in the emergency department should be
Systemic scleroderma (SS) causes a hardening of aimed at differentiating the far more common urgent
the skin and subcutaneous tissues. Raynaud phenomenon, mucocutaneous
and emergent traumatic and infectious complaints
Polyarteritis nodosa (PAN) causes necrotizing inflammation, chest pain, muscle weakness, and
from CVD or malignancy.
inflammation of small- and medium-sized arteries. back pain
Sjogrens syndrome is associated with lymphocytic r Duration of symptoms at the time of diagnosis is Initial Lab Tests
r Serial inflammation labs: CBC, ESR, and C-reactive
infiltration of exocrine glands. quite variable (5).
r Fever, malaise, and myalgias may be complaints in protein are useful in the emergency department to
Mixed connective tissue disease (MCTD) is a
screen for infection vs. CVD. Infections typically
generalized disorder with overlapping clinical PAN.
r Dry eyes and mouth can indicate Sjogren syndrome. cause transiently high ESR, but CVDs cause
features of other CVD.
r Recurrent buccal apthous and genital ulcers and persistently high values.
Behcet disease and Wegener granulomatosis
A normal ESR does not exclude a CVD diagnosis
(WG) are vasculitides that are rare in children. uveitis with hypopion suggest Behcet disease.
r CVD is a complicated topic, and the reader is (5).
r A persistent dry cough may be the earliest symptom r Urinalysis to detect proteinuria and hematuria,
encouraged to peruse the Additional Readings of SS. associated with SLE and vasculitis
section for more information on these diseases. r Raynaud phenomenon may be a primary disorder or r The antinuclear antibody (ANA) test is positive in
EPIDEMIOLOGY due to SS, SLE, MCTD, and overlapping rheumatoid certain syndromes:
Prevalence syndromes (1,6). All patients with MCTD, 90% of patients with
r Pediatric rheumatic conditions are relatively rare, r Abnormal gait may indicate JIA, SLE, other arthritis,
SS, 67% with Sjogren syndrome, and >90% with
affecting <0.5% of children in the U.S. dermatomyositis, or orthopedic problems. SLE (2,6,7)
r Conditions that must be distinguished from CVDs, r Inability to walk is an emergent condition and may However, a positive ANA can be found in
however, are prevalent: 20% of urgent pediatric be a sign of acute decompensation due to SS or PAN. nonrheumatic diseases and with certain drugs
visits involve musculoskeletal complaints. (eg, phenytoin and procainamide).
r 300,000 children in the U.S. have CVD: PHYSICAL EXAM
r General appearance: Follow-Up Lab Tests
85,000 have arthritis: Systemic JIA, psoriatic r Most of the evaluation may be done in the
Depressed affect suggesting psychiatric disease
arthritis, polyarthritis, oligoarthritis, and rather than CVD outpatient setting by the primary care provider. Early
enthesitis-related including ankylosing spondylitis Lack of, or abnormal, movement may be due to diagnosis is now more likely due to new tests:
(AS) muscle weakness, arthritis, CNS disease, or Immunologic labs such as CH50 , C3, and C4 are
25,000 have SLE (3). skeletal abnormality. low in SLE and vasculitis syndromes.
The rest have the other CVDs. r 90% of patients with PAN will have a mild to Lactate dehydrogenase may be elevated in CVD,
moderate elevation of BP. but marked elevations indicate malignancy.
RISK FACTORS
r Genetic predisposition, in association with the The presence of anti-Scl 70 antibodies is more
commonly associated with SS.
presence of certain multiple HLA and other genetic
The presence of specific antibodies to Sjogren
alleles, has been noted.
r Family history of CVD syndromerelated antigens (7)
r Environmental factors such as blood transfusions, Antineutrophilic cytoplasmic antibody in WG (8)
A high titer of anti-U1-RNP antibodies is critical in
smoking, and ultraviolet light exposure (4) the diagnosis of MCTD.
r Female gender
An association with HLA-B5, and HLA-B51 is clear
in Behcet disease.
r Consider appropriate tests to rule out the other
causes of symptoms.
178
COLLAGEN VASCULAR DISEASE
Imaging
r Chest radiographs may show:
Issues for Referral
r Stable patients can be given a referral for outpatient
REFERENCES
Increased reticulation or a honeycombed rheumatology but should have prompt follow-up by 1. DeSilva TN, Kress DW. Management of collagen
appearance in SS a primary care provider and/or subspecialist. vascular diseases in childhood. Dermatol Clin.
Globular enlargement of the cardiac silhouette is r Refer patients to a center with: 1998;16(3):579592.
seen in PAN. Pediatric rheumatology 2. Silverberg NB, Paller AS. Collagen vascular diseases
r Bone scan and MRI with gadolinium may reveal Other subspecialists as needed for anticipated in children. Curr Probl Dermatol. 2000;12(4):
joint findings and may be done in the inpatient or complications of the disease 177182.
outpatient setting. Physical therapy and nutritionists 3. Arthritis Foundation Disease Center database
2009.
C
Diagnostic Procedures/Other COMPLEMENTARY & ALTERNATIVE
ECG is necessary in patients with SS and PAN: 4. Bengtson AA, Rylander L, Hagmar L, et al. Risk
THERAPIES
r Pulmonary HTN may cause ventricular hypertrophy. r Sun avoidance and protection factors for developing systemic lupus
r Cardiac involvement in PAN may show ST r Physical therapy erythematosis: A case control study in southern
r Psychosocial therapy Sweden. Rheumatology. 2002;41:563571.
depression and inverted T waves (6).
r Keep hands warm with polyester, plastic, or 5. Adib N, Hyrich K, Thornton J, et al. Association
DIFFERENTIAL DIAGNOSIS between duration of symptoms and severity of
Malignancy, infection, muscular dystrophies, viral sheepskin gloves during cold exposure for Raynaud diseases at first presentation to paediatric
myositis, school phobias, postinfectious reactive phenomenon (1). rheumatology. Rheumatology. 2008;47(7):
r Biofeedback training may help decrease the
arthritis, traumatic arthritis, torn meniscus, 991995.
hemarthrosis, osteochondritis, Legg-Calve-Perthes, frequency of Raynaud syndrome attacks (2). 6. Callen JP. Collagen vascular diseases. J Am Acad
r Nutritional evaluation and guidance
osteomyelitis, neuropathy, and periodic fever Dermatol. 2004;51(3):427439.
syndromes 7. Fox RJ. Sjogrens syndrome. Lancet. 2005;366:
FOLLOW-UP 321331.
8. Akikusa JD, Schneider EA, Harvey D, et al. Clinical
TREATMENT FOLLOW-UP RECOMMENDATIONS features and outcome of pediatric Wegeners
INITIAL STABILIZATION/THERAPY Discharge instructions and medications: granulomatosis. Arthritis Rheum. 2007;57(5):
r The complexity and the systemic nature of CVD r 12 day follow-up for patient reassessment and to 837844.
should be kept in mind when such patients present make appropriate referrals
to the emergency department. PROGNOSIS ADDITIONAL READING
r If the patient is unstable, support the ABCs. r CVDs have a variable course, and findings at
r An integrated multisystem approach (eg, r Furst DE, Breevald FC, Kalden JR, et al. Updated
presentation are usually not predictive.
rheumatology, immunology, and orthopedics) is r The course of CVD varies from mild disease with few consensus statement on biological agents for the
recommended for patients with CVD. complications to multiorgan disease leading to treatment of rheumatic diseases, 2007. Ann Rheum
death (eg, PAN, SS). Dis. 2007;66(Suppl 3):iii2iii22.
MEDICATION r Wagener JS, Soep JB, Hay TC. Collagen vascular
r Arthralgia and myalgia are generally treated with r Sjogren syndrome develops and progresses slowly
but has an increased risk of lymphoma. disorders. In Taussig LM, Landau LI, eds. Pediatric
salicylates or NSAIDs (2).
r Corticosteroids (oral and/or IV) used early in the r Patients with MCTD have milder symptoms and Respiratory Medicine. 2nd ed. Philadelphia, PA:
Mosby; 2008:693703.
course of these diseases may help attenuate fewer complications than other CVDs.
inflammation (2,6). COMPLICATIONS
r Artificial tears, oral lozenges, and fluids in patients r Raynaud phenomenon can be severe enough to lead
with Sjogren syndrome may be used to limit damage
CODES
to gangrenous changes that can lead to
from decreased secretions (7). autoamputation or osteomyelitis of the digits.
r In PAN, mild to moderate HTN is treated with r Pulmonary HTN and fibrosis is seen in SS with ICD9
r 446.0 Polyarteritis nodosa
diuretics, hydralazine, and beta-blockers. respiratory decompensation. r 446.20 Hypersensitivity angiitis, unspecified
r Cyclophosphamide and methotrexate are needed for r Pulmonary hemorrhage and upper airway r 710.1 Systemic sclerosis
life-threatening illness; cyclosporin can also be used. obstruction is seen in PAN. r 710.9 MCTD
r Cutaneous nodules in PAN may ulcerate and are at
DISPOSITION r 714.0 Rheumatoid disease
Admission Criteria risk of infection.
r Inpatient admission should be considered when r Enlarging granulomas in WG can disrupt local
immediate subspecialty care is needed. anatomy, causing orbital invasion or deafness. PEARLS AND PITFALLS
r Unstable patients (eg, hypertensive encephalopathy r Pericarditis is seen in PAN and SS.
r Blindness is seen in Behcet disease due to posterior r Sjogren syndrome patients have greater problems
or CHF in PAN)
r Critical care admission criteria: uveitis. with corticosteroids, including acceleration of
Unstable patients (eg, severe HTN with r Renal complications may gradually lead to chronic periodontal disease and thrush (7).
renal failure in SS, PAN, and Behcet. r PAN may present with acute scrotal pain and
encephalopathy or CHF in PAN) should be
admitted to the ICU. purpura with dysuria.
r Behcet disease may mimic numerous other
Discharge Criteria
r Well appearing and in no distress conditions seen commonly in the emergency
r Acute symptoms controlled in the emergency department and should be considered when
appropriate.
department r WG may present as an orbital pseudotumor or
r Reliable follow-up
severe sinusitis (8).
179
COMPARTMENT SYNDROME
Michael L. Epter

BASICS r Extrinsic (exert pressure on the compartment):
Lab
Pressure dressing r No lab investigation is required to diagnose
DESCRIPTION Casts (circumferential) compartment syndrome.
r Compartment syndrome is a surgical emergency. Burn eschar r Complications resulting from muscle necrosis may
r Most commonly associated with trauma, specifically Intramuscular hematoma warrant the following:
fractures: Limb compression Creatine phosphokinase
Tibia r Intrinsic (increased volume of compartment
Urinalysis
Supracondylar space): Electrolytes
Forearm Fracture (open is more common than closed) Renal function
Wrist Reperfusion after ischemia
r The anterior compartment of the lower leg is most Vascular injury Imaging
Thrombosis Indicated for suspected fracture
commonly affected.
r Diagnosis is challenging in the pediatric population Burns Diagnostic Procedures/Other
Hereditary bleeding disorders r Measurement of compartment pressures:
because of difficulty in assessing compartment
pressures, communication, cooperation, and poor Snake and spider bite/envenomation Consider analgesia or sedation
reliability of physical exam (eg, 2-pt discrimination). Viral infection (influenza, enterovirus) Options available: Slit catheter, wick catheter,
r Keys to ensuring good outcome: Sepsis (arthritis, meningococcemia) needle manometer, arterial line,
High clinical suspicion Allergic reaction intracompartmental pressure monitor (eg, Stryker,
Early surgical/orthopedic consultation Iatrogenic: Stryker Instruments, Kalamazoo, MI)
Intraosseous infusion r Stryker technique (used most often):
Measurement of compartment pressures
Prompt surgical decompression IV infiltration (especially in ICU patients) Aseptic preparation
Local anesthetic (eg, lidocaine): Only SC (IM will
RISK FACTORS COMMONLY ASSOCIATED CONDITIONS
r Fractures cause false positive)
Trauma
18-gauge needle attached to the monitor
r Crush injuries +/ fractures (hand/foot)
Enter into compartment adjacent to area of
r Excessive exercise DIAGNOSIS greatest pressure.
r Hypotension, especially low diastolic BP Ensure placement into the compartment by
HISTORY squeezing the muscle and/or passively stretch the
GENERAL PREVENTION History of any of the following: muscle (causes transient increase in pressure).
Avoid compressive casts in fracture management. r Trauma Inject <1 cc saline.
PATHOPHYSIOLOGY r Fever/Infection Take multiple pressures.
r Increased intracompartmental pressure impaired r Coagulopathy Record the highest pressure for determining the
perfusion disruption of skeletal muscle r IV/IM medications need for fasciotomy.
metabolism cytolysis increase in fluid from r Suspected abuse
plasma to interstitium further increase in r Persistent pain with increasing analgesic ALERT
r Tissue pressure should be measured within 5 cm
pressure compromised blood supply/nerve
requirement of the zone of maximum pressure (injury site) to
conduction: r Apprehension, crying, agitation, inability to console
Sensory nerves: C fibers (most susceptible) > avoid false negatives.
motor nerves/muscles > fat > skin (least PHYSICAL EXAM r Intracompartmental pressures:
susceptible) r May be unreliable due to confounding factors: Fixed values are more applicable for
r Muscle injury (can be irreversible) rhabdomyolysis If equivocal measure compartment pressures unconscious patients:
myoglobinuria renal failure r 6 Ps: <1012 mm Hg: Normal pressure
Pain: >20 mm Hg: Compromised capillary flow
Disproportionate to physical exam 3040 mm Hg: Risk of ischemic necrosis of
Pressure (pain on palpation): muscles/nerves
Pain with passive stretch
Compartment may or may not be tense.
Paresthesias:
Loss of 2-point discrimination (early)
Paresis
Pallor
Pulselessness (late and not reliable):
Shiny, erythematous skin
Swelling (may or may not be present)
Consider measuring circumference of extremity
180
COMPARTMENT SYNDROME
Pathological Findings Issues for Referral ADDITIONAL READING

Muscle necrosis All patients who are sent home with fractures and/or
soft tissue injuries (eg, crush) should be referred to r Choi PD, Rose RK, Kay RM, et al. Compartment
DIFFERENTIAL DIAGNOSIS syndrome of the thigh in an infant: A case report.
r Arterial insufficiency/occlusion their primary care provider within 24 hr to assess for
r Thrombophlebitis development of compartment syndrome. J Orthop Trauma. 2007;21(8):587590.
r Elliott KG, Johnstone AJ. Diagnosing acute
r Myositis/Fasciitis
compartment syndrome. J Bone Joint Surg Br.
r Lymphangitis FOLLOW-UP 2003;85(5):625632.
r Cellulitis r Grottkau BE, Epps HR, Di Scala C. Compartment
r Osteomyelitis FOLLOW-UP RECOMMENDATIONS
r Discharge instructions and medications: syndrome in children and adolescents. J Pediatr
C
Patients who sustain traumatic/soft tissue injury Surg. 2005;40(4):678682.
r Perron AD, Brady WJ, Keats TE. Orthopedic pitfalls in
TREATMENT must be given strict instructions to return to the
emergency department for any new or worsening the ED: Acute compartment syndrome. Am J Emerg
symptoms (eg, increasing pain, paresthesias, Med. 2001;19(5):413416.
INITIAL STABILIZATION/THERAPY r Ramos C, Whyte CM, Harris BH. Nontraumatic
r Correct extrinsic factors, if applicable (eg, swelling).
cast/dressing removal). Pain control as appropriate. Use caution with compartment syndrome of the extremities in
r Elevate affected limb to the level of the heart. opioids, as these may mask signs of compartment children. J Pediatr Surg. 2006;41(12):e5e7.
r Correct underlying hypotension. syndrome. See Also (Topic, Algorithm, Electronic
r Activity:
r Application of ice or raising the affected limb above Media Element)
Restrict activity that may increase pain/swelling. r Deep Vein Thrombosis
the heart will compromise circulation.
Patient Monitoring r Rhabdomyolysis
MEDICATION All patients with suspected compartment syndrome
r Pain control (eg, morphine 0.1 mg/kg IV/IM/SC PRN)
r Steroids/vasodilators have no proven benefit. with elevated pressures should be admitted for
observation: CODES
SURGERY/OTHER PROCEDURES r Serial physical exams +/ compartment pressures
r Emergent fasciotomy is the treatment of choice: should be performed given the evolving nature of ICD9
Indications: this syndrome. r 958.8 Other early complications of trauma
Clinical signs of compartment syndrome (most r Lab evaluation for rhabomyolysis should occur. r 958.91 Traumatic compartment syndrome of upper
important) extremity
PROGNOSIS
Pressure measurements (controversial): r 958.92 Traumatic compartment syndrome of lower
Absolute pressure >30 mm Hg Functional loss and complication rate are directly
proportional to the time to diagnosis and extremity
Delta pressure (diastolic BPcompartment
pressure) 30 decompression:
Differential pressure (mean arterial r Fasciotomy at 6 hr of establishing the diagnosis is
pressurecompartment pressure) 30 associated with a good recovery. PEARLS AND PITFALLS
r Prompt consultation with orthopedics/surgery r Poor clinical outcomes are expected if fasciotomies r Delayed diagnosis is more common when the cause
should be initiated once the diagnosis is suspected. are delayed >12 hr. of compartment syndrome is not related to fracture
r 110% of patients with compartment syndrome
and/or is complicated by altered mental status.
DISPOSITION develop Volkmann ischemic contracture. r Increasing analgesia/sedation requirement may be
Admission Criteria
COMPLICATIONS the only indicator of compartment syndrome.
Clinical signs/symptoms of compartment syndrome r Tissue necrosis r Lack of assessment of compartment pressures is the
with elevated pressure
r Infection most common factor associated with a missed
Discharge Criteria r Neurologic deficit diagnosis.
r No clinical signs/symptoms of compartment
r Delayed fracture healing (if applicable)
syndrome
r Normal pressures as determined by r Ischemic contracture
r Amputation
intracompartmental measuring device
r Rhabdomyolysis
r Hyperkalemia
r Acidosis
r Renal failure
181
CONCUSSION
Emily Schapiro

BASICS Usually involves blunt force trauma to the head: r Brain contusion
r Primarily associated with falls in younger children r Epidural and subdural hemorrhage
DESCRIPTION and contact sports in older children and teenagers r Skull fracture
r Concussion is any alteration in neurologic or r Other causes include motor vehicle accidents, r Cerebral edema/increased intracranial pressure
cognitive function after head trauma, with or pedestrian/auto accidents, biking accidents, r The differential for children with altered mental
without loss of consciousness (LOC). assaults, and child abuse.
r The term concussion is most frequently used to refer status includes:
Seizure with postictal state
to mild head injuries with little alteration in level of Intoxication
consciousness. DIAGNOSIS Hypoglycemia
r LOC, if present, is usually brief. There are usually no
HISTORY Central nervous system infection
focal deficits on neurologic exam. r A Sports Concussion Assessment Tool (2) may be
r Grading of concussion is no longer recommended
useful in detecting common and uncommon
(1,2). Rather, an individualized approach to the
symptoms:
TREATMENT
patients clinical presentation and needs is
Confusion PRE HOSPITAL
appropriate.
r Children who suffer a concussion may develop a Headache Attention to stabilizing airway, breathing, and
Nausea, vomiting circulation and cervical immobilization prior to
postconcussive syndrome in which symptoms of Dizziness
varying severity may persist for several months and transport
Blurred vision
may affect school performance: Fatigue INITIAL STABILIZATION/THERAPY
Symptoms may include headaches, confusion, Delayed verbal response r Every effort should be focused on minimizing the
difficulty concentrating, irritability, and mood Poor coordination possibility of secondary brain injury.
changes. Repetitive questioning r Attention to vital signs, perfusion, and oxygenation,
EPIDEMIOLOGY Sensitivity to light and noise as necessary
Drowsiness r If there is persistent vomiting, IV hydration and
Incidence
r It is estimated that there are >600,000 emergency Difficulty falling asleep administration of antiemetics, as needed
department visits for traumatic brain injuries in More emotional r Analgesics may be indicated.
children <18 yr of age annually in the U.S. (3). Irritability r A search should be done for other injuries.
r About 62,000 high school athletes experience Sadness r Evaluation of the cervical spine should be
concussions yearly, with 63% of these being Nervous or anxious performed:
r There may be retrograde and anterograde amnesia.
associated with football (4). If the patient is alert and there are no distracting
r There may or may not be a period of LOC.
RISK FACTORS injuries, the cervical spine may be cleared clinically.
r Brief seizure activity may be noted at the time of
r Impact sports, motor vehicle accidents, biking Otherwise, plain radiographs should be obtained.
injury.
accidents MEDICATION
r Age at time of injury (younger brains are more PHYSICAL EXAM r Ondansetron 0.1 mg/kg may be used for nausea
r Altered cognition is frequently present, even in and vomiting.
susceptible, and high school athletes are at greater
risk than college athletes) seemingly minor injuries. r Acetaminophen 1015 mg/kg up to 650 mg for
r History of previous concussion r There are usually no focal neurologic findings. headache
r Alcohol or drug intoxication r Search for signs of a basilar skull fracture such as r Try to avoid analgesics, such as opioids, that will
r Shaking impact syndrome mastoid or periorbital ecchymoses or alter the mental status.
hemotympanum.
GENERAL PREVENTION r Determine if the child has cervical spine tenderness DISPOSITION
r Safety equipment, such as helmets, during impact Admission Criteria
or ligamentous laxity.
sports and biking Critical care admission criteria:
r Safety education DIAGNOSTIC TESTS & INTERPRETATION r Any patient with focal neurologic findings, unstable
Lab vital signs, or significantly abnormal findings on CT
PATHOPHYSIOLOGY Initial Lab Tests
r Concussion is on the continuum of traumatic brain should be admitted to the ICU for close observation.
No routine lab testing is recommended in most r Children with persistently severe headaches or
injury ranging from mild to severe. concussive injuries.
r Rotational and shearing forces cause axonal injury intractable vomiting should be admitted to the
and disruption of the electrophysiologic activities of Imaging general ward.
r The decision to image the brain is multifactorial:
neurons. Discharge Criteria
r Cerebrovascular autoregulation and alterations in The mechanism of injury, patients signs and r Most children with a concussion do not require
cerebral metabolism have been shown in concussed symptoms, physician experience, parent comfort hospitalization.
animal models. level, and patient age are all factors used in r Patients with a relatively minor mechanism can be
r MRI may show evidence of brain contusion or making the decision to obtain a head CT. safely discharged home.
r Patients with altered mental status and signs of r Obtaining a head CT is not necessary prior to
diffuse axonal injury even in the presence of normal
CT imaging. skull fracture have an increased risk of abnormal discharge if the child does not meet criteria for
r Neuropsychological testing may reveal abnormalities findings on head CT. having a head CT.
r If the patient has a normal mental status, no
in cognition for up to a week even in minor
concussions: evidence of skull fracture, and a nonfocal exam, CT
These abnormalities persist for longer periods with is not recommended in the absence of persistent
more severe injury. vomiting, severe mechanism of injury, persistent
Younger children have a higher risk for persistent severe headache, or worsening symptoms (4).
symptoms.
Amnesia for the event at the time of presentation
is also a risk factor for persistent symptoms.
182
CONCUSSION
Issues for Referral COMPLICATIONS

r Anticipatory guidance and education concerning r Some patients develop postconcussive syndrome CODES
concussion and postconcussion syndrome with symptoms of confusion, poor concentration,
r Follow-up with a neurologist for neuropsychological headaches, depression, and poor school ICD9
testing is indicated if symptoms persist beyond performance that may persist for weeks to months. r 850.0 Concussion with no loss of consciousness
r Second impact syndrome is a rare and poorly r 850.11 Concussion, with loss of consciousness of
7 days.
understood phenomenon that has been observed in 30 minutes or less
COMPLEMENTARY & ALTERNATIVE some athletes who have suffered a second injury r 850.12 Concussion, with loss of consciousness from
THERAPIES
r Neuropsychological testing should be performed for soon after an initial concussion (6):
Presumably, altered cerebrovascular
31 to 59 minutes C
those with persistent symptoms: autoregulation from the initial event leads to a
Ideally, young athletes should have baseline, catastrophic response with the 2nd insult, which
preconcussion testing performed before the sports PEARLS AND PITFALLS
can lead to sudden death (4,6).
season begins (5). r Most children who sustain a concussion do not have
r The optimal timing of testing is unknown, as
an associated LOC.
neurocognitive findings may be worse a week after REFERENCES r Grading of concussion as simple or complex is no
the injury. longer recommended.
1. Erlanger D, Kaushik T, Cantu R. Symptom-based
r Most children will have resolution of concussive
assessment of the severity of a concussion. J
FOLLOW-UP Neurosurg. 2003;98:477484. symptoms within 7 days of the injury.
r Most children with a concussion do not have an
2. McCrory P, Meeuwisse W, Johnston K, et al.
FOLLOW-UP RECOMMENDATIONS Consensus Statement on Concussion in Sport; 3rd associated intracranial hemorrhage.
r Discharge instructions and medications: r After a concussion, a postconcussive syndrome
International Conference on Concussion in Sport.
Discharge instructions should include signs and November 2008. Clin J Sport Med. involving neuropsychiatric changes may result.
symptoms of progressing injury and specific 2009;19:185195. r Recommendations to avoid contact sports after
instructions for when to return to the emergency concussion are used to prevent morbidity and
3. Kupperman N, Holmes JF, Dayan PS, et al.
department. mortality due to second impact syndrome.
Identification of children at very low risk of
Anticipatory guidance is important, as many
clinically-important brain injuries after head
patients with even mild concussions may have
trauma: A prospective cohort study. Lancet.
persistent symptoms for days to months
2009;374(9696):11601170.
(postconcussive syndrome).
r Activity: 4. Powell JW, Barber-Foss KD. Traumatic brain injury in
high school athletes. JAMA. 1999;282:958963.
Rest and gradual return to activity are essential in
patients who have been concussed because of the 5. Guskiewicz KM, Bruce SL, Cantu RC, et al. National
concern that the concussed brain is more Athletic Trainers Association Position Statement:
susceptible to repeat injury. This may be Management of Sport-Related Concussion. J Athl
particularly true in younger patients. Train. 2004;39:280282.
A number of guidelines have been developed to 6. Guskiewicz KM, McCrea M, Marshall SW, et al.
help determine the timing of the return of athletes Cumulative effects associated with recurrent
to their sports activities safely. concussion in collegiate football players: The NCAA
Return to activity must be individualized, but in concussion study. JAMA. 2003;290:25492555.
general the patient should be asymptomatic for at
least 1 wk before return to sports (2). Response to
exercise should be monitored closely.
Cognitive rest may be necessary for some children.
Activities such as attending school, watching
television, or using computers may cause
symptoms may need to be avoided for days or
weeks after a concussion.
183
CONGENITAL ADRENAL HYPERPLASIA

Shilpa Patel
Dewesh Agrawal

BASICS r Endocrinology: r Classic severe salt-wasting 21OHD presents with:
21OH is a cytochrome p450 enzyme that is Hypotension
DESCRIPTION responsible for converting Shock
r Congenital adrenal hyperplasia (CAH) represents a 17-hydroxyprogesterone (17-OHP) to Hyponatremia
group of autosomal recessive disorders resulting in a 11-deoxycortisol, a precursor of cortisol, as well as Hyperkalemia
deficiency of 1 of 5 enzymes necessary for cortisol progesterone to 11-deoxycorticosterone, a Hypoglycemia
synthesis: precursor of aldosterone. Metabolic acidosis
9095% are 21-hydroxylase deficiency (21OHD) Cortisol deficiency leads to hypoglycemia and Hypothermia
5% are 11-hydroxylase deficiency (11-OHD) hypotension. Altered sensorium
<5% are 3-hydroxysteroid dehydrogenase At the pituitary gland, there is a lack of negative Dehydration
deficiency (3-HSD), 17-hydroxylase deficiency, feedback normally provided by cortisol, resulting Abnormal genitalia:
and 20,22-desmolase deficiency. in increased adrenocorticotropin hormone (ACTH) Ambiguous genitalia in a genotypic female with
r This topic focuses on 21OHD because it makes up production, secondary adrenal hyperplasia, and a large clitoris, rugated and partly fused labia
9095% of CAH. shunting of adrenal hormone enzymatology to majora, and common urogenital sinus in place
r CAH caused by 21OHD is characterized by cortisol produce excess androgens. of a separate vagina and urethra
deficiency, with or without aldosterone deficiency r Genitourinary: Androgen excess causes virilization A severely virilized female may have been
and androgen excess: of the external genitalia beginning in utero. incorrectly classified as male and therefore could
There are three typical presentations of 21OHD r Nephrology: Aldosterone deficiency results in the have what appears to be a normal phenotypic
(see History section): inability to reabsorb sodium and excrete potassium male appearance without palpable gonads.
Classic severe salt wasting in the renal tubules, thus leading to hyponatremia, A genotypic male may have a large penis and
Classic simple virilizing hyperkalemia, and hyperreninemia (lack of negative subtle hyperpigmentation.
Nonclassic feedback to the renin-angiotensin-aldosterone r Classic simple virilizing 21OHD presents with:
system). Premature puberty: Pubic hair, body odor, acne,
EPIDEMIOLOGY
and rapid linear growth
Incidence ETIOLOGY Hirsutism, clitoromegaly, and virilization are noted
r Classic 21OHD occurs in 1:15,000 of live births A family of autosomal recessive disorders of adrenal in females.
worldwide, but incidence varies according to steroidogenesis leading to a deficiency of cortisol Premature isosexual development is noted in
geographic area and ethnicity: production males with hyperpigmentation and phallic
75% is classic severe salt wasting. enlargement, usually with small testes.
25% is classic simple virilizing. r Nonclassic 21OHD usually presents with:
r Data on the incidence of nonclassic 21OHD is DIAGNOSIS
Females: Acne, hirsutism
lacking because neonatal screening does not HISTORY Males: Acne, large penis with small testes
accurately detect it. r Classic severe salt-wasting 21OHD presents within
Prevalence the 1st 4 wk of life with:
r Nonclassic 21OHD occurs in 1:1,000 of the Lethargy, decreased activity, or fatigue Lab
general Caucasian population. Prevalence varies Unresponsiveness Typical findings of classic severe salt-wasting 21OHD
according to ethnicity with a rate as high as 3% in Poor feeding/weak suck include hyponatremia, hyperkalemia, hypoglycemia,
those of Ashkenazi Jewish decent and people of Vomiting and/or metabolic acidosis.
Yugoslavian heritage. Dehydration Initial Lab Tests
r Nonclassic 21OHD is much more common than Failure to thrive r Stat tests:
classic 21OHD and is thought to be the most Seizures Serum glucose
common autosomal recessive disorder. r Classic simple virilizing 21OHD presents in Serum sodium
childhood with: Serum potassium
GENERAL PREVENTION Precocious pubarche Serum bicarbonate
r Genetic counseling for parents who have CAH may
Rapid growth acceleration and adult short stature pH
result in an early prenatal diagnosis. secondary to early skeletal maturation If there is a known diagnosis of CAH, no further
r Obstetricians may consider prenatal treatment with diagnostic labs are necessary.
Virilization in females
dexamethasone during the 1st trimester for fetuses r Nonclassic 21OHD presents in adolescence or r Emergent labs in order of importance (before
at a high risk of having CAH in order to minimize the adulthood: treatment with steroids if possible) to accurately
degree of virilization. Females usually present with acne, menstrual diagnose the cause if diagnosis is unknown:
r Screening: Serum cortisol level, 17-OHP, and ACTH
irregularities (oligomenorrhea or infertility), and
Neonatal screening is present in all U.S. states and hirsutism. Plasma renin and aldosterone
territories for classic 21OHD (1). In males, acne may be the only presenting Urine sodium and potassium
There is a high rate of false positives, especially in symptom. Imaging
sick or preterm infants.
Pelvic US to visualize internal reproductive organs and
ALERT adrenal glands can be done at a later time and is not
Failure to maintain a high index of suspicion for necessary emergently.
CAH in any ill-appearing vomiting infant can lead to
a delay in treatment with a subsequent increase in
morbidity and mortality.
184
CONGENITAL ADRENAL HYPERPLASIA
r Electrolyte correction is usually not necessary, as

r Classic 21OHD is characterized by markedly elevated
REFERENCES
electrolytes should normalize with steroid
17-OHP and low basal cortisol (<10 g/dL). In administration. However, if hyperkalemia is severe, 1. National Newborn Screening Status Report.
infants with classic 21OHD, basal levels of 17-OHP there are ECG changes, or there is renal Updated 11/29/10. National Newborn Screening
are often >10,000 ng/dL (normal levels <100 insufficiency: and Genetics Resource Center. Available at
ng/dL). Patient should be placed on a continuous cardiac http://genes-r-us.uthscsa.edu/nbsdisorders.pdf.
r In consultation with an endocrinologist, an ACTH monitor. 2. Speiser P, White P. Congenital adrenal hyperplasia.
stimulation test may be done as an outpatient or Treat hyperkalemia. (See Hyperkalemia topic.) N Engl J Med. 2003;349(8):776788.
r In a patient previously diagnosed with 21OHD, stress
inpatient once the patient has been stabilized in the
emergency department. dosing is required for an acute illness or procedure
3. Consensus Statement on 21-Hydroxylase Deficiency
from the Lawson Wilkins Pediatric Endocrine
C
r Karyotype to determine genotypic sex can be sent (severe illness such as fever 38 C, vomiting, Society and the European Society for Paediatric
once the patient is stable. diarrhea, lethargy, surgery, trauma, dental work): Endocrinology. J Clin Endocrinol Metab.
Give 2 to 3 times the regular dose per day IV 2002;87:40484053.
DIFFERENTIAL DIAGNOSIS divided t.i.d. or per the consensus guidelines (3):
r Classic severe salt-wasting 21OHD: 4. Gmyrek GA, New MI, Sosa RE, et al. Bilateral
<3 yr: 25 mg followed by 2530 mg/day laparoscopic adrenalectomy as a treatment for
Formula intolerance 312 yr: 50 mg followed by 5060 mg/day congenital adrenal hyperplasia attributable to
Gastroenteritis/Dehydration >12 yr: 100 mg followed by 100 mg/day 21-hydroxylase deficiency. Pediatrics.
Pyloric stenosis r For an infant presenting in acute adrenal 2002;109(2):e28.
Sepsis and septic shock
(addisonian) crisis, it is important to monitor BP,
CHF
electrolytes, and response to therapy.
Inborn error of metabolism ADDITIONAL READING
Methemoglobinemia Second Line
Infantile botulism The goal of maintenance therapy for classic severe r Antal Z, Zhou P. Congenital adrenal hyperplasia:
Nonaccidental head trauma salt-wasting 21OHD is to suppress adrenal androgen Diagnosis, evaluation and management. Pediatr
Acquired adrenal insufficiency secretion enough to prevent virilization; optimize Rev. 2009;30(7):e49e57.
CAH: 3-HSD growth; and protect potential fertility by the r Merke D, Bornstein S. Congenital adrenal
Poisoning administration of daily glucocorticoid, hyperplasia. Lancet. 2005;365:21252136.
r Classic simple virilizing 21OHD: mineralocorticoid, and salt supplementation. r Shulman DI, Palmert MR, Kemp SF; Lawson Wilkins
Precocious puberty SURGERY/OTHER PROCEDURES Drug and Therapeutics Committee. Adrenal
Virilizing tumor r Bilateral adrenalectomy may be indicated for insufficiency: Still a cause of morbidity and death in
CAH: 11-OHD individuals with classic 21OHD who have a history of childhood. Pediatrics. 2007;119(2):e484e494.
r Nonclassic 21OHD:
poor control with hormonal replacement therapy (4).
Polycystic ovarian syndrome r Genotypic females who are virilized at birth may
require feminizing genitoplasty, if the family decides CODES
to raise the infant as a female. This surgery is
TREATMENT controversial, and there is much debate regarding ICD9
PRE HOSPITAL the timing of the procedure, though historically it 255.2 Adrenogenital disorders
Rapid clinical recognition and correction of was recommended between 2 and 6 mo of age (2).
hypotension and hypoglycemia: Issues for Referral PEARLS AND PITFALLS
r IV fluid bolus for hypotension r Patients should be followed by pediatric
r Check glucose level, and treat if hypoglycemic. endocrinology. r Consider CAH in any infant who presents with
r Those with ambiguous genitalia will likely need a severe vomiting or shock in the 1st few weeks of life.
INITIAL STABILIZATION/THERAPY surgical/urologic and psychological evaluation. r CAH may be missed if newborn screen results are
r Rapid fluid resuscitation with isotonic saline to treat r Parents should be referred for genetic counseling. still pending or if genitalia are not noticeably
hypotension and hypovolemia ambiguous (male infants).
r Administration of glucose as necessary to correct r The 4 rare causes of CAH (see Description section)
hypoglycemia FOLLOW-UP are not routinely tested in every state as part of
MEDICATION FOLLOW-UP RECOMMENDATIONS neonatal screening and thus may be missed.
r Severe hyponatremia may be delayed in the classic
First Line Patients should be instructed to wear a bracelet
r Administration of high-dose stress steroids after stating they have adrenal insufficiency with their severe salt-wasting form and therefore not as
obtaining the aforementioned labs: normal required stress steroid dose determined by apparent on presentation in the 1st 2 wk of life.
Hydrocortisone 5075 g/m2 IV once followed by their endocrinologist.
hydrocortisone 100 g/m2 IV divided q.i.d. for Patient Monitoring
2448 hr until the acute stressed phase has In treated individuals, 17-OHP levels will remain
passed higher than normal, though renin levels should return
Treatment should not be withheld if the diagnosis to normal for age.
is known or suspected.
PROGNOSIS
Most individuals live relatively normal lives on lifelong
steroid replacement.
COMPLICATIONS
r Refractory shock
r Hypoglycemic/Hyponatremic seizures
r Intractable hyperkalemia and arrhythmias
185
CONGENITAL HEART DISEASE

Calvin G. Lowe

BASICS r The exact cause of CHD is unknown.
Lab
r Some factors are associated with an increased risk r Serum electrolytes, calcium, glucose, and CBC:
DESCRIPTION of CHD: Maternal risk factors, chromosomal Electrolyte abnormalities (hyponatremia and
r Patients with congenital heart disease (CHD) present
abnormalities, and single gene defects hypochloremia) can occur.
with symptoms in 2 typical age groups: r A multifactorial etiology is a theoretical basis for calcium can present as prolongation of the QT
Ductal dependent lesions will present within the most forms of CHD. interval, CHF, hypotension.
1st mo of life (see Ductal Dependent Cardiac Hypoglycemia may also cause weakness and
Emergencies topic). COMMONLY ASSOCIATED CONDITIONS fatigue.
r 58% of children with CHD have an association
Left (L) to right (R) shunting lesions will present in Depending on the heart lesion, polycythemia
the 26 mo age range. with a chromosomal abnormality. (from chronic hypoxemia) or anemia (dilutional
r Undiagnosed CHD patients can present to the r Examples include trisomy 21 (Down syndrome),
effects) can be present.
emergency department in extremis at any age. trisomy 18, trisomy 13, Turner syndrome, cri-du-chat r A blood gas sample should be obtained to determine
r There are 35 types of CHD. syndrome, Wolf-Hirschhorn syndrome, the degree of hypoxemia and metabolic acidosis.
velocardiofacial syndrome, and/or DiGeorge r Cardiac enzymes, such as creatine phosphokinase
EPIDEMIOLOGY sequence and Williams syndrome.
Incidence r Single gene defects such as Marfan syndrome (CPK), the cardiac fraction (CPK-MB) as well as the
r CHD occurs in 8 per 1,000 live births within the troponins, specifically troponin T (cTnT) and troponin
Smith-Lemli-Opitz syndrome, Ellis-van Creveld, I (cTnI) may be helpful.
1st yr of life. Holt-Oram syndrome, Noonan syndrome, and the
r Incidence is the same among premature and term mucopolysaccharidoses are associated with CHD. Imaging
infants. Chest radiographic imaging is essential:
r Premature infants have a greater incidence of patent r The heart size in CHD can be small, normal, or large.
ductus arteriosus (PDA). DIAGNOSIS r Some types of CHD will show characteristic findings
r Parental or sibling history of CHD increases on chest radiography:
HISTORY
incidence to 16 per 1,000 live births. r Depending on the cardiac lesion, the age at The classic boot-shaped heart of TOF
Prevalence presentation will vary greatly: The 3 sign secondary to a prominent aortic
r The prevalence of CHD at birth ranges from 15 per PDA-dependent lesions will clinically manifest knob and poststenotic dilation of the descending
1,000 live births. within the 1st days of life. aorta is indicative of aortic coarctation.
r In North America, the observed prevalence of CHD Lesions that have a VSD may not become evident The snowman or figure of 8 sign is seen in
until 46 wk of age. supracardiac anomalous return.
in children rose from 6.88 per 1,000 people in 1985
to 11.89 per 1,000 in 2000. r Symptoms can vary from benign to CHF to shock. The egg on a string is seen in TGA.
r The most common presentations are acute Various degrees of ventricular hypertrophy and
RISK FACTORS pulmonary congestion will depend on the type of
respiratory distress and cyanotic episodes.
Maternal risk factors: r CHF (fatigue, poor appetite, and diaphoresis during CHD.
r Infection (rubella)
feeding, tachypnea, tachycardia, S3 heart sound, Diagnostic Procedures/Other
r Medication use (anticonvulsants, lithium) r Any suspected CHD should have a pediatric
hepatomegaly, pallor), failure to thrive (FTT),
r Drug abuse (ethanol) cardiology consult.
irritability, dehydration, and recurrent lung infections
r Disease states (phenylketonuria, insulin-dependent r An echo should be performed on patients suspected
are common signs and symptoms.
diabetes mellitus, systemic lupus erythematosus) of having CHD.
PHYSICAL EXAM r A 12-lead ECG should be obtained. Depending on
PATHOPHYSIOLOGY r General appearance and color is the most important
r CHD can be classified as either acyanotic or cyanotic the lesion, the ECG may show various arrhythmias,
part of the exam:
hypertrophy, R or L axis deviations, and bundle
lesions. Blue color indicates a cyanotic heart lesion and a
r Acyanotic lesions can be further classified as L to R branch blocks.
R to L shunt. r A hyperoxia test can differentiate between cyanotic
shunts or obstructive lesions: Grey color indicates outflow obstruction, systemic
hypoperfusion, and shock. cardiac and pulmonary disease. For a description of
L to R shunt lesions: Oxygenated blood from the L
r BP should be measured with an appropriate-sized the hyperoxia test, see the Cyanotic Heart Disease
side of the heart or aorta is shunted to the R heart
topic under Diagnostic Procedures/Other.
via an intra-arterial or intraventricular septal cuff:
defect or a PDA. BPs should be measured in both upper and lower DIFFERENTIAL DIAGNOSIS
The additional blood in the R side of the heart extremities. r In neonates, sepsis must be suspected prior to a
can increase the pulmonary blood flow and Lower extremity BP > upper extremity BP definitive diagnosis of CHD.
pulmonary BP. suggests aortic coarctation. r Dilated cardiomyopathy
The higher the degree of shunting, the greater r Tachycardia and tachypnea may be out of proportion r Myocarditis
the degree of symptoms. to the patients general appearance. r Supraventricular tachycardia
Lesions in this category include atrial septal r Cool skin and delayed capillary refill indicates shock r Arrhythmias
defect, ventricular septal defect (VSD), and PDA. from severe cardiac disease. r Hypoglycemia
Obstructive lesions result in blood flow r Absent or distal pulses suggest aortic arch r Structural heart disease
obstruction without shunting. A pressure gradient obstruction. r Persistent pulmonary HTN
evolves resulting in pressure overload proximal to r Assessment of hydration status, mucosal color,
the obstruction, resulting in ventricular r Apparent life-threatening event
auscultation of the heart and lungs, palpation of the r Pneumonia
hypertrophy and CHF.
r Cyanotic lesions cause varying degrees of R to L precordium, and a survey for organomegaly should r Inborn errors of metabolism
be performed.
shunting of deoxygenated venous blood: r Heart murmurs with or without thrills can suggest
Pulmonary blood flow may be , normal, or .
CHD.
>5 g/dL of deoxygenated hemoglobin in blood r Gallop rhythms may also be heard.
will result in clinical cyanosis. r CHF is a common presentation: Tachypnea,
Examples of cyanotic heart lesions include:
Tetralogy of Fallot (TOF), transposition of the great hyperactive precordium, chest congestion, and
arteries (TGA), tricuspid atresia, total anomalous hepatomegaly.
r Recognition of dysmorphic features consistent with
pulmonary venous return (TAVPR), and truncus
arteriosus. a genetic abnormality
186
CONGENITAL HEART DISEASE
DISPOSITION REFERENCE
r Any CHD patient with an O requirement over 1. Meckler GD, Lowe CG. To intubate or not to
2
INITIAL STABILIZATION/THERAPY baseline, acute respiratory distress, or worsening intubate? Transporting infants on prostaglandin E1.
r Immediate evaluation and treatment of the ABCs CHF not responsive to emergency department Pediatrics. 2009;123(1):e25e30.
and continuous pulse oximetry are crucial. therapy should be admitted.
Administer oxygen (O2 ) judiciously. r Patients with confirmed or symptomatic respiratory
Establish IV access: >1 site is recommended. syncitial virus should be admitted for observation.
ADDITIONAL READING
r Obtain blood and urine samples. r Critical care admission criteria: r Gewitsz MH, Woof PK. Cardiac emergencies. In
r Small, frequent IV boluses of normal saline or Any patient who is intubated and/or requiring Fleisher GR, Ludwig S, Herentig FM, eds. Textbook of
C
lactated Ringer solution of 10 cc/kg are indicated to vasopressor support should be promptly admitted Pediatric Emergency Medicine. 6th ed. Philadelphia,
treat hypotension. to a pediatric ICU (neonatal, pediatric, or PA: Lippincott Williams & Wilkins; 2010.
r 4 extremity BPs should be measured. cardiothoracic). r Penny DJ, Shekerdemian LS. Management of the
r A full sepsis evaluation should be initiated and The decision to admit should be made in neonate with symptomatic congenital heart disease.
antibiotics empirically started after the appropriate conjunction with a pediatric cardiologist. Arch Dis Child Fetal Neonatal Ed. 2001;84(3):
cultures are obtained in infants <23 mo of age Discharge Criteria F141F145.
who are exhibiting signs and symptoms of sepsis: r Rudolf AM. Congenital Diseases of the Heart:
A patient who has been evaluated by a pediatric
Fever >38.0 C, irritability, respiratory distress, cardiologist and deemed to be stable may be Clinica-Physiological Considerations. 2nd ed.
lethargy. discharged home with outpatient cardiology Armonk, NY: Futura Publishing Company; 2001.
r Caution must be used if a lumbar puncture is follow-up. r Savitsky E, Alejos J, Votey S. Emergency department
indicated, especially in an unstable cyanotic child. Issues for Referral presentations of pediatric congenital heart disease. J
r If a patient requires a higher level of care at a Emerg Med. 2003;24(3):239245.
MEDICATION r Silverbach M, Hannon D. Presentation of congenital
First Line tertiary pediatric center, then arrangements for
transport should be made. heart disease in the neonate and young infant.
In a cyanotic patient who may have ductal-dependent r A specialized pediatric critical care transport team Pediatr Rev. 2007;28:123131.
CHD, a prostaglandin (PGE1 ) infusion should be r Wylie TW, Sharieff GQ. Cardiac disorders in the
initiated. may be necessary to facilitate the transport.
r Infusion rates should be started at 0.050.1 pediatric patient. Emerg Med Rep. 2005;10:112.
g/kg/min with a max rate of 0.4 g/kg/min. FOLLOW-UP
r A common side effect of PGE is apnea; prompt
intubation may be necessary.
1
FOLLOW-UP RECOMMENDATIONS CODES
r Elective intubation of patients on PGE for transport Discharge instructions and medications:
1
may increase the risk of transport complications (1). r Parents should be instructed to look for worsening ICD9
r 745.5 Ostium secundum type atrial septal defect
r Other occurrences associated with PGE include signs and symptoms of the patients CHD.
1
r Discharge medications should be based upon the r 746.9 Unspecified congenital anomaly of heart
hyperthermia, flushing, arrhythmias, hypotension, r 747.0 Patent ductus arteriosus
and seizures. recommendations of the consulting pediatric
Second Line cardiologist.
r A child with CHF may benefit from a dose of r A follow-up appointment with a pediatric
cardiologist should be made. PEARLS AND PITFALLS
furosemide at 0.51 mg/kg.
r If a urine output of 35 cc/kg/hr is not achieved r A combination of cyanosis, murmur, and abnormal
PROGNOSIS
within 12 hr after the 1st dose of furosemide, Prognosis is based on the patients initial acuity, CHD pulses is associated with a PGE1 -sensitive CHD
repeat doses of 1 mg/kg can be given at hourly type, and need for surgical treatment. lesion.
intervals to a max of 35 mg/kg. r Routine intubation of patients on PGE is not
1
r If hypotension persists after IV fluid boluses, COMPLICATIONS necessary.
r Hypoxic brain injury
dopamine should be initiated at 5 g/kg/min and r Administration of high levels of O may worsen a
r FTT 2
titrated up to a max of 20 g/kg/min. r Severe metabolic acidosis patient with cyanotic CHD:
r For further inotropic support, dobutamine can be O2 can act as a pulmonary vasodilator; hence,
r Multiple organ failure
added with an initial rate of 5 g/kg/min with caution is warranted when administering O2 in a
r Cardiopulmonary arrest
titration to a max rate of 20 g/mg/min. suspected CHD patient.
r Caution should be used with higher doses of
dobutamine because of its vasodilator effects that
may lead to precipitous drops in BP, especially in the
hypovolemic CHD patient.
187
CONGESTIVE HEART FAILURE

Travis K. F. Hong
Calvin G. Lowe
ETIOLOGY
BASICS r Varies by age of presenting symptoms and DIAGNOSIS
functional classification
DESCRIPTION r 1st day of life: HISTORY
r Presentation is usually related to the increased
CHF is the inability of the heart to provide an Cardiac dysfunction: Hypoglycemia, sepsis,
adequate level of tissue perfusion to meet metabolic hypocalcemia, myocarditis, birth asphyxia metabolic energy requirement in CHF.
requirements. r Changes in infant feeding habits:
Structural: Valvular regurgitation, extracardiac
arteriovenous malformation Increase in feeding time, >3060 min for a bottle
EPIDEMIOLOGY (regardless of amount)
Conductional: Supraventricular tachycardia,
Incidence Caloric intake <75 kcal/kg/day
r 12,000 cases of pediatric heart failure occur in the congenital heart block
Hematologic: Hyperviscosity states (eg, Increased work of breathing
U.S. each year (1): Early fatigue, agitation, or irritability
polycythemia), anemia
61% of cases were associated with congenital r 1st wk of life: Diaphoresis, especially with feeds
heart disease (CHD) or cardiac surgery. r Prolonged general fatigue and malaise
82% of cases occur in infants. Structural: Persistent pulmonary HTN of the
r Weight loss, anorexia, or nausea
r For primary cardiomyopathies in structurally normal newborn, aortic coarctation, critical aortic stenosis
(AS), hypoplastic left heart syndrome (HLHS), r Decreased exercise tolerance or activity
hearts, the incidence is 0.87 per 100,000 infants (2). r Tachypnea, orthopnea, or paroxysmal nocturnal
critical pulmonary stenosis (PS), interrupted aortic
RISK FACTORS arch (IAA), transposition of the great arteries orthopnea
r CHD, especially conditions with left-to-right (TGA), obstructed total anomalous venous return r Chronic cough
shunting or left-sided obstruction (TAPVR), pulmonary atresia, patent ductus r Frequent lower respiratory tract infections
r Dilated or hypertrophic cardiomyopathy arteriosus (PDA) r Above symptoms associated with excessive salt or
r Previous cardiac surgery Metabolic: Adrenal insufficiency, hyperthyroidism fluid intake
r Metabolic or renal disorders Renal: Systemic HTN, renal failure
Cardiac dysfunction and conductional PHYSICAL EXAM
PATHOPHYSIOLOGY abnormalities r Sinus tachycardia
r CHF physiology is due to volume overload, pressure r 1st 2 mo of life: r Systemic hypotension
overload, inadequate inotropic state, alteration in Structural: Ventricular septal defect (VSD), r Murmurs may be present depending on location and
chronotropic state, or a combination. atrioventricular canal, single ventricle, atrial septal size of defect or lesion (see Heart Murmur topic).
r Cardiac output (CO) equals heart rate (HR) r Increased precordial activity in shunt lesions
defect, PDA, nonobstructed TAPVR, truncus
multiplied by stroke volume (SV): arteriosus, AS, IAA, anomalous coronary artery, r S3 or ventricular gallop
HR is controlled by neurologic and intrinsic cardiac HLHS r S4 or atrial kick due to ventricular hypertrophy
conduction input. Myocardial: Cardiomyopathy, myocarditis, Pompe r Cool or mottled extremities
SV depends on cardiac muscle contractility, disease r Decreased peripheral pulses or capillary refill
preload, and afterload. Pulmonary: Pulmonary HTN, central
r Preload is the volume that must be ejected from the r Pulsus paradoxus
hypoventilation syndromes, upper airway
r Jugular venous distension
left ventricle (LV) at the end of diastole, which obstruction (eg, tracheomalacia),
depends on venous return. A larger filling volume bronchopulmonary dysplasia r Tachypnea
causes increased contractility via the Frank-Starling Other: Hypothyroidism, renal and metabolic r Cyanosis, central or peripheral
mechanism. causes as above r Persistent hacking cough
r Afterload is the pressure required to eject preload r Childhood and beyond: r Grunting, retractions, or nasal flaring
volume from the LV, typically measured as systolic Acquired causes: Sepsis, infective endocarditis, r Wheezing, and less commonly rales
aortic pressure. rheumatic heart disease, cocaine toxicity r Hepatomegaly or liver tenderness
r Clinical manifestations of CHF are primarily caused Genetic: Noonan syndrome, Marfan syndrome, r Jaundice in infants
by alterations in fluid retention and adrenergic Hurler syndrome, Duchenne muscular dystrophy, r Peripheral edema or ascites in older children
activity: Friedreich ataxia
Inadequate systemic perfusion results in fluid Unrepaired CHD: Valvular insufficiency, DIAGNOSTIC TESTS & INTERPRETATION
retention via the kidneys and renin-angiotensin Eisenmenger syndrome, Ebstein anomaly, severe Lab
system. PS r Diagnosis is primarily clinical, but certain lab assays
After initial brief improvement in preload, dilated Repaired CHD: Fontan procedure may cause may be useful.
cardiomyopathy occurs and increases ventricular protein-losing enteropathy and CHF. r Glucose and ionized calcium levels should be
wall stress, pressure, and myocardial oxygen Failure of surgical palliation: Large systemic to measured and monitored.
demand. pulmonary artery shunt, pulmonary atresia with r Hyponatremia, hypochloremia, or anemia may be
Compensatory cardiac hypertrophy then reduces large VSD, prosthetic valve failure, ventricular present during volume overload.
contractility and thus CO. failure following TGA arterial switch operation, r Blood gas measurement may demonstrate metabolic
r Increased -adrenergic tone augments HR and reopened VSD, aortic insufficiency following
acidosis and hypoxemia.
contractility but causes many of the typical signs and valvotomy or truncus arteriosus repair, mitral r Elevated troponin or creatine phosphokinase levels
symptoms of CHF due to an increased sympathetic insufficiency after endocardial cushion repair,
myocardial ischemia following operative arrest, PS may be seen in myocardial inflammation or ischemia.
state. r The role of brain natriuretic peptide (BNP) levels is
or outflow tract obstruction, pulmonary
insufficiency unclear in children:
Collagen vascular disease: Systemic lupus Elevation may aid in distinguishing respiratory
erythematosus, juvenile idiopathic arthritis distress as cardiac or respiratory.
Other: Kawasaki disease, neuromuscular BNP >300 pg/mL is strongly correlated with poor
weakness, hypo/hyperthyroidism, renal disease, outcome (3).
end-stage cystic fibrosis, systemic HTN
188
CONGESTIVE HEART FAILURE
Imaging r Inotropic agents as indicated for hypotension:

r Chest radiograph is essential and may show the Caution with high-dose dopamine FOLLOW-UP
following: (>10 g/kg/min) due to an increase in
Cardiomegaly is nearly always present. myocardial oxygen consumption FOLLOW-UP RECOMMENDATIONS
r Correct electrolyte and laboratory abnormalities. r Consultation with a pediatric cardiologist is
Increased pulmonary vascular markings
Pleural effusion, especially in right-sided CHF r Consultation with a pediatric cardiologist and/or recommended.
Pericardial effusion r If the patient is stable for discharge home, an urgent
critical care specialist is recommended.
r Echo provides a quick, noninvasive, and relatively follow-up with a pediatric cardiologist is strongly
MEDICATION recommended.
inexpensive method to gather anatomic and
physiologic data: First Line C
Furosemide 1 mg/kg IV, repeat q612h PRN: COMPLICATIONS
Provides essential details of cardiac anatomy r Cardiac arrhythmias, especially ventricular
Color Doppler echo can detect and quantify r No pediatric data exist for thiazide diuretic
tachycardia or fibrillation
valvular insufficiency, stenosis, or intracardiac monotherapy. r MI
shunting. Second Line r Cardiac arrest
Ejection fraction is used to estimate left ventricular r Digoxin, initial total digitalizing dose (IV): r Hypoxemic brain injury
function by measuring the ratio of blood volume 3-dose regimen: Give 50% of total digitalizing r Pulmonary edema and respiratory failure
during diastole and systole. dose (TDD), then 25% of TDD 2 q612h
r Cardiac MRI is helpful for 3D imaging and r Respiratory or metabolic acidemia
Preterm infants: 20 g/kg r Renal insufficiency or failure
assessment of right ventricle and single ventricle Term infants: 25 g/kg
function: r Hepatic dysfunction, including coagulopathies and
1 mo to 2 yr: 30 g/kg
Limited use in emergent or acute situations 210 yr: 25 g/kg delayed pharmacologic metabolism and clearance
r Digoxin toxicity
Diagnostic Procedures/Other 10 yr to adult: 0.51 mg
r ECG: r Digoxin, maintenance dose (IV): r Loop diureticinduced hypokalemia, hyponatremia,
Nonspecific indicator of cardiac abnormality Preterm infant: 2.5 g/kg b.i.d. contraction alkalosis, and ototoxicity (usually in
Useful when an arrhythmia or myocardial ischemia Term infants: 2.54 g/kg b.i.d. chronic use)
is present. 1 mo to 2 yr: 46 g/kg b.i.d.
Increased QRS amplitude in precordial leads may 210 yr: 2.54.5 g/kg b.i.d.
indicate ventricular wall hypertrophy. 10 yr to adult: 125500 g per day REFERENCES
Decreased QRS amplitude in precordial leads may r Digoxin: Dosages for CHF management only.
1. Webster G, Zhang J, Rosenthal D. Comparison of
indicate myocarditis. Equivalent oral dose is 125% of IV form. the epidemiology and co-morbidities of heart
In anomalous left coronary artery from the r Consultation with a pediatric cardiologist is strongly failure in the pediatric and adult populations: A
pulmonary artery (ALCAPA), an anterolateral recommended prior to initiating therapy. retrospective, cross-sectional study. BMC
infarct pattern is seen. Cardiovasc Disord. 2006;6:23.
r Cardiac catheterization: SURGERY/OTHER PROCEDURES
r Indications for surgical intervention are varied 2. Andrews RE, Fenton MJ, Ridout DA, et al.
Used when interventional procedures are required New-onset heart failure due to heart muscle
(eg, biopsy, balloon septostomy) depending on the specific etiology of CHF.
r Pacemaker therapy in CHD is indicated for disease in childhood: A prospective study in the
Provides detailed hemodynamic and anatomic United Kingdom and Ireland. Circulation.
data symptomatic bradycardia, atrioventricular
asynchrony, or intra-atrial reentrant 2008;117:7984.
Emergent utility has decreased with advent of
tachyarrhythmias. 3. Price JF, Thomas AK, Grenier M, et al. B-type
color Doppler echo.
r Implanted defibrillator in CHD is indicated for natriuretic peptide predicts adverse cardiovascular
DIFFERENTIAL DIAGNOSIS ventricular tachycardia or syncope. events in pediatric outpatients with chronic left
r Myocardial infarction ventricular systolic dysfunction. Circulation.
r Mechanical ventricular assist devices may be used in
r Sepsis 2006;114:10631069.
end-stage CHF as a bridge to heart transplantation.
r Malnutrition r Heart transplantation is indicated in refractory 4. Rosenthal D, Chrisant MR, Edens E, et al.
r Cardiac tamponade International Society for Heart and Lung
end-stage CHF:
r Thyrotoxicosis 1-yr posttransplant survival is 85% (4).
Transplantation: Practice guidelines for
r Pulmonary thromboembolism management of heart failure in children. J Heart
20-yr posttransplant survival is 40% (4).
r Intracardiac thrombus Lung Transplant. 2004;23:13131333.
r Pulmonary HTN DISPOSITION
r Cardiac neoplasm Admission Criteria
r All patients with either new-onset CHF or an acute CODES
r Kawasaki disease
worsening of chronic CHF should be admitted for
r Pregnancy diuretic therapy and supportive care.
r Cardiotoxic drugs (eg, doxorubicin, daunorubicin,
ICD9
r Consider admission in the newly presenting neonate 428.0 Congestive heart failure, unspecified
cyclophosphamide, 5-fluorouracil) or infant for further workup and treatment of
possible undiagnosed CHD.
r Critical care admission criteria: PEARLS AND PITFALLS
TREATMENT Consider critical care admission in patients with r CHF in neonates or infants is often due to an
hemodynamic instability or pulmonary
INITIAL STABILIZATION/THERAPY undiagnosed congenital heart defect.
r Assess and stabilize airway, breathing, and compromise. r As in most cases of cardiogenic shock, exercise
circulation: caution during fluid resuscitation in order to avoid
Judicious IV fluid resuscitation as needed to volume overload.
maintain adequate BP
5 mL/kg boluses of isotonic fluid as needed with
frequent reassessment of intravascular volume
status
189
CONJUNCTIVAL INJURY
Donald T. Ellis, II
Sandip A. Godambe
BASICS DIAGNOSIS r Pronounced conjunctival chemosis
r Epithelial loss
DESCRIPTION HISTORY r Corneal edema and opacification
r The conjunctival membranes represent the thin, r Most cases are readily identifiable from the history;
translucent covering of the white sclera of the globe however, burns from UV light may present with DIFFERENTIAL DIAGNOSIS
severe pain hours after the event. r Corneal abrasion
(bulbar conjunctiva) and the inside of the eyelids
(palpebral conjunctiva). r Pain r Infectious conjunctivitis
r The most common conjunctival injuries include r Photophobia r Allergic conjunctivitis
direct trauma and burns from chemical irritants or r Foreign body sensation r Foreign body
radiant energy, as with ultraviolet (UV) light. r Conjunctival redness and tearing r Glaucoma
r Scleritis/Episcleritis (such as in systemic lupus
EPIDEMIOLOGY PHYSICAL EXAM
Incidence r Epiphora erythematosus, Wegener granulomatosis,
r The annual incidence of all forms of eye injury has r Chemosis rheumatoid arthritis, and inflammatory bowel
been reported at 1% (1). r Hyperemia disease)
r Conjunctival and corneal abrasions comprised r Corneal clouding
16.5% of the ocular injuries in the same study (1). r Scleral pallor TREATMENT
RISK FACTORS r Teardrop pupil (as seen with ruptured globe)
As with trauma in general, conjunctival injury is more r Foreign body (Eyelid eversion is critical when PRE HOSPITAL
r Trauma: An eye shield (not eye patch) should be
common in males than females. evaluating for potential presence of foreign bodies.)
r UV keratitis may present with punctuate lesions over placed if there is concern for a ruptured globe or if
GENERAL PREVENTION accommodation is painful.
r Eye protection is critical to reducing the risk of any the corneal surface (seen on fluorescein staining) (3). r Thermal: Copious irrigation and rapid cooling of the
eye injury. ALERT ocular structures
r It has been postulated that 90% of eye injuries are r Chemical (alkali, acid): Copious irrigation with
Strong acids may be associated with pale
preventable. conjunctiva and corneal clouding, which may be buffered solution (such as Diphoterine or lactated
PATHOPHYSIOLOGY followed by desquamation. The absence of Ringer):
r Traumatic injury occurs from direct trauma from an hyperemia may then obscure the degree of tissue However, if none is available, use any sterile,
object or foreign body. injury. nontoxic solution (such as normal saline).
r Alkaline substances induce liquefactive necrosis, Tap water is a preferable alternative to delayed
which can allow the chemical to reach into the irrigation and may be utilized immediately
deeper tissues in the anterior chamber (2). following the injury:
Lab However, hypotonic solutions are associated
r Acids are typically responsible for superficial injury,
Initial Lab Tests with a risk of increasing the depth of
as they cause coagulation of the tissues, which Other lab testing is usually not indicated in penetration.
prevents them from reaching deeper layers in the conjunctival injury.
eye (2): INITIAL STABILIZATION/THERAPY
Substances with a pH of 2.5 cause penetrating Imaging r All conjunctival injuries:
injury similar to that seen with alkalis. Imaging is generally not helpful unless orbital or other Administer topical anesthetic drops to provide
Hydrofluoric acid, in particular, has been known to facial fractures are suspected. comfort and to facilitate examination (once
cause deep, alkalilike eye injuries. Diagnostic Procedures/Other ruptured globe has been ruled out).
r Fluorescein staining is strongly encouraged when r Chemical burns:
ETIOLOGY
r Trauma: the differential diagnosis includes entities such as Irrigate (see above) until pH has normalized for 30
corneal abrasion, retained foreign body, herpetic min. Normal pH should be 6.57.5.
Play or sports activity
keratitis, and UV burns. Irrigation using a Morgan lens is recommended to
Motor vehicle accidents r pH testing may be used in chemical burns, but
Foreign body (dirt, sand, glass, etc.) achieve adequate reaching of areas under the
Self-inflicted (rubbing eye, scratching eye) irrigation should never be delayed. eyelids.
r Alkali: Oven cleaners, fireworks, dishwashing r pH testing of the lacrimal fluid should be 6.57.5. Never attempt to neutralize alkali burns with
Wait several minutes after discontinuing irrigation of acidic solutions and vice versa.
detergent
r Acid: Battery acid, bathroom cleaners, rust-removal the eye before testing to obtain an accurate result. Do not remove contact lenses during irrigation, as
r Visual acuity should also be determined at baseline, these may serve as physical barriers to block
agents, automotive wheel cleaners deeper penetration of the corrosive substance.
r UV: Welding light, tanning beds, outdoor activities but as with pH testing, it should not delay irrigation.
r Must consider performing slit lamp exam with Remove after completion of irrigation.
at increased elevation Evert the lids to ensure that no foreign material
r Thermal: Fire, steam, hot liquids fluorescein staining and measurement of intraocular
pressure remains.
r Thermal burns:
r Conjunctival injury may also be associated with As with chemical burns, irrigate liberally (see
corneal abrasion, hyphema, open globe injury, above) and remove any foreign matter.
facial/airway burns, and facial injury, including Remove contact lenses.
fractures. May need to remove eschar from eyelids
r See respective topics on Fracture, Orbital; Corneal Ensure that any perioral or airway burns are
Abrasion; Hyphema; Foreign Body, Cornea; and addressed.
Burn, Chemical.
190
CONJUNCTIVAL INJURY

First Line FOLLOW-UP r Ehlers JE, Shah CP. The Wills Eye Manual. 5th ed.
r Topical anesthetic (such as 0.5% proparacaine or
tetracaine) in the emergency department. Do not FOLLOW-UP RECOMMENDATIONS Philadelphia, PA: Lippincott Williams & Wilkins;
use repeated doses upon discharge, as this may Discharge instructions and medications: 2008.
r Follow up with the primary care provider for repeat r Spector J, Fernandez WG. Chemical, thermal, and
impair corneal healing.
r Parenteral analgesics (such as morphine 0.1 fluorescein testing within 24 hr. biological ocular exposures. Emerg Med Clinic N
mg/kg/dose, up to 46 mg) to adequately control r Follow up with an ophthalmologist in the next Am. 2008;26(1):125136.
r Xiang H, Stallones L, Chen G, et al. Work-related eye
pain initially. Oral narcotics may be necessary for
patients if discharged.
2448 hr for significant injuries.
r Ophthalmic lubricant to reduce the risk of injuries treated in hospital emergency departments
C
r Topical antibiotics (eg, erythromycin ointment or symblepharon in the US. Am J Ind Med. 2005;48(1):5762.
trimethoprim/polymixin drops q.i.d.) should be a r Topical ophthalmic antibiotic ointment or drops as
consideration. See Corneal Abrasion topic. noted in the Medication section.
r For chemical and thermal burns, assess tetanus
Patient Monitoring
CODES
immunization status and update if appropriate. Outpatient monitoring of healing and assessing for
secondary complications should be done by the ICD9
Second Line r 918.2 Superficial injury of conjunctiva
r Both systemic and topical steroids (such as oral primary care provider. r 921.1 Contusion of eyelids and periocular area
prednisone 2 mg/kg/day, up to 60 mg) remain PROGNOSIS r 940.3 Acid chemical burn of cornea and conjunctival
controversial but may be used after consultation r Most patients with conjunctival injury from trauma
with ophthalmology. sac
r After consultation with ophthalmology, medications do well if injuries are isolated to the conjunctiva.
r Both thermal and UV lightassociated injuries are
to lower intraocular pressure (such as
acetazolamide, dose not established for pediatrics)
relatively self-limited problems when compared to PEARLS AND PITFALLS
those burns from chemical exposures (3).
may be needed if glaucoma develops. r Alklali burns tend to be the most severe; however,
r Cycloplegics (such as homatropine 2% 12 drops; COMPLICATIONS
r Dry eyes hydrofluoric acid burns may also cause
may use every 1520 min as needed) have been sight-threatening injury.
r Infection
used with chemical, thermal, and UV injuries, but r Assessment and documentation of visual acuity and
evidence supporting this practice is limited. r Glaucoma
r Conjunctival adhesions deficit are critical.
DISPOSITION r Use a Morgan lens to achieve adequate irrigation
r Scarring
Admission Criteria for caustic or thermal burns.
Hospital admission is not needed unless there are r Pinhole refraction may be used in visual acuity
severe burns (such as with hydrofluoric acid or alkaline REFERENCES testing in patients whose corrective lenses are
substances), concurrent facial (or significant systemic) unavailable at the time of the emergency
injuries, or social concerns. 1. Fea A, Bosone A, Rolle T, et al. Eye injuries in an department evaluation.
Discharge Criteria Italian urban population: Report of 10620 cases
r Minor burns (most 1st-degree burns by thermal admitted to an eye emergency department in
injury) Torino. Graefes Arch Clin Exp Ophthalmol.
r UV injuries 2008;246:175179.
2. Wagoner MD. Chemical injuries of the eye: Current
Issues for Referral concepts in pathophysiology and therapy. Surv
Transfer to a regional burn center may be required for Ophthalmol. 1997;41(4):275280.
those with severe burns or with extraorbital injuries. 3. Rihawi S, Frentz M, Becker J, et al. The
COMPLEMENTARY & ALTERNATIVE consequences of delayed intervention when
THERAPIES treating eye burns. Graefes Arch Clin Exp
r Cool compresses may provide a measure of relief for Ophthalmol. 2007;(10):15071513.
thermal burns.
r Eye patches remain controversial.
191
CONJUNCTIVITIS
Audrey H. Le
Sandip A. Godambe
r Bacterial conjunctivitis is suggested by a history of DIAGNOSTIC TESTS & INTERPRETATION

BASICS sticky eyelashes or eyelids in the morning and the Lab
presence of purulent eye discharge or crusting of the Initial Lab Tests
DESCRIPTION eyelashes or eyelid on exam. r Except in neonatal infections, lab tests are limited to
Conjunctivitis denotes inflammation of the r In neonates, Neisseria gonorrhoeae infection those cases that are particularly severe or refractory
conjunctiva, a membrane that overlies the outer globe, acquired by vertical transmission typically presents to treatment.
or bulbar surface, and reflects back to cover the inner between 2 and 5 days of age, and Chlamydia r Neonates should have cultures:
eyelids, the palpebral surface. trachomatis between 5 and 14 days of age. Other Consider full sepsis workup with gonococcal
EPIDEMIOLOGY pathogens acquired perinatally or postnatally may infections.
present at 57 days. In contrast, chemical Chlamydia infection mandates evaluation for
Incidence
conjunctivitis may be seen 12 days after birth as a pulmonary infection.
Conjunctivitis occurs in 1.612% of newborns.
result of perinatal ocular prophylaxis, particularly
Prevalence with silver nitrate. Diagnostic Procedures/Other
r Bacterial conjunctivitis is more prevalent during the r Outside the neonatal period, N. gonorrhoeae and In herpetic infections, fluorescein staining of the eye
winter season, while viruses predominate during the and exam with a cobalt blue light may reveal the
C. trachomatis infections occur mostly in young,
fall. classic dendritic pattern.
sexually active individuals, spread from the genital
r Bacterial conjunctivitis is more common in children Pathological Findings
area to the eye via hand contact.
<6 yr of age, whereas adenovirus accounts for more r Viral conjunctivitis is usually hailed by irritation r Staining scrapings of the conjunctival surface with
infections in those >6 yr. beginning in 1 eye and spreading to the other within Hansel or Giemsa stains reveals eosinophils in
a few days via hand-eye contact. Some patients may 2080% of patients with allergic conjunctivitis.
GENERAL PREVENTION r Chlamydial infections may be diagnosed via Giemsa
r Frequent hand washing have concurrent upper respiratory tract symptoms.
r Wearing gloves for health care workers r Viral conjunctivitis has symptoms that overlap both stain, direct fluorescent antibody, ELISA testing, or
allergic and bacterial conjunctivitis, although itching PCR. Culture is the preferred method.
PATHOPHYSIOLOGY is not as prevalent as in allergic conjunctivitis, and
r The conjunctiva, as the outer covering of the globe, DIFFERENTIAL DIAGNOSIS
mucoid production is less common than in bacterial r Nasolacrimal duct obstruction
is subject to environmental irritants and infectious conjunctivitis. r Glaucoma
agents, which trigger an inflammatory response, r Pharyngoconjunctival fever caused by some r Intraocular tumors
causing redness and edema. adenovirus species presents abruptly with fever,
r Allergic conjunctivitis is an IgE-mediated reaction in r Subconjunctival hemorrhage
pharyngitis, and bilateral conjunctivitis. r Episcleritis
which exposure to environmental allergens triggers r Herpes simplex virus (HSV) conjunctivitis is usually
an allergic cascade, including mast cells and r Scleritis
unilateral, painful, and associated with a foreign r Uveitis
histamine release. body sensation.
r Periorbital cellulitis
ETIOLOGY PHYSICAL EXAM r Orbital cellulitis
r The most common etiologies for acute conjunctivitis r Symptoms of allergic conjunctivitis are expectedly
are allergic, bacterial, and viral. r Eye irritation
r Bacterial conjunctivitis is most commonly caused by mild, and chemosis may be more impressive than
redness.
Streptococcus pneumoniae, Staphylococcus aureus, r Bacterial infections will cause bulbar conjunctival
Haemophilus influenzae, and Pseudomonas TREATMENT
injection that may be more pronounced at the
aeruginosa. fornices. A mucopurulent discharge is usually seen:
r A number of different organisms have been Patients with contact lenses should be advised to stop
N. gonorrhoeae causes hyperacute conjunctivitis: wearing them until symptoms have resolved.
implicated in viral conjunctivitis, among them Marked conjunctival injection, chemosis, lid
adenovirus and herpesvirus. swelling, globe tenderness, and profuse purulent MEDICATION
r Allergic conjunctivitis may be treated with comfort
discharge.
Pseudomembranes are associated with chlamydial measures including cool compresses, artificial tears,
DIAGNOSIS infection, but this is not specific. and avoidance of triggers. Topical medications may
r Viral conjunctivitis may include injection, provide relief (1):
HISTORY
r Common symptoms seen include itching, burning, nonpurulent watery discharge, follicular reaction of First line: Naphcon-A, Occuhist (naphazoline
the palpebral conjunctiva, and preauricular hydrochloride/pheniramine maleate) 12 gtt
red eye (redness), foreign body sensation,
lymphadenopathy: q.i.d.: Over-the-counter combination
discharge, or sticky eyelids.
r Patients with allergic conjunctivitis will almost Epidemic keratoconjunctivitis caused by decongestant and antihistamine for children >6 yr
adenovirus species presents with conjunctival Second line:
invariably present with itching with or without Azelastine 0.05% (Optivar) 1 gtt b.i.d.: H1
associated rhinorrhea or watery eyes. The edema, petechial hemorrhages, a
pseudomembrane, and corneal subepithelial receptor antagonist for children 3 yr
predominant symptom in allergic conjunctivitis is Lodoxamide tromethamine 0.1% (Alomide)
itching. Watery eyes are also common. A personal or infiltrates causing decreased visual acuity.
HSV conjunctivitis may have associated corneal 12 gtt q.i.d.: Mast cell stabilizer
family history of atopy or the absence of sick
contacts in patients with symptoms suggests allergic ulceration or vesicular lesions on an erythematous
conjunctivitis. base involving the eyelid and surrounding skin.
r Bacterial and viral conjunctivitis generally starts
abruptly in 1 eye and spreads to the contralateral
side within 2 days.
192
CONJUNCTIVITIS
r Simple bacterial conjunctivitis can be treated with DISPOSITION 3. AAP Subcommittee on Management of Acute Otitis
topical antibiotics (2): Admission Criteria Media. Diagnosis and management of acute otitis
First line: r Consider sepsis evaluation and/or hospitalization of media. Pediatrics. 2004;113:14511465.
Trimethoprim/Polymixin B (Polytrim) 12 gtt neonates with gonococcal, chlamydial, or HSV 4. CDC. Sexually transmitted diseases treatment
q.i.d. for 1 wk: Broad spectrum, inexpensive, infections. guidelines. 2006. Morb Mortal Wkly Rep.
minimal side effects r Consider admission for any patient with gonococcal 2006;55(RR-11):3849.
Aminoglycosides (gentamicin, tobramycin, conjunctivitis. 5. Wilhelmus K. Therapeutic interventions for herpes
erythromycin) 0.5-inch ribbon q.i.d. for 1 wk. simplex virus epithelial keratitis. Cochrane
Discharge Criteria
The 1st 2 have good gram-negative coverage
but are ineffective for Chlamydia. Erythromycin
r Simple bacterial infections in immunocompetent Database Syst Rev. 2008;(1):cd002898.
6. Patel PB, Diaz MC, Bennett JE, et al. Clinical
C
has good activity against Chlamydia but poor children may be managed on an outpatient basis
with appropriate treatment. features of bacterial conjunctivitis in children. Acad
activity against gram-negative organisms and
r Close follow-up with an ophthalmologist for HSV Emerg Med. 2007;14:15.
Staphylococcus species.
Sodium sulfacetamide 10% (Bleph-10) 13 gtt infection
q23h while awake for 1 wk: Good coverage of Issues for Referral ADDITIONAL READING
gram-positive organisms but may cause r Epidemic keratoconjunctivitis requires follow-up
r Bielory L, Friedlaender MH. Allergic conjunctivitis.
significant local irritation within 7 days with an ophthalmologist since keratitis
Second line: is a potential complication. Immunol Allergy Clin North Am. 2008;28:4358.
Fluoroquinolones (ciprofloxacin 0.3%, r Patients with viral infections who do not show r Ehlers JE, Shah CP. The Wills Eye Manual. 5th ed.
ofloxacin) 12 gtt q.i.d. for 1 wk: Broad improvement within 710 days should be referred Philadelphia, PA: Lippincott Williams & Wilkins;
spectrum but more expensive to an ophthalmologist. 2008.
4th-generation fluoroquinolones (gatifloxacin r Mahmood AR, Narang AT. Diagnosis and
0.3% 12 gtt q2h (max 8 times per day) while management of the acute red eye. Emerg Med Clin
awake for 2 days, then q.i.d. for 5 days; FOLLOW-UP North Am. 2008;26:3555.
moxifloxacin 0.5% 1 gtt t.i.d. for r Prentiss KA, Dorfman DH. Pediatric ophthalmology
1 wk): Broad spectrum with increased efficacy FOLLOW-UP RECOMMENDATIONS in the emergency department. Emerg Med Clin
against gram-positive organisms; expensive Discharge instructions: North Am. 2008;26:181198.
r Conjunctivitis-otitis syndrome is most often r Allergic conjunctivitis should have follow-up within r Robinett DA, Kahn JH. The physical examination of
attributable to nontypeable H. influenzae, and may weeks depending on the response to treatment. the eye. Emerg Med Clin North Am. 2008;26:116.
be treated with antibiotics alone (3): r Simple bacterial conjunctivitis should follow up r Wagner RS, Aquino M. Pediatric ocular
Amoxicillin/Clavulanate: High dose (dosed as within 34 days if symptoms do not improve. inflammation. Immunol Allergy Clin North Am.
amoxicillin) 8090 mg/kg/day PO divided b.i.d. or r Patients with HSV, chlamydia, or gonococcal
2008;28:169188.
t.i.d. infection should follow up within 2 days.
Cefdinir 14 mg/kg/day given once daily or divided r Hand washing and other hygiene is critical to
b.i.d., max 600 mg/day prevent spread of infection. CODES
Cefpodixime 10 mg/kg/day divided b.i.d., max
800 mg/day PROGNOSIS
r Gonococcal conjunctivitis is treated with a single Most cases of conjunctivitis resolve without ICD9
complications. r 077.3 Other adenoviral conjunctivitis
dose of parenteral ceftriaxone (2550 mg/kg, max r 372.14 Other chronic allergic conjunctivitis
125 mg) and saline eye lavage (4). COMPLICATIONS r 372.30 Conjunctivitis, unspecified
r Chlamydial infection can be treated with: r Corneal ulcers
Erythromycin ophthalmic ointment and oral r Scarring
erythromycin 50 mg/kg/day divided q.i.d. for r Keratitis
14 days in neonates: PEARLS AND PITFALLS
A 2nd course is occasionally required. r Treating HSV conjunctivitis with steroids can cause
Adolescents and adults may be treated with REFERENCES uncontrolled viral proliferation and increase the risk
topical antibiotics for conjunctivitis, along with of secondary infection.
systemic antibiotics (eg, azithromycin 1 g PO, 1. Owen CG, Shah A, Henshaw K, et al. Topical r Patients with allergic conjunctivitis treated with
erythromycin base 500 mg q.i.d. for 7 days, or treatment for seasonal allergic conjunctivitis:
Systemic review and meta-analysis of efficacy and topical steroids require close supervision, and
doxycycline 100 mg b.i.d. for 7 days) for genital
effectiveness. Br J Gen Prac. 2004;54(503): treatment should be limited to 2 wk to decrease the
disease (4).
r Most cases of viral conjunctivitis can be treated with 451456. risk for complications.
r Gonococcal and chlamydial infections should be
supportive care including cold compresses and 2. Sheikh A, Hurwitz B. Antibiotic versus placebo for
acute bacterial conjunctivitis. Cochrane Database considered in every neonate presenting with eye
artificial tears.
r Treatment of HSV includes cool compresses and Syst Rev. 2007;(4):cd001211. discharge.
r Patients should discontinue use of contact lenses
topical antiviral medications (eg, trifluridine 1%
while being treated for any conjunctivitis.
drops, vidarabine ointment). Severe cases may
require oral antiviral medications and/or topical
cycloplegic medications (5), given in cooperation
with an ophthalmologist.
193
CONJUNCTIVITIS, NEONATAL
Emily Schapiro
r The substitution of erythromycin or tetracycline DIAGNOSTIC TESTS & INTERPRETATION

BASICS ointment in place of silver nitrate has resulted in a Lab
decreased incidence of chemical conjunctivitis (3). Initial Lab Tests
DESCRIPTION r Dacryostenosis may also present with conjunctivitis: r Diagnosis is made by sending a swab or scraping
r Ophthalmia neonatorum (ON) is any inflammatory
Stenosis may lead to dacryocystitis, a bacterial from the conjunctiva for Gram stain and bacterial
(infectious or noninfectious) process affecting the infection of the nasolacrimal duct. and viral culture.
conjunctiva that occurs within the 1st month of life. r STIs such as Chlamydia trachomatis, Neisseria r The presence of gram-negative, intracellular
r This includes those causes that have potential for
gonorrhoeae, and herpesvirus are the most common diplococci is highly indicative of gonococcal
serious and permanent damage to the eye and for organisms causing infectious ON. infection.
systemic complications. r Skin flora such as Staphylococcus or Pseudomonas r Chlamydia trachomatis may be diagnosed using a
EPIDEMIOLOGY species may also cause ON. direct immunofluorescence test or polymerase chain
Incidence COMMONLY ASSOCIATED CONDITIONS reaction analysis. Also, Giemsa staining of epithelial
r In the U.S. and Europe, the incidence of ON has cells scraped from the tarsal conjunctivae may show
Chlamydial ON may be associated with chlamydia
fallen dramatically due to screening pregnant pneumonitis. typical intracytoplasmic inclusions.
r In the ill-appearing or septic infant or one with a
women for STIs and instilling antibiotics into infants
eyes shortly after birth (1). clinical picture suggestive of gonococcal disease,
r In the U.S., chlamydia ON occurs in 8.2/1,000 births, DIAGNOSIS clinicians should order a CBC, blood culture, and
while gonococcal ON has an incidence of 0.3/1,000 CSF for analysis and culture.
HISTORY
live births (2). r A history of STIs in the mother should raise the Imaging
r However, ON remains a more significant problem in r Imaging is not necessary in uncomplicated ON and
concern for infectious ON.
developing countries where prenatal health care, r Inquire about fever. should be performed only as indicated for a given
STI screening, and newborn prophylaxis are less r Inquire about excessive tearing. clinical situation.
commonly available. r A CXR should be performed if chlamydial disease is
r The time from birth to symptom onset can be helpful
RISK FACTORS suspected and the infant presents with cough.
r Infectious ON is most commonly acquired as the in diagnosis, though presumptive treatment should r A CT of the head may be indicated in a
not be based on this alone:
infant is exposed to organisms in an infected mother septic-appearing child in whom herpetic disease is
Chemical conjunctivitis from silver nitrate usually
during passage through the birth canal. suspected.
presents within the 1st day after instillation of the
r Premature or prolonged rupture of membranes and Diagnostic Procedures/Other
solution and spontaneously remits within
prolonged labor increase the chance of r Gram stain and culture
2448 hr.
transmission; postdelivery exposures to Gonococcal infection usually becomes r Lumbar puncture as indicated by the clinical picture
microorganisms may also occur. symptomatic within 35 days after birth but can
GENERAL PREVENTION present later. r Noninfectious causes for ON including chemical
Prenatal screening and treatment for maternal STIs The incubation period for chlamydia is 514 days,
irritation
and prophylaxis by administering antibiotic agents so this infection tends to become symptomatic r Dacryostenosis
dramatically decrease the incidence of ON. later with milder symptoms than gonorrheal r Dacryocystitis
disease.
PATHOPHYSIOLOGY r A history of marked lid swelling, chemosis, and r Infectious ON including gonococcal, chlamydial, and
r Gonococcal infection has the propensity to spread herpes viruses
copious amounts of purulent discharge is indicative
and become vision threatening: r Other bacterial causes including Staphylococcus or
of gonococcal disease.
Corneal involvement may occur with progression Pseudomonas species
to perforation, leading to blindness. PHYSICAL EXAM
r Conjunctival injection
There is also potential for development of systemic
r Gonorrheal disease presents with marked eyelid
disease, including meningitis and sepsis.
r Untreated chlamydial infection may lead to eyelid swelling, chemosis, and copious amounts of purulent
scarring and pannus formation and may result in eye discharge. Corneal involvement may occur.
r Chlamydial disease usually presents with mild
blindness, though it is generally less invasive than
gonococcal disease. discharge, but chemosis and pseudomembrane
formation may occur. Untreated infection may lead
ETIOLOGY to eyelid scarring and pannus formation.
r ON may arise from both infectious and
r Herpetic conjunctivitis usually presents as part of a
noninfectious causes.
r The most common etiology of noninfectious ON is more generalized infection. There may be vesicles
surrounding the eye and corneal epithelial
chemical irritation from 1% silver nitrate solution involvement. More seriously, life-threatening CNS
instilled in the eyes at birth to prevent infectious infection may present in a septic-appearing infant.
causes (3).
194
CONJUNCTIVITIS, NEONATAL
Discharge Criteria ADDITIONAL READING

TREATMENT A subset of newborns with conjunctivitis may be
r Lambert SR. Conjunctivitis of the newborn
considered for outpatient therapy:
INITIAL STABILIZATION/THERAPY r This would include any newborns not meeting (ophthalmia neonatorum). In Wright KW, Spiegel
r Fluid stabilization in a septic-appearing infant as admission criteria above. PH, eds. Pediatric Ophthalmology and Strabismus.
indicated r These infants should be started on presumptive 3rd ed. Philadelphia, PA: Elsevier Saunders;
r ON is an ocular emergency requiring systemic therapy for chlamydial infection, which may often be 2005:146148.
r Malika PS, Asok T. Neonatal conjunctivitisa
treatment. safely managed on an outpatient basis.
MEDICATION
r Treatment of suspected gonococcal ON should not
Issues for Referral
r Referral to a neonatologist may be appropriate in
review. Malaysian Family Physician. 2008;3(2):
77-81.
C
r Nelson LB, Harley RD. Disorders of the conjunctiva.
be delayed pending culture results. most cases.
r In cases where neither disease can be conclusively r Patients with chlamydia pneumonia should be In Harleys Pediatric Ophthalmology. 4th ed.
Philadelphia, PA: WB Saunders; 1998:202214.
excluded on clinical grounds, the World Health referred to a neonatologist or pulmonologist with
Organization (WHO) guidelines call for treating experience in managing this disease.
infants with ON for both gonococcal and chlamydial
infection since the coinfection rates are estimated to
CODES
be 2% (4). FOLLOW-UP
r Treatment of chlamydial ON is oral erythromycin ICD9
FOLLOW-UP RECOMMENDATIONS r 098.40 Gonococcal conjunctivitis (neonatorum)
50 mg/kg/day in 4 divided doses for 14 days. Topical r 771.6 Neonatal conjunctivitis and dacryocystitis
erythromycin or tetracycline can be used as COMPLICATIONS
r Corneal ulcer
adjunctive therapy (4). r Glaucoma
r In areas with endemic penicillinase-producing
r Blindness PEARLS AND PITFALLS
strains of gonorrhea, a 3rd-generation
r Meningitis
cephalosporin should be used. The WHO r Infants at risk for gonococcal ON include those in
recommends a single dose of ceftriaxone 50 mg/kg r Pneumonia
r Arthritis the 1st week of life, with fever or mucopurulent eye
IM/IV (max 125 mg) (4,5). discharge, or a maternal history of gonorrhea.
r In areas where most gonococcal disease is penicillin r Osteomyelitis r If gonococcal disease is suspected, do not delay
sensitive, treatment can consist of penicillin G, r Bacteremia
treatment awaiting culture results.
100,000 U/kg/day IV for 7 days. r Sepsis r Chlamydia ON may result in pneumonia; therefore,
r The infants eyes should be frequently irrigated with
PROGNOSIS systemic rather than topical therapy is indicated.
normal saline to clear discharge. r ON typically responds well to antibiotic therapy and r Response to treatment for pneumonia associated
r Herpetic ON should be treated with systemic
usually resolves without sequelae. with chlamydia ON often takes several days to a
acyclovir 30 mg/kg/day PO in divided doses for at r Pneumonia associated with chlamydia typically week to begin demonstrable improvement.
least 2 wk.
responds more slowly to antibiotic therapy than
DISPOSITION other bacterial pneumonias, whether IV or PO
Admission Criteria antibiotics are used.
r All infants with suspected gonococcal ON should
receive a full evaluation for sepsis and be admitted
for systemic treatment. Included would be those REFERENCES
with any of the following features:
1. Schaller UC, Klauss V. Is Credes prophylaxis for
In the 1st week of life
ophthalmia neonatorum still valid? Bull World
Febrile
Health Organ. 2001;79(3):262266.
Mucopurulent eye discharge
Gram stain revealing gram-negative, intracellular 2. Olitsky SE, Hug D, Smith L. Disorders of the
diplococci conjunctiva. In Kliegman RM, Behrman RE, Jenson
Maternal history of gonorrhea HB, et al., eds. Nelson Textbook of Pediatrics.
r Critical care admission criteria: 18th ed. Philadelphia, PA: WB Saunders; 2007:
25882589.
Infants with signs of sepsis may require admission
to a critical care unit. 3. Laga M, Plummer FA, Piot P, et al. Prophylaxis of
Infants with severe chlamydia pneumonia may gonococcal and Chlamydia ophthalmia
require management in a critical care unit. neonatorum. N Eng J Med. 1988;318(11):
653657.
4. World Health Organization. Guidelines for the
Management of Sexually Transmitted Infections.
Geneva, Switzerland: Author; 2003:198.
5. Haase Da, Nash Ra, Nsanze H, et al. Single-dose
ceftriaxone therapy of gonococcal ophthalmia
neonatorum. Sex Transm Dis. 1986;13(1):5355.
195
CONSTIPATION
Besh Barcega
Mary Jane Piroutek

BASICS r The majority of children with constipation beyond
Lab
the neonatal period have functional constipation: r No other specific lab tests are recommended unless
DESCRIPTION Most commonly an acquired behavior, resulting particular organic causes are suspected:
r Constipation can be broadly defined as infrequent from the child purposefully withholding stool in Thyroid-stimulating hormone and free T4 if
bowel movements with at least one of the following: order to prevent further painful defecation concerned about hypothyroidism
Painful defecation, hard stools, purposeful fecal Common triggers include changes in routine or Stool for botulinum toxin if concerned for botulism
retention, fecal soiling, or encopresis. diet, toilet training, starting school, stressful r Stool for occult blood may be useful if history and
r The normal frequency of stools varies with age and events, and postponing defecation because the exam are suggestive for an organic etiology such as
diet (1): child is too busy or does not want to use a public failure to thrive (1).
Newborns may pass stool with every feed, but the toilet.
frequency varies with an average of 4 stools/day r Delayed passage of meconium or constipation in a Imaging
r Routine abdominal radiographs are not
during the 1st wk of life. newborn is organic in nature until proven otherwise:
1.7 stools/day by age 2 yr Organic constipation: Varies due to underlying recommended for initial evaluation but may be
1.2 stools/day by age 4 yr, which remains cause useful to determine the extent of fecal impaction (1).
r Abdominal radiographs should be obtained if a
unchanged throughout adulthood
r Functional constipation is constipation without any COMMONLY ASSOCIATED CONDITIONS sacral dimple is found on exam to look for spinal
See the Differential Diagnosis below of organic causes abnormalities.
evidence of an organic cause:
of constipation.
It is also known as idiopathic constipation, fecal DIFFERENTIAL DIAGNOSIS
withholding, nonorganic constipation, and r Infant dyschezia: Immature coordination of
functional fecal retention.
r Fecal impaction is characterized as a palpable hard
DIAGNOSIS contraction of abdominal musculature and
relaxation of the pelvic floor muscles during
mass in the lower abdomen, a dilated rectum filled HISTORY defecation:
r The child typically presents with a chief complaint of
with stool, or excessive stool in the colon seen on an Typically presents with infant crying, grunting, and
abdominal radiograph. hard pelletlike stools, difficulty or pain with straining prior to having a soft normal bowel
r Constipation accounts for 3% or all general defecating, abdominal pain, abdominal distention, movement. Infants should have a stooling pattern
pediatric outpatient visits and 25% of all pediatric vomiting, or anorexia. within the limits of normal.
r Parents often describe previous similar episodes of Reassure parents that symptoms will resolve with
gastroenterology referrals.
central abdominal pain that improve with a large time as the infants neuromuscular system
EPIDEMIOLOGY bowel movement. becomes more developed.
Incidence r Parents often know when the child is resisting the r Functional causes of constipation: Dietary
r Peak incidence is between 2 and 4 yr of age.
urge to defecate, describing behavior such as transitions, toilet training, acquired behavior
r This is coincident with the typical age of toilet
squatting, standing on toes, or squeezing buttocks. secondary to painful defecation, fecal
training. r Inquire about the childs: retention/withholding behavior, or sexual abuse
Prevalence Previous stooling pattern r Organic causes of constipation:
r 3% in the 1st yr of life (2) Current pattern, consistency, and caliber of stools Anatomic: Anal fissures, strictures, or stenosis;
r 10% in the 2nd yr of life (2) Presence of blood on stools imperforate or anteriorly displaced anus;
r Most studies report similar prevalence rates in boys Associated abdominal pain, vomiting, change in abdominal or pelvic mass; rectal polyps, abscess,
and girls. appetite, and weight loss or foreign body
Recent dietary or social changes Endocrine/Metabolic: Meconium ileus, cystic
RISK FACTORS r Delayed passage of meconium, constipation since fibrosis, hypothyroidism, dehydration, or cows
r Patients with anorectal anomalies such as
birth, significant abdominal distention, bloody stools milk protein intolerance
imperforate anus and patients with neuromuscular (unless an anal fissure is present), abnormal Neuromuscular: Spina bifida, cerebral palsy,
diseases such as spina bifida tend to have development, weight loss, and failure to thrive are Hirschsprung disease, infantile botulism, or spinal
constipation despite corrective surgery. red flags for an underlying organic cause. cord lesion
r Patients with metabolic abnormalities and patients r In the neonate or young infant, include questions Drugs: Antacids, anticholinergics, opiates,
taking medications, such as narcotics, tend to have about strength of suckle, feeding, and muscle tone. antidepressants, antiepileptics, antihypertensives,
constipation. iron, or lead poisoning
PHYSICAL EXAM
GENERAL PREVENTION r Look for abdominal distention; palpate for
Anticipatory guidance regarding diet, toilet training, abdominal masses and tenderness TREATMENT
and toileting behaviors may prevent or ameliorate r Assess the location of the anus, and examine the
functional constipation. sacral area to look for anatomic malformations. r Treatment typically involves acute disimpaction and
PATHOPHYSIOLOGY r Look for the presence of anal fissures if there is a then maintenance therapy in order to keep the
r Withholding stool leads to incomplete rectal history of bloody stools. rectum empty and allow the rectum to return to its
emptying and stool impaction. Impacted stool r Check for the presence of an anal wink and normal size:
becomes firm and dry as fluid reabsorption cremasteric reflexes. Also check extremity tone, Maintenance therapy is often needed for several
continues in the colon. strength, and deep tendon reflexes. Absence or months.
r Retained stool in the rectum causes distention and diminished presence of these are suggestive of a r Parental education, behavior modification, and close
dilation of the rectum. This results in a higher neuromuscular abnormality. follow-up are essential to prevent recurrence.
threshold of stimulation to signal the need for r At least 1 digital anorectal exam is recommended r If an organic cause is found, treatment involves
defecation and also leads to weakening of the (1): addressing the underlying problem.
sphincter muscle, which further impedes stool If a rectal exam is done, an empty rectum on
evacuation and leads to soiling and encopresis. physical exam is concerning for an organic cause.
r When the child does finally defecate, painful large, In the neonate, focus on suckle, bulbar findings,
hard stool is passed, reinforcing further withholding and muscle tone.
behavior.
196
CONSTIPATION
MEDICATION DISPOSITION REFERENCES

Disimpaction by either the oral or rectal route is Admission Criteria
effective: r Children with abdominal pain and colons full of 1. Constipation Guideline Committee of the North
r Oral route is preferred but may be limited by stool requiring whole bowel irrigation American Society for Pediatric Gastroenterology,
compliance issues. r Failed disimpaction Hepatology, and Nutrition. Evaluation and
r Rectal route yields results more quickly but is r Concern for an undiagnosed organic cause of treatment of constipation in infants and children:
Recommendations of the North American Society
invasive. constipation necessitating further workup
for Pediatric Gastroenterology, Hepatology, and
First Line Discharge Criteria Nutrition. J Pediatr Gastroenterol Nutr.
Polyethylene glycol (PEG) 3350: r Sufficient amount of stool evacuated 2006;43:e1e13. C
r Disimpaction: 11.5 g/kg/day for 3 days r Child able to tolerate food orally 2. Loening-Baucke V. Prevalence, symptoms and
r Maintenance: 1 g/kg/day outcome of constipation in infants and toddlers.
Issues for Referral
Referral to pediatric gastroenterology when J Pediatr. 2005;146:359363.
Second Line
r Osmotic agents: management is complex, therapy fails, or there is 3. Pashankar DS, Loening-Baucke V, Bishop WP.
Lactulose or sorbitol 70% solution: concern for an undiagnosed organic disease. Safety of polyethylene glycol 3350 for the
13 mL/kg/day in divided doses treatment of chronic constipation in children. Arch
COMPLEMENTARY & ALTERNATIVE Pediatr Adolesc Med. 2003;157:661664.
May cause abdominal cramping and flatulence
THERAPIES 4. Loening-Baucke V, Pashankar DS. A randomized,
Magnesium hydroxide 400 mg/5 mL liquid: r For infants, dietary changes:
13 mL/kg/day prospective, comparison study of polyethylene
Up to 4 ounces of sorbitol-containing juice (pear,
Potential for acute magnesium toxicity glycol 3350 without electrolytes and milk of
prune, white grape, or apple) daily. May dilute 1:1 magnesia for children with constipation and fecal
Magnesium citrate: with water.
<6 yr old: 13 mL/kg/day; 612 yr old: r Behavior modification incontinence. Pediatrics. 2006;118:528535.
100150 mL/day; >12 yr old: 150300 mL/day r Biofeedback therapy
in single or divided doses
Potential for acute magnesium toxicity ADDITIONAL READING
Phosphate enema: FOLLOW-UP r Bulloch B, Tenenbein M. Constipation: Diagnosis
Disimpaction: 2 yr old: 6 mL/kg up to 135 mL and management in the pediatric emergency
Use with caution in children with kidney FOLLOW-UP RECOMMENDATIONS department. Pediatr Emerg Care. 2002;18:
problems because of cases of lethal r Follow up with pediatrician in 23 days.
254258.
hyperphosphatemia and hypocalcemia. r Discharge instructions and medications: r Van den Berg MM, Benninga MA, Di Lorenzo C.
r Lubricant: For children eating table food, increase water and Epidemiology of childhood constipation: A
Mineral oil: fiber content of diet. Bran, psyllium, or systematic review. Am J Gastroenterol. 2006;
Disimpaction: 1530 mL per year of age orally methylcellulose supplementation may help. 101:24012409.
to max of 240 mL/day Encourage scheduled time to sit on the toilet for r Youssef NN, Peters JM, Henderson W, et al. Dose
Maintenance: 13 mL/kg/day 10 min after each meal. response of PEG 3350 for the treatment of childhood
Not recommended <1 yr old; causes lipoid Return promptly to medical care for vomiting, fecal impaction. J Pediatr. 2002;141:410414.
pneumonia if aspirated fever, severe abdominal pain, anorexia, or any
r Stimulants: Use for acute disimpaction for 35 days: other concerns. See Also (Topic, Algorithm, Electronic
Senna (8.8 mg sennosides/5 mL): Media Element)
26 yr old: 2.57.5 mL/day; 612 yr old: PROGNOSIS r Anal Fissure
r Months of treatment are usually required.
515 mL/day r Botulism
r Roughly 50% recurrence rate:
May cause abdominal pain. Side effects include r Hirschsprung Disease
idiosyncratic hepatitis, melanosis coli, 1 yr recovery rate 3060% regardless of
hypertrophic osteoarthropathy, and analgesic laxative chosen (4)
nephropathy. COMPLICATIONS CODES
Bisacodyl: Chronic abdominal pain, rectal fissures, enuresis,
2 yr old: 13 tablets (5-mg tablet) or 0.51 encopresis, urinary tract infection, rectal prolapse, and ICD9
suppository (10-mg suppository) per dose social stigmata r 560.32 Fecal impaction
Side effects include abdominal pain, diarrhea, r 564.00 Constipation, unspecified
hypokalemia, and proctitis. r 564.09 Other constipation
Glycerin suppository:
Rarely of value in children >6 mo old
PEG-electrolyte solution:
Disimpaction: 25 mL/kg/hr (up to 1 L/hr) by NG PEARLS AND PITFALLS
tube until effluent is clear or 20 mL/kg/hr for r Constipation should be a diagnosis of exclusion in
4 hr/day patients with acute abdominal pain.
Maintenance: 510 mL/kg/day r A normal stooling history per the patient should
Usually requires hospital admission
not be taken at face value, and appropriate
historical questions may reveal abnormal stooling
patterns that the patient has accepted as normal.
197
CONSTRICTING BAND/TOURNIQUET SYNDROME

Carl K. Hsu
Bradley Pecker

r Primary constricting band: A band of any type of r A crying, inconsolable infant without obvious cause
r Pain and swelling, most commonly a finger or toe, Remove rings and other potential constricting bands, if
material such as metal, fabric, or hair tightened possible, before the development of tourniquet
around an appendage that causes swelling and pain with or without visualization of a constricting band syndrome.
(eg, a hair knotted around a toddlers toe). (eg, a knotted hair that may be buried within the
r Secondary constricting band: Injury or disease edema) INITIAL STABILIZATION/THERAPY
r Other locations: Wrist, ankle, toe, umbilicus, ear r Pain management and conscious sedation may be
process that causes the swelling and edema
resulting in tightness against the band (eg, an lobe, nipple, septum or nares of nose, uvula, penis, necessary.
r Removal of ring or constricting band
impacted ring with an underlying fracture of the scrotum, vaginal labia, or tongue
finger) r In older children and adolescents, inquire about
MEDICATION
r If left untreated, the constricting band may become duration of constriction, any associated trauma, and r Local anesthetic:
embedded and interrupt skin integrity and attempts at removal prior to the emergency Nerve blockade with local anesthetic is preferred.
circulation to the affected appendage. department visit. Lidocaine 1% or 2%, max 5 mg/kg (without
r For rings, inquire as to the type of metal, since new epinephrine)
RISK FACTORS r Opioids:
r Poor hygiene styles of rings made of ultrahard metals such as
r Long hair titanium or tungsten or ceramic cannot be removed Removal of ring or constricting band usually
r Child abuse using standard ring cutters and must be removed by results in significant immediate reduction in pain,
cracking. and systemic analgesics are typically unnecessary.
GENERAL PREVENTION PHYSICAL EXAM Morphine 0.1 mg/kg IV/IM/SC q2h PRN:
r Good hygiene Initial morphine dose of 0.1 mg/kg IV/IM may
Perform a thorough visual and neuromuscular exam of
r Short hair be repeated q1520min until pain is controlled,
the swollen affected appendage, with high suspicion
r Avoidance of tight-fitting rings or small objects that of a hair tourniquet if no constricting band is seen. then q2h PRN
can be potentially be slipped onto an appendage Codeine/Acetaminophen dosed as 0.51 mg/kg of
DIAGNOSTIC TESTS & INTERPRETATION codeine component PO q4h PRN
PATHOPHYSIOLOGY Lab r NSAIDs:
r Primary constricting band: Constricting band or ring
Initial Lab Tests Consider NSAID medication in anticipation of
impedes return of lymphatic and venous fluid, Usually not indicated for acute treatment: prolonged pain and inflammation.
resulting in edema r Occasionally, CBC and C-reactive protein may be Ibuprofen 10 mg/kg/dose PO/IV q6h PRN
r Secondary constricting band: Underlying injury,
used to differentiate between edema and cellulitis of Ketorolac 0.5 mg/kg IV/IM q6h PRN
typically traumatic but sometimes infectious, causes an involved digit or appendage. Naproxen 5 mg/kg PO q8h PRN
swelling and edema r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN
Imaging r Administer tetanus prophylaxis if indicated.
ETIOLOGY X-ray may be needed to assess for underlying fracture
Tourniquet syndrome may result from underlying or foreign body after band removal. SURGERY/OTHER PROCEDURES
allergic, dermatologic, iatrogenic, endocrinologic, r The distal swollen finger, especially the proximal
infectious, malignant, metabolic, physiologic, or Diagnostic Procedures/Other
Measurement of electrolytes, BUN and creatinine, interphalangeal joint, presents an important
traumatic conditions or be related to pregnancy.
thyroid function tests, and Tzanck smear of vesicular obstacle in constricting band removal.
COMMONLY ASSOCIATED CONDITIONS lesions may be useful in the diagnosis of secondary r Distal to proximal edema reduction by these
r Trauma sequential compression methods:
constricting band.
r Any process causing edema and swelling Self-adherent tape is wrapped distal to proximal
to form a smooth and compressed area over
Pain, swelling, edema, cyanosis, prolonged capillary
which the band is advanced.
refill, neurapraxia, or necrosis
A Penrose surgical drain or a finger cut from a
DIFFERENTIAL DIAGNOSIS small glove is stretched to fit over the distal
r Primary vs. secondary constricting band swelling before the attempted removal:
r Cellulitis With lubrication, the proximal end of the drain is
r Tenosynovitis pulled under the ring to form a cuff around the
ring; the cuff with distal traction applied
advances the band over the decompressed area.
Suture material (no. 0 silk, dental floss, or
umbilical tape) is wrapped under tension in a tight
layer advancing over the edema in a distal to
proximal direction; the proximal tail of the suture
material (or floss) is tucked under the ring; with
lubrication, the tail under tension is pulled distally
and unwound, forcing the ring over the layered
suture material and decompressed area.
198
CONSTRICTING BAND/TOURNIQUET SYNDROME
r Constricting band removal by manual division: Cracking ring:

Scissors may be used to lift and then cut the Rings made of ceramic or tungsten are removed FOLLOW-UP
offending fibrous band constricting a toddlers toe by cracking them.
or penis. Tungsten is the hardest metal used in jewelry FOLLOW-UP RECOMMENDATIONS
A no. 11 scalpel blade with the cutting surface up and cannot be cut but can be cracked due to
may be sufficient to cut constricting bands formed poor malleability. Wound check if skin disruption
by hair, fibers, or plastic ties. To do so, a vice or vice pliers is needed. Acetaminophen, ibuprofen, or opiates for pain
A topical commercially available depilatory agent Tighten the vice pliers/grip onto the ring, Appropriate medications for underlying medical
causes
may be used to divide a tourniquet formed by a
suspected hair obscured by local edema.
remove and then tighten the vice by a turn of
the tightening screw. r Activity: C
A handheld wire cutter/stripper may readily divide Clamp onto the ring, and repeat this process of As tolerated
small-girth metallic rings with minimum slightly narrowing the width of the vice until Patient Monitoring
discomfort: when the vice is closed onto the ring, cracking r Social work referral
This type of removal may impart a crush defect occurs. r Report for suspected child abuse
to the ring, making repair difficult. More than 1 crack may be required, and
A long-handled bolt cutter available in most cracking in more than 1 location may be PROGNOSIS
operating rooms or in the hospital engineering required. r Varies with duration and degree of constriction
department may be used to divide large-girth, Use this same technique for ceramic rings, and/or tourniquet syndrome
broad-sized rings: taking care that no portion of the ring may fly r Generally well tolerated if constricting band did not
Longer handles provide significant mechanical out and strike the patient or staff. cause prolonged ischemia of the affected appendage
advantage needed to cut large rings.
The reinforced cutting blades may not fit DISPOSITION COMPLICATIONS
Admission Criteria r Loss of function, neurapraxia, or necrosis.
through a constricting band with adjacent r Loss of function, tissue ischemia or necrosis, or r Associated injury from attempts at removal
swollen tissue and skin.
A standard hand-powered, medically approved neurovascular compromise
r Suspected child abuse
ring cutter (Steinmann pin cutter with a
MacDonald elevator) may be used to divide
ADDITIONAL READING
Discharge Criteria
small-girth metallic constricting bands made of r Successful removal with restoration of circulation r Hsu CK, Neblett M, Mansur M, et al. Hair tourniquet
soft metals such as gold or silver: and function syndrome: Division by a topical deplilatory agent.
This method has the advantage of a cleaner cut r Decreased pain and edema Unpublished data.
for subsequent repair of the ring. r Peckler B, Hsu CK. Tourniquet syndrome: A review
The disadvantage is that the handheld ring Issues for Referral
r Underlying fractures: Orthopedics, hand, or podiatry of constricting band removal. J Emerg Med.
cutter is labor intensive and may aggravate the 2001;20(3):253262.
r Ischemia of appendage: Hand surgery, urology
pain of an underlying injury. r Rosen P, Chan TC, Vilke GM, et al. Atlas of
Constricting band removal by motorized COMPLEMENTARY & ALTERNATIVE Emergency Procedures. St. Louis, MO: Mosby; 2001.
cutting: THERAPIES
A motorized high revolution per minute (RPM) r Treatment is directed at removal of the constricting See Also (Topic, Algorithm, Electronic
cutting device may be used to rapidly divide band either by advancing the constricting band Media Element)
constricting bands irrespective of girth and size distally or by division. Tungsten and titanium ring removal instruction can be
of the ring: It may be battery-powered, r These adjuvant methods may be used alone or in found at http://www.titaniumstyle.com
AC-powered, or pneumatically driven in the
combination:
operating suite.
Elevation of the affected extremity may help
Motorized cutting procedure:
decrease vascular congestion. CODES
Protective eyewear should be worn by all
Cooling the extremity with ice or cold water to
persons present, including the patient. ICD9
Place a thin aluminum splint (shaped to the reduce edema and erythema
Lubrication with soap or mineral oil to allow for 782.3 Edema
curvature of the ring) between the patients skin
slippage of tourniquet over an inflamed or
and the ring as a shield to protect underlying
edematous area
tissue from heat and debris. PEARLS AND PITFALLS
Cool the splint and cutting surface with ice
r Crying or inconsolable infants should be carefully
water irrigations before and during the cutting
procedure. evaluated for a hair tourniquet.
The high-RPM cutting wheel is then used to cut r Constricting bands or rings may result in tourniquet
through the band over the volar aspect of the syndrome and permanent injury.
finger. r Administration of local anesthesia or analgesic is
Because of heat generation, limit cutting with appropriate.
the motorized device to 5-sec intervals with r Rings made of titanium may take a long time to cut
60-sec intervals of ice water cooling. using a ring cutter, or a ring cutter may fail.
A tenaculum may be used to spread the band r Tungsten cannot be removed using a ring cutter and
made of softer metals after the 1st cut. must be cracked using a vice.
A 2nd cut may be made by rotating the ring 180
degrees and again cutting on the volar aspect.
This method may fail when used for ultrahard
metal rings such as titanium.
Tungsten rings cannot be cut using a ring cutter.
199
CONTACT DERMATITIS
Solomon Behar

Usually a clinical diagnosis
DESCRIPTION HISTORY
r Contact dermatitis is an inflammatory condition of r Ask about the following exposures: Diagnostic Procedures/Other
the skin leading to an eczematous rash. Hygiene products Refractory cases of ACD or those involving the
r Two major types: Clothing/Diapers face/hands should have patch testing against various
Footwear allergens by a dermatologist or allergist.
Irritant contact dermatitis (ICD), which accounts
for 80% of cases Jewelry DIFFERENTIAL DIAGNOSIS
Allergic contact dermatitis (ACD) Cosmetics r Atopic dermatitis
Fragrances r Acrodermatitis enteropathica
EPIDEMIOLOGY Deodorants r Cutaneous mycosis
Incidence Medicines (systemic and topical) r Impetigo
r Allergy sensitization rates: Nonprescription medicinal supplements
r Scabies
1320% of all children (1,2) Home remedies
24.5% in children 6 mo to 5 yr of age (3) r Past medical history r Photodermatitis
More common in infants and younger children r Elicit history of known allergies r Psoriasis
r Prevalence increases with age due to cumulative r Ask about: r Herpes simplex virus infection
exposure to allergens and sensitizations. Sporting and other extracurricular activities r Chemical burn
Hobbies r Nummular eczema
RISK FACTORS
Timing and distribution of rash r Seborrheic dermatitis
Previous exposure to antigen primes the immune
system to react to re-exposures. Pain and/or itching
Prior history of allergic reactions
GENERAL PREVENTION Lip licking TREATMENT
Avoiding known allergens or irritating substances Prior history of rashes
Respiratory symptoms INITIAL STABILIZATION/THERAPY
PATHOPHYSIOLOGY Allergen avoidance is the single most important
r ICD: Nonimmunologic inflammatory reaction to any
PHYSICAL EXAM treatment in ICD/ACD. All other therapies are adjuvant
substance irritating the skin r ICD: Large red patches in discrete patterns matching and not for chronic use.
r ACD: Type IV T-cellmediated hypersensitivity distribution of causative agent exposure
reaction: r ACD: Red, edematous areas usually in the same MEDICATION
Allergen penetrates skin and activates Langerhans distribution as ICD but can have vesicles and First Line
cell within skin, which presents the antigen to T r Topical moisturizers (petroleum jellies, lotions)
papules present
cells (sensitization) r Generalized rash may occur in ACD (called id r Barrier creams (in diaper ICD), such as zinc oxide,
Upon re-exposure to allergen, memory T cells reaction) applied each diaper change to affected area
activate the allergic response. r Special conditions: r Topical steroids:
ETIOLOGY Lip-lickers dermatitis: Perioral ICD after excessive Low potency: Hydrocortisone 1% cream applied
r ICD: Saliva, feces, urine, foods, detergents, soaps, licking around lips to affected areas b.i.d. until improved
wipes, bubble baths, nickel, cobalt Rhus dermatitis: ACD appearing as a Moderate potency: Mometasone 1% cream or
r ACD: Certain plants (poison ivy, sumac, oak); nickel; vesicobullous eruption after exposure to poison ointment applied to affected area per day until
ivy, sumac, or oak improved. Do not use >7 days on the face.
thimerosal; and a wide variety of synthetic chemicals r Antihistamines:
in rubber, metals, dyes, and preservatives Shoe dermatitis: ACD affecting dorsa of feet,
sparing the skin between the toes Generally not necessary but may be used for
COMMONLY ASSOCIATED CONDITIONS Juvenile plantar dermatosis: ICD usually affecting severe pruritis
Atopic dermatitis (associated with ACD) prepubertal children; dermatitis on plantar surface Diphenhydramine 1 mg/kg/dose PO q6h PRN for
with painful fissuring itching OR
Hydroxyzine 1 mg/kg/dose PO q6h PRN for itching
(ACD has been described with this medicine in
case reports, so use with caution.) OR
Loratadine: Age 25 yr, 5 mg PO per day >5 yr,
10 mg OR
Cetirizine: Age 612 mo, 2.5 mg PO per day
15 yr, 2.55 mg PO per day >6 yr, 510 mg PO
per day
200
CONTACT DERMATITIS
Second Line COMPLICATIONS

r Topical calcineurin inhibitors: Tacrolimus 0.03% or Secondary skin infections from itching can occur. CODES
pimecrolimus 1% applied to affected area b.i.d.
PRN: ICD9
Should be short-term use REFERENCES r 692.4 Contact dermatitis and other eczema due to
Only for children >2 yr of age 1. Weston WL, Weston JA, Kinoshita J, et al. other chemical products
Avoid in immune-suppressed patients (4) Prevalence of positive epicutaneous tests among r 692.5 Contact dermatitis and other eczema due to
r Oral steroids for severe flares:
infants, children and adolescents. food in contact with skin
A 5-day burst of 1 mg/kg/day per day or divided Pediatrics.1986;78:10701074. r 692.9 Contact dermatitis and other eczema, C
b.i.d 2. Barros MA, Baptista A, Correia M, et al. Patch unspecified cause
In rhus dermatitis, a 14-day course (7 days at testing in children: A study of 562 school children.
1 mg/kg/day followed by 7-day taper) is Contact Dermatitis. 1991;25:156159.
sometimes used. 3. Bruckner AL, Weston WL, Morelli JG. Does PEARLS AND PITFALLS
DISPOSITION sensitization to contact allergens begin in infancy? r The location of the rash may give clues as to what
Discharge Criteria Pediatrics. 2000;105:e3.
the offending substance may be that is causing the
Unless complicated by severe infection, all contact 4. Fonacier L, Spergel J, Leung DYM, et al. Report of
rash (eg, rash on the lower abdomen under the
dermatitis patients may safely be discharged home. the Topical Calcineurin Inhibitor Task Force of the
jeans button leads one to consider a nickel contact
Issues for Referral American College of Allergy, Asthma and
allergic dermatitis).
Refer refractory cases to dermatology or allergy Immunology and the American Academy of Allergy, r Palmar and plantar surfaces of the hands and feet
specialists. Asthma and Immunology. J Allergy Clin Immunol.
2005;115:12491253. are generally not affected by ACD.
r Ask about products used by parents and siblings.
FOLLOW-UP Children often will experiment with these
ADDITIONAL READING substances on their own skin, leading to ICD/ACD.
FOLLOW-UP RECOMMENDATIONS r Nickel is the most common allergen in ACD. Topical
r Eczema. In Behrman RE, Kliegman RM, Jenson HB,
Discharge instructions and medications: neomycin is the second most common allergen.
r Keep fingernails clean and short. eds. Nelson Textbook of Pediatrics. 16th ed. r Make sure parents send instructions on allergen
r Avoid known allergens/irritants. Philadelphia, PA: WB Saunders; 2000.
r Militello G, Jacob SE, Crawford GH. Allergic contact avoidance to daycare providers and teachers.
r Follow up with primary care provider in 12 wk.
dermatitis in children. Curr Opinion Pediatr.
DIET 2006;18(4):385390.
Exclude foods thought to be associated with r Nijhawan RI, Matiz C, Jacob SE. Contact dermatitis:
outbreaks of dermatitis. From basics to allergodromes. Pediatr Ann.
2009;38(2):99108.
PROGNOSIS
Contact dermatitis is a chronic condition that has a
good prognosis as long as avoidance of exacerbating
substances is practiced.
201
CONVERSION DISORDER
Allison A. Keller
D. Richard Martini
Charles W. Pruitt

BASICS r Psychodynamic theory: r A detailed neurologic exam is necessary to evaluate
An unconscious process by which psychosocial for organic disease.
DESCRIPTION needs conflict or stresses are expressed as somatic r Positive signs of conversion disorder in motor
Conversion disorder is a type of somatoform disorder symptoms disturbances:
that typically affects voluntary motor or sensory Conversion symptoms develop to defend against Movement during sleep
functions. The symptom or deficit: unacceptable impulses. Movement after noxious stimuli
r Is not intentionally produced or feigned The conversion symptom binds anxiety and keeps Automatic behaviors such as dressing oneself
r Cannot be fully explained by: a conflict internal. are preserved.
r Learning theory: Avoidance of hurting oneself (when dropping the
A general medical condition
The direct effects of a substance Conversion symptom is seen as a classically paralyzed arm over the childs face)
A culturally sanctioned behavior conditioned learned behavior: Symptoms of illness Hoover test: If a patient in supine position is truly
r Causes clinically significant distress or impairment in are used as a means of coping with an otherwise making an effort to lift a weak or paralyzed leg,
social or occupational functioning, or warrants perceived impossible situation. the examiner will note pressure under the
medical evaluation Secondary gain may be an important factor: contralateral heel.
r Is not limited to pain symptoms Children with illness and disability become the Giveaway weakness: A patients motor strength
r Is not better accounted for by another cause focus for family attention. demonstrates resistance followed by a sudden loss
r Is a mental disorder (1) of resistance (in contrast to true weakness, where
the patient exerts constant resistance).
Occurs in the presence of other psychiatric illness r Positive signs of conversion disorder in gait
EPIDEMIOLOGY including depression, anxiety, and personality
Incidence disorders (6) disturbances:
Annual incidence rate for all ages is 522/100,000 May walk normally when not being observed
(2). May attempt to fall vs. attempt to support self
Prevalence DIAGNOSIS Atasia-abasia: Inability to stand despite normal
r Child psychiatrists report a prevalence of 13% of ability to move legs when sitting
r Conversion disorder is not a diagnosis of exclusion. r Positive signs of conversion reaction with sensory
their patients (3). r The diagnosis should be made on the basis of
r 1% of patients admitted for neurologic problems deficits:
negative organic findings and positive evidence of Sensory loss does not conform to dermatomal
have conversion symptoms (2).
conversion reaction. See positive signs of conversion distribution.
RISK FACTORS reactions in the Physical Exam section. Sharply demarcated boundaries that involve all
r More common in females than males across all age localized sensory modalities (pain, temperature,
HISTORY
groups r The physical impairment interferes with daily life. light touch, proprioception, and vibration)
r The onset of conversion disorder is from late Reaction to sensation while asleep
r Symptoms often mimic those of a close friend or
childhood to early adulthood and is rare before age Inconsistent findings on repeated sensory exams
relative. r Pseudoseizure characteristics:
10 yr or after age 35 yr. r A medical illness may have occurred prior to the
r Children who have been exposed to violence or Thrashing about with trunk rather than
development of the unexplained symptom. tonic-clonic movement
sexual abuse are more likely to experience r Psychological stressor within hours to weeks of
conversion symptoms. Absence of incontinence, tongue biting, or
r High frequency of recent familial stress, family symptom onset postictal state
r Symptoms may cause more distress to the parents
communication problems, unresolved grief reactions, Resistance toward examiner opening eyelids
and school-related and social disturbances (4) than to the patient. during the event
r May have coexisting medical and neurologic La belle indifference is lack of concern or Avoidance of noxious stimuli, such as sternal rub,
indifference to physical disability that would cause or other painful stimuli
disorders: r Positive signs of conversion reaction with severe
great psychological distress to others with the
May be modeled after previous or current illness,
same new-onset disability. bilateral blindness:
or the illness of a family member r Frequently reported symptoms:
Intact pupillary responses
PATHOPHYSIOLOGY Weakness or paralysis Sudden flash of bright light results in patient
r Conversion reactions usually mimic lesions in the Paresthesias flinching
voluntary motor or sensory pathways. Gait disturbances Instruction to Look at your hand and the
r Some data implicate biologic and Pseudoseizures patient does not look there (Blindness does not
neuropsychological factors in the development of Visual disturbance affect looking in the appropriate direction.)
conversion symptoms: r Conversion reaction vs. organic etiology: Instruction to Touch your index fingers and the
Functional MRI studies have shown different Sleep or other vital functions often are not patient is unable to perform (Blind people can do
activation patterns in patients with conversion interrupted. this via proprioception.)
symptoms vs. healthy control subjects. Occurs more during or preceding school hours
These imaging findings are thought to be Occurs more around other people rather than in
consistent with the involuntary nature of isolation
conversion symptoms (5). Brought on by emotional stresses rather than
specific events or physical actions (7)
202
CONVERSION DISORDER
DIAGNOSTIC TESTS & INTERPRETATION DISPOSITION 4. Zeharia A, Mukamel M, Mimouni M, et al.

Lab Admission Criteria Conversion reaction: Management by the
r In all cases, consider the possibility of organic Consider admission for patients when further pediatrician. Eur J Pediatr. 1999;158:160164.
disease processes. evaluation is required to exclude organic etiology. 5. Stone J, Zeman A, Simonotto E, et al. FMRI in
r Consider lab evaluation to exclude: patient with motor conversion symptoms and
Discharge Criteria
Electrolyte disturbances r No evidence of acute medical or neurologic disorder controls with simulated weakness. Psychosom
Hypoglycemia Med. 2007;69(9):961969.
requiring inpatient treatment
Renal dysfunction r Appropriate follow-up established 6. Pehlivanturk B, Unal F. Conversion disorder in
Systemic infection
Toxicologic exposures/ingestions Issues for Referral
children and adolescents. A four-year follow up
study. J Psychosom Res. 2002;52:187191.
C
r Consider CSF analysis to evaluate for infection. r Neurologic consultation may be helpful if the
7. Schecker NH. Childhood conversion reactions in the
neurologic findings are equivocal: ED: Part IIgeneral and specific features. Pediatr
Imaging May be necessary in the emergency department
r CT scan or MRI may rule out lesions of the brain or Emerg Care. 1990;6:4651.
If an emergency medical condition has been 8. Schecker NH. Childhood conversion reactions in the
spinal cord. excluded, consider a neurology referral for further
r EEG may help distinguish true seizures from emergency department: Diagnostic and
evaluation of a possible seizure disorder or for an management approaches within a biopsychosocial
pseudoseizures. equivocal neurologic exam.
r Psychiatric consultation may be helpful if an organic framework. Pediatr Emerg Care. 1987;3:202208.
r Neurologic disorders: cause is largely excluded.
Toxins, dystonic reaction, neuroleptic agents r Referrals may be made to behavioral pediatricians or ADDITIONAL READING
Intracranial hemorrhage child psychiatrists. r Dula DJ, DeNaples L. Emergency department
Brain or spinal cord tumor or abscess
Encephalitis presentation of patients with conversion disorder.
Degenerative disease FOLLOW-UP Acad Emerg Med. 1995;2:120123.
r Glick TH, Workman TP, Gaufberg SV. Suspected
Guillain-Barre syndrome FOLLOW-UP RECOMMENDATIONS
MS r Close follow-up with the primary care physician and conversion disorder: Foreseeable risks and avoidable
Myasthenia gravis errors. Acad Emerg Med. 2000;7:12721277.
psychiatrist, if the patient is undergoing psychiatric
Myopathy care, is recommended to assess for persistence of
Optic neuritis symptoms, missed organic etiologies, or continued
Polymyositis psychosocial stressors.
CODES
Vestibular neuronitis r The patient should be encouraged to return to
Creutzfeldt-Jakob disease ICD9
r Psychologic disorders: age-appropriate levels of functioning as soon as
possible. 300.11 Conversion disorder
Factitious disorder or malingering
Munchausen syndrome or Munchausen by proxy PROGNOSIS
r Many children with conversion reactions have PEARLS AND PITFALLS
Hypochondriasis
Pain disorder or other somatoform disorder spontaneous remission or require only brief r Conversion disorder is not simply a diagnosis of
psychotherapy.
r Full recovery occurs in >85% of children. exclusion:
TREATMENT r Favorable prognostic features include a recent onset Rather, it requires a negative workup for organic
etiologies as well as positive signs of conversion
PRE HOSPITAL of symptoms, a single symptom manifestation, and reaction.
Treat patients as if the symptoms are resulting from no other comorbidities. r Anxiety, depression, exposure to violence or sexual
r Early recognition is associated with a quicker
organic disease. abuse, and social/familial stress all predispose to
recovery. conversion disorder.
INITIAL STABILIZATION/THERAPY r Children with conversion disorder may have
r The emergency physician must initially evaluate the COMPLICATIONS
r Disuse atrophy and contractures are rare but coexisting medical or neurologic illness:
patient as if the symptoms are resulting from
organic disease. reported in cases of prolonged conversion disorder Children presenting with pseudoseizures often
r However, consider both physiologic and psychosocial with limb disuse. have an underlying seizure disorder.
r Unnecessary diagnostic tests and unsuccessful Patients with chronic illnesses or recovering from
contributions to presenting symptoms (8).
r Emergency physicians should: medical interventions illness may develop conversion symptoms.
r School absence r Limited time available in the emergency department
Accept that patients can have distressing physical
symptoms without feigning symptoms. makes the diagnosis of conversion disorder difficult.
Avoid telling patients that their symptoms are Consider early neurologic or psychiatric consultation.
imaginary but empathize with the stress of their
REFERENCES r Ensure adequate follow-up to assess missed organic
condition. etiologies or continued psychosocial stressors.
1. American Psychiatric Association. Diagnostic and
Avoid focusing on organic diagnosis or Statistical Manual of Mental Disorders. 4th ed.
psychologic diagnosis alone but rather emphasize Washington DC: Author; 1994.
a concurrent physiopsychologic approach to 2. Marsden CD. Hysteriaa neurologists view. Psych
evaluation (8). Med. 1986;16:277288.
r Suggestive therapy: Symptoms remit spontaneously
3. Leary PM. Conversion disorder in
with simple suggestion that symptoms should childhooddiagnosed too late, investigated too
resolve soon. much? J R Soc Med. 2003;96:436438.
203
CORNEAL ABRASION
Nicole D. Porti
Karen Franco
r Trachoma r If the exam is limited by pain, a topical anesthetic

BASICS r Lid surgery should be used (tetracaine or proparacaine: See
r Anesthesia Medications).
DESCRIPTION r UV keratitis r Slit lamp exam:
r The cornea is the transparent cover of the anterior
r Chemical exposures Reveals defect in the corneal epithelium
portion of the eye that functions to protect the eye r Spontaneous Reveals depth of corneal defect
and provide refraction. r Iatrogenic factors Identifies associated injuries
r A corneal abrasion is an acquired defect in the Utility limited by age (ability to cooperate) and
cornea, specifically the corneal epithelium. size of patient (ability to adjust slit lamp to size of
EPIDEMIOLOGY DIAGNOSIS patient)
Should be used in conjunction with the fluorescein
Incidence HISTORY exam (see Diagnostic Procedures/Other)
Corneal abrasions are common, but the exact r Symptoms usually include:
incidence is unknown: DIAGNOSTIC TESTS & INTERPRETATION
r In a survey of ophthalmic emergencies in a general Eye pain
FB sensation Imaging
hospital emergency department in the U.K., 66% Tearing If there is concern about a retained FB, ocular CT or
presented with trauma, with 80% of those patients Comfort increased with eye closing MRI may be needed:
having minor trauma, mainly abrasions or foreign r Metallic FBs are a contraindication to MRI.
Blurred vision
bodies (FBs) (1). Isolated crying in the infant
r In a pediatric study, nonperforating anterior globe Diagnostic Procedures/Other
r Details of antecedent trauma or FB often given: Fluorescein exam confirms the diagnosis of corneal
injuries were the most frequent injury encountered Injury: Finger or fingernail, paper, tree branch, abrasion. This dye stains the basement membrane,
(93%). 83% of those were corneal abrasions (2). sand which is exposed in the area of the epithelial defect:
RISK FACTORS Exposure: Chemical, makeup application r Techniques:
r Obtain history of contact lens use
Not wearing protective eyewear when appropriate Place a fluorescein paper strip over the inferior
(eg, during sports activities) PHYSICAL EXAM cul-de-sac of eye, and use saline or a topical
r Exclude penetrating trauma. If unable to open the anesthetic to moisten the strip and allow dropping
PATHOPHYSIOLOGY
The cornea is composed of 5 layers (anterior to eye, gently retract the lids without applying pressure into the eye. Once the patient blinks, the dye is
posterior): The corneal epithelium, Bowman layer, to the globe: spread. Do not touch the cornea with the
corneal stroma, Descemet membrane, and the corneal Confirm the pupil is central and round. fluorescein paper strip. OR
endothelium: Confirm the anterior chamber is grossly clear with Moisten the fluorescein strip with saline. Touch
r A corneal abrasion is a violation of the most normal contour. the strip to the palpebral conjunctivae, avoiding
Elicit pupillary response to light: the bulbar conjunctivae. Once the patient blinks,
superficial layer. the dye is spread.
Assess for an irregular pupil, large nonreactive
ETIOLOGY r When using either the cobalt blue filter on an
pupil, extruded ocular contents, loss of normal
r Traumatic: ophthalmoscope, slit lamp, or a Wood lamp, an
contour, hyphema (blood), or hypopyon (pus).
Sports-related injury The pupil may be small from a reactive miosis. abrasion will appear as yellow-green.
Blowing dust, sand, or debris r Assess extraocular movement. r If there is penetrating trauma, then leaking aqueous
Mechanical injury: r Assess visual acuity: humor may be seen (Seidel sign).
Direct injury (eg, from a finger or tree branch)
Use an age-appropriate eye chart.
May be occult, as in a 1-mo-old infant who
Visual acuity may be affected if the abrasion is
presents with crying (inadvertent) over the visual axis.
FB related r Inspect for FB. Make sure the eyelids are flipped in
Contact lens trauma
order to look for the object (see Foreign Body,
Cornea topic).
204
CORNEAL ABRASION
r Corneal ulceration
Second Line
r Topical antibiotics:
REFERENCES
r Conjunctivitis Sulfacetamide 10% solution: 12 gtt q2h 1. Edwards RS. Ophthalmic emergencies in a district
r Keratitis Polymyxin/Trimethoprim solution: 12 gtt q2h general hospital casualty department. Br J
r Corneal perforation Ciprofloxacin solution: 12 gtt q2h Ophthalmol. 1987;71:938942.
r Ruptured globe r Ibuprofen 10 mg/kg/dose PO q6h 2. Nelson LB, Wilson TW, Jeffers JB. Eye injuries in
r Recurrent corneal erosion r Acetaminophen/Oxycodone 0.1 mg/kg/dose q6h childhood: Demography, etiology, and prevention.
r Corneal foreign body Pediatrics. 1989;84:438441.
r Chemical burn r None 3. Peyman GA, Rahimy MH, Fernandes ML. Effects of
morphine on corneal sensitivity and epithelial
C
r Iritis r Treating simple corneal abrasions by patching does
wound healing: Implications for topical ophthalmic
not improve healing or reduce pain (4). analgesia. Br J Ophthalmol. 1994;78(2):138141.
TREATMENT DISPOSITION 4. Turner A, Rabiu M. Patching for corneal abrasion.
Corneal abrasions are managed on an outpatient Cochrane Database Syst Rev. 2006;(2):cd004764.
INITIAL STABILIZATION/THERAPY basis.
r Cover the globe with a protective shield if
penetrating trauma is suspected. ADDITIONAL READING
r Apply a topical anesthetic for patient comfort and to FOLLOW-UP
facilitate the exam. FOLLOW-UP RECOMMENDATIONS Media Element)
Discharge instructions: r Conjunctivitis
MEDICATION
r Instruct the patient to use antibiotics as prescribed r Foreign Body, Cornea
First Line
r Topical antibiotics are the mainstay of treatment. or until asymptomatic (may be shorter duration than
Ointment is better than drops since it acts as a 35 days).
r Repeat eye exam in 24 hr. CODES
lubricant and is administered less often. Duration of
treatment is typically 35 days: r If symptoms persist >4 hr, re-exam by an
Bacitracin ointment 0.5 ribbon to lower eyelid ophthalmologist is warranted. ICD9
q48h r Advise eye rest. Significant eye movement may 918.1 Superficial injury of cornea
Erythromycin ointment: 0.5 ribbon to the lower interfere with healing.
eyelid q48h Patient Monitoring
Sulfacetamide ointment: 0.5 ribbon to the lower Follow up for fluorescein testing in 2448 hr to ensure
PEARLS AND PITFALLS
eyelid q48h healing. May be done by optometry, ophthalmology, a r A patient with eye pain, FB sensation, and tearing
r Topical NSAIDs have been found to be useful in
primary care provider, or the emergency department with preceding trauma or FB likely has a corneal
reducing pain:
PROGNOSIS abrasion or more significant injury.
Ketorolac tromethamine 0.5%: 1 gtt q.i.d. for up r Rule out penetrating trauma 1st:
to 2 wk Healing within 2448 hr is to be expected. The
r Topical anesthetics: prognosis is excellent in most cases. Emergent referral to ophthalmology is warranted
if penetrating trauma exists.
Use a minimal amount in the emergency COMPLICATIONS r Topical antibiotics are the treatment of choice, with
department, and do not let the patient take drops r Deeper abrasions involving the visual axis may heal
home. These agents can compromise wound resolution of abrasion expected in 12 days.
with a scar, leading to loss of visual acuity. r Follow-up for fluorescein testing in 2448 hr should
healing (3) and blunt normal corneal reflex and r Allergic conjunctivitis secondary to ophthalmic
sensation. be ensured to assess for healing.
medications
Tetracaine 0.5% ophthalmic solution: r Recurrent corneal erosions may occur in area of
Apply 12 gtt x 1; may repeat once
healed abrasion if reinjured.
Proparacaine 0.5% ophthalmic solution:
Apply 12 gtt x 1; may repeat up to 57 times
205
COSTOCHONDRITIS
Abu N.G.A. Khan
Faiz Ahmad
BASICS DIAGNOSIS r Tietze syndrome is similar to costochondritis, except
for the presence of significant swelling, frequently at
DESCRIPTION HISTORY the right sternoclavicular or costochondral junction.
r Costochondritis is an inflammatory process of the The onset of costochondritis is often insidious. Chest It is usually due to minor trauma and responds to
costochondral or costosternal joints that causes wall pain with a history of repeated minor trauma or NSAIDs.
localized pain and tenderness. unaccustomed activity (eg, painting, moving furniture) r Muscle strain is common, especially if there is a
r It is a benign cause of chest pain and is an is common. Pain may be described as follows: history of sports participation or exertion, although
important consideration in the differential diagnosis r Sharp, nagging, aching, or pressurelike
quite often there is no known precipitating event.
of chest pain: r Affects the anterior chest wall Blunt trauma may cause recurrent pain long after
Although the term costochondritis often is used r Usually unilateral (left side more frequent than the the event. Chronic or paroxysmal coughing can
interchangeably with fibrositis and Tietze right side) cause muscle strain or even rib fractures.
syndrome, these are distinct diagnoses. r Usually localized but may extend or radiate r Precordial catch, or Texidor twinge, is a
EPIDEMIOLOGY extensively relatively frequent cause of sharp pain of short
r Exacerbated by trunk movement, deep inspiration, duration in healthy teenagers and young adults. It is
Incidence
and/or exertion often related to exercise and is characterized by a
The exact prevalence of a musculoskeletal etiology for
r Lessens with decreased movement, quiet breathing, brief, sharp, shooting pain that pinpoints to the left
chest pain is not known, although overall prevalence
or change of position substernal border or apex. The onset is sudden, with
of a musculoskeletal etiology for chest pain was
1030%. r May be severe a momentary hesitation on inspiration, then shallow
r May wax and wane breathing resumes until the pain subsides, usually
RISK FACTORS within a minute. The pain may recur frequently or
r Girls are affected more often than boys. PHYSICAL EXAM remain absent for months.
r Peak age for chest pain in children is 1214 yr of r Pain with palpation of affected costochondral joints r Chest wall pain from herpes zoster follows a
age. is a consistent finding in costochondritis. dermatomal pattern and may precede the rash by
r Typically, the 2nd to 5th costochondral junctions are 12 days. This is rare in adolescents and children.
GENERAL PREVENTION r Bornholm disease: Also known as epidemic
involved; in 90% of patients, >1 junction is
Modify improper posture or ergonomics at home,
involved. pleurodynia or Devils grip. Its usually caused by
school, or the workplace. r Surprisingly, patients may not be aware of the chest some strains of coxsackievirus or echovirus and is
PATHOPHYSIOLOGY wall tenderness until exam. due to inflammation of pleural lining or intercostal
r Costochondritis is an inflammatory process of the r The diagnosis should be reconsidered in the absence muscles. Pain is spasmodic, lasting 1530 min.
costochondral or costosternal joints. of local tenderness to palpation: Symptoms may last from 26 days. Complications
r The 2nd to 5th costochondral junctions most Tietze syndrome is characterized by are rare but may include orchitis, pericarditis,
commonly are involved. nonsuppurative edema. myocarditis, and aseptic meningitis. Treatment is
r >1 site is affected in 90% of cases. Costochondritis has no palpable edema. pain control with NSAIDs.
r Other diagnoses:
r The etiology of costochondritis is not well defined. Cardiovascular: Myocardial ischemia, pericarditis,
Lab supraventricular tachycardia
r Costochondritis is often preceded by an upper No specific diagnostic studies exist for costochondritis. Pulmonary: Asthma/Bronchospasm, pneumonia,
respiratory infection or exercise. The clinical scenario and the most likely differential pneumothorax, pneumomediastinum
r Repetitive minor trauma has been proposed as the diagnoses should guide which laboratory tests are to GI: Reflux, esophagitis
most likely cause. be obtained: Rheumatoligic: Fibromyalgia, rheumatoid arthritis
r Bacterial or fungal infections of these joints occur r An ECG may be helpful to rule out cardiac pathology. Oncologic: Leukemia, sarcoma, etc.
uncommonly, usually in patients who are IV drug Miscellaneous: Psychogenic chest pain (stress,
Imaging
users or those who have had thoracic surgery. r Chest radiograph is not routinely warranted but is anxiety), breast development (both sexes)
r Costochondritis, among others, is a common
sometimes obtained to rule out differential
noncardiac cause of chest pain in athletes. diagnoses for chest pain.
r Some case reports exist where bone (gallium) scans
have been used to confirm the clinical diagnosis.
206
COSTOCHONDRITIS

TREATMENT FOLLOW-UP Media Element)
r Chest Pain
r NSAIDs for pain control r Trauma, Chest
Assess and address any compromise of airway, r Reassure patients of the benign nature of the
breathing, or circulation. problem, and instruct them regarding avoidance of
MEDICATION
provoking activities. CODES
r Provide patients with a good understanding of the
First Line
Ibuprofen 10 mg/kg PO q6h, drug of choice for initial
proper use and potential adverse effects of NSAIDs.
r Primary care follow-up with persistent symptoms
ICD9 C
therapy. 733.6 Tietzes disease
r Other NSAID options include flurbiprofen, r The prognosis for patients with costochondritis is
excellent.
PEARLS AND PITFALLS
mefenamic acid, ketoprofen, and naproxen. r After 1 yr, 1/2 of patients still may have discomfort
r Narcotic analgesics generally are not required but r Always consider serious causes of chest pain in the
may be used if necessary, such as morphine 0.1 and 1/3 report tenderness with palpation. differential diagnosis (myocardial ischemia or
mg/kg IV/SC/IM, repeated as necessary. infarction, pulmonary embolism, pericarditis,
r Local infiltration of local anesthetic, steroid, or pneumonia, etc.).
ADDITIONAL READING r Parents and patients often have significant anxiety
intercostal nerve block (reserved for refractory cases)
r Brown RT, Jamil K. Costochondritis in adolescents: A and concern that the cause of chest pain is cardiac
COMPLEMENTARY & ALTERNATIVE in nature. It is essential to assuage such concerns.
follow-up study. Clin Pediatr. 1993;32:499500.
THERAPIES r Disla E, Rhim HR, Reddy A, et al. Costochondritis. A r Consider costochondral infection in IV drug abusers.
r Local heat r Costochondritis is an important cause of school
r Stretching of the pectoralis muscles 23 times a day prospective analysis in an emergency department
setting. Arch Intern Med. 1994;154(21): absence.
may be beneficial.
24662469. r Adolescents tend to limit physical activity
r Avoid repetitive misuse of muscles.
r Fam AG, Smythe HA. Musculoskeletal chest wall unnecessarily for long periods.
r Modify improper posture or ergonomics at home, r Restriction of activities is usually not required.
pain. Can Med Assoc J. 1985;133(5):379389.
school, or the workplace. r Fraz M. Pediatric Respiratory Disease: Diagnosis and
DISPOSITION Treatment. Philadelphia, PA: WB Saunders;
Admission Criteria 1993:162172.
An isolated costochondritis patient does not need to r Gotway MB, Marder SR, Hanks DK, et al. Thoracic
be admitted unless there is an underlying systemic complications of illicit drug use: An organ system
illness that requires hospitalization. approach. Radiographics. 2002;22:S119S135.
r Kocis KC. Chest pain in pediatrics. Pediatr Clin North
Am. 1999;46:189203.
r Mendelson G, Mendelson H, Horowitz SF, et al. Can
(99m)technetium methylene diphosphate bone
scans objectively document costochondritis? Chest.
1997;111:16001602.
r Selbst DM. Chest pain in children: Consultation with
the specialist. Pediatr Rev. 1997;18:169173.
r Sik EC, Batt ME, Heslop LM. Atypical chest pain in
athletes. Curr Sports Med Rep. 2009;8(2):5258.
207
COUGH
Eileen Murtagh Kurowski
Lynn Babcock Cimpello
r Other focal infections: Sinusitis, tonsillitis, laryngitis, PHYSICAL EXAM

BASICS laryngotracheitis, tracheitis, pneumonia, r Vital signs including pulse oximetry (SpO )
2
bronchiolitis, pleuritis, bronchiectasis, airway or r Perform a full physical exam with particular focus on
DESCRIPTION pulmonary abscess lung, cardiac, and ENT exams
r Cough is forced expiration that can be stimulated by r Structural: Pneumothorax, atelectasis due to mucus r Lungs:
multiple receptors in the airways mucosa or may be plugging, usually from infectious etiologies Asymmetric breath sounds suggest pneumonia,
produced voluntarily. r Congenital: Laryngotracheomalacia, atelectasis, FB, or mass.
r Cough can be divided into:
tracheoesophageal fistula Rales (crackles) or rhonchi indicate atelectasis or
Acute: <4 wk r Suppurative lung disease: Cystic fibrosis, chronic infiltrate.
Chronic: >4 wk aspiration, immunodeficiency Increased work of breathing including grunting,
EPIDEMIOLOGY r Asthma, allergy, or vasomotor rhinitis nasal flaring, retractions, or abdominal breathing
r Aspiration, including foreign body (FB) is found in children with respiratory compromise.
Incidence
r According to the 2006 National Hospital Ambulatory r Physical/Chemical irritation: Tobacco/Wood smoke, Wheezing can be found in asthma, bronchiolitis,
dry/dusty environment, volatile chemicals or FB aspiration.
Medical Care Survey, 6.6% (1.4 million) of
r Iatrogenic: Angiotensin-converting enzyme (ACE) Stridor occurs in upper airway obstruction from
emergency department visits among children <15
edema, mass, infection, or FB.
yr of age were for the chief complaint of cough (1). inhibitors
r School-aged children typically have 46 r Other: Paroxysmal cough suggests pertussis or atypical
pneumonia.
symptomatic upper respiratory tract infections Habit or psychogenic r Cardiac: Assess for signs of CHF and/or
(URTIs) per year (2). 50% recover by 10 days, 90% CHF
hemodynamic compromise including:
by 25 days, and 10% will have persistent symptoms Mediastinal mass
Tachycardia
into the 3rd and 4th wk (3). GERD
Prolonged capillary refill
Prevalence Relentlessly progressive cough (increasing
Presence of S3, S4, or gallop
r The exact prevalence is unknown. frequency and severity >23 wk) is concerning
Diminished or unequal central and distal pulses
r According to 1 community-based survey, reported for pertussis, retained inhaled FB, expanding
(especially important in infants with concern of
cough without colds has a prevalence of 28% in mediastinal neoplasm, or lobar collapse secondary
congenital heart disease)
boys and 30% in girls (4). to mucous plug or TB. r ENT: Assess for signs of URTI, allergies, irritants, or
GENERAL PREVENTION FB:
Use measures to prevent spread of infections: DIAGNOSIS Nasal congestion or rhinorrhea
r Hand washing Erythema of posterior pharynx, which may
r Cover your cough, coughing into your elbow. The combination of the history and physical exam indicate postnasal drip
defines the etiology of cough in most cases. Inspection of the ear for matter in the external
PATHOPHYSIOLOGY canal or fluid within the middle ear
r Cough can be divided into 3 phases: HISTORY Lymphadenopathy
r Obtaining a detailed history will help elucidate the
Inspiratory: Inhaling lengthens expiratory muscles. etiology of the cough. DIAGNOSTIC TESTS & INTERPRETATION
Compressive: Very brief closure of the glottis to r Chronicity: Lab
maintain lung volumes as intrathoracic pressure r None routinely indicated
Most children will present with acute onset of
builds due to isometric contraction of expiratory r Tests to consider include:
cough, especially with URTI and most infections
muscles
Chronic cough (>4 wk) is concerning for asthma, Pertussis culture or PCR if spasmodic or whooping
Expiratory: Opening of glottis, releasing brief
postnasal drip due to allergic rhinitis, GERD, cough.
supramaximal expiratory flow followed by lower
retained FB, pertussis, TB, or mediastinal mass. CBC may show a lymphocytosis.
expiratory flows r Nature/Quality:
r Dynamic collapse of airways occurs: Sputum Gram stain/culture if productive cough to
Barky: Croup aid in diagnosis of pneumonia
Can be voluntary or involuntary
Brassy: Tracheomalacia, habit, or viral PPD and/or acid fast bacilli (AFB) culture if there is
May be triggered as part of a laryngeal expiratory
Paroxysmal: Pertussis clinical concern for TB. Consider referral for
reflex when the larynx is stimulated by foreign
Productive cough, especially with hemoptysis, early-morning gastric aspirate samples for
material. Laryngeal cough is thought to protect
concerning for bronchiectasis diagnosis.
the airways from aspiration. r Absence of cough during sleep is suggestive of habit
Chemo- or mechanical receptors in the lower Imaging
cough. r Obtain a CXR if:
airways may also act as a trigger for cough and r Triggers: Smoke, cold, pets, plants
function primarily in airway clearance and Red flags on history are present
r Family history: Respiratory diseases, atopy Hemoptysis
maintenance of the mucociliary apparatus.
r Medication use: ACE inhibitors can cause cough. Concern for FB aspiration
ETIOLOGY r Red flags: Uncertain about the diagnosis of pneumonia
r Most commonly due to URTIs:
Neonatal onset: Congenital malformation, r Consider CXR for occult pneumonia for children
Usually caused by viruses: Respiratory syncytial
aspiration, or perinatal infection <5 yr of age, with temperature >39 C, and WBC
virus, human metapneumovirus, parainfluenza,
Cough with feeding: Aspiration >20,000/mcL (5).
influenza, adenovirus
Bacterial: Streptococcus, Haemophilus, Moraxella, Chronic moist cough: Bronchiectasis Diagnostic Procedures/Other
Associated night sweats/weight loss: Malignancy r Urgent bronchoscopy is indicated if there is concern
Chlamydia (infants), pertussis, Mycobacterium
Fungal or TB for aspirated FB.
TB Signs of chronic lung disease: Failure to thrive, r Consider spirometry in children 6 yr of age with
finger clubbing, overinflated chest, or chest chronic cough that is concerning for asthma.
deformity
208
COUGH
COMPLEMENTARY & ALTERNATIVE 8. Udezue E. Lidocaine inhalation for cough

TREATMENT THERAPIES suppression. Am J Emerg Med. 2001;19(3):
Honey (between 1/2 and 2 teaspoons/dose depending 206207.
PRE HOSPITAL on the age of the child) has been shown to decrease 9. American Academy of Pediatrics, Subcommittee
Assess and support ABCs. symptoms in children 218 yr of age with acute URTIs on Diagnosis and Management of Bronchiolitis.
when given prior to bedtime, as compared to placebo Diagnosis and management of bronchiolitis.
INITIAL STABILIZATION/THERAPY (10).
r Assess and stabilize airway, breathing, and Pediatrics. 2006;118:17741793.
circulation. Issues for Referral 10. Paul IM, Beiler J, McMonagle A, et al. Effect of
r Treat the underlying cause of cough. Outpatient referral to pulmonology, honey, dextromethorphan, and no treatment on
nocturnal cough and sleep quality for coughing
C
r Consider symptomatic treatment such as a cool-mist allergy/immunology, cardiology, psychiatry, surgery,
and others, as is appropriate to the patient children and their parents. Arch Pediatr Adol Med.
humidifier and/or increased fluid intake. 2007;161(12):11401146.
MEDICATION
The U.S. FDA Nonprescription Drugs and Pediatric FOLLOW-UP
Advisory Committees recommend against the use of ADDITIONAL READING
over-the-counter (OTC) cough and cold medications in r If a definitive diagnosis is not obtained in the r Bachur RG. Cough. In Fleisher GR, Ludwig S, eds.
infants and children <6 yr, citing a lack of safety and Textbook of Pediatric Emergency Medicine. 6th ed.
efficacy data in these children (6). emergency department, follow-up with the primary
care provider is recommended. Philadelphia, PA: Lippincott Williams & Wilkins;
First Line r If an empiric trial of asthma therapy is started for 2010.
r Treat the underlying cause of cough: r Shields MD, Bush A, Everard ML, et al. British
cough, follow-up must be scheduled and medication
See the Asthma topic for dosing of stopped if no improvement is seen. Thoracic Society Cough Guideline Group.
bronchodilators. r Other discharge instructions, medications, and Recommendations for the assessment and
See the Pneumonia topic for dosing of antibiotics. follow-up is disease specific. management of cough in children. Thorax.
r Dextromethorphan: 2007;63:115.
Not recommended for children <6 yr PROGNOSIS
r Most coughs resolve spontaneously or with See Also (Topic, Algorithm, Electronic
Children 612 yr: 510 mg PO q4h or 15 mg PO
q68h PRN treatment of the underlying cause. Media Element)
r 10% of children will have persistent cough after r Asthma
>12 yr: 1030 mg PO q8h PRN r Foreign Body Aspiration
viral illness for up to 1 mo.
Second Line r Pneumonia
r Codeine: COMPLICATIONS r Wheezing
Not recommended for children <6 yr r Interference with sleep, school function, and play
Children 612 yr: 2.55 mg PO q46h PRN r Parental anxiety
>12 yr: 1020 mg PO q46h PRN r Other complications are dependent upon the
r No strong evidence of efficacy of dextromethorphan underlying etiology.
CODES
or codeine in acute cough in children (7).
r For pertussis, macrolides should be initiated within ICD9
12 wk of the onset of symptoms to reduce the REFERENCES 786.2 Cough
period of infectivity.
r A small study showed that nebulized lidocaine 1. Pitts SR, Niska RW, Xu J, et al. National Hospital
Ambulatory Medical Care Survey: 2006 PEARLS AND PITFALLS
(0.25% solution given q46h, preceded by a emergency department summary. Natl Health Stat
bronchodilator) was able to decrease persistent r Appropriate treatment of cough depends on
Report. 2008;(7):138.
cough in adults (8). identification of the underlying etiology.
2. Monto AS, Sullivan KM. Acute respiratory illness r OTC cough and cold remedies are not recommended
SURGERY/OTHER PROCEDURES in the community. Frequency of illness and the
Emergent laryngoscopy and bronchoscopy if concern agents involved. Epidemiol Infect. 1993;110(1): for children <6 yr of age.
for aspirated FB 145160.
DISPOSITION 3. Hay AD, Wilson A, Fahey T, et al. The duration of
acute cough in pre-school children presenting to
Admission Criteria primary care: A prospective cohort study. Fam
r Significant increased work of breathing
r Frequent albuterol treatment requirement Pract. 2003;20(6):696705.
r Hypoxemia with increased oxygen requirement from 4. Burr ML, Anderson HR, Austin JB, et al.
Respiratory symptoms and home environment in
baseline children: A national survey. Thorax. 1999;54(1):
r Significant dehydration and/or inability to maintain
2732.
hydration status 5. Rutman MS, Bachur R, Harper MB. Radiographic
pneumonia in young, highly febrile children with
Intubation for respiratory failure leukocytosis before and after universal conjugate
Severe asthma with need for continuous albuterol pneumococcal vaccination. Pediatr Emerg Care.
and concern for decompensation 2009;25(1):17.
Discharge Criteria 6. Kuehn BM. Citing serious risks, FDA recommends
r Well appearing without respiratory distress no cold and cough medicines for infants. JAMA.
r At baseline oxygenation level: 2008;299(8):887888.
For young, previously healthy children with 7. Taylor JA, Novack AH, Almquist JR, et al. Efficacy
bronchiolitis, SpO2 90% is acceptable for of cough suppressants in children. J Pediatr.
discharge (9). 1993;122(5 Pt 1):799802.
For children with other lung processes (eg, asthma
or pneumonia), many clinicians use SpO2
9293% as discharge criteria.
r Well hydrated and able to tolerate oral fluids
209
CROUP
Mary Jane Piroutek
Lilit Minasyan
PHYSICAL EXAM DIFFERENTIAL DIAGNOSIS

BASICS r Stridor may be present at rest or with agitation: Other causes of stridor should be considered:
Stridor may be inspiratory or biphasic in severe r Epiglottitis:
DESCRIPTION cases. Lower incidence since the Haemophilus influenzae
r The term croup is used to describe r Barky cough, hoarse voice type b vaccine
laryngotracheobronchitis, or infectious croup, as well r Fever Toxic appearing, severe distress, drooling,
as spasmodic croup. r Varying degrees of tachypnea or respiratory distress dysphagia, sniffing or tripod position
r Infectious croup is an acute respiratory illness r Minimal to no pharyngitis, normal epiglottis r Laryngomalacia or tracheomalacia
characterized by barky, seallike cough, fever, r Impending respiratory failure marked by severe r Retropharyngeal or peritonsillar abscess
sometimes with inspiratory stridor, and mild to r Foreign body aspiration
retractions, significant hypoxemia, cyanosis, fatigue,
severe respiratory distress due to obstruction of the r Angioedema or allergic reaction
or decreased level of consciousness
larynx. r A croup severity score has been developed (2): r Anatomic abnormality of airway:
EPIDEMIOLOGY Mild: Subglottic stenosis
r Peak incidence is between 6 mo and 3 yr of age (1). Occasional barky cough, no stridor at rest, mild Respiratory laryngeal papillomatosis (human
r Occurs in 5% of children in 2nd yr of life or no retractions papillomavirus verrucae growth in airway)
r Typically seen in fall and winter seasons Moderate: Atrioventricular malformation
r 85% of children seen in emergency departments Frequent barky cough, stridor at rest, retractions r Bacterial tracheitis:
have mild croup, and <1% have severe croup (2). Severe: Should be considered in severe cases that do not
Frequent cough, prominent stridor, marked respond to routine treatment
GENERAL PREVENTION distress and retractions Toxic-appearing patient
Hand washing and routine personal protective
DIAGNOSTIC TESTS & INTERPRETATION Drooling or dysphagia
equipment can help control transmission.
r Lab or imaging studies are generally not indicated in
PATHOPHYSIOLOGY mild or moderate cases of croup.
r Acute laryngotracheobronchitis: Erythema and r The diagnosis can be made based on historical and TREATMENT
edema of walls and inflammatory cells within exam findings.
respiratory lumen PRE HOSPITAL
r Edema of vocal cords and luminal narrowing leads Lab Attention to airway patency and oxygenation
r No routine lab testing is necessary, as croup is a
to characteristic cough, hoarseness, and stridor. INITIAL STABILIZATION/THERAPY
r Spasmodic croup: Noninflammatory edema of clinical diagnosis. r Assess airway patency, oxygenation, and degree of
r Viral studies are generally not useful, as disease is
subglottic trachea respiratory distress.
self-limited: r Take care not to upset or agitate the patient, as this
ETIOLOGY May be helpful in cohorting admitted patients or
Viral croup: may worsen stridor and respiratory distress.
in severe cases, especially if the patient does not r Oxygen as necessary
r Parainfluenza type 1 is the most common causative respond to routine management r Prompt treatment with appropriate medications
organism (1). Imaging r Careful airway management with consideration for
r Other viruses have also been implicated, including r Radiographs are not routinely indicated.
parainfluenza types 2 and 3, respiratory syncytial r X-rays of the neck may show narrowing of the need of endotracheal intubation as indicated
virus, adenovirus, influenza, and measles (1): subglottic space (steeple sign) on AP or lateral views. MEDICATION
Influenza has been associated with more severe First Line
cases. Diagnostic Procedures/Other r Nebulized epinephrine:
Pulse oximetry should be obtained:
r May have hypoxemia in severe cases Recommended in patient with stridor at rest
DIAGNOSIS Temporary relief of symptoms of airway
obstruction
HISTORY Repeat treatments may be needed in severe cases.
r Acute onset of barky cough, shortness of breath, Recommended dose: 2.25% 0.5 mL in 2.5 mL of
fever, stridor or noisy breathing saline
r Symptoms are typically worse at night.
r Prodrome of fever, rhinorrhea, and cough may be
present.
210
CROUP
r Corticosteroids: ADDITIONAL READING

Recommended for moderate or greater severity, FOLLOW-UP r Cherry JD. Croup. N Engl J Med. 2008;358:
typically patients with increased work of breathing
or stridor at rest FOLLOW-UP RECOMMENDATIONS 384391.
Shown to decrease emergency department length Discharge instructions and medications: r Donaldson D, Poleski D, Knipple E, et al.
of stay, rates of admission, and return visits r For children who present early with croup that is Intramuscular versus oral dexamethasone for the
Associated with decreased need for intubation in mild and does not warrant corticosteroid therapy, a treatment of moderate-to-severe croup; a
severe cases prescription for a burst dose of steroid (prednisone randomized, double blind trial. Acad Emerg Med.
2003;10:1621.
Oral or IM route of corticosteroids is equal or more
effective than an inhaled route (3).
12 mg/kg/day for 24 days) may be given to the
parent with instructions to use if the child develops r Johnson DW, Jacobson S, Edney PC, et al. A C
Recommended dose: stridor at rest. comparison of nebulized budesonide, intramuscular
Dexamethasone 0.6 mg/kg single dose PO or IM r Return for worsening dyspnea, stridor at rest, dexamethasone, and placebo for moderately severe
(4) excessive drooling, dysphagia, fatigue, or cyanosis croup. N Engl J Med. 1998;339:498503.
Nebulized budesonide 2 mg in 4 mL saline r Generally, no further home medications, other than r Klassen TP, Craig WR, Moher D, et al. Nebulized
Nebulized L-epinephrine (1:1,000) solution antipyretics, are indicated unless there is a comorbid budesonide and oral dexamethasone for the
diluted in 5 mL saline condition such as: treatment of croup. JAMA. 1998;279:16291632.
Otitis media requiring antibiotics r Waisman, Y, Klein BL, Boenning DA, et al.
ALERT
Humidified air or cool mist has repeatedly been Asthma exacerbation may need additional Prospective randomized double-blind study
demonstrated to be ineffective as a therapy for corticosteroids. comparing L-epinephrine and racemic epinephrine
Patient Monitoring aerosols in the treatment of laryngotracheitis
croup (5):
r Evidence-based practice clearly does not warrant The croup severity scale may be used to monitor (croup). Pediatrics. 1992;89:302306.
r Zhang L, Sanguebsche LS. The safety of nebulization
use of this therapy on an inpatient or outpatient response to treatment.
with 3 to 5 ml of adrenaline (1:1000) in children: An
basis. PROGNOSIS evidence based review. J Pediatr (Rio J).
r Self-limited illness usually lasting <1 wk, peaking
Second Line 2005;81:193197.
on day 23 of illness
Heliox (helium/oxygen mixture): r <5% require hospitalization; of these, 12% See Also (Topic, Algorithm, Electronic
r May be equally effective but more expensive than Media Element)
require intubation.
treatment with racemic epinephrine (6) Tracheitis
r Caution should be used when using heliox, as it COMPLICATIONS
allows a greater quantity of epinephrine to be Complications are uncommon but may include:
delivered to the alveoli. r Hypoxemia CODES
SURGERY/OTHER PROCEDURES r Dehydration ICD9
Intubation and mechanical ventilation in cases of r Secondary bacterial infections: r 464.4 Croup
severe respiratory compromise or failure: r 478.75 Laryngeal spasm
r May need smaller endotracheal tube due to edema Otitis media
Sinusitis r 490 Bronchitis, not specified as acute or chronic
around the glottic and subglottic structures
Pneumonia
DISPOSITION
Admission Criteria PEARLS AND PITFALLS
r Minimal or no improvement 24 hr after steroids REFERENCES
r Most cases of croup are mild to moderate cases and
given 1. Bjornson CL, Johnson DW. Croup. Lancet.
r Recurrence of respiratory distress during observation self-limited.
2008;371:329339. r Rapid administration of corticosteroids and use of
period 2. Bjornson CL, Johnson DW. Croup-treatment
r Persistent stridor at rest racemic epinephrine are mainstays of therapy.
update. Pediatr Emerg Care. 2005;21:863870. r If intubation is needed, be prepared to use an
r Requiring multiple nebulized epinephrine treatments
3. Russell KF, Wiebe N, Saenz A, et al. Glucocorticoids endotracheal tube that is 0.51.0 size smaller than
r Critical care admission criteria: for croup. Cochrane Database Syst Rev. would normally be used due to tracheal edema.
Severe symptoms with poor response to treatment 2004;(1):cd001955. r Dexamethasone may be given orally with equal
Suspected bacterial croup or tracheitis 4. Bjornson CL, Klassen TP, Williamson J, et al. A efficacy as IM administration.
Impending respiratory failure or need for randomized trial of a single dose of oral
mechanical ventilation dexamethasone for mild croup. N Engl J Med.
Discharge Criteria 2004;351:13061313.
r No stridor at rest 5. Moore M, Little P. Humidified air inhalation for
r No respiratory distress treating croup. Cochrane Database Syst Rev.
r Normal color/perfusion or pulse oximetry 2006;(3):cd002870.
r Reliable follow-up 6. Weber JE, Chudnofsky CR, Younger JG, et al. A
r Moderate cases may be discharged after treatment randomized comparison of helium-oxygen mixture
and 24 hr of observation: (heliox) and racemic epinephrine for the treatment
Observation time after racemic epinephrine is not of moderate to severe croup. Pediatrics.
well studied or defined. 2001;107:e96.
Issues for Referral

May need pediatric ENT consultation for suspected
abscess or for congenital or anatomic abnormalities
211
CRYING/COLIC
Seth L. Brindis
Marianne Gausche-Hill
r Look for signs of physical injury/trauma:

BASICS DIAGNOSIS Inspect for bruising.
Palpate for tenderness along the long bones.
DESCRIPTION HISTORY Hair tourniquets:
r Rule of 3: Colic is defined as crying in an infant r Suggestive of colic:
Fingers: Swollen and edematous finger or toe
who is well fed and healthy that is: 1st born distal to the tourniquet
>3 hr per day Late afternoon and evening crying Genitals (penis or clitoris) swollen or
>3 days a week Increasing after 34 wk of age erythematous distal to the tourniquet
For >3 wk Peak crying at 6 wk of age Fluorescein-aided corneal exam to detect abrasion
r 1030% of infants are affected. Periods of normal/happy behavior Retinal exam in suspected child abuse
r Begins at 24 wk, peaks at 6 wk, and resolves No fever r Observe feeding.
typically by 4 mo of age Able to be soothed r Assess the emotional state of the parents: Presence
r Diurnal pattern, with increased crying late afternoon Mothers mood, symptoms of postnatal depression
r Suggestive of organic cause: of fatigue, depression, anger, or agitation.
and early evening
r Most common in 1st-born infants Preterm DIAGNOSTIC TESTS & INTERPRETATION
Complications in the perinatal period Lab tests and radiographic examinations usually are
PATHOPHYSIOLOGY History of underlying conditions unnecessary if the patient is growing well and has a
The unifying pathophysiology of colic is largely History of possible ingestions/exposures normal exam.
unknown, though it has been attributed to: Fever Lab
r GI disorders Apnea The extent of lab evaluation will depend on the clinical
r Normal variances in temperament Cyanosis presentation and suspicion for illness or injury.
r Psychosocial and neurodevelopmental disorders Respiratory distress
Rash Imaging
ETIOLOGY Forceful vomiting Imaging may be indicated based on clinical
r <5% of excessive crying is due to an organic cause, Recent illness presentation:
but this must be ruled out. r Other important history points: r Consider CXR in children with respiratory distress.
r Infection: Allergies r Consider appropriate plain x-rays of deformed or
Meningitis Attempted medical treatments tender long bones.
Sepsis Homeopathic, natural, cultural treatments r Consider urgent head CT if concerned about child
Otitis media/externa Stooling pattern abuse or if there is a history of trauma.
Urinary tract infection Family history
Viral illness Sibling temperament
Thrush TREATMENT
PHYSICAL EXAM
Gingivostomatitis r Plot child on growth chart: Height, weight, and
r GI: PRE HOSPITAL
head circumference. Failure to gain weight and poor Advise EMS personnel to reassure the parents,
Constipation growth are likely to point to an organic/infectious
Cows milk protein intolerance allowing the parents to ride with the child to the
cause. hospital.
GERD r Vital signs: With a temperature >38 C, consider
Lactose intolerance INITIAL STABILIZATION/THERAPY
infectious etiologies. r ABCs: Ensure that the patient is adequately
Anal fissure r Observation of the child being held by a parent gives
Intussusception protecting his or her airway, and stabilize breathing
Hernia clues to parent bonding and also consolability of the
and circulation abnormalities.
r Neurologic: infant. r Reassure the parents, allowing them to watch your
r Remove all clothing.
CNS abnormality (Chiari type 1) r Thorough cardiac, respiratory, abdominal, and skin exam and explaining what you are examining.
Infantile migraine Discuss reassuring findings (eg, Your baby is
Subdural hematoma exams to look for signs of systemic illness: growing well.).
Seizure Lethargy, tachypnea, or poor profusion are signs r Once organic causes are excluded:
r Trauma: of serious illness.
Acknowledge the difficulties the parents are
Fractures Rashes
facing.
Nonaccidental trauma Orifices: Tight phimosis, fissure, white patches in
Inquire how they are doing.
Corneal abrasions oropharynx, erythematous ear canal or tympanic
Ensure that they have some emotional support.
r Other causes: membrane, scleral injection
Encourage parents to take breaks away from
Neurologic exam: Normal baby reflexes
Diaper rash the crying baby:
Tight phimosis Division of labor: Alternate caretakers, allow
Teething one to leave the home
Hair tourniquet (extremities, penis, clitoris) Single parent: Put the baby in the crib (back to
Torsion (testicular, ovarian, appendix testis) sleep) and close a door.
Supraventricular tachycardia
212
CRYING/COLIC
r Hydrolyzed formula (hypoallergenic formula) has

Reassure parents that colic is a benign process ADDITIONAL READING
that will improve with infant growth and been shown to be effective in reducing crying times
maturation. in a small randomized controlled trial. However, r Garrison MM, Christakis DA. A systematic review of
Encourage breast-feeding. hypoallergenic-labeled formulas cost up to 3 times treatments for infantile colic. Pediatrics.
Change to hypoallergenic formulas in infants with more than standard formulas (5). 2000;106:184190.
signs of cows milk intolerance, such as loose or r Infant massage is equal to the use of a crib vibrator r Roberts DM, Ostepchuk M, OBrien JG. Infantile
bloody stools, and dermatitis. in decreasing crying 4748%. It has also been colic. Am Fam Physician. 2004;70:735742.
Instruct parents on infant calming techniques shown to have benefits on motherinfant r Rogovik AL, Goldman RD. Treating infants colic.
using the 5 Ss:
Nonnutritive Sucking/pacifier
interaction, infant sleeping, and crying (6).
r 12% sucrose solution has been shown to reduce
Can Fam Physician. 2005;51:12091211.
r Rosen LD, Bukutu C, Le C, et al. Complementary, C
Swinging or bouncing baby symptoms by 63% compared to water. The effect is holistic, and integrative medicine: Colic. Pediatr Rev.
Shushing or hushing baby short lived (<30 min), so frequent redosing would 2007;28(10):381385.
Singing to baby be needed if crying persists (7). r Wessel MA, Cobb JC, Jackson EB, et al. Paroxysmal
Swaddling fussing in infancy, sometimes called colic. Pediatrics.
Encourage a stable emotional environment. 1954;14(5):421435.
Holding the infant for >3 hr a day has been FOLLOW-UP
shown to decrease intensity but not the duration
of cry. FOLLOW-UP RECOMMENDATIONS
Follow up with primary care provider in 23 days: CODES
MEDICATION r Recheck crying symptoms.
There are no proven medications. r Evaluate for evolving organic etiology. ICD9
ALERT r Assess parental state of mind. 789.7 Colic
Colic is a diagnosis of exclusion in well-appearing
COMPLICATIONS
patients in which organic causes have been
There is a high correlation between colic and excessive PEARLS AND PITFALLS
excluded. crying with postpartum depression. Infantile colic at 2 r Gas does not cause colic. Excessive crying that
DISPOSITION mo of age has been associated with high maternal
accompanies colic usually leads to aerophagia.
depression scores 4 mo later (8). r Excessive crying has been linked to parental distress
Admission Criteria
r Significant vital sign abnormalities
and in rare instances infant abuse.
r Respiratory distress REFERENCES r Simple maneuvers and soothing techniques can help
r Inability of caretaker to care for patient relieve symptoms. (See the 5 Ss in the Initial
1. Metcalf TJ, Irons TG, Sher LD, et al. Simethicone in
Issues for Referral Stabilization/Therapy section.)
the treatment of infant colic: A randomized, r Medications are not routinely recommended for
r Consultation with social work services for referral to
placebo controlled, multicenter trial. Pediatrics.
parenting support groups or classes 1994;94:2934. colic.
r Psychiatry referral if the mother is exhibiting r Sucrose solutions may help relieve symptoms, but
2. Grunseit F. Evaluation of the efficacy of dicyclomine
symptoms of severe postnatal depression hydrochloride (Merbentyl) syrup in the treatment the effects are short lived.
r Primary care referral for all patients who do not r Parental reassurance and support remain the
of infant colic. Curr Med Res Opin.
already have a pediatrician. They need follow-up 1977;5:258261. mainstay of treatment of infantile colic. The majority
checks, well-baby care, and immunizations. 3. Weizman Z, Alkrinawi S, Goldfarb D, et al. Efficacy of colic symptoms eases by the 4th mo of life
of herbal tea preparation in infantile colic. J without treatment.
THERAPIES Pediatr. 1993;122:650652.
r Simethicone (Mylicon, Gas-X): An oral agent that 4. Savino F, Pelle E, Palumeri E, et al. Lactobacillus
reduces surface tension and purportedly reduces reuteri (American Type Culture Collection Strain
gas but has not been shown to be more effective 55730) versus simethicone in the treatment of
than placebo (1) infantile colic: A prospective randomized study.
r Dicyclomine (Bentyl): An anticholinergic medication Pediatrics. 2007;119:e124e130.
shown to be more effective than placebo in reducing 5. American Academy of Pediatrics Committee on
crying. However, it is associated with apnea, Nutrition. Hypoallergenic infant formulas.
seizures, and coma and is contraindicated in infants Pediatrics. 2000;106:346349.
(2). 6. Huhtala V, Lehtonen L, Heinonen R, et al. Infant
r Herbal tea of fennel, chamomile, vervain, licorice, massage compared with crib vibrator in the
and lemon has been shown to reduce crying when treatment of colicky infants. Pediatrics.
compared to placebo (3). 2000;105:e84e89.
r Probiotics: Lactobacillus reuteri has been shown to 7. Markestad T. Use of sucrose as a treatment for
be more effective than simethicone in reducing infant colic. Arch Dis Child. 1997;76:356358.
infant crying. 95% in a treatment group were 8. Vik T Grote V, Escribano J, et al. European
treatment responders. However, it cannot be safely Childhood Obesity Trial Study Group. Infantile colic,
recommended for immunocompromised or severely prolonged crying and maternal postnatal
debilitated patients (4). depression. Acta Paediatr. 2009;98(8):13441348.
213
CRYPTORCHIDISM
Marie Waterhouse
Deborah R. Liu

BASICS Normal testicular migration proceeds in 2 phases: Lab
r Abdominal phase (815 wk gestation): Androgens r Generally not necessary in the emergency
DESCRIPTION mediate regression of the cranial suspensory department
r Cryptorchidism is failure of the testis to descend to r If bilateral UDT, karyotype and hormonal stimulation
ligament. This, in addition to firm caudal attachment
its normal anatomic location at the base of the of the testis to the inguinal ring by the testing is recommended on an outpatient basis to
scrotum. gubernaculum, allows the testis to descend into the confirm the presence of testicular tissue.
r Unilateral (90%) or bilateral (10%)
lower abdomen.
r Testis may be palpable (80%): r Inguinoscrotal phase (usually complete by Imaging
r In general, imaging is not recommended due to poor
High in scrotum 2834 wk gestation): Testosterone causes the sensitivity and reliability. It does not replace the
Inguinal canal (peeping) gubernaculum to enlarge and widen within the diagnostic and therapeutic ability of laparoscopy.
Ectopic (eg, perineal, anterior to symphysis pubis) inguinal canal. This facilitates passage of testis, r US is limited by intestinal gas and obesity.
r Testis may be nonpalpable (20%): aided by abdominal pressure, into the scrotum. r MRI is poorly sensitive and requires sedation in
Truly cryptorchid or hidden testis
Located in the abdomen ETIOLOGY young children.
r Complex combination of genetic and environmental r Small studies suggest that gadolinium-enhanced
EPIDEMIOLOGY factors MRA may be more reliable (4).
Incidence r Disruption of normal testicular migration by r May consider imaging in obese patients (where a
r Most common genitourinary anomaly in boys interference with androgen sensitive pathways normal exam is difficult) or if a history of multiple
r 34% of term newborn males (1,2) r Preterm birth (prior to completion of testicular intrabdominal surgeries or adhesions make
r 1530% of preterm infants (3) migration) will result in a temporary lack of descent. laparoscopy difficult or dangerous
r Identifiable genetic mutation in only a small subset
Prevalence Diagnostic Procedures/Other
Falls to 1% by age 3 mo, indicating that most of patients Diagnostic laparoscopy is the gold standard.
undescended testes (UDT) will self-resolve by this age Pathological Findings
(1) DIAGNOSIS Cryptorchid testes exhibit multiple histopathologic
RISK FACTORS changes including:
r Birth factors: HISTORY r Germ cell loss
r Pregnancy history: Gestational age, birth weight,
Low birth weight r Leydig cell loss
Small for gestational age maternal diabetes, smoking, estrogen or other r Testicular fibrosis
Intrauterine growth retardation steroid use
r Results of the scrotal exam at birth DIFFERENTIAL DIAGNOSIS
Twin gestation
r Family history: Other relatives with cryptorchid testis, All of the following carry histopathologic changes and
Preterm birth
r Family history: 23% of cryptorchid patients will have hypospadias, other genitourinary anomalies require urologic evaluation:
r History of endocrinopathy or intracranial pathology r Retractile testis:
a male relative with the disorder
r Maternal tobacco exposure affecting hypothalamic-pituitary function Can be manipulated into normal anatomic
r Gestational diabetes position during exam and stays there after being
PHYSICAL EXAM
r Conditions of impaired androgen synthesis or effect r Best accomplished with relaxed patient, in seated released
r Disorders affecting hypothalamic-pituitary-adrenal frog-legged position Possibly due to hyperactive cremaster muscle (eg,
r With warm hands, examine the contralateral testicle cerebral palsy)
axis r Acquired UDT:
r Disorders of abdominal musculature: first for size and consistency.
r Sweep the nondominant hand from the anterior Normal testicular position at birth but
Prune-belly syndrome
reascends in early childhood due to failure of
Gastroschisis superior iliac spine medially across the groin to push
spermatic cord to elongate as child grows
Omphalocele testis into the inguinal canal.
r Once the testis is palpated, grasp gently with the Acquired UDT cannot be placed into the correct
Down syndrome
anatomic position during the exam. If forced, pain
Prader-Willi syndrome dominant hand and bring the testis into the scrotum.
r Caudal developmental defects: results and the testis immediately reassumes the
r Hold this position for 1 min to fatigue the cremaster
prior position when released.
Spina bifida muscle, then release and observe. r Atrophic or vanishing testis:
r Other chemical exposures: r If the testis stays in the scrotum, it is retractile.
Testicular tissue damaged by spermatic cord
Organochlorine compounds r If the testis reassumes a high position, it is torsion or other cause of ischemic injury
Pesticides undescended. Atrophic testicular remnant remains in either
Diethylstilbestrol r Exam under anesthesia may locate the nonpalpable anatomic or ectopic location
testis in 20% of cases. r Absent testis (monorchia or anorchia):
Due to congenital defect or chromosomally female
patient
Consider the virilized female in congenital adrenal
hyperplasia.
214
CRYPTORCHIDISM
REFERENCES
TREATMENT FOLLOW-UP
1. Berkowitz G, Lapinski RH, Dolgin SE, et al.
Most pediatric urologists consider surgery to be FOLLOW-UP RECOMMENDATIONS Prevalence and natural history of cryptorchidism.
r Follow up with a pediatric urologist or surgeon. Pediatrics. 1993;92:4449.
first-line treatment for simple cryptorchidism. r No limitations on physical activity 2. Pettersson A, Richiardi L, Nordenskjold A, et al.
MEDICATION Age at surgery for undescended testis and risk of
Human chorionic gonadotropin or Patient Monitoring
Encourage routine self-exams by the patient or testicular cancer. N Engl J Med.
gonadotropin-releasing hormone therapies:
r Overall success rates are extremely variable primary caretaker for testicular malignancy. 2007;356:18351841.
3. Tasian GE, Hittelman AB, Kim GE, et al. Age at
C
(675%) but comparable for the 2 hormones. PROGNOSIS orchiopexy and testis palpability predict germ cell
r Higher success rates in older patients (>5 yr), r Dependent on multiple factors, including location of
and Leydig cell loss: Clinical predictors of adverse
bilateral UDT, and retractile testis testis, uni- or bilateral, and age at discovery histological features of cryptorchidism. J Urol.
r Adverse effects include impaired spermatogenesis r Correction before 2 yr of age may lower future
2009;182:704709.
and/or precocious puberty. infertility risks. 4. Yeung CK, Tam YH, Chan YL, et al. A new
r Correction before puberty lowers future malignancy
management algorithm for impalpable
SURGERY/OTHER PROCEDURES risk.
r Laparoscopic or open orchiopexy to secure the testis undescended testis with gadolinium enhanced
COMPLICATIONS magnetic resonance angiography. J Urol.
in the scrotum
r Orchiopexy: Recommended age of operation at r Testicular malignancy: 1999;162:9981002.
It is unclear whether lack of descent itself 5. Lee P, OLeary LA, Songer NJ, et al. Paternity after
312 mo:
increases the malignancy risk or underlying unilateral cryptorchidism: A controlled study.
Orchiopexy allows better routine self-exams for
intrinsic pathology is responsible for both. Pediatrics. 1996;98:676679.
malignancy monitoring.
The surgical plan must balance the anesthesia risk Relative risk of malignancy is 2.758 (if
against the potential malignancy risk. uncorrected) (2):
r Orchiectomy for selected patients, particularly those Falls to 23 if surgically corrected before ADDITIONAL READING
with atrophic or hypertrophic testis, in which the puberty (2) r Bonney T, Hutson J, Southwell B, et al. Update on
malignancy risk is higher Higher risk if bilateral UDT, abdominal location, congenital versus acquired undescended testes:
r The decision to observe, remove, or repair a UDT in abnormal karyotype, or coexistent endocrinopathy Incidence, diagnosis, and management. ANZ J Surg.
Seminoma is the most common (70% of 2008;78:10101013.
the postpubertal male is complex, since the
malignancy and fertility benefit from surgery may be
malignancies in uncorrected patients, 30% in r Esposito C, Caldamone AA, Settimi A, et al.
corrected patients) malignancy. Management of boys with nonpalpable
limited.
Embryonal carcinoma, teratocarcinoma, and undescended testis. Nat Clin Pract Urol.
DISPOSITION choriocarcinoma are also seen. 2008;5:252260.
Admission Criteria r Infertility: r Schneck FX, Bellinger MF. Abnormalities of the
r Cryptorchidism not associated with underlying Germ cell development in UDT begins to testes and scrotum and their surgical management.
medical conditions rarely requires admission to the deteriorate after 1 yr of age. In Wein AJ, Kavoussi LR, Novick AC, et al., eds.
hospital. Infertility risk increases with age. Campbell-Walsh Urology. 9th ed. Philadelphia, PA:
r Cryptorchidism as a sign of an undiagnosed medical Early surgical correction (between 3 and 12 mo of Saunders; 2007.
condition (eg, congenital adrenal hyperplasia or age) is important. r Virtanen HE, Toppari J. Epidemiology and
prune-belly syndrome) may require admission for There is a lack of paternity in 10% of formerly
pathogenesis of cryptorchidism. Human Reprod
further evaluation. cryptorchid males compared to 5% of controls (5).
r Surgical complications include postoperative edema, Update. 2008;14:4958.
Discharge Criteria r Wood HM, Elder JS. Cryptorchidism and testicular
Patients not experiencing pain, in whom torsion is not inflammation, and tension of the spermatic cord:
cancer: Separating fact from fiction. J Urol.
suspected, can generally be discharged with These can lead to ischemic injury and testicular
2009;181:452461.
appropriate follow-up. atrophy.
r Testicular torsion is rare in cryptorchid patients but
Issues for Referral
should be suspected in any male with acute
All patients with a testis located outside of normal
abdominal pain and an empty ipsilateral
CODES
anatomic position should be referred to a pediatric
hemiscrotum:
urologist or surgeon upon diagnosis. ICD9
If suspicious for torsion, obtain an immediate US
and/or urological or surgical consultation. 752.51 Undescended testis
PEARLS AND PITFALLS

r Cryptorchidism is a very common developmental
anomaly that may be found in the process of exam
for unrelated complaints.
r Proper clinical exam with a relaxed patient is the key
to diagnosis with an appropriate referral to pediatric
urology or surgery.
r Imaging has little role in the diagnosis.
r Though rare, torsion of UDT constitutes a surgical
emergency.
215
CUSHING SYNDROME
Todd P. Chang
Imaging
BASICS DIAGNOSIS r Imaging is typically not done emergently.
r On plain films, bone age is typically delayed.
DESCRIPTION HISTORY r CT or MRI of the abdomen can locate and
r Cushing syndrome (CS) is a constellation of signs r Inquire about medication use.
r Weight gain and growth failure can occur insidiously differentiate an adrenocortical tumor or adrenal
and symptoms from excessive glucocorticoids, with hyperplasia.
typical cushingoid features, cardiovascular, over time and are more prevalent in infants and r MRI of the sella turcica can confirm a pituitary
hematologic, and endocrine effects. younger children.
r Cushingoid features include: r Facial and body fat changes adenoma, though only half of microadenomas are
r Disproportionate skin pigmentation, increased visible by MRI (3).
Facial fat deposition (moon facies)
Posterior neck fat deposition (buffalo hump) sweating, or acne Diagnostic Procedures/Other
r Headache, depression, emotional lability, or r ECG to evaluate for myocardial ischemia chest pain
Abdominal striae (stretch marks)
Truncal obesity with thin extremities psychosis or if other suggestive symptoms exist
r Cushing disease refers to CS caused by a pituitary r Muscle pain, frequent fractures r An endocrinologist can confirm CS through a 24-hr
adenoma that produces excess adrenocorticotropin r Hirsutism, amenorrhea, virilization, and other urine cortisol screen, serial circadian cortisol levels,
hormone (ACTH), which is the most common cause and/or dexamethasone suppression testing.
pubertal disturbances may have occurred.
of CS in children 5 yr. DIFFERENTIAL DIAGNOSIS
PHYSICAL EXAM r Obesity
EPIDEMIOLOGY r Elevated body mass index and poor growth: Children
r DM
Incidence with CS are shorter than regular obese children (2). r Hypothyroidism
r Pediatric CS is significantly more rare than r HTN
r Cushingoid features are almost always present in r Polycystic ovarian syndrome
adult-onset CS.
r Occurs in females more often than males
older children.
r Adrenocortical tumors account for most cases of CS r Skin findings include acanthosis nigrans, generalized
in children <7 yr.
TREATMENT
hyperpigmentation, hyperhidrosis, and striae:
r Incidence has been reported to be 15% in patients Cafe-au-lait spots with distinct, jagged edges PRE HOSPITAL
of all ages with diabetes mellitus (DM) or HTN (1). coast of Maine are found with Assess the patient, and support airway, breathing, and
RISK FACTORS McCune-Albright syndrome circulation until hospital arrival.
r Focal neurologic signs are rare but can suggest
Chronic oral or IV glucocorticoid use for other INITIAL STABILIZATION/THERAPY
underlying inflammatory conditions ischemia or infarct: r Check for signs of acute addisonian crisis if a patient
Papilledema may be present with associated
PATHOPHYSIOLOGY is under stress (infection, trauma, etc.).
pseudotumor cerebri. r In a patient with CS who appears ill or toxic:
r Excess hypercortisolemia causes characteristic r Evidence of inappropriate androgen activity, such as
changes to adipose tissue, hair follicles, and skin. Crystalloid or colloid IV resuscitation as needed to
hirsutism, acne, body odor, and virilization may be
r Hypercortisolemia can come from abnormalities in maintain perfusion
seen in prepubertal children.
any portion of the hypothalamus-pituitary-adrenal Broad-spectrum antibiotic therapy
axis or from a purely exogenous source. DIAGNOSTIC TESTS & INTERPRETATION Vasopressors as necessary
Lab MEDICATION
ETIOLOGY Initial Lab Tests
r Causes of CS are divided into ACTH dependent or r Lab tests are needed if the patient appears ill or First Line
ACTH independent: r Hydrocortisone for addisonian crisis: 12 mg/kg IV
r ACTH dependent: toxic.
r With suspected sepsis, shock, or addisonian crisis: bolus, then 100 mg/m2 /day divided or as an
Pituitary adenoma (Cushing disease) infusion. See Adrenal Insufficiency topic.
CBC may show lymphopenia despite elevated r Broad-spectrum antibiotic therapy:
Ectopic ACTH-producing tumor WBCs.
r ACTH independent: Ceftriaxone 50 mg/kg IV q12h, adult max single
Chemistries may show hypernatremia and
Exogenous glucocorticoid use or abuse is the most dose 2,000 mg OR
hypokalemia from mineralocorticoid effects.
common cause of pediatric CS. Meropenem 20 mg/kg IV q8h, adult max single
Blood culture
Adrenal adenoma or carcinoma: dose 1,000 mg OR
Free cortisol level will be low or undetectable in
Beckwith-Weidemann syndrome Piperacillin/Tazobactam 100 mg/kg IV q8h, adult
crisis.
Primary adrenocortical hyperplasia: r Recommended nonemergent labs for CS include a max single dose 3,000 mg
Carney complex Consider adding vancomycin 10 mg/kg IV q6h
workup for pituitary involvement:
Multiple endocrine neoplasia type 1 (adult max single dose 1,000 mg) if MRSA or if
Free T4
Primary pigmented adrenocortical disease, also local antibiotic resistance of Streptococcus
Thyroid-stimulating hormone pneumoniae warrants.
known as micronodular adrenal disease Prolactin
McCune-Albright syndrome
Luteinizing hormone
Macronodular adrenal hyperplasia
Follicle-stimulating hormone
Free testosterone
Androstenedione
Dehydroepiandrosterone sulfate (DHEA-S)
Beta-hCG
216
CUSHING SYNDROME
Second Line
r Antihypertensive agents for uncontrolled
ADDITIONAL READING
FOLLOW-UP
hypertension (see Hypertension topic): Nicardipine Chan LF, et al. Pediatric Cushings syndrome: Clinical
(5 mg/kg/min IV, then titrated 13 mg/kg/min) has FOLLOW-UP RECOMMENDATIONS features, diagnosis, and treatment. Arq Bras
minimal risk of hypotension. Discharge instructions and medications: Endocrinol Metabol. 2007;51(8):12611271.
r Medications to lower serum cortisol levels such as r Taper steroids as soon as possible.
bromocriptine or ketoconazole should be
PROGNOSIS CODES
administered only under the guidance of a pediatric
Untreated CS can lead to DM, HTN, dyslipidemia, and
endocrinologist.
hypercoagulability in adults (4).
ICD9
C
r Transphenoidal resection for pituitary adenoma 255.0 Cushings syndrome
r Acute addisonian crisis
r Adrenalectomy(-ies) for adrenal causes
r Obesity
r Radiation may be useful for certain neoplasms. PEARLS AND PITFALLS
r Growth arrest
DISPOSITION r Pubertal arrest r Consider corticosteroid use or abuseeither
Admission Criteria r Osteoporosis
intentional or unintentional
r Admission should be considered in children with r MI r Consider a relative acute addisonian crisis in a
symptomatic HTN, toxic or septic appearance, or r Cerebrovascular ischemia patient who appears cushingoid
high suspicion of neoplasm. r Sepsis and septic shock r CS in infancy is almost always associated with
r Critical care admission criteria: r Pathologic and stress fractures McCune-Albright syndrome.
Septic shock requiring significant fluid r DM and hyperosmolar coma r Obesity with growth failure warrants endocrinologic
resuscitation (>60 mL/kg), pressors, or positive evaluation.
pressure ventilation
Discharge Criteria REFERENCES
r No evidence of acute addisonian crisis
r No symptomatic HTN 1. Baid SK, Rubino D, Sinaii N, et al. Specificity of
screening tests for Cushings syndrome in an
Issues for Referral overweight and obese population. J Clin Endocrin
r Because pediatric CS differs in etiology and workup Metab. 2009;94(10):38573864.
from adult CS, a pediatric endocrinologist is 2. Greening JE, Storr HL, McKenzie SA, et al. Linear
preferred to an adult endocrinologist. growth and body mass index in pediatric patients
r Most lab testing for CS takes a significant time to with Cushings disease or simple obesity. J
process; it may be beneficial to patient care to begin Endocrinol Invest. 2006;29(10):885887.
the lab workup in the emergency department for the 3. Magiakou MA, Mastorakos G, Oldfield EH, et al.
endocrinologist follow-up. Cushings syndrome in children and adolescents.
Presentation, diagnosis, and therapy. N Engl J Med.
1994;331(10):629636.
4. Boscaro M, Arnaldi G. Approach to the patient with
possible Cushings syndrome. J Clin Endocrinol
Metab. 2009;94:31213131.
217
CUTANEOUS LARVA MIGRANS

Craig A. McElderry

BASICS r The life cycle of the parasites begins when eggs are r Pruritic, erythematous, edematous papules and/or
passed from animal feces into warm, moist, sandy vesicles with serous fluid
DESCRIPTION soil, where the larvae hatch. After two molts in the r Serpiginous (snakelike), slightly elevated,
Cutaneous larva migrans (CLM) is an acquired soil, larvae become infective. By using their erythematous tunnels that are 23 mm wide and
dermatosis caused by infection with the infective proteases, larvae penetrate through follicles, track 34 cm from the penetration site
larvae of various nematode parasites. It is one of the fissures, or intact skin of the new host. r Creeping dermatitis
most common helminth (hookworm) infections r In their natural animal hosts, the larvae are able to r Bullae
acquired from subtropical and tropical regions of the penetrate into the dermis and are transported via r Secondary impetiginization
world. the lymphatic and venous systems to the lungs. They r Most frequent anatomic locations of CLM lesions
EPIDEMIOLOGY break through into the alveoli and migrate to the
are on the feet in >50% of individuals, followed by
trachea, where they are swallowed. In the intestine,
Incidence buttock and thigh (3).
r These small, round, blood-sucking worms infest they mature sexually, and the cycle begins again as r Tract advancement of several millimeters to a few
their eggs are excreted.
700 million people worldwide each year. r Humans are accidental hosts. The larvae lack the centimeters a day
r Rated 2nd to pinworms among helminth infections
collagenase enzymes required to penetrate the DIAGNOSTIC TESTS & INTERPRETATION
in developed countries
r The CLM parasite can be found in the southeastern basement membrane to invade the dermis and thus Lab
are confined to the skin. There, they are unable to r Labs are generally not necessary.
and Gulf states of the U.S. and in the tropical complete their life cycle, as they would do in cats r Some patients may develop a peripheral
countries of the Caribbean, South America, and and dogs.
Southeast Asia. eosinophilia and elevated levels of IgE.
r Rarely, in infections with a large burden of parasites,
pneumonitis (Loeffler syndrome) and myositis may
r Hookworm-related CLM is significantly more Biopsy may be considered, but this rarely identifies the
follow skin lesions.
prevalent during rainy seasons (1). r Occasionally, the larvae reach the intestine and may parasites since the anterior end of the track does not
r In 1 study of CLM in Brazil, the prevalence varied necessarily indicate the location of the larvae (1).
cause an eosinophilic enteritis.
from 4.4% in the rainy season to 1.7% in the dry Pathological Findings
season (2). ETIOLOGY May show a larva (periodic acid-Schiff positive) in a
r Infective larvae of cat and dog hookworms:
r Most patients with hookworm-related CLM seen by suprabasalar burrow, basal layer tracts, spongiosis
Ancylostoma braziliense, found in the central and with intraepidermal vesicles, necrotic keratinocytes,
health workers in developed countries are travelers
southern U.S., Central America, South America, and an epidermal and upper dermal chronic
returning from the tropics and subtropics (1).
r One study including 17,000 travelers who returned and the Caribbean inflammatory infiltrate with many eosinophils
Ancylostoma caninum, found in Australia
ill showed that hookworm-related CLM occurred in Uncinaria stenocephala, found in Europe DIFFERENTIAL DIAGNOSIS
23% of them, with the highest prevalence of the r Other skin-penetrating nematodes are less common Most of the following can be ruled out with a good
condition in those returning from Caribbean clinical history of recent exposure to moist sand
causes.
destinations, followed by Southeast Asia and frequented by cats or dogs and physical exam
Central America (1). findings of intensely pruritic, serpiginous lesions that
RISK FACTORS DIAGNOSIS advance:
More common in children, gardeners, farmers, r Impetigo
HISTORY r Tinea pedis
sunbathers, carpenters, and those whose hobbies or r Tingling/prickling at the site of exposure within
occupations involve contact with warm, moist, sandy r Photoallergic dermatitis
30 min of penetration of larvae
soil contaminated with cat or dog feces r Intense pruritis (98100% of patients) (3) r Scabies
r Erythematous, slightly elevated, linear track that r Cercarial dermatitis (schistosomiasis)
GENERAL PREVENTION
r Avoid skin contact with moist soil contaminated moves forward in an irregular pattern r Allergic contact dermatitis
with animal feces. r Often associated with a history of sunbathing, r Epidermal dermatophytosis
r Protective footwear should be worn at all times walking barefoot on the beach, or similar activity in r Migratory myiasis
while walking on the beach. a tropical location r Larva currens caused by Strongyloides stercoralis
r When lying on beaches frequented by cats and r Erythema migrans of Lyme borreliosis
dogs, areas of sand washed by the tide are
preferable to dry areas.
r Mattresses are preferable to towels.
218
CUTANEOUS LARVA MIGRANS
ADDITIONAL READING
TREATMENT FOLLOW-UP r American Academy of Pediatrics. Red Book: 2006
PROGNOSIS Report of the Committee on Infectious Diseases.
The condition is benign and self-limited but can cause
The prognosis is excellent. Hookworm-related CLM is 27th ed. Elk Grove Village, IL: Author; 2006:272.
severe pruritus. The intense pruritis and risk for r Juzych LA, Douglass MC. Cutaneous larva migrans.
infection often mandate treatment. a self-limiting disease. Human beings are accidental
hosts, with the larva dying and the lesions resolving eMedicine Dermatology. 2008. Available at
MEDICATION within 48 wk. Rarely, the disease can last for years. http://emedicine.medscape.com/article/998709-
First Line overview.
r The drug of choice is ivermectin. A single dose COMPLICATIONS
r Secondary infections
C
(200 g per kg of body weight) kills the migrating r Allergic reactions
larva effectively and relieves itching quickly (24). r Erythema multiforme CODES
r Cure rates after a single dosage range from
77100%. ICD9
r Contraindicated in children who weigh <15 kg (or 126.9 Ancylostomiasis and necatoriasis, unspecified
REFERENCES
<5 yr of age) and in pregnant and breast-feeding
women 1. Heukelbach J, Feldmeier H. Epidemiological and
r Off-label use in children has been shown to be safe. clinical characteristics of hookworm-related PEARLS AND PITFALLS
cutaeous larva migrans. Lancet Infect Dis. r Clinical diagnosis based on history of contact with
Second Line 2008;8(5):302309.
r Albendazole 400800 mg/day (according to weight) warm, moist sand and physical findings of pruritic,
for 3 days (1,3,4); for children <2 yr, 200 mg/day 2. Heukelback J, Jackson A, Ariza L, et al. Prevalence serpiginous erythematous tunnels that advance
for 3 days and repeat in 3 wk, if necessary and risk factors of hookworm-related cutaneous r Though a self-limited disease, the intense pruritis
r Topical tiabendazole (thiabendazole) in a larva migrans in a rural community in Brazil. Ann
often mandates treatment.
Trop Med Parasitol. 2008;102:5361. r The best way to prevent CLM is to wear protective
concentration of 1015% t.i.d. for 57 days is as
effective as oral treatment with ivermectin (1). 3. Hochedez P, Caumes E. Hookworm-related
footwear at all times while on the beach.
r Antistaphylococcal/Streptococcal antibiotics for cutaneous larva migrans. J Travel Med.
2007;14(5):326333.
secondary bacterial infections/impetiginization:
Cephalexin 25100 mg/kg/day divided q68h, 4. Mosel G, Caumes E. Recent developments in
max dose 4 g/day dermatolgical syndromes in returning travelers.
Clindamycin 1030 mg/kg/day divided q68h, Curr Opin Infect Dis. 2008;21(5):495499.
max dose 1.8 g/day
Additional Therapies
As an alternative therapy, liquid nitrogen cryotherapy
can be applied to the progressive end of the larval
burrow. This is considered obsolete by some since it is
painful, ineffective, and may cause ulcerations (1).
DISPOSITION
Generally treated on an outpatient basis
Admission Criteria
Consider admission for severe secondary infections
not adequately treated with oral antibiotics.
219
CYANOSIS
Joshua Nagler
ETIOLOGY
BASICS r Respiratory: DIAGNOSIS
High altitude or any other reason for decreased
DESCRIPTION amount of inspired oxygen HISTORY
r Cyanosis is a blue tint of the skin and mucous r Acute or chronic/recurrent (duration of symptoms)
Neurologic causes of respiratory depression:
membranes that appears to be due to deoxygenated Apnea of prematurity, central apnea, seizure, r Birth history (eg, gestational age, problems with
blood near the skin surface. breath-holding, respiratory depression due to delivery, neonatal ICU stay, group B streptococcus
r Cyanosis becomes apparent when the amount of medication or toxin (eg, morphine, alcohol, status, mechanical ventilation, etc.)
deoxygenated hemoglobin (Hgb) is >5 g/dL. etc.), increased intracranial pressure r History of underlying conditions/surgeries
r Central cyanosis is defined by blue discoloration of Restrictive lung process: r History of aspiration
the skin and mucous membranes (particularly lips, External compression, pneumothorax, r Respiratory distress
mouth, head, and torso). hemothorax, pleural effusion or empyema, r Problems feeding, sweating with feeds
r Peripheral or acrocyanosis is a bluish tint of the skin mediastinal or lung mass, flail chest, congenital r History of possible ingestions/exposures
of the distal extremities and around the lips, which diaphragmatic hernia, diaphragmatic paralysis, r Current medications
may be a normal finding in neonates. congenital cystic adenomatoid malformation, r Systemic symptoms: Fevers, rash, etc.
r Causes of cyanosis range from benign and transient pulmonary sequestration, congenital lobar r Neurologic symptoms: Weakness, difficulty with
(eg, breath-holding spell) to severe and life emphysema
Neuromuscular disease such as spinal muscular movements
threatening (eg, congenital heart disease [CHD]). r Family history
For specific details of the various etiologies, please atrophy, botulism, Guillain-Barre syndrome,
transient myelitis, muscular dystrophy r Allergies
see the respective topics in this textbook.
r Cyanosis can be acute or long-standing, transient or Obstructive lung process: PHYSICAL EXAM
Asthma, bronchiolitis, croup, pertussis, foreign r Vital signs:
persistent, depending on its etiology.
body aspiration, epiglottitis, tracheitis, Tachypnea will be most commonly present:
EPIDEMIOLOGY laryngomalacia, tracheomalacia, anaphylaxis If tachypnea is not present and the patient is
Incidence Congenital obstruction secondary to a mass,
hypoxemic, assess for apnea or fatigue and
The incidence of cyanotic CHD is 0.1%, though with choanal atresia, Pierre Robin and other impending respiratory failure.
current prenatal screening, few of these children structural abnormalities Patients with long-standing cyanosis may not
initially present in the emergency department (1). Vocal cord paralysis, tracheostomy obstruction,
appear in distress but will have a mild baseline
hemorrhage tachypnea.
RISK FACTORS Diffusion abnormalities across the
r There are risk factors for specific conditions that Tachycardia will be commonly present.
alveolar-capillary wall: Fever can point to infectious causes such as
cause cyanosis. Some of these include: CLD or bronchopulmonary dysplasia
Advanced maternal age and gestational diabetes pneumonia, epiglottitis, etc.
Surfactant deficiency, acute respiratory distress
for CHD Hypotension can be present with septic or
syndrome, cystic fibrosis, pneumonia, acute cardiogenic shock.
Prematurity for chronic lung disease (CLD), apnea chest syndrome in sickle cell anemia, pulmonary
and asthma r Skin exam: Distinguish between central and
hemorrhage/edema
Cerebral palsy/developmental delay for aspiration r Cardiovascular: peripheral cyanosis:
pneumonias, seizures, and central apnea If peripheral, is it distributed equally on the upper
r Polycythemia will make patients appear cyanotic at Cardiac: and lower extremities? (Infants with coarctation of
Cardiogenic shock, CHF, pulmonary HTN,
a normal oxygen saturation even though they are the aorta and an open patent ductus arteriosus
persistent pulmonary HTN of the newborn (PDA) may have cyanosis in just the lower
not hypoxemic. Congenital cyanotic heart disease:
extremities.)
Atrioventricular canal defect, Ebstein anomaly,
PATHOPHYSIOLOGY r HEENT exam looking for evidence of choanal
r Central cyanosis is usually a manifestation of hypoplastic left heart syndrome, pulmonary
atresia, features of craniofacial abnormalities
hypoxemia, which appears when the amount of atresia/severe stenosis, tetralogy of Fallot, r Respiratory exam:
unsaturated Hgb is >5 g/dL, which at normal Hgb total anomalous pulmonary venous return,
transposition of the great arteries, tricuspid Tracheal deviation
levels corresponds to 7378% (2).
atresia, truncus arteriosus, severe aortic Diaphragmatic excursion
Such hypoxemia may result from:
Inadequate oxygen intake coarctation may cause cyanosis in the lower Stridor
Poor oxygen absorption from the lungs to the extremities Increased respiratory effort including grunting,
flaring, or retractions
circulation Vascular:
Intracardiac or intrapulmonary shunting, which Acrocyanosis of the newborn, cold exposure, Wheezing, crackles, or rales
Egophony
causes some blood to bypass oxygenation in the Raynaud syndrome (if only affecting fingers and
Assessment of tracheostomy, if present
lungs toes), pulmonary embolism (PE), septic shock r Cardiac exam:
r Methemoglobinemia may manifest as central r Other:
Evidence of heave, lift, or thrill
cyanosis but is not a result of hypoxemia. See Methemoglobinemia:
Congenital hemoglobin M or abnormalities in Evaluation of heart sounds with splitting
Methemoglobinemia topic. Sulfhemoglobinemia is
Presence of murmur
very rare dyshemoglobinemia that results in cyanosis methemoglobin reductase
Exposure to toxins/drugs such as quinines, Check for pulses and presence of radiofemoral
without hypoxemia.
delay
benzocaine, sulfonamide antibiotics r Neurologic exam: Thorough exam including an
assessment for decreased strength or tone and deep
tendon reflexes
220
CYANOSIS
DIAGNOSTIC TESTS & INTERPRETATION Issues for Referral

r The most important initial test is a pulse oximetry Consultation from the emergency department should
TREATMENT be done as necessary. Outpatient follow-up may be
(SpO2 ) reading, which serves as a noninvasive
surrogate of blood gas oxygenation: PRE HOSPITAL scheduled after consultation:
SpO2 may be falsely high when forms of Hgb are r Assess and stabilize airway, breathing, and r Cardiology for CHD
present other than oxyhemoglobin and circulation. r Pulmonology for chronic lung conditions
deoxyhemoglobin. r Regularly reassess ABCs. r Toxicology for ingestions or drug overdoses
SpO2 may be falsely low when the patients r Administer supplemental oxygen unless r Neurosurgery for cases of suspected increased
circulation to the extremities is inadequate
because of cold, shock, etc.
contraindicated. intracranial pressure
r Otorhinolaryngology for airway obstruction
C
r Transient cyanosis that has resolved, with a normal INITIAL STABILIZATION/THERAPY r Surgery for thoracic masses, flail chest, etc.
SpO2 reading, may not require further evaluation. r Neurology for seizures, suspected central apnea,
circulation.
Lab r Administer supplemental oxygen as needed to and severe breath-holding spells. The latter two may
Initial Lab Tests be manifestations of seizures and may require EEG
r A blood gas analysis should be obtained. In many correct low oxygen saturation and improve cyanosis.
r If the ABCs are secure, the SpO reading is normal, testing.
cases, venous blood gas sampling will be adequate, 2
and the patient is in no distress, further treatment
but arterial blood gas provides more information
may proceed judiciously. FOLLOW-UP
about both oxygenation and ventilation:
PaO2 <80 mm Hg on room air confirms ALERT
hypoxemia. FOLLOW-UP RECOMMENDATIONS
r The following tests are indicated selectively: In infants in whom heart disease is suspected, avoid As noted in the Issues for Referral section
administration of 100% oxygen during the
Hgb level if concerned about anemia or resuscitation, as it can induce closure of the PDA in COMPLICATIONS
polycythemia Patients who experience a prolonged episode of
neonates and cause overcirculation in the lungs in
In infants and patients with lethargy or sepsis, hypoxemia may have end-organ damage including the
older infants. These patients require only enough
consider a capillary blood glucose measurement. kidney, liver, and/or brain.
If concerned about sepsis, obtain CBC, supplemental oxygen delivery to achieve adequate
disseminated intravascular coagulation panel, and oxygenation (3). Examples of ductal-dependent
appropriate cultures. lesions are (see Patent Ductus Arteriosus): REFERENCES
r Tricuspid atresia
If methemoglobinemia, consider blood 1. Hoffman JI, Kaplan S. The incidence of CHD. J Am
co-oximetry. r Pulmonary atresia
Coll Cardiol. 2002;39(12):18901900.
If drug ingestion, consider basic metabolic panel r Transposition of the great arteries
2. Martin L, Kahil H. How much reduced hemoglobin
and toxicology screen. r Mitral valve atresia with hypoplastic left ventricle is necessary to generate central cyanosis? Chest.
Imaging r Aortic valve atresia 1990;97(1):182185.
r Chest radiograph to assess for pneumonia, lung r Pulmonary artery hypoplasia 3. Steinhorn RH. Evaluation and management of the
parenchymal abnormality, effusion, foreign body r Severe coarctation of the aorta cyanotic neonate. Clin Pediatr Emerg Med.
aspiration, pneumothorax, widened mediastinum, or 2008;9(3):169175.
enlarged cardiac silhouette MEDICATION
r Chest CT if concerned for a lung mass, pulmonary r Choice of medications will depend on the etiology of
hemorrhage, or PE (CT angiography). cyanosis, for example: ADDITIONAL READING
r Consider echo for concern of CHD. Status asthmaticus requires bronchodilator Stack AM. Cyanosis. In Fleisher GR, Ludwig S, eds.
Diagnostic Procedures/Other therapy such as albuterol. Textbook of Pediatric Emergency Medicine. 6th ed.
r ECG Seizures require antiepileptic medications, often Philadelphia, PA: Lippincott Williams & Wilkins; 2010.
r Consider a hyperoxia test to distinguish between benzodiazepines acutely.
cardiac and respiratory causes. See Cyanotic Heart If cyanotic CHD is suspected in a neonate, an IV
infusion of prostaglandin E2 may be required
Disease topic, Diagnostic Procedures/Other.
emergently.
CODES
DIFFERENTIAL DIAGNOSIS r See specific topics for recommended treatment for
r See Etiology. ICD9
other diagnoses. r 770.83 Cyanotic attacks of newborn
r Some conditions can be confused with cyanosis:
SURGERY/OTHER PROCEDURES r 782.5 Cyanosis
Polycythemia can be mistaken for cyanosis. r Dependent on the etiology of cyanosis:
The blue dye of clothing can cause an appearance
of cyanosis. Intubation or even an emergent tracheostomy may
Large pigmentary lesions such as Mongolian spots be necessary for respiratory failure. PEARLS AND PITFALLS
may be confused for cyanosis. Tracheostomy management: Suctioning or
changing the tube if necessary r Pearls:
Amiodarone therapy or silver ingestion can cause
Thoracentesis or thoracostomy for pleural effusion Cyanosis is not a direct correlate of oxygen
a bluish tint to the upper body.
or pneumothorax saturation and depends on the absolute Hgb level.
Laryngoscopy and bronchoscopy for foreign body In patients with anemia, cyanosis will be apparent
aspiration at much lower oxygen saturation levels than with
r See specific topics for recommended treatment for a normal or high Hgb concentration.
other diagnoses. r Pitfalls:
Overoxygenation of neonatal patients with
DISPOSITION ductal-dependent lesions and older patients with
Admission Criteria heart disease
r Any patient who presents with acute, unresolved
cyanosis will require admission to the hospital.
Any patient requiring ventilatory support
Impending cardiac or respiratory failure
Any infant requiring prostaglandin E2 infusion
221
CYANOTIC HEART DISEASE

Calvin G. Lowe
The lone arterial trunk sits over a large VSD. DIAGNOSTIC TESTS & INTERPRETATION
BASICS Pulmonary vascular resistance (PVR) and Lab
blood flow indicate pulmonary HTN. Initial Lab Tests
DESCRIPTION r Hypoplastic left heart syndrome (HLHS): r Serum electrolytes, calcium, glucose, and CBC:
r Varying degrees of deoxygenated venous blood
Hypoplasia of the L ventricle Electrolyte abnormalities ( sodium, chloride) can
shunting from the right (R) to left (L) side of the Hypoplastic aortic arch occur.
heart or circulation occurs in cyanotic heart disease Aortic and mitral valvular stenosis Calcium can present as prolongation of the QT
(CyHD). r Ebstein anomaly: interval, CHF, hypotension.
r Cyanosis occurs when >5 mg/dL of deoxygenated
Tricuspid valve leaflets are abnormally attached to Hypoglycemia can cause weakness and fatigue.
blood is in the capillary beds. its annulus. Depending on the heart lesion, polycythemia
EPIDEMIOLOGY An enlarged RA and smaller R ventricle = R to L (from chronic hypoxemia) or anemia (dilutional
shunting and pulmonary blood flow. effects) can be present.
Incidence r An arterial blood gas sample can determine the
In 2005, the CDC reported that CyHD occurred in 56.9 ETIOLOGY
per 100,000 live births in the U.S. r Exact cause of CyHD is unknown. degree of hypoxemia and metabolic acidosis.
r Factors associated with an increased risk of CyHD: Imaging
Prevalence r Chest radiographic imaging is essential.
CyHD accounts for 25% of all congenital heart Maternal risk factors, chromosomal abnormalities,
and single gene defects r Various degrees of ventricular hypertrophy and
disease (CHD).
r A multifactorial etiology is the theoretical basis for pulmonary congestion depend on CyHD type:
RISK FACTORS most forms of CyHD. A boot-shaped heart is seen in TOF.
Maternal risk factors: Snowman or figure of 8 sign = TAPVR.
r Infection (rubella) COMMONLY ASSOCIATED CONDITIONS Egg on a string sign = TGA.
r DiGeorge syndrome: TA, TOF
r Medication use (eg, anticonvulsants, lithium)
r Noonan syndrome: Supravalvular (SV) PS Diagnostic Procedures/Other
r Drug abuse (ethanol) r An echo should be performed on patients suspected
r Williams syndrome: SV aortic stenosis, pulmonary
r Disease states (phenylketonuria, systemic lupus of having CyHD.
artery stenosis r A 12-lead ECG should be obtained. Depending on
erythematosis, diabetes mellitus)
GENERAL PREVENTION the lesion, the ECG may show various arrhythmias,
Adequate prenatal care: Prenatal US can diagnose DIAGNOSIS hypertrophy, R or L axis deviations, and bundle
CyHD in utero. After delivery, transport to an branch blocks.
HISTORY r A hyperoxia test can differentiate between cyanotic
appropriate tertiary care center is warranted. r Not all CyHD is clinically evident at birth.
cardiac and pulmonary disease:
PATHOPHYSIOLOGY r Presence of a PDA can mask severe pulmonary or
r Tetralogy of Fallot (TOF): A baseline R radial artery (preductal) blood gas
systemic flow obstruction. sample is obtained on room air.
4 basic lesions: r Presentation in 1st 2 wk of life: AS, HLHS, TGA, A 2nd blood gas is obtained after a 10-min
Ventricular septal defect (VSD) TAPVR, TA, and TrA administration of 100% oxygen (O2 ).
R ventricular outflow obstruction from r Presentation within the 1st mo: TrA A PaO2 >200 mm Hg on 100% O2 makes
pulmonary stenosis (PS) r Presentation within 6 wk to 6 mo: TrA cyanotic CHD unlikely.
Overriding aorta r Patients can be stable, in CHF, or in shock. A PaO2 <150 mm Hg on 100% O2 suggests
R ventricular hypertrophy = pulmonary flow
r The most common presentations are acute CyHD with complete mixing without pulmonary
resulting in R to L shunting. blood flow restriction.
Pink TOF: Mild PS and L to R shunting respiratory distress and cyanotic episodes.
r Signs of CHF (fatigue, poor appetite and diaphoresis A PaO2 <50 mm Hg indicates a mixing lesion
TOF hypercyanotic spells or Tet spells: with restrictive pulmonary blood flow.
Agitated patient has extreme cyanosis in during feeding, pallor, tachypnea, tachycardia),
situations with sympathetic activity. failure to thrive, irritability, dehydration, and DIFFERENTIAL DIAGNOSIS
R ventricular outflow tract obstruction worsens recurrent lung infections are common signs and r In neonates, sepsis must be suspected prior to a
with infundibular septum spasms. symptoms. definitive diagnosis of CyHD.
Tet spells may cause end-organ damage, are r CHF is due to lesions that cause pulmonary flow: r Tracheal or bronchial foreign body
unpredictable, and potentially are lethal. TGA, TOF, TA, HLHS, and TAPVR. r Congenital anomalies: Vascular malformations,
r Transposition of the great arteries (TGA): hypoplastic mandible
PHYSICAL EXAM r Apparent life-threatening event
The aorta originates from the R ventricle, and the r Evaluation of general appearance and color is the
main pulmonary artery (PA) arises from the L r Pneumonia/Empyema/Effusion
most important part of the exam.
ventricle. r Pink color = CyHD (pink Tet), L to R shunt. r Pulmonary edema
A patent ductus arteriosus (PDA), atrial septal r Blue color typically = CyHD with R to L shunt. r Diaphragmatic hernia
defect (ASD), or VSD is critical for survival and r Grey color indicates outflow obstruction, systemic r Congenital pulmonary hypoplasia
allows mixing of the 2 systems to move r Breath-holding
oxygenated blood to the systemic system. hypoperfusion, and shock.
r Tachycardia and tachypnea may be out of proportion r Methemoglobinemia
r Total anomalous pulmonary venous return (TAPVR):
Pulmonary veins return oxygenated blood from to the patients general appearance.
r Cool skin and delayed capillary refill indicates shock
the lungs to the right atrium (RA).
An ASD or patent foramen ovale is needed to associated with severe cardiac disease.
r Distal pulses imply aortic arch obstruction.
cause mixing and shunting of blood to the L side
of the heart for survival. r Hydration status, mucosal color, and lung/heart
r Tricuspid atresia (TA): sounds should be assessed along with palpation of
Atresia of the tricuspid valve causes the R ventricle the precordium and a survey for organomegaly.
to be hypoplastic or absent. r Heart murmurs with or without thrills and gallop
The RA will become hypertrophied. rhythms suggest CyHD.
An ASD, VSD, or PDA is critical to survival. r CHF: Tachypnea, hyperactive precordium, S3 heart
R to L shunting occurs to drain the RA. sound, chest congestion, and hepatomegaly
r Truncus arteriosus (TrA): Failure of separation of the
aorta and PA leads to a single arterial trunk arising
from both ventricles:
222
CYANOTIC HEART DISEASE
SURGERY/OTHER PROCEDURES DIET

r Surgical options are lesion specific for CyHD.
TREATMENT r Atrial septostomy creates intra-atrial mixing
Diet may include fluid and salt restrictions based upon
pediatric cardiology suggestions.
A pediatric cardiologist should be consulted for between atria in TGA and TA. PROGNOSIS
evaluation and treatment recommendations. r Modified Blalock-Taussig (BT) shunt: Artificial tubing
Prognosis is based on the patients initial acuity, CyHD
sewn between the subclavian or carotid artery to the type, and need for surgical treatment.
r Immediate evaluation and treatment of the ABCs corresponding side branch PA.
r Similarly, the Sano shunt redirects blood directly COMPLICATIONS
and continuous pulse oximetry is crucial: r Without immediate treatment, anoxic brain injury,
Administer O2 judiciously. from the R ventricle to the PA.
r The Glenn shunt: Superior vena cava (SVC) to PA severe metabolic acidosis, multiple organ failure,
C
Establish IV access: >1 site is suggested. and cardiopulmonary arrest may ensue.
r Small, frequent IV boluses of normal saline or shunt for infants with pulmonary resistance r CyHD is associated with brain abscesses.
r The Fontan procedure used in HLHS and TA:
lactated Ringer solution of 10 cc/kg are indicated to
treat hypotension. Anastomosis of SVC to R PA along with the
r A full sepsis evaluation should be initiated and anastomosis of the RA and/or IVC to the PAs REFERENCES
r Norwood procedure: 2-stage HLHS repair:
antibiotics administered empirically in infants <23
mo of age who are exhibiting signs and symptoms Stage 1: Proximal main PA to the aorta and a 1. Meckler GD, Lowe CG. To intubate or not to
of sepsis: Fever >38.0 C, irritability, respiratory modified right BT shunt or Sano shunt to intubate? Transporting infants on prostaglandin E1.
distress, lethargy: pulmonary blood flow. Pediatrics. 2009;123(1):e25e30.
Caution must be used when considering lumbar An ASD is also created to allow L to R flow. 2. Penny DJ, Shekerdemian LS. Management of the
puncture in a cyanotic child. Stage 2: Bidirectional Glenn to reduce the volume neonate with symptomatic congenital heart
overload of the single R ventricle. disease. Arch Dis Child Fetal Neonatal Ed.
MEDICATION Fontan procedure follows to correct cyanosis. 2001;84(3):F141F145.
First Line r Arterial switch of Jantene: TGA repair 3. Rao PS. Diagnosis and management of cyanotic
Prostaglandin (PGE1 ) should be initiated on patients congenital heart disease: Part 1. Indian J Pediatr.
with a ductal-dependent CyHD: DISPOSITION
2009;76(1):5770.
r 0.050.1 g/kg/min should be initiated with a max Admission Criteria
r Inpatient floor admission criteria:
rate of 0.4 g/kg/min.
r A common side effect of PGE is apnea; prompt O2 requirement, acute respiratory distress, ADDITIONAL READING
1
worsening CHF unresponsive to emergency
intubation may be necessary.
department therapy or confirmed/symptomatic r Gewitsz MH, Woof PK. Cardiac emergencies. In
r Elective intubation of patients on PGE for transport
1 respiratory syncitial virus Fleisher GR, Ludwig S, eds. Textbook of Pediatric
may increase the risk of transport complications (1). r Critical care admission criteria: Emergency Medicine. 6th ed. Philadelphia, PA:
r Other occurrences associated with PGE include
1 Any patient who is intubated and/or requiring Lippincott Williams & Wilkins; 2010.
hyperthermia, flushing, arrhythmias, hypotension, vasopressor support should be admitted to a r Rudolf AM. Congenital Diseases of the Heart:
and seizures. pediatric ICU. Clinical-Physiological Considerations. 2nd ed.
Second Line The decision to admit should be made in Armonk, NY: Futura Publishing Company; 2001.
r A child with signs or symptoms of CHF may benefit conjunction with a pediatric cardiologist. r Silverbach M, Hannon D. Presentation of congenital
from furosemide at 0.51 mg/kg. If a urine output of Discharge Criteria heart disease in the neonate and young infant.
35 cc/kg/hr is not achieved within 12 hr after the r Patients may be discharged home with follow-up if Pediatr Rev. 2007;28:123131.
1st dose of furosemide, repeat doses of 1 mg/kg can r Yee L. Cardiac emegencies in the first year of life.
deemed stable by pediatric cardiology.
be given at hourly intervals to a max of 35 mg/kg. r A TOF patient with a Tet spell that is corrected Emerg Med Clin North Am. 2007;25(4):9811008.
r If hypotension persists after IV fluid boluses,
without pharmacologic intervention may be
dopamine should be initiated at 5 g/kg/min and considered for discharge directly from the
titrated up to a max rate of 20 g/kg/min. emergency department. CODES
r Dobutamine can be added for inotropic support with
an initial rate of 5 g/kg/min with titration to a max Issues for Referral
r Transfer to a tertiary care center if needed. ICD9
rate of 20 g/mg/min. r 745.2 Tetralogy of fallot
r Tet spell treatment includes several options: r A specialized pediatric critical care transport team
r 745.4 Ventricular septal defect
O2 reduces hypoxemia and decreases PVR. may be necessary to facilitate the transport. r 746.9 Unspecified congenital anomaly of heart
Calming the child decreases PVR.
IV fluids provides volume resuscitation. FOLLOW-UP
Knee-chest position: Venous return, systemic PEARLS AND PITFALLS
vasculature resistance (SVR) FOLLOW-UP RECOMMENDATIONS
Morphine sulfate 0.10.2 mg/kg SC/IM/IV Discharge instructions and medications: r HLHS patients can present with pulmonary blood
venous return, PVR, relaxes infundibulum r Parents must be instructed to look for any flow at the expense of systemic blood flow.
Phenylephrine 0.02 mg/kg IV increases SVR worsening signs and symptoms of the CyHD. r Therefore, the O saturation will be >90%, but
2
Propanolol 0.150.25 mg/kg, slow IV push r Discharge medications should be based upon peripheral perfusion and pulses will be decreased.
decreases inotropic effect and may SVR. r These patients should not be given supplemental O
pediatric cardiology recommendations. 2
Sodium bicarbonate (1 mEq/kg IV) reduces r Cardiology follow-up should be arranged. but should be on room air since hypoxemia is a
metabolic acidosis. potent pulmonary vasoconstrictor.
r Hyperoxia testing requires blood sampling; an
attempt to use a pulse oximetry reading on the right
hand may give a falsely reassuring reading.
223
CYCLIC VOMITING
Richard G. Boles
r 50% of patients have cyclical episodes at Imaging

BASICS regular intervals, and the others have episodes Imaging is not helpful to diagnose CVS but is used to
triggered by stressors, or apparently at random. exclude other emergent diagnoses, if indicated:
DESCRIPTION r The duration of episodes varies from a few hours to r Upper GI series with small bowel follow-through to
r A cyclic vomiting pattern is defined as the presence
several days, with a median of 2 days. rule out etiologies such as malrotation should be
of multiple stereotypical episodes of nausea and r The frequency of episodes varies from every several performed at least once (5).
vomiting separated by intervals without these months to twice a week, with a median of 1 mo. r Abdominal/Renal US to rule out non-CVS etiologies
symptoms: r The age of onset varies from neonates into should be performed at least once.
Some patients, particularly adolescents and adults, adulthood, with a median of 4 yr for those r Brain imaging to rule out non-CVS etiology in cases
have lesser degrees of nausea between episodes. presenting to pediatricians.
r 90% of patients with a cyclic vomiting pattern do with altered mental status or abnormal neurologic
r CVS is frequently associated with other functional findings (5)
not have an alternative definable diagnosis (see disorders such as:
Differential Diagnosis) and are given the diagnosis DIFFERENTIAL DIAGNOSIS
Migraine headache r The differential includes the broad differential
of cyclic vomiting syndrome (CVS) (1). Irritable bowel syndrome
diagnoses of vomiting, which can be found in the
EPIDEMIOLOGY Other chronic pain syndromes
Vomiting topic.
Prevalence Chronic fatigue syndrome r Malrotation
CVS was present in 2% of school-age children in 2 GERD r Unilateral ureteral obstruction
studies conducted in Australia (2) and Scotland (3): Postural orthostatic tachycardia syndrome
r Pancreatitis (but can be comorbid with CVS)
r CVS is likely less common in nonEuropean-derived Depression (unipolar or bipolar)
Anxiety disorder r Intracranial mass
populations. r 1/3 of cases have chronic neuromuscular disease r Ornithine transcarbamylase deficiency:
PATHOPHYSIOLOGY (termed as CVS+), including: Other urea cycle disorders
r CVS is a functional disorder of multifactorial r Organic acidemias
Mental retardation
pathogenesis, related to migraine and irritable Seizure disorders r Fatty acid oxidation disorders
bowel syndrome (4,5): Hypotonia r Congenital defects of glycosylation
Many consider CVS to be a migraine variant. Autistic spectrum disorders r Pregnancy
r CVS and the associated functional disorders are
PHYSICAL EXAM r Marijuana cyclical emesis
associated with abnormal autonomic nervous r Between episodes: r Fictitious disorder (unlikely)
system function.
r In many cases, these same disorders are associated Usually normal
May have subtle signs of a skeletal myopathy ALERT
with mitochondrial dysfunction (46): A minority of cases have findings related to 1 r New neurologic findings should prompt additional
Some cases have frank mitochondrial disease. comorbid disorders listed in the History section. workup for a metabolic disorder and/or
Clinical manifestations are generally intermittent r During episodes: intracranial mass (7).
and typically occur at times of high-energy r Acute abdomen or abdominal pain worse than
Acute distress with lethargy
demand, including fasting, viral infection,
Often with abdominal pain, with or without usual for that patient should prompt workup for
overexercise, psychological stress, and
tenderness a surgical cause, especially malrotation (7).
environmental temperature extremes.
Occasionally with fever, diarrhea, photophobia
ETIOLOGY and/or phonophobia
r Unknown in most cases but presumably
multifactorial
DIAGNOSTIC TESTS & INTERPRETATION TREATMENT
r Many cases have mutations in the maternally Lab
r If done, standard lab testing will be normal between Avoid fasting by administration of calories, including
inherited mitochondrial DNA (mtDNA), usually fruit juices, chocolate milk, etc.
mutations not assayed by standard mtDNA episodes in almost all cases.
r Lab abnormalities are common during vomiting
screening tests (5,6): INITIAL STABILIZATION/THERAPY
In many cases, maternal-side relatives who share episodes, as reflected below. r IV normal saline bolus if dehydrated
the same mtDNA sequence are affected with a Initial Lab Tests r IV fluids with 10% dextrose 0.45% normal saline at
variety of dysautonomic, functional, and r Chemistry panel: Anion gap metabolic acidosis a high rate of 1.52 times maintenance:
psychiatric conditions (4,5). r Urine dipstick: Ketosis (at onset of episode) Reduce glucose content if glucose >250300
r ALT, GGT, lipase: Rule out potential non-CVS mg/dL; hyperglycemia triggers insulin, resulting in
etiologies: mitochondrial anabolism.
DIAGNOSIS Mild elevations, up to about twice the upper limit r Darkened and quiet room
HISTORY of the normal range, in transaminases are
r Within each patient, episodes are stereotypical common in CVS.
(similar). Pancreatitis can coexist with CVS.
r Associated findings during episodes include: r Beta-hCG in the appropriate setting
r Quantitative urine organic acids should be
Nausea
Vomiting performed at least once early in an episode for
Lethargy potential mitochondrial disease and organic
r Other findings that may be present include: acidemias.
r Quantitative plasma amino acids should be
Abdominal pain
Diarrhea performed at least once early in an episode for
Fever potential urea cycle defects.
Headache
Photophobia and/or phonophobia
224
CYCLIC VOMITING
MEDICATION COMPLEMENTARY AND ALTERNATIVE REFERENCES

Acute treatment (7): MEDICINE
r Ondansetron for nausea/vomiting at 0.30.4 r Riboflavin: 1. Li BU, Murray RD, Heitlinger LA, et al.
mg/kg/dose (adult dose 1216 mg) given by 100 mg/day, or one B100 tablet/day Heterogeneity of diagnoses presenting as cyclic
standard routes (IV or oral dissolving tablet): r Food allergen elimination diets (in selected cases vomiting. Pediatrics. 1998;102:583587.
Patients do not generally respond to the lower with suspected food triggers) (7) 2. Cullen K, Macdonald WB. Periodic syndrome: Its
doses but usually respond to higher doses. nature and prevalence. Med J Aust. 1963;5:
r Some cases respond to triptan therapy if caught DISPOSITION 167173.
Admission Criteria
early:
Sumatriptan (Imitrex):
r Inability to stop emesis 3. Abu-Arafeh IA, Russell G. Migraine and cyclical
vomiting syndrome in children. Headache Quart.
C
r Significant dehydration, no urine output
Intranasal: 5-, 10-, or 20-mg spray in 1 nostril 1997;8:122125.
r Failure to maintain adequate hydration
for adolescents; may repeat in 2 hr, max dose 4. Boles RG, Adams K, Li BU. Maternal inheritance in
r Sodium <130 mEq/L cyclic vomiting syndrome. Am J Med Genet.
40 mg/day
SC: <30 kg, 3 mg; >30 kg, 6 mg; may be r Serum anion gap 20 mM (sodium minus chloride 2005;133A:7177.
repeated once in 1 hr minus HCO3 ): 5. Zaki EA, Freilinger T, Klopstock T, et al. Two
r Sedation with lorazepam or diphenhydramine Serum anion gap 1819 is borderline. common mitochondrial DNA polymorphisms are
(possibly with a phenothiazine) for comfort in cases r Large urine ketones (>40 mg/dL): highly associated with migraine headache and
not responding to D10-containing IV fluids and Moderate ketones (40 mg/dL) is borderline. cyclic vomiting syndrome. Cephalalgia. 2009;29:
ondansetron: r Loss of abilities, altered mental status (relative to 719728.
Start with lower dosages and observe, as patients baseline), or new neurologic finding 6. Boles RG, Powers ALR, Adams K. Cyclic vomiting
with CVS have a high incidence of side effects r Acute abdomen syndrome plus. J Child Neurol. 2006;21:182188.
from sedation. r Pancreatitis 7. Li BUK, Lefevre F, Chelimsky GG. NASPGHAN
Lorazepam 0.05 mg/kg/dose PO/IV q6h PRN Consensus Statement on the Diagnosis and
Diphenhydramine 1 mg/kg/dose q6h PRN Discharge Criteria Management of CVS. J Pediatr Gastroenterol Nutr.
r Acute nausea and pain may improve with r Ability to tolerate adequate enteral intake
r Patients know when the episode is over and can 2008;47:379393.
acid-reducing agents, such as proton pump 8. Boles RG, Lovett-Barr MR, Preston A, et al.
inhibitors: resume a regular diet. Treatment of cyclic vomiting syndrome with
Lansoprazole 0.81.5 mg/kg/day up to 30 mg co-enzyme Q10 and amitriptyline, a retrospective
b.i.d. FOLLOW-UP study. BMC Neurology. 2010;10:10.
Omeprazole 0.81 mg/kg/day up to 20 mg b.i.d.
r Abdominal painmoderate: See Also (Topic, Algorithm, Electronic
Ketorolac 1 mg/kg/dose (max single dose 30 mg) r Follow the management plan recommended by the Media Element)
r http://www.cvsaonline.org
q6h PRN specialist. r http://www.umdf.org
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN r Return for:
r http://www.curemito.org
Naproxen 5 mg/kg PO q8h PRN Signs of dehydration
Acetaminophen 15 mg/kg/dose PO/PR q4h PRN New neurologic findings
Prophylaxis: Abdominal pain more severe than usual
r First line (7) Other worrisome findings CODES
r Counsel patient to avoid other identifiable triggering
Amitriptyline is the first-line drug used for
prophylaxis in patients 5 yr: factors as much as feasible: ICD9
0.51 mg/kg/day qhs Viral illnesses 536.2 Persistent vomiting
Higher dosages are often needed; check blood Allergy and sinusitis
level. Anticipatory positive stress
Consider ECG prior to and 12 wk after starting PEARLS AND PITFALLS
Patient Monitoring
to detect prolonged QTc. r Mental status r Pearls:
Other tricyclic antidepressants may not be as r Abdominal pain CVS is treatable in most cases. Referral to a CVS
effective. r Urine ketones specialist is often appropriate.
Cyproheptadine is the first-line drug used for r Serum anion gap, if very ill Simple measures like frequent snacking and
prophylaxis in patients 4 yr: cofactor/vitamin therapy are often helpful.
0.250.5 mg/kg/day qhs PROGNOSIS r Pitfalls:
Co-enzyme Q10 was found to be as effective as In most cases, episodes can be substantially reduced Drug therapy often appears to fail because only
amitriptyline with fewer side effects in 1 in frequency and severity on the appropriate low dosages were tried.
retrospective study (8) and is effective in all therapeutic regimen. Episodes can coalesce together into status CVS,
ages: which requires expert intervention.
10 mg/kg/day b.i.d. (adult dose 200 mg b.i.d.) COMPLICATIONS
r SIADH Many adolescents and adults self-treat nausea
r Second line:
r Urinary obstruction with marijuana. While of apparent efficacy in
Propranolol 0.251.0 mg/kg/day b.i.d. (adult dose r HTN some, cannabis abuse can precipitate cyclic
generally 10 mg b.i.d. or t.i.d.) (7) r Bowel obstruction (especially in opiate use): vomiting in others.
L-carnitine 50100 mg/kg/dose (adult dose 1
r Complications of mitochondrial disease in the
g/dose) b.i.d.
Oral contraceptives may improve catamenial CVS subpopulation with that etiology.
but may exacerbate vomiting episodes in some:
Low dose types are better tolerated.
Chronic nausea is often secondary to GERD and
responds to proton pump inhibitors.
225
CYSTIC FIBROSIS: EXACERBATION

Craig A. McElderry
ETIOLOGY r Periodic screening for pancreatic dysfunction should

BASICS r Many patients with CF will experience an be done in all patients with CF:
exacerbation with no obvious new organism or Random glucose concentration
DESCRIPTION obvious precipitant. A yearly oral glucose tolerance test is thought to
r Cystic fibrosis (CF) is an autosomal recessive disease r Some known precipitating factors for pulmonary be the best screening method for those 10 yr of
caused by mutations in the cystic fibrosis exacerbations include (3): age.
transmembrane conductance regulator (CFTR) gene Nonadherence to maintenance treatment Imaging
that results in abnormal viscous mucoid secretions New bacterial infection r Chest radiography:
in multiple organs. Viral infection:
r Exacerbations of pulmonary symptoms (eg, cough, Remains the primary imaging modality used in the
Respiratory syncytial virus (RSV) follow-up of patients with CF
wheeze, sputum production) in patients with CF Influenza A Used to evaluate for new infiltrate or lobar or
must be recognized early and treated vigorously in Fungal infection/allergic bronchopulmonary segmental collapse
order to maintain pulmonary function and relieve aspergillosis (ABPA)seen in 215% of patients Not sensitive in detecting bronchiectasis
symptoms. with CF r CT of the chest:
r Pulmonary exacerbations in patients with CF have Mucus plugging CT typically is used as a supplemental modality
an important negative impact on quality of life and Lobar/Segmental collapse when specific, fine anatomic detail is necessary.
survival. Atypical mycobacteria: Detects even mild bronchiectasis
r Pulmonary insufficiency is responsible for at least Mycobacterium avium complex
Serial CT scans allow assessment of the evolution
80% of CF-related deaths (1). Mycobacterium abscessus or Mycobacterium
of pulmonary abnormalities in patients with CF.
fortuitum CT has advantages over pulmonary function tests
EPIDEMIOLOGY Mycobacterium kansasii
See Cystic Fibrosis: New Diagnosis topic. and clinical scoring in the depiction of pulmonary
changes over time.
RISK FACTORS
Factors shown to have an adverse effect on patients DIAGNOSIS Diagnostic Procedures/Other
with CF include: Bronchoalveolar lavage, though unlikely to become
r Exposure to tobacco smoke This section will focus on the diagnosis of pulmonary part of routine clinical monitoring, can be used to
exacerbations in patients with CF. identify lower respiratory tract infections when sputum
r Poor socioeconomic status
HISTORY is unavailable.
GENERAL PREVENTION The most reliable indicators for a pulmonary DIFFERENTIAL DIAGNOSIS
r Adherence to maintenance treatment
exacerbation include (3): See Cystic Fibrosis: New Diagnosis topic.
r Good nutrition r Decreased exercise tolerance
PATHOPHYSIOLOGY r Shortness of breath
r See Cystic Fibrosis: New Diagnosis topic. r Difficulty breathing TREATMENT
r Patients with CF typically become chronically r Increased wheeze or cough r Treatment of CF includes therapies for maintenance
infected soon after birth. r Increased sputum
r The presence of lower respiratory infection is of lung (including suppression of chronic infection),
r Absence from school or work
pancreatic, and nutritional health and management
associated with: r Decreased appetite of pulmonary exacerbations.
More frequent symptoms (eg, wheeze) r See Cystic Fibrosis: New Diagnosis topic for
Increased levels of inflammatory mediators PHYSICAL EXAM
r Increased work of breathing manifested by maintenance of lung and management of pancreatic
Increased air trapping and nutritional health.
r 1 study showed that 98% of a cohort of 40 infants tachypnea, retractions, dyspnea, etc. r This section will focus on exacerbations:
r Increased adventitial sounds on lung examination
with CF had serologic or culture evidence of Many patients with CF will develop pulmonary
Pseudomonas aeruginosa by 3 yr of age (2). (eg, crackles, rhonchi)
r Chronic infection leads to: r Hypoxemia exacerbations in the presence of chronic lower
respiratory infection, often with P. aeruginosa.
Generation and secretion of chemotactic cytokines DIAGNOSTIC TESTS & INTERPRETATION Determining which factor(s) may have triggered
Cytokines recruit large numbers of Lab an exacerbation is essential for effective
polymorphonuclear cells into the airways. Initial Lab Tests management of the exacerbation.
r P. aeruginosa amplifies the cycle of infection and r Respiratory tract culture (oropharyngeal or sputum):
inflammation. INITIAL STABILIZATION/THERAPY
r P. aeruginosa has the ability to establish chronic
Sample should be labeled as a CF culture, as many r Consider advanced airway management such as
microbiology labs handle CF samples differently positive pressure ventilation for patients with
infection through biofilm formation on damaged from routine samples in order to ascertain the
respiratory epithelium. respiratory failure.
r Symptoms of an exacerbation may be secondary to
presence of CF-specific organisms. r Treatment for pulmonary exacerbations often
Consider viral, fungal, and mycobacterial cultures.
release of organisms from this biofilm. r Diagnosis of ABPA is likely if: includes:
r This chronic infection/inflammation makes the Antibiotics (PO, inhaled, or IV)
One can demonstrate a 4-fold rise in the level of Increased used of airway clearance techniques
patient with CF especially vulnerable to other IgE, accompanied by positive aspergillus Improved nutrition
factors, which may trigger an exacerbation. (See precipitins
Etiology.) Clinical and radiologic deterioration despite
appropriate antibiotics
226
CYSTIC FIBROSIS: EXACERBATION
MEDICATION COMPLEMENTARY & ALTERNATIVE

Antibiotic treatment of pulmonary exacerbations is THERAPIES FOLLOW-UP
guided by identification of specific organisms from the r Airway clearance techniques (should be augmented
airways. with inhaled dornase alfa, if the patient is not FOLLOW-UP RECOMMENDATIONS
already receiving this): Follow-up in CF clinic should be arranged within
First Line several weeks of an exacerbation to assure that lung
r Antibiotics: Combination antibiotic treatment Postural drainage and clapping
Vibrating mechanical vests function has improved.
(generally with antipseudomonal activity) with
agents that have different modes of action is Forced expiratory technique and autogenic Patient Monitoring
preferred to single-agent treatment to avoid
emergence of resistant strains, with treatment
drainage: A technique characterized by breathing
control, in which the individual adjusts the rate,
Close attention to respiratory status as well as use of
pulse oximetry should be considered in patients with
C
lasting about 14 days. depth, and location of respiration in order to clear CF exacerbations.
r Consider a beta-lactambased antibiotic and an the chest of secretions independently
r Supplemental oxygen DIET
aminoglycoside. See Cystic Fibrosis: New Diagnosis topic.
r Antipseudomonal: SURGERY/OTHER PROCEDURES
Ceftazadime (IV) 50 mg/kg/dose IV q8h r For management of mucus plugging when COMPLICATIONS
Tobramycin (IV) 46.6 mg/kg/dose IV per day physiotherapy and IV antibiotics have been r Death
Meropenem (IV) (also has activity against unsuccessful, consider flexible bronchoscopy with
Staphylococcus aureus and Burkholderia cepacia) suction.
40 mg/kg/dose IV q8h r Percutaneous drainage may be necessary for
Ciprofloxacin (PO): May be sufficient for milder
REFERENCES
pulmonary abscesses complicating severe
exacerbations in combination with inhaled bronchiectasis. 1. OSullivan BP, Freedman SD. Cystic fibrosis. Lancet.
antibiotics: 2009;373:18911904.
1 mo to 5 yr: 15 mg/kg/dose PO q12h DISPOSITION
2. Burns J, Gibson R, McNamara S, et al. Longitudinal
518 yr: 20 mg/kg/dose PO q12h Admission Criteria
r Critical care admission criteria: assessment of Pseudomonas aeruginosa in young
Tobramycin (inhaled): children with cystic fibrosis. J Infect Dis.
Infant/Toddler: 1020 mg in 24 mL normal Endotracheal intubation
2001;183:444452.
saline nebulized b.i.d. Positive pressure ventilation
Children: 2040 mg in 23 mL normal saline r Inpatient admission criteria: 3. Smyth A, Elborn JS. Exacerbations in cystic fibrosis:
3management. Thorax. 2008;63(2):180184.
nebulized b.i.d. Failure of outpatient antibiotic therapy
r Antistaphylococcal: Dyspnea
Oxacillin (IV) 100200 mg/kg/day in divided doses Deteriorating pulmonary exam
IV q6h Deteriorating pulmonary function tests (including CODES
Linezolid (IV or oral) for MRSA: 10 mg/kg/dose blood gas values)
q8h Deteriorating chest radiograph appearance ICD9
r Anti-Stenotrophomonas maltophilia: Anorexia or weight loss r 277.00 Cystic fibrosis without mention of meconium
Trimethoprim/Sulfamethoxazole (TMP/SMX) (PO): Need to initiate and teach home IV treatment ileus
Lobar or segmental atelectasis r 277.02 Cystic fibrosis with pulmonary
>2 mo: 1520 mg/kg/day (based on TMP) PO
t.i.d.q.i.d. for 14 days Right heart failure manifestations
Massive hemoptysis
Second Line Hypoxemia or initiation of home oxygen therapy
r Antifungal agents: Consider in patients with
Pneumothorax PEARLS AND PITFALLS
indwelling access devices who develop high, spiking Respiratory failure
fevers while on appropriate IV antibiotics: r Early recognition and vigorous management of
SIADH
Amphotericin B liposome IV (better tolerated than Superimposed respiratory illness: pulmonary exacerbations in the patient with CF is
conventional amphotericin B): Influenza vital to the maintenance of lung function, good
Start: 1 mg/kg/day IV as a once-daily infusion RSV quality of life, and survival.
Increase by: 1 mg/kg/day IV to a max dose of Aspergillosis r One should consider the etiology of an exacerbation
5 mg/kg/day as a once-daily infusion Legionnaire disease in each patient.
Prednisone or prednisolone PO (treatment of Status asthmaticus r Appropriate antibiotic therapy, as well as attention
ABPA) 0.51 mg/kg once daily for 23 wk, New onset P. aeruginosa colonization to airway clearance and nutrition, is essential.
followed by the same dose alternating daily for Initiation of treatment for MRSA
23 mo if there is improvement in clinical and Initiation of comprehensive pulmonary treatment
radiologic features in a newly diagnosed patient
r Antimycobacterium: Treatment guided by specific
organism. At least 3 drugs started sequentially. Discharge Criteria
Treatment is required for at least 12 mo. Use of IV antibiotics does not require hospitalization.
Similar results can be achieved with home IV
treatment provided that appropriate patients are
selected and adequate community support for patients
and families is available.
227
CYSTIC FIBROSIS: NEW DIAGNOSIS

Craig A. McElderry

BASICS r Mutation in a gene that encodes CFTR protein, r While most patients with CF present with classic
which is expressed in many epithelial cells and blood features of malabsorption, malnutrition, and chronic
DESCRIPTION cells respiratory symptoms, some patients may have only
r Cystic fibrosis (CF) is an autosomal recessive disease r Autosomal recessive a few or even just 1 clinical sign.
caused by mutations in the cystic fibrosis r Clinical features seen in CF patients include:
transmembrane conductance regulator (CFTR) gene COMMONLY ASSOCIATED CONDITIONS
Salty taste to skin
that results in abnormal viscous mucoid secretions See History.
Wheezing
in multiple organs. Signs of pulmonary infection (eg, crackles,
r The main clinical features characteristic of CF are decreased aeration)
DIAGNOSIS
pancreatic insufficiency and chronic endobronchial Nasal polyps
infection. Current diagnostic criteria for CF (2) are: Digital clubbing
EPIDEMIOLOGY r 1 characteristic phenotypic features (see History) Rectal prolapse
OR Failure to thrive
Incidence Edema (secondary to hypoproteinemia and
r CF is the most common life-threatening genetic r A history of CF in a sibling OR
r A positive newborn screening test PLUS fat-soluble vitamin deficiency)
condition in the Caucasian population.
r It is most common in populations of northern r Evidence of abnormal CFTR function as DIAGNOSTIC TESTS & INTERPRETATION
European descent. demonstrated by one of the following: The following tests would be performed as an
r Birth incidence (affected/number of live births): Elevated sweat chloride 60 mmol/L inpatient in the ill child or as an outpatient in the
Non-Hispanic, Caucasian: 1/2,5003,500 Abnormal nasal transepithelial ion transport clinically stable child. Consider consultation with a
Hispanic: 1/4,00010,000 Identification of 2 disease-causing CFTR gene pulmonologist.
African: 1/15,00020,000 mutations Lab
Asian: 1/100,000 HISTORY Initial Lab Tests
r Sweat chloride testing should be performed by
Prevalence The diagnosis of CF should be considered in any child
r 1 in 31,000, or 0.0000322% or adult who presents with signs or symptoms of (1): experienced personnel:
r According to the Cystic Fibrosis Foundation, 30,000 r Salty-tasting skin Quantitative pilocarpine iontophoresis testing
children and adults in the U.S. (70,000 worldwide) r Clubbing of fingers or toes (QPIT) is the only acceptable method of sweat
are affected. r Mucoid P. aeruginosa isolated from airway testingdetermines concentration of chloride in
the sweat:
PATHOPHYSIOLOGY secretions <40 mmol/L: Unaffected
There are several hypotheses regarding how the CFTR r Hypochloremic metabolic alkalosis 40 and 59 mmol/L: Indeterminate
gene mutation leads to the phenotypic disease known r Meconium ileus 60 mmol/L: Elevated/diagnostic of CF
as CF. It is possible that all four of the following r Protracted jaundice Indeterminate test results require evaluation for
contribute to the pathogenesis of the disease. r Abdominal or scrotal calcifications other clinical features of CF:
r Low volume hypothesis: r Intestinal atresia Consider respiratory tract cultures, fecal
Inhibition of epithelial sodium channels leads to r Persistent infiltrates on chest radiographs elastase.
excess sodium and water reabsorption r Failure to thrive Because men with CF have obstructive
Results in dehydration of airway surface materials r Anasarca or hypoproteinemia azoospermia, a semen analysis can be helpful.
Results in loss of lubricating layer between r Nasal potential difference measurementscan be
r Chronic diarrhea
epithelium and mucus r Abdominal distention helpful in cases where sweat chloride levels are
Results in compression of cilia by mucus indeterminate and genetic analysis unrevealing.
r Cholestasis r Genetics testing:
Inhibition of normal ciliary and cough clearance of
mucus r S. aureus pneumonia
Mutations in CTFR gene were identified in 1989
Mucus forms plaques with hypoxic niches that r Idiopathic intracranial HTN (vitamin A deficiency) as the genetic basis of CF.
harbor bacteria, particularly Pseudomonas r Hemolytic anemia (Vitamin E deficiency can cause Over 1,400 mutations may cause CF.
aeruginosa. RBC fragility.) Clinical relevance of some of the more rare
r High-salt hypothesis: r Chronic pansinusitis or nasal polyposis mutations and polymorphisms is not known.
Excess sodium and chloride are retained in airway r Steatorrhea Complexity between CF genotype and phenotype
surface liquid. r Rectal prolapse limits diagnostic utility but may be helpful in some
The increased concentration of chloride in the r Distal intestinal obstruction cases of indeterminate sweat tests.
periciliary layer disrupts the function of innate r Newborn screening:
r Idiopathic recurrent or chronic pancreatitis
antibiotic molecules, allowing bacteria to persist. r Liver disease Not diagnostic/not available everywhere
r Dysregulation of the host inflammatory response Sweat testing or other appropriate diagnostic
r Allergic bronchopulmonary aspergillosis
hypothesis: tests should always be performed in patients
r Bronchiectasis
Abnormally high concentrations of inflammatory where CF is suspected regardless of newborn
mediators are seen in CF cell cultures and r Hemoptysis screening results.
uninfected ex vivo tissue samples. r Pneumothorax
r Primary predisposition to infection hypothesis: Imaging
r Portal HTN r Chest/Sinus radiographs: Limited value for diagnosis
An increase in asialo-GM1 in apical cell r Delayed puberty but often first line in evaluation of exacerbations
membranes allows increased binding of r Azoospermia secondary to congenital bilateral r Chest CT: To evaluate for bronchiectasis and to
P. aeruginosa and Staphylococcus aureus to absence of the vas deferens assess evolution of pulmonary abnormalities
airway epithelium (1).
228
CYSTIC FIBROSIS: NEW DIAGNOSIS
Pathological Findings r Oral ibuprofen: DIET

r Lungs are normal at birth but progressively become For patients 6 yr, with FEV1 >60% predicted (3) r Good nutrition is mandatory for CF patients.
infected and inflamed. 2030 mg/kg/dose: Consider risks of bleeding r Pancreatic enzyme supplementation should be used
r Polymorphonuclear cells are seen in and potential adverse effects on renal function. in patients with pancreatic insufficiency.
bronchoalveaolar lavage specimens. r Oral azithromycin (3): r Fat-soluble vitamin supplementation is necessary in
r Bronchiectasis For patients 6 yr and with P. aeruginosa all patients with pancreatic insufficiency.
r Haemophilus influenzae or S. aureus, or both, persistently present in airway cultures r Breast-feeding should be encouraged for infants
rapidly colonize infants with CF. SURGERY/OTHER PROCEDURES with CF.
r Within a short time, P. aeruginosa becomes the r Liver biopsy to look for evidence of biliary cirrhosis r Supplemental nutrition should be strongly C
predominant organism. (highly suggestive of CF) considered (orally or by gastrostomy tube) in any
r Other organisms commonly seen in patients with CF r Gastrostomy tube placement as needed for patient with suboptimal growth.
include Burkholderia cepacia, Stenotrophomonas supplemental nutrition PROGNOSIS
maltophilia, and atypical mycobacteria. r Lung transplantation for end-stage lung disease r The U.S. Cystic Fibrosis Foundations projected life
DIFFERENTIAL DIAGNOSIS DISPOSITION expectancy for patients has increased from 31 yr to
r Malnutrition 37 yr over the past decade.
r Hypogammaglobulinemia Admission Criteria r For children born with CF today, a U.K. model
r Consider for patients with:
r Immotile cilia syndrome predicts their life span to be 50 yr (1).
Failure to thrive
r Asthma Metabolic disturbances COMPLICATIONS
r Celiac disease Pancreatitis See History section and Cystic Fibrosis: Exacerbation
r Shwachman-Diamond syndrome Meconium ileus topic.
r Adrenal insufficiency Significant respiratory distress
r Anorexia nervosa Failure of outpatient antibiotic and respiratory
r Hypothyroidism therapy REFERENCES
r Congenital metabolic diseases r Critical care admission criteria:
1. OSullivan BP, Freedman SD. Cystic fibrosis. Lancet.
See Cystic Fibrosis: Exacerbation topic. 2009;373:18911904.
Issues for Referral 2. Flume PA, Stenbit A. Making the diagnosis of cystic
TREATMENT As a complex and multisystemic disease, CF is best fibrosis. Am J Med Sci. 2008;335(1):5154.
managed by a specialty center with multidisciplinary 3. Flume PA, OSullivan BP, Robinson, et al. Cystic
MEDICATION care teams (i.e., CF centers). Fibrosis Foundation, Pulmonary Therapies
This section will focus on chronic medications used for Committee. Cystic fibrosis pulmonary guidelines:
maintenance of lung health in patients with CF. See COMPLEMENTARY & ALTERNATIVE
Chronic medications for maintenance of lung
Cystic Fibrosis: Exacerbation topic for therapies used THERAPIES
health. Am J Respir Crit Care Med.
for treatment of new infections/exacerbations of CF. Airway clearance techniques:
r Postural drainage and clapping 2007;176(10):957969.
First Line
r Inhaled tobramycin (high dose): r Vibrating mechanical vests
Especially for patients 6 yr old who have r Forced expiratory technique ADDITIONAL READING
moderate to severe lung disease and with P. r Autogenic drainage: A technique characterized by
Voter KZ, Ren CL. Diagnosis of cystic fibrosis. Clin Rev
aeruginosa persistently in airway cultures breathing control, in which the individual adjusts
Allergy Immunol. 2008;35:100106.
Children 6 yr and adults: 300 mg every 12 hr; the rate, depth, and location of respiration in order
administered in repeated cycles of 28 days on to clear the chest of secretions independently
drug, followed by 28 days off drug (3)
Lower dosages can be used in infants and children CODES
<6 yr of age. FOLLOW-UP
r Inhaled recombinant human DNase (dornase alfa or ICD9
FOLLOW-UP RECOMMENDATIONS r 277.00 Cystic fibrosis without mention of meconium
Pulmozyme):
Especially for patients 6 yr with moderate to
Patient Monitoring ileus
Patients should be monitored in the CF clinic every r 277.01 Cystic fibrosis with meconium ileus
severe lung disease (3)
Children 6 yr and adults: 2.5 mg once daily
23 mo with the following goals: r 277.02 Cystic fibrosis with pulmonary
r Maintenance of growth and development
using a recommended nebulizer manifestations
Recommended also for patients who are r Maintenance of as nearly normal lung function as
asymptomatic or those with mild disease (3) possible
r Intervention and retardation of the progression of PEARLS AND PITFALLS
Second Line
r Inhaled -adrenergic receptor agonists (3) lung disease via suitable use of antibiotics, r Common clinical features characteristic of CF are
2
r Inhaled hypertonic saline: bronchodilators, and airway clearance techniques
r Clinical evaluation to monitor GI tract involvement chronic endobronchial infection and pancreatic
Used to increase hydration of airway surface insufficiency.
liquid, improving mucociliary clearance and presence of malabsorption and to provide r Presence of mucoid P. aeruginosa in airway
Improves quality of life and reduces pulmonary enzyme and nutrition supplementation
r Monitoring for complications secretions is strongly suggestive of CF.
exacerbations
r Addressing psychosocial issues r Refer to CF center.
Dosage: 7% solution, 10 mL nebulized twice daily
(3)
229
CYSTIC HYGROMA
Joseph B. House
Stuart A. Bradin
ETIOLOGY Imaging
BASICS Unknown r MRI is study of choice:
Best soft tissue detail
DESCRIPTION COMMONLY ASSOCIATED CONDITIONS
r Infection of cyst Delineate relationship to underlying structures
r A cystic hygroma is a congenital malformation of the Differentiates hemangiomas from lymphangiomas
r Hypertrophy of both bone and soft tissue:
lymphatic system with dilated lymphatic channels. Hyperintense signal in T2-weighted images
r Synonymous with macrocystic lymphatic Frequently seen as progressive distortion of Ring enhancement with contrast use
malformation and cystic lymphangioma mandibular body, can cause underbite and r CT scanning:
r Not a neoplasm open-bite deformity (5)
r First trimester often associated with trisomies 13, Faster than MRI
r Usually found in the posterior triangle of the neck, Detail is lost if surrounding tissue of similar
18, and 21; second trimesters often associated with attenuation
but can be in other neck locations as well as axillae,
monosomy X Contrast helps to enhance cyst wall
groin, popliteal fossae, or torso
r Can grow rapidly within the first few weeks r US:
r Categorized as unilateral or bilateral and suprahyoid DIAGNOSIS Least invasive
or infrahyoid (1): No radiation exposure
Stage I: Unilateral infrahyoid HISTORY Useful demonstrating relationship with
r Symptoms vary based on lesion location. surrounding structures
Stage II: Unilateral suprahyoid
r May present after sudden appearance of neck Limited in assessing mediastinal and
Stage III: Unilateral supra- and infrahyoid
Stage IV: Bilateral suprahyoid swelling secondary to infection or intralesional retropharyngeal lesions
Stage V: Bilateral supra- and infrahyoid bleeding Can be used in utero in the late 1st trimester: May
r Classification based on size (1): r Rarely, new-onset obstructive sleep apnea or stridor appear as excess nuchal fluid, largest in the
Microcystic or capillary lymphangiomas: <1 cm or cyanosis nuchal region, and may extend along entire length
Macrocystic: >1 cm r Feeding difficulties or failure to thrive: of the fetus
r Plain radiography: Generally unhelpful but may
May be early sign of impending airway obstruction
EPIDEMIOLOGY r Pelvic lesions cause bladder outlet obstruction, delineate gross airway compromise
Incidence constipation, or recurrent infection.
r 1 case per 6,00016,000 live births (2) Pathological Findings
r Large irregular sinuses with single layer of flattened
r 5065% evident at birth, with 90% detected at PHYSICAL EXAM
r Often, overlying skin is normal or has bluish hue. epithelial lining and fibrous adventitial coats:
<2 yr of age Hemorrhage within the cystic spaces is common
r Equal frequency in males and females r Less common, puckering or deep cutaneous
after trauma or with spontaneous intralesional
r Equal frequency in ethnic groups dimpling
r Soft, painless compressible mass bleeding.
r Most commonly occurs in head and neck (75%) r Thickness of vessel wall varies with striated and
r About 20% of cystic hygromas occur in the axilla r In contrast to thyroid cysts, does not move with
smooth muscle components.
In neck, most commonly in posterior triangle swallowing
50% of fetuses with cystic hygroma have an r Typically transilluminates DIFFERENTIAL DIAGNOSIS
r Microcystic form appears as clusters of clear, black, r Teratoma
abnormal karyotype, and chromosomal r Germ cell tumor
abnormalities are more frequent in septated or red vesicles on buccal mucosa or tongue.
r Macrocystic lesions usually are found above level of r Branchial cleft cyst
cystic hygroma (4):
r Thyroglossal duct cyst
Karyotypes include Klinefelter syndrome, Turner mylohyoid muscle and involve oral cavity, lip, and
tongue. r Goiter
syndrome, Down syndrome, trisomy 13 and 18,
Noonan syndrome, Fryns syndrome, multiple r Life-threatening airway compromise may present as r Soft tissue tumor
pterygium syndrome, and achondroplasia. noisy breathing, cyanosis, or tracheal deviation. r Neck abscess
r Those that develop in the third trimester or r Inspect the tongue and oral cavity for lesions that r Lymphadenopathy
postnatally usually are not associated with a may lead to airway compromise. r Lymphadenitis
chromosomal abnormality (3). r Lesions in the forehead and orbit can cause r Parotitis
r 33% of fetuses with cystic hygroma have a proptosis.
structural abnormality (4). r Diffuse thoracic lymphatic anomalies or
Prevalence abnormalities of thoracic duct can manifest as
r In 1st trimester, overall about 1 in 100 fetuses: recurrent pleural or pericardial chylous effusion or
Septated cystic hygroma occurs in 1 in 285 fetuses. ascites.
r Some authors believe all cystic hygromas are present r Lesions in an extremity may cause diffuse or
at birth (2). localized swelling or gigantism with soft tissue and
skeletal overgrowth.
RISK FACTORS r Diffuse soft tissue and skeletal lesions may cause
r Intrauterine substance exposure, including alcohol
progressive osteolysis, called Gorham-Stout
(2) syndrome, or disappearing bone or phantom bone
r Maternal viral infections, including parvovirus (3)
disease.
r Maldeveloped localized lymphatic network
r Combination of: Lab
Initial Lab Tests
Failure of lymphatics to connect to venous system r No initial lab testing is routinely required.
Abnormal budding of lymphatic tissue r Check white blood cell count and/or C-reactive
Sequestered lymphatic rests that retain embryonic protein, and check blood culture if infection of cyst
growth potential is suspected.
230
CYSTIC HYGROMA
r Airway obstruction 1. Gross EG, Sichel J. Congential neck lesions. Surg
INITIAL STABILIZATION/THERAPY r Superinfection of lesion Clin North Am. 2006;86:383392.
r If airway compromise, consider aspiration: r Pericardial or pulmonary chylous effusions or ascites 2. Acevedo JL, Shah RK. Cystic hygroma. eMedicine
Prepare for a difficult airway if compromise is r Observation of rapidly expanding cyst Pediatrics: Surgery. July 18, 2008. Available at
suspected. http://emedicine.medscape.com/article/994055-
Emergent otolaryngology or anesthesiology Issues for Referral overview.
Referral to surgeon or surgical subspecialist depending
consult may be needed for airway evaluation.
Aspiration with large-bore (18- to 20-gauge) on anatomic location
3. Emory University School of Medicine. Cystic
Hygroma. 2008.
C
needle may temporarily alleviate immediate COMPLEMENTARY & ALTERNATIVE 4. Simpson LL. First trimester cystic hygroma and
airway compromise. THERAPIES enlarged nuchal translucency. UpToDate. May
Save aspirate for culture if necessary. r Observation: 15% spontaneous regress (1) 2008.
r If signs of infection, treat with antibiotics: r Laser resection: 5. Cummings CW. In Flint PW, Haughey BH, Lund VJ,
IV antibiotic indicated CO2 laser or et al, eds. Cummings Otolaryngology: Head & Neck
Treat with antibiotics for oral pathogens in head Neodymium:yyttrium-aluminum-ganet laser Surgery. 5th ed. Philadelphia, PA: Mosby; 2010.
and neck lesions. May be MRI controlled 6. Christison-Lagay ER, Fishman SJ. Vascular
Treat with antibiotics for enteric pathogens in the Oral cavity, tongue, and airway most amenable anomalies. Surg Clin North Am. 2006;86:393425.
trunk and perineum. 7. Townsend CM Jr., Beauchamp RD, Evers BM, et al,
r Bleeding may be treated with analgesics:
eds. Sabiston Textbook of Surgery. 18th ed.
Prophylactic antibiotics should be prescribed if FOLLOW-UP Philadelphia, PA: Saunders; 2008.
there is a large collection of intraluminal blood.
MEDICATION Discharge instructions and medications:
Sclerotherapy: r Follow up with a surgical consult.
ADDITIONAL READING
r OK-432: Inactive strain of group A Streptococcus Al-Dajani N, Wootton SH. Cervical lymphadenitis,
pyogenes Patient Monitoring suppurative parotitis, thyroiditis, and infected cysts.
r Airway compromise
Mechanism: Inflammatory response r Signs of cyst infection Infect Dis Clin North Am. 2007;21:523541.
Option for large unilocular cysts
r Alcohol: Works well in vascular malformations with See Also (Topic, Algorithm, Electronic
PROGNOSIS Media Element)
low flow; often painful and may need general r Spontaneous resolution is uncommon.
r Recurrence is rare when gross disease is removed. Lymphangioma
anesthesia and postprocedural pain medication; can
result in local necrosis blistering and neuropathy; r If residual tissue is left behind after surgery, the
systemic absorption may lead to cardiac arrest, recurrence rate is about 15%.
pulmonary vasoconstriction, or systemic hypotension CODES
(6) COMPLICATIONS
r Fibrin sealant: r Intralesional bleeding ICD9
r Cyst infection 228.1 Lymphangioma, any site
Edema post-injection associated with prolonged
recovery and increased therapeutic effect r Cellulitis
Better results with macrocystic type lesions as r Airway compromise
compared to poor or absent results in microcystic r Deformation of surrounding bony structures or teeth PEARLS AND PITFALLS
type (7) if left untreated r Rapid enlargement may cause respiratory distress.
r Adverse psychosocial effects may result from social r Early administration of antibiotics is indicated for
Surgical resection:1 stigmatization in cysts resulting in deformation. superinfection.
r Primary treatment
r Macrocystic lesions: Ideally removed in 1 procedure,
repeated excisions complicated by fibrosis and
anatomic distortions
r Microcystic lesions: Most difficult to resect, no
distinct tissue planes between malformed and
normal structures
r Exception to excision at diagnosis includes close
proximity to crucial neurovascular structures; may
need to wait until child is older.
r Since not a neoplasm, removal of surrounding blood
vessels and nerves is not indicated.
231
LWBK822-driver-D LWBK822-Hoffman ch115.xml April 19, 2011 0:56
DACRYOCYSTITIS/DACRYOSTENOSIS
Donald T. Ellis II
Sandip A. Godambe
Kimberly A. Randell

BASICS r Bacteria most often associated with dacryocystitis r Apply gentle pressure to bilateral lacrimal sacs to
include Staphylococcus (especially aureus and attempt to express discharge from lacrimal punctum.
DESCRIPTION epidermidis) and Streptococcus pneumoniae. r Assess for impairment of extraocular movements
r Dacryocystitis describes inflammation of either the However, other organisms such as diptherioids, and for proptosis.
lacrimal duct or sac. Escherichia coli, Pseudomonas species, Actinomyces r Assess for any facial tenderness, especially sinus or
r Infection occurs as the stasis of tears promotes species, and TB have been implicated as well. nasal problems.
bacterial overgrowth. r Viruses (eg, Epstein-Barr virus and human r Epiphoria is present in most cases.
r Classifications: papillomavirus) and fungi (eg, Candida species) r Fever and decreased activity may be seen in some
Congenital dacryocystitis is associated with have also been reported as causative agents. patients.
infection. r Acquired dacryocystitis is caused by a variety of r Mattering is due to the inability to effectively drain
Acquired: conditions including the following: the mucoid portion of tears.
Acute dacryocystitis is commonly associated Nearby infection (eg, sinusitis or rhinitis) r Conjunctivitis can also be seen.
with pain, erythema and swelling of the lower Structural defects (eg, deviated septum) r Tenderness and erythema near the medial canthus
eyelid, excessive tearing, eye discharge, and Trauma
fever. indicate acute dacryocystitis.
Nasal foreign body r Chronic dacryocystitis may present with merely
Chronic dacryocystitis is not normally associated Neoplasm
with infection; however, it may develop tearing Dacryolithiasis mucoid or purulent discharge from the upper and/or
and discharge. Iatrogenic (eg, postoperative complication) lower puncta.
r Dacryostenosis: Blocked tear duct (also called r Photophobia suggests other etiologies (in neonates,
COMMONLY ASSOCIATED CONDITIONS consider congenital glaucoma).
nasolacrimal duct (NLD) impotency or stenosis) r Conjunctivitis is frequently seen in conjunction with
EPIDEMIOLOGY dacryocystitis with both acute and chronic forms. DIAGNOSTIC TESTS & INTERPRETATION
Incidence r Orbital cellulitis is uncommon but may occur with Lab
Bimodal, most often diagnosed in neonates and adults congenital and acute dacryocystitis. Initial Lab Tests
r A dacryocystocele or amniotocele is a bluish mass, r The diagnosis of dacryocystitis is most frequently
>40 yr
which represents a collection of amniotic fluid from determined on clinical grounds.
Prevalence r The presence of peripheral leukocytosis may provide
r A recent study of 15,398 neonates found the fetal development and may be seen with
dacryocystitis: further evidence for dacryocystisis.
prevalence for congenital dacryocystitis to be r Cultures of the lacrimal discharge should preferably
0.146% (1). Dacryocystoceles may cause nasal obstruction and
r Congenital dacryostenosis is found in 620% of all subsequent respiratory distress in the newborn. be collected prior to the administration of
r Acute dacryocystitis may be associated with fistula antibiotics; blood cultures are rarely indicated.
neonates (2,3) r Nasal and/or conjunctival cultures may provide
r Dacryocystitis found in 2.9% of infants with formation from the lacrimal sac to the overlying skin.
r Autoimmune disease additional assistance in determining bacterial
dacryostenosis, 60% of infants with dacryocystocele r Sjogren syndrome susceptibility.
(4,5) r In febrile neonates, obtain blood, urine and
RISK FACTORS cerebrospinal fluid cultures prior to initiating
r Brachycephaly, narrow facial structure, flattened DIAGNOSIS antibiotics (strongly consider in afebrile neonates).
nose, and dacryoceles are recognized as risk factors
HISTORY Imaging
for the development of dacryocystitis. r In acute and congenital dacryocystitis, there is r If facial deformity or posttraumatic obstruction of
r Caucasians are thought to be at an increased risk
usually a history of tenderness, swelling, and tear outflow is suspected, plain radiographs may be
relative to blacks. obtained.
erythema over the lacrimal sac, located medial to
GENERAL PREVENTION r CT scan (with axial and coronal views) of the orbit
the medial canthus (1,6).
Warm compresses and lacrimal massage have been r Chronic dacryocystitis is characterized by a more and paranasal sinuses may be necessary in atypical
suggested as possible techniques to decrease the rate indolent course (7). or severe cases of dacryocystitis, in patients with
of infection in the setting of nasolacrimal duct r Elicit history of previous episodes, systemic illness, or orbital cellulitis, or when concern for neoplasm.
dysfunction. r CT scans are generally preferred over MRIs when
other HEENT infections
PATHOPHYSIOLOGY r Dacryostenosis: Onset of tearing or mucoid eye investigating the possibility of neoplasm resulting in
r All forms of dacryocystitis are caused by the discharge days-weeks after birth, 1/3 are bilateral, obstruction.
r CT scans may also assist in differentiating preseptal
stagnation of tears, which promotes bacterial the conjunctiva are usually clear
overgrowth: from orbital cellulitis due to dacryocystitis.
Can see secondary conjunctivitis. Diagnostic Procedures/Other
r Congenital obstruction results from failed atrophy of Flourescein disappearance test can confirm diagnosis
adhesion between the ductal epithelium and nasal place dye in lower conjunctival fornix, blotting excess
mucosa: solution/tears away. Examination after 5 min with
Most common site of obstruction is at the valve of cobalt blue filter identifies residual fluorescein in
Hasner (the opening of the lacrimal duct into the children with dacryostenosis (90% sensitive, 100%
inferior meatus of the nose) specific).
r Acquired cases frequently involve obstruction of the
inferior nasolacrimal system.
232
DACRYOCYSTITIS/DACRYOSTENOSIS
DIFFERENTIAL DIAGNOSIS DISPOSITION 4. Pollard ZF. Treatment of acute dacyrocystitis in

r Dacryocystitis: neonates. J Pediatr Ophthalmol Strabismus.
Admission Criteria
Conjunctivitis r Inpatient treatment should be strongly considered 1991;28:341343.
Preseptal or orbital cellulitis for all infants and children who present with 5. Paysse EA, Coats DK, Bernstein JM, et al.
Dacryocystocele systemic signs (eg, fever), preseptal cellulitis, orbital Management and complications of congenital
Blepharitis cellulitis, meningitis, or ill appearance. dacryocele with concurrent intranasal mucocele.
Ethmoid or maxillary sinusitis r Disposition should be planned in conjunction with J AAPOS. 2000;4:4653.
Insect bite input from ophthalmology, who will likely admit 6. Mueller JB, McStay CM. Ocular infection and
Neoplasm most congenital and acute cases for IV antibiotics inflammation. Emerg Med Clin North Am. 2008;
r Dacryostenosis: 26:5772.
and DCR.
Lacrimal fistula r Critical care admission criteria: 7. Wright KW, Tearing. In: Wright KW (ed): Pediatric
Impatent/absent puncta Patients with ill appearance, especially with Ophthalmology for Primary Care Providers. Elk
Congenital glaucoma abnormal vital signs or change in mental status, Grove, IL: American Academy of Pediatrics, 1999,
Corneal abrasion
Foreign body
may need intensive care services. 151157.
8. Prentiss KA, Dorfman DH. Pediatric ophthalmo-
D
Discharge Criteria
r Well-appearing, afebrile patients with dacryocystitis logy in the emergency department. Emerg Med
Clin North Am. 2008;26:181198.
TREATMENT can be discharged if they do not meet the
aforementioned admission criteria. 9. Wald E. Periorbital and orbital infections. Pediatr
INITIAL STABILIZATION/THERAPY r All patients with dacryostenosis may be treated as Rev. 2004;25:312319.
Especially in the newborn, airway, breathing, and outpatients. 10. Kapadia MK, Freitag SK, Woog JJ. Evaluation and
circulation should be assessed and stabilized due to management of congenital nasolacrimal duct
Issues for Referral obstruction. Otolaryngol Clin N Am. 2006;39:
the potential for respiratory distress (eg, with r Since dacryocystitis is definitively treated by DCR,
obstruction as with a dacryocystocele) or sepsis. 959977.
consider referral to ophthalmology.
MEDICATION r Ophthalmology referral if congenital dacryostenosis
First Line persists beyond 6 mo ADDITIONAL READING
r For dacryostenosis, caregivers should provide
r Gilliland G. Dacryocystitis. eMedicine. September
nasalacrimal massage several times daily (gentle
downward pressure along lacrimal duct, beginning FOLLOW-UP 26, 2007. Available at http://emedicine.medscape.
just below the medial canthus). No antibiotics are com/article/1210688-overview. Accessed July 30,
FOLLOW-UP RECOMMENDATIONS 2009.
indicated.
r For acute dacryocystitis, systemic antibiotics should Discharge instructions and medications: r Hurwitz JJ. The lacrimal drainage system. In Yanoff
r Afebrile well-appearing patients with dacryocystitis
be initiated (following acquisition of blood and M, Duker JS, eds. Ophthalmology. 3rd ed.
can be discharged: Philadephia, PA: Mosby; 2004.
lacrimal fluid cultures).
r Parenteral antibiotics should be used in any patient If being discharged, patients should have a clear r Lui D, Lee S. Lids, lashes, and lacrimal disorders. In
plan for follow-up with ophthalmology (ideally Loewenstein J, Lee S. Ophthalmology: Just the Facts.
with systemic signs (8). Antibiotics with within 2448 hr).
antistaphylococcal activity are preferred: Columbus, OH: McGraw-Hill; 2003.
Patients should return for fever; clear discharge r Vincente G, Katz B. Eye infections. In Gershon AA,
Clindamycin 2540 mg/kg/day divided q68h; (as seen with CSF leak after DCR); or increased
max daily dose 4.8 g/day Katz S, Hotez PJ, eds. Krugmans Infectious Diseases
pain, erythema, or swelling. of Children. 11th ed. Philadelphia, PA: Mosby; 2004.
Vancomycin 4060 mg/kg/day IV divided q68h; r Patients with dacryostenosis can follow up with their
max daily dose 4 g/day r Wald ER. Periorbital and orbital infections. In Long
r Although antibiotics are indicated for congenital primary physician without specialist referral. SS, Pickering LK, Prober CG, eds. Principles and
and acute forms, they are somewhat controversial in PROGNOSIS Practice of Pediatric Infectious Diseases. 3rd ed.
chronic dacryocystitis. r Following an initial episode of acute dacryocystitis, Philadelphia, PA: Churchill Livingstone; 2003.
2/3 of patients may experience recurrence. See Also (Topic, Algorithm, Electronic
Second Line r DCR has a success rate of 90%.
r Naphazoline 0.05%: 612 yr, 1 gtt q6h PRN; Media Element)
r Congenital dacryostenosis: 90% will spontaneously r Conjunctivitis
>12 yr, 2 gtt q6h PRN; do not use in children under
6 yr: resolve by 812 mo of age when treated with r Orbital cellulitis
May be used for a max of 5 days but should be lacrimal sac massage (10) r Periorbital cellulitis
discontinued thereafter due to the risk of atrophic COMPLICATIONS
rhinitis r Orbital cellulitis
r Antihistamines have been used to decrease the r Periorbital cellulitis CODES
amount of lacrimal secretions. r Brain abscess
SURGERY/OTHER PROCEDURES r Meningitis ICD9
r Dacryocystorhinostomy (DCR) remains the definitive r Cavernous sinus thrombosis r 375.30 Dacryocystitis, unspecified
treatment. r Sepsis r 375.32 Acute dacryocystitis
r Nasolacrimal duct probing, incision and drainage, r Cutaneous fistula r 771.6 Neonatal conjunctivitis and dacryocystitis
and DCR have historically been performed following
clinical improvement with systemic antibiotics.
However, DCR has been suggested as an alternative REFERENCES PEARLS AND PITFALLS
treatment even in the acute phase (9). r Uncomplicated dacryostenosis may be associated
r Dacryostenosis: Probing of the NLD is not needed 1. Nie WY, Wu HR, Qi YS, et al. A pilot study of
ocular diseases screening for neonates in China. with scant mucoid drainage; the absence of
unless stenosis persists beyond 612 mo; in the
Zhonghua Yan Ke Za Zhi. 2008;4(6):497502. conjunctival injection distinguishes this from
majority of infants, adhesions within the NLD
2. Kapadia MK, Freitag SK, Woog JJ. Evaluation and conjunctivitis. If photophobia is present, evaluate for
undergo spontaneous atrophy
management of congenital nasolacrimal duct congenital glaucoma.
obstruction. Otolaryngol Clin N Am. 2006;39: r Be aware of the uncommon, yet potentially
959977. devastating, complications of dacryocystitis (eg,
3. MacEwen CJ, Phillips MG, Young JDH. Value of orbital cellulitis, brain abscess, meningitis, cavernous
bacterial culturing in the course of congenital sinus thrombosis, and sepsis). Hospitalize any
nasolacrimal duct (NLD) obstruction. J Pediatr patient with systemic signs or toxicity.
Ophthalmol Strabismus. 1994;31:246250.
233
DECOMPRESSION SICKNESS
Carl P. Kaplan

BASICS r The main component of compressed air is nitrogen, r Musculoskeletal pain, often at joints, is typical.
which, unlike oxygen, poorly and slowly diffuses into r Dermal findings may include lymphedema, cutis
DESCRIPTION tissues and remains in the circulation. marmorata.
r Decompression sickness (DCS) primarily affects r Decompression with rapid ascent allows the r GI findings may include abdominal pain, nausea,
scuba divers and is referred to as the bends. formation of nitrogen bubbles in the and vomiting.
r It may also present in caisson workers or microcirculation leading to right to left shunting and r Pulmonary findings may include dyspnea, cough, or
high-altitude aviators. local inflammatory response. substernal pressure.
r It derives from a complex interaction of physical gas r Larger amounts of gas may enter the circulation r CNS findings:
properties and physiologic processes. mechanically through pulmonary barotrauma. Altered mental status
r The pressure of a gas is inversely proportional to its r Larger gas emboli may form in severe cases. Focal neurologic deficits
volume (Boyle law). When inert nitrogen (the r Intracardiac shunts may allow CAGE (most Motor weakness or sensory loss
predominant gas in compressed air) is rapidly commonly in the middle cerebral artery and r PNS findings
exposed to a lower pressure (during ascent), vertebrobasilar artery).
bubbles may form in tissue capillary beds as its DIAGNOSTIC TESTS & INTERPRETATION
volume expands, resulting in microvascular ischemia ETIOLOGY Lab
r Inexperience or inebriation of divers
and local inflammatory response. No lab assays are required, but consider:
r Type I DCS: Also termed pain only, primarily affects r Diving-related trauma r CBC
r Equipment failure r Basic metabolic profile, creatine phosphokinase,
periarticular areas and tendons (the bends),
lymphatics, and the skin r Breath-holding on ascent (panic)
troponin I
r Type II DCS: Consists of vestibular, cardiopulmonary, r Dangerous conditions necessitating rapid ascent r Urinalysis
CNS, or peripheral nervous system (PNS) r Air travel following diving r Venous blood gas analysis:
manifestations Arterial analysis is typically unnecessary.
r Arterial gas embolism (AGE), or cerebral arterial gas COMMONLY ASSOCIATED CONDITIONS
r Major trauma
embolism (CAGE), is the most severe form of DCS. Imaging
r Near drowning r CXR
EPIDEMIOLOGY r Barotrauma (paranasal sinuses, pneumothorax, r Consider brain CT +/ angiography for CNS
Incidence pneumomediastinum, tympanic membrane rupture) pathology.
r Male to female ratio: 34:1 r Nitrogen narcosis r Consider chest CT +/ angiography for suspected
r Around 16 cases per year in patients <19 yr. r Dehydration pulmonary embolism.
r Sport divingassociated DCS (all ages): r Headache
Warm water: 13.4:100,000 dives r Vertigo ECG
Cold water: 10.5:100,000 dives
r 2.7/100,000 in healthy divers with strict adherence DIFFERENTIAL DIAGNOSIS
r Cerebrovascular accident
to published dive tables DIAGNOSIS
r Traumatic brain or spinal cord injury
RISK FACTORS HISTORY r Near drowning
r Caisson work r Recent diving (depth, length of dive, time of each
r Dehydration
r High-altitude aviation dive, use of dive tables or dive computers, number r Hypothermia
r Pre-existing cardiovascular disease of dives)
r Air travel r Ciguatera poisoning from consumption of reef fish
r Intracardiac shunts
r Difficulty breathing, chest pain r Envenomation: Jellyfish, corals, stingrays
r Dehydration
r Loss of consciousness
GENERAL PREVENTION r Headache
r Avoidance of rapid ascents during diving
r Adherence to published dive tables r Weakness or paresthesias
r Maintenance of cabin pressure in airplanes and r Vertigo
r Extremity pain or swelling
caissons
r Scheduled maintenance of equipment r Recent meals containing reef fish
r Associated dive trauma, such as coral abrasions,
envenomations, blunt trauma
234
DECOMPRESSION SICKNESS
r Tube thoracostomy for associated pneumothorax
ADDITIONAL READING
TREATMENT r Myringotomy tube placement for patients with r Bennett MH, Lehm JF, Mitchell SJ, et al.
PRE HOSPITAL altered mental status undergoing HBO. (Others are Recompression and adjunctive therapy for
r Assess and stabilize airway, breathing, and able to use maneuvers to equilibrate eustachian decompression illness. Cochrane Database Syst Rev.
circulation. tube pressure.) 2007;(2):cd005277.
r Recompression dive to 60-foot seawater depth with r DeGorordo A, Vallejo-Manzur F, Chanin K, et al.
DISPOSITION Diving emergencies. Resuscitation. 2003;
slow ascent (only feasible with stable divers and
experienced oversight)
Admission Criteria 59:171180.
r Administer 100% oxygen. Critical care admission criteria: r MacDonald RD, ODonnell C, Allan GM, et al.
r Pulmonary complications such as pneumothorax,
r Maintain supine position. Interfacility transport of patients with decompression
r Administer isotonic fluids. acute respiratory distress syndrome, or endotracheal illness: Literature review and consensus statement.
r Avoid hypothermia. intubation Prehosp Emerg Care. 2006;10:482487.
r All patients requiring HBO should be considered for r Tintinelli JE , Gabor D, Stapczynski JS, et al., eds.
ALERT admission as an inpatient. Emergency Medicine: A Comprehensive Study D
r Divers Alert Network (DAN) Discharge Criteria Guide. 6th ed. New York, NY: McGraw-Hill;
r Emergency Hotline (800) 446-2671 r Resolution of symptoms within 46 hr following 2003:12131217.
r Tsung JW, Chou KJ, Martinez C, et al. An adolescent
r Transport assistance (800) DAN-EVAC (326-3822) prehospital 100% oxygen
r Stable patients with mild symptoms may be scuba diver with 2 episodes of diving related injuries
discharged after HBO therapy. requiring hyperbaric oxygen recompression therapy.
r Assess and stabilize airway, breathing, and Pediatr Emerg Care. 2005;21(10):681686.
Issues for Referral
circulation. r Availability of HBO therapy See Also (Topic, Algorithm, Electronic
r Administer 100% oxygen. r Air transport should only occur if cabin altitude can Media Element)
r Identify and treat associated trauma. r http://www.diversalertnetwork.org
be maintained below 500 feet (152 meters) above
r Isotonic volume resuscitation the extraction point. r Pain, Extremity
r Rewarming as necessary
MEDICATION FOLLOW-UP CODES

First Line
r Hyperbaric oxygen (HBO) should be administered to FOLLOW-UP RECOMMENDATIONS
r Discharge instructions and medications: ICD9
all patients with DCS. U.S. Navy Treatment Table 6 is
Keep well hydrated. 993.3 Caisson disease
the standard first-line therapy and may be modified
r Activity:
as needed.
r Multiple treatments with HBO or different tables Avoid further diving for 46 wk. (Consider
cessation of diving with severe disease.)
PEARLS AND PITFALLS
may be employed by experts in refractory cases.
Avoid air travel for 4872 hr. r Traumatic brain injury, anoxic brain injury, and DCS
Second Line
r NSAIDs: PROGNOSIS can present similarly or simultaneously in divers.
r 5070% of patients achieve total resolution of r Marine envenomations or ciguatera toxin may cause
Consider NSAID medication in anticipation of
prolonged pain and inflammation. symptoms. neurologic symptoms mimicking DCS.
NSAIDS may reduce the duration of hyperbaric r 30% achieve temporary relief of symptoms that may
therapy by modifying inflammation in the CNS or wax and wane.
PNS. r 1.3 deaths per 100,000 warm water dives
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN r 2.9 deaths per 100,000 cold water dives
Naproxen 5 mg/kg PO q8h PRN COMPLICATIONS
r Neurocognitive deficits
r Focal neurologic deficits
r Opioids:
r Hearing loss
Morphine 0.1 mg/kg IV/SC/IM q2h PRN: r Dysbaric osteonecrosis
r Chronic pain
then q2h PRN.
Codeine or codeine/acetaminophen dosed as
PO q46h PRN
r Local anesthetic:
Lidocaine 1.52 mg/kg IV bolus followed by
infusion 1 mg/min
May alleviate inflammatory response associated
with severe CNS or PNS involvement, improve
nerve conduction, decrease intracranial HTN, and
improve spinal cord blood flow
235
DEEP VEIN THROMBOSIS

Kevin D. Buckley

BASICS r Congenital:
Lab
Deficiencies of the regulatory proteins: Protein C, r CBC, PT, PTT, and type and cross-match should be
DESCRIPTION protein S, antithrombin III, and plasminogen monitored prior to initiation of therapy.
r Thrombotic events in deep veins are relatively rare in Synthesis of a procoagulant protein unable to be r D-dimer may be useful as an exclusionary test, but a
children, typically occurring in children with inhibited by regulatory protein (eg, factor V positive result is highly nonspecific.
associated comorbidities and risk factors. Leiden) r There are no screening tests for hereditary
r Healthy children appear to be at a significantly Elevated levels of procoagulant protein; predisposition to thrombosis. Specific testing is
lower risk than adults, and there may even be some prothrombin mutation (G20210A), elevated factor required for protein C, protein S, antithrombin III,
protective mechanisms. Adults have at least a 7-fold VIII levels factor V Leiden, prothrombin 20210, and plasma
increase in relative risk for deep vein thrombosis Elevated levels of a toxic organic acid (eg, homocysteine levels.
(DVT) compared to children (1). homocysteinemia)
r Health and cost burdens of DVT and its long-term r Acquired conditions that increase risk: Imaging
r Real time US is noninvasive and is effective in
complications are disproportionately higher in Obstruction to flow from indwelling lines,
children since children live 6080 yr following DVT, pregnancy, polycythemia, dehydration demonstrating the presence or absence of residual
and postthrombotic syndrome (PTS) limits aerobic Immobilization, injury, trauma, surgery blood flow in DVTs in extremities, particularly the
activities necessary for normal healthy development. Inflammation: Inflammatory bowel disease (IBD), jugular and subclavian veins but not in the
vasculitis, infection, Behcet syndrome intrathoracic veins:
EPIDEMIOLOGY Venous duplex US has now replaced venography
Hypercoagulability: Pregnancy, malignancy,
Incidence antiphospholipid syndrome, nephrotic syndrome, as the diagnostic study of choice.
r Peaks in newborn/infants and adolescents r Impedance plethysmography (IPG) is valuable for
oral contraceptives, L-asparaginase, elevated
r Newborn 5.1/10,000 patients with suspected recurrent DVT because the
factor VIII levels
r Childhood venous thrombosis 0.070.14/10,000 in r Rare other entities: test returns to normal earlier in patients with
the general population Congenital: Dysfibrinogenemia blocks clot lysis proximal VT than compression US.
r 5.3/10,000 child hospitalizations r Less-used imaging modalities include CT and MRI,
Acquired: Paroxysmal nocturnal hemoglobinuria,
r 0.51/10,000 births thrombocythemia, grafts but the cost and use of IV contrast limits its use.
r 0.24/10,000 neonatal admissions r If suspicious for pulmonary emboli, a spiral CT is
COMMONLY ASSOCIATED CONDITIONS recommended.
r CVLs are the most common risk factor for VTE, with
RISK FACTORS
r Previous thrombosis 3.5/10,000 pediatric admissions: DIFFERENTIAL DIAGNOSIS
r Children with DVT likely have multiple thrombophilia CVL is the sole reason for increased frequency of r Muscle strain or tear
VTE in the upper venous system of children (80% r Direct twisting injury of the leg
traits. In a recent study of those with thrombosis,
of DVT in newborns, and 60% in older children). r Lymphangitis or lymphatic obstruction
19% had no abnormality, 27% had a single trait,
r Umbilical vein catheters are associated with thrombi r Venous reflux
and 54% had multiple traits (3).
r Obesity and sedentary lifestyle or prolonged in the inferior vena cava and portal vein. r Popliteal cyst
r Common risk factors for inflammation: Lupus r Cellulitis
immobilization, such as from a cast or even long air
travel anticoagulant, CVLs, acute infection, chronic r Pyomyositis
r Ongoing risk factors: Genetic thrombophilia, protein inflammation, and IBD r Necrotizing fasciitis
r Activated protein C resistance is the most common
S,C and antithrombin III deficiency, factor V Leiden, r Leg swelling in a paralyzed limb
primary or secondary antiphospholipid antibodies, hereditary abnormality predisposing to VT. r Abnormality of the knee joint
inflammatory diseases such as ulcerative colitis or r Factor V Leiden autosomal dominant inheritance is
systemic lupus erythematosus, prosthetic cardiac 5% in the Caucasian population but 16% in
valves, sickle cell disease, malignancy, central patients with their 1st episode of DVT. TREATMENT
venous lines (CVLs)
r Age-specific risk factors in adolescents include INITIAL STABILIZATION/THERAPY
smoking and the use of oral contraception. DIAGNOSIS Management should be directed at anticoagulation
r Nephrotic syndrome and/or antithrombolytics.
HISTORY
r Pregnancy is a risk factor. r Classic signs and symptoms of DVT are associated
MEDICATION
PATHOPHYSIOLOGY with obstruction to venous drainage, including First Line
r Venous thrombi (VT) are composed mainly of fibrin extremity pain and swelling. r Standard unfractionated heparin or
r Clinical diagnosis of DVT is difficult.
and RBCs. low-molecular-weight heparin (LMWH) is indicated
r Formation, growth, and breakdown of venous r 50% of those with DVT have no symptoms, and DVT for DVTs that are neither massive nor complicated or
thromboemboli (VTE) reflect a balance between cannot be excluded or diagnosed based upon if thrombolytics are contraindicated:
thrombogenic stimuli and protective mechanisms. clinical findings. Both are metabolized more rapidly in newborn
r Thrombogenic stimuli are: infants.
PHYSICAL EXAM
Venous stasis r Clinical features of VT include leg tenderness, Heparin, standard unfractionated:
Activation of blood coagulation 5075 U/kg by IV bolus FOLLOWED BY:
warmth, swelling, a palpable cord, discoloration,
Vein damage 2030 U/kg/hr in newborns OR 1525 U/kg/hr
venous distention, prominence of superficial veins,
r Protective mechanisms are: and cyanosis. in older children and adults
Inactivation of activated coagulation factors by r Clinical diagnosis of DVT is nonspecific, since LMWH:
1.5 mg/kg q12h SC for newborns
circulating inhibitors (eg, antithrombin III, symptoms may also be from nonthrombotic 1 mg/kg q12h SC for older children/adults
activated protein C) disorders.
Clearance of activated coagulation factors and LMWH needs less monitoring.
r Warfarin (Coumadin):
soluble fibrin polymer complexes by the liver and
reticuloendothelial system 0.3 mg/kg/day PO for newborns
Lysis of fibrin by the fibrinolytic system 0.15 mg/kg/day PO for older children
r Inflammation in the most common risk factor.
236
DEEP VEIN THROMBOSIS
Second Line SURGERY/OTHER PROCEDURES DIET

r Thrombolytics (ie, tissue plasminogen activator r Inferior vena cava filters are indicated for patients Adjust warfarin if increasing intake of vitamin K.
[T-PA]) are indicated for (4): with acute DVT and:
PROGNOSIS
Extensive DVT An absolute contraindication to anticoagulant
8% recur in 1 yr, and up to 18% recur within 7 yr.
Massive pulmonary embolism (PE), with therapy
respiratory compromise Rare for a patient with massive PE who survives COMPLICATIONS
Free-floating thrombi on the outer surface of but in whom a recurring PE may be fatal r DVT has high risk for PE: 80/466, or 17%.
indwelling central venous catheters Rare for a patient with objectively recurrent DVT r 2.2% chance of death
Consider first line in patients with all of the during adequate anticoagulant therapy r Being overweight predisposes to PTS (88%).
following: Acute DVT (<14 days), occlusive Patient with recent (<6 wk) proximal VT who
iliofemoral thrombi, significant pain, swelling, and requires emergency surgery
no contraindications. r Filter increases incidence of recurrent DVT REFERENCES
r Contraindications: r Thrombectomy has little role in children.
Active bleeding r Bleeding concerns: 1. Vu LT, Nobuhara KK, Lee H, et al. Determination of
Surgery or organ biopsy within 10 days Local or minor bleeding: Compress; topical
risk factors for deep venous thrombosis in
hospitalized children. J Pediatr Surg. 2008;43(6):
D
Neurosurgery within the previous 3 wk thrombin, topical collagen, or combination
Underlying bleeding diathesis 10951099.
Major or life-threatening bleeding on T-PA: Stop
r Dosing of T-PA: No consensus exists. Either low-dose T-PA and heparin, and give cryoprecipitate.
2. Sandoval J, Sheehan MP, Stonerock CE, et al.
or high-dose TPA (4,5) can be used: Incidence, risk factors, and treatment patterns for
Reversal of the thrombolytic process is by
Children >3 mo, start 0.03 mg/kg/hr, max deep venous thrombosis in hospitalized children:
E-aminocaproic acid (Amicar) at a dose of
2 mg/hr; no loading dose An increasing population at risk. J Vasc Surg.
100 mg/kg IV or orally (max single dose 4 g).
Monitor labs every 12 hr and radiographic 2008;47:837843.
If only heparin, stop heparin and give protamine:
evidence of fibrinolysis every 24 hr. If there is no Dose is 1 mg per 100 units of heparin given in the 3. Manco-Johnson MJ, Goldenberg NA. Thrombosis in
evidence of improvement in blood flow, adjust the past 2 hr. the Pediatric Patient: Unique Risk Factors,
infusion rate upward to 0.06 mg/kg/hr. If on warfarin, stop and give fresh frozen plasma. Diagnosis and Management Issues. Surgeon
Neonates may require higher starting doses Generals Workshop on Deep Vein Thrombosis, May
(0.06 mg/kg/hr), if there is no improvement in 24 DISPOSITION 89, 2006.
r Inpatient admission criteria:
hr, double to 0.12 mg/kg/hr. 4. Wang M, Hays T, Balasa V, et al. Pediatric
A low dose can be used 6 hr to 4 days. Monitor All newly diagnosed DVT patients should be Coagulation Consortium. Low-dose tissue
blood flow every 24 hr, discontinuing T-PA as soon admitted to the inpatient ward for anticoagulation plasminogen activator thrombolysis in children.
as clot lysis has been achieved. with heparin. J Pediatr Hematol Oncol. 2003;25(5):379386.
High-dose T-PA may be given for a shorter 5. Raffini L. Thrombolysis for intravascular thrombosis
duration at 0.50.6 mg/kg/hr for 6 hr and has Patients on T-PA will need ICU monitoring. in neonates and children. Curr Opin Pediatr.
higher bleeding complications. There is Patients who are hypoxemic with a PE need ICU 2009;21(1):914.
controversy over a 2nd 6-hr treatment. admission. 6. Monagle P, Adams M, Mahoney M, et al. Outcome
r Unfractionated heparin has been shown to be Discharge Criteria of pediatric thromboembolic disease: A report from
helpful in adults with T-PA but is not well studied in r Patients should be transitioned after 3 days of the Canadian Childhood Thrombophilia Registry.
children. T-PA should be accompanied by low-dose anticoagulation to oral warfarin with a goal INR of Pediatr Res. 2000;47:763766.
standard unfractionated heparin at 510 U/kg/hr 23 for DVT, or 34 for PE or massive DVT.
without a loading dose: r LMWH may be discontinued when INR is 23.
If renal function is impaired, the infusion rate of
Issues for Referral CODES
heparin should be lowered to 2.55 U/kg/hr
Consider hematology referral for congenital risk
because of the greater bioavailability of heparin. ICD9
factors. r 453.40 Acute venous embolism and thrombosis of
Both dosing strategies are associated with similar
levels of efficacy. unspecified deep vessels of lower extremity
r When T-PA therapy is discontinued, start FOLLOW-UP r 453.41 Acute venous embolism and thrombosis of
immediately on LMWH, with b.i.d. dosing, as noted deep vessels of proximal lower extremity
above. FOLLOW-UP RECOMMENDATIONS r 453.42 Acute venous embolism and thrombosis of
r Monitor platelet counts because of a small risk for Discharge instructions and medications:
r Patients should be on oral warfarin for 36 months, deep vessels of distal lower extremity
thrombocytopenia.
r On day 3 of LMWH, convert to oral warfarin. maintaining an INR of 23.
r For fibrinogen levels <80 mg/dL, consider r Longer or indefinite therapy should be considered
PEARLS AND PITFALLS
cryoprecipitate 0.2 bags/kg. for the presence of congenital risk factors.
r Monitor platelet levels: Platelet transfusion may be r Refrain from contact sports or high-risk physical r VT of the lower extremities, which occurs at an early
required if platelets are <50,000/L and bleeding activity because of the bleeding risk. age and peaks in the 2nd decade of life, is the most
r Counsel the patient on the use of other medications, common symptom in antithrombin deficiency.
occurs.
including over-the-counter medications, that may r Negative US of lower extremities and negative
change the effectiveness of warfarin. D-dimer does not require repeat US in 7 days.
r If there is a negative US with risk factors, r Poor outcome is defined as recurrent DVT within
recommend a repeat US in 37 days to confirm 2 yr, presence of residual thrombosis, or
there is no DVT. development of PTS.
Patient Monitoring
r Maintain INR between 2 and 3.
r IPG returns to normal in 65% of patients in 3 mo,
85% by 6 mo, and 95% in 1 yr compared to US,
which has returns of 30%, 45%, and 60%.
237
DEHYDRATION
Alan L. Nager

BASICS r Decreased intake (voluntary or involuntary): r The physical exam should be performed looking at
Anatomic or pathologic diseases (pharyngitis, signs that may reflect dehydration.
DESCRIPTION stomatitis, cleft lip/palate, facial dysmorphism, r Vital signs may show evidence of tachycardia or
r Dehydration is a physiologic response to many airway obstruction) tachypnea, which are signs characteristic of
diseases and conditions. Neurologic diseases (meningitis, encephalitis, moderate dehydration.
r It is the result of a negative fluid balance resulting brain tumor, seizures) r Hypotension may be present, which is a classic
from: Febrile illnesses finding in hypovolemic shock.
Decreased and/or inadequate intake AND/OR r Increased output: r Further evidence of the degree of dehydration may
Increased output, such as GI, renal, or insensible GI losses (vomiting and/or diarrhea) be discovered by finding evidence of lethargy or
losses from systemic responses to specific disease Renal losses: listlessness; a sunken fontanel; sunken eyes or
states, such as burns or sepsis Osmotic (diabetic ketoacidosis, acute tubular absent or diminished tears; dry or sticky mucous
r A spectrum of signs and symptoms can be seen in necrosis) membranes; tachypnea; a scaphoid or distended
dehydration, with categorization ranging from Nonosmotic (renal diseases, electrolyte abdomen; skin that is cool and/or mottled with
asymptomatic or mild to severe dehydration with or disturbance, diabetes insipidus, adrenal disease, delayed capillary refill time, diminished pulses; or
without hypovolemic shock. diuretics, kidney disease, evidence of neurologic dysfunction such as seizures
r In the U.S., acute gastroenteritis remains the most pseudohypoaldosteronism) (2).
significant cause of dehydration. Insensible losses (fever, heat, respiratory diseases,
diaphoresis, thyroid disease, cystic fibrosis): DIAGNOSTIC TESTS & INTERPRETATION
EPIDEMIOLOGY Moderate to severe burns Lab
Prevalence Secondary ascites r Utility of routine lab testing for patients thought to
r In the U.S., >1.5 million outpatient visits occur Respiratory disease, peritonitis (medical or be mildly or moderately dehydrated is unclear.
annually for gastroenteritis, resulting in 200,000 surgical) r Different underlying mechanisms may result in
hospitalizations and 300 deaths per year. Anaphylaxis varying lab abnormalities.
r Worldwide, diarrheal disease remains the leading r No specific lab test is consistently predictive of
cause of morbidity and mortality, with 1.5 billion COMMONLY ASSOCIATED CONDITIONS
Some patients have underlying disease for which fluid dehydration severity in lieu of a clinical assessment
episodes and 1.52.5 million deaths occurring for the mildly and moderately dehydrated patient.
annually in patients <5 yr (1). requirements and losses are unique, such as diabetes, r Obtain electrolytes, BUN, creatine, and glucose
cystic fibrosis, thyroid disease, neurologic diseases
RISK FACTORS (tumor, pituitary dysfunction, or diabetes insipidus), for:
r Sun exposure, humidity, insensible losses, exercise, adrenal diseases affecting electrolytes, metabolic Severe illness
young age diseases, heat-related illnesses, moderate or major Severe dehydration
r Excessive losses burns, or chronic GI illnesses. Patients with chronic diseases
r Insufficient intake (voluntary or involuntary) Patients whose diet may cause electrolyte changes
(eg, rice water or improperly mixed formula)
GENERAL PREVENTION DIAGNOSIS Adjunct means to assess bicarbonate level or
r Fluid intake on a regular and adequate basis acidemia such as blood gas analysis or
r Protection against risk factors HISTORY capnography are of potential value.
r Monitoring input and output r The history should include the environment in which
symptoms developed the manifestation of the DIFFERENTIAL DIAGNOSIS
PATHOPHYSIOLOGY disease and prior treatment. See Etiology.
r Dehydration causes total body water and electrolyte r Intake and output should be ascertained:
losses in the intracellular fluid and extracellular fluid Intake history should include quantifying questions
compartments. related to oral intake, such as types and amounts.
TREATMENT
r Dehydration is often referred to in relation to serum Output history should include such questions as PRE HOSPITAL
sodium concentrations: the amount and frequency of urination, presence In most cases, normal saline or lactated Ringer solution
Isonatremic: Sodium 130150 mEq/L or absence of vomiting and/or stooling should be used for IV fluid resuscitation as needed.
Hyponatremic: Sodium <130 mEq/L (description, amounts, frequency), tear production
Hypernatremic: Sodium >150 mEq/L (none, minimal, streaming), and the presence or INITIAL STABILIZATION/THERAPY
r Isonatremic dehydration is the most common form absence of sweating. r Fluid administration can be given PO, IV, or NG:
of dehydration, with hyponatremic or hypernatremic r Other questions that should be asked include the Decision to rehydrate orally or parenterally is
dehydration occurring much less frequently. level of activity; evidence of a sunken fontanel; based on severity of dehydration; ability to
fever; presence of saliva; difficulty swallowing, tolerate oral fluid; and preference of clinician,
drooling; respiratory symptoms; pallor, cyanosis or patient, and parent:
changes in skin warmth, texture, or integrity; Severe rehydration is typically treated with IV
hematemesis, melena, or hematochezia; penile fluid.
swelling or changes in urinary stream pattern; Mild dehydration is typically treated with PO
changes in mental status, neurologic function, or fluid.
seizure; appetite or thirst changes; Oral rehydration solution should be given in small,
antibiotic/medication use; possible toxic ingestion; frequent amounts.
travel history; and change in weight. IV fluid can be given in 2050 mL/kg boluses over
1 hr (clinician preference).
NG fluid should be given 20 mL/kg over 1 hr,
which can be repeated to a max of 50 mL/kg (3).
238
DEHYDRATION
r Maintenance hydration can be given based on the 3. Nager AL, Wang VJ. Comparison of nasogastric and
4-2-1 rule: FOLLOW-UP intravenous methods of rehydration in pediatric
For patients <10 kg, administer 4 mL/kg/hr. patients with acute dehydration. Pediatrics.
For patients between 10 and 20 kg, administer FOLLOW-UP RECOMMENDATIONS 2002;109:566572.
[40 + 2 (weight 10)] mL/hr. 4. Allen C, Etzwiler L, Miller M, et al. Recombinant
For patients >20 kg, administer [60 + 1 Follow-up should occur when additional guidance human hyaluronidase-enabled subcutaneous
(weight 20)] mL/hr. is needed or if a hydration check is deemed pediatric rehydration. Pediatrics. 2009;124:
Additional fluid requirements (eg, 11/2 x appropriate. e858e867.
maintenance) can also be given. Instruct the patient and caregivers about hand 5. Nager A, Wang V. Comparison of ultra-rapid versus
hygiene and contagiousness. rapid intravenous hydration in pediatric patients
MEDICATION r Activity:
First Line with acute dehydration. Am J Emerg Med.
As tolerated 2010;28:123129.
Antiemetics such as ondansetron (Zofran) may be
attempted: Patient Monitoring 6. American Academy of Pediatrics. Practice
r <4 yr: 0.15 mg/kg/dose IV/PO q68h
r 412 yr: 4 mg 23 times/day IV/PO, max dose
Parent instructions should include watching for
diminished tears, decreased urine output including
parameter: The management of acute
gastroenteritis in young children. Pediatrics.
D
concentrated or bright yellow urine, diminished 1996;97:424436.
12 mg/day alertness, lethargy, and seizures.
r >12 yr: 8 mg 23 times/day IV/PO, max dose
24 mg/day DIET ADDITIONAL READING
r Encourage small amounts of oral rehydration fluids,
Second Line such as Pedialyte, Gatorade, or other sport drinks. World Health Organization. The treatment of diarrhea.
r Hyaluronic acid (Hylenex) 150 U single dose SC
r Give bland, nonspicy foods and avoid food or liquids WHO CDD/SER/80.2. Geneva, Switzerland: Author;
several minutes prior to SC fluid administration (4): 1995.
known to cause diarrhea, such as beans,
In preliminary stages of clinical use without clearly
high-fructosecontaining juices, and caffeinated
defined role in therapy
drinks (6).
Facilitates rehydration without IV use in children r BRAT (bananas, rice, applesauce, toast) diet may be CODES
For use with difficult or expected difficult vascular
access or based on clinician or patient/parent helpful.
preference
ICD9
PROGNOSIS r 276.51 Dehydration
r Other antiemetics such as diphenhydramine or r Most patients will recover within 35 days, although
r 775.5 Other transitory neonatal electrolyte
metoclopromide have limited use in nononcologic recovery time may vary depending on the cause of
the dehydration. disturbances
patients.
r Infectious agents causing diarrhea and dehydration
DISPOSITION
may require antibiotics (see Diarrhea topic).
Admission Criteria r The vast majority of patients recover without PEARLS AND PITFALLS
r Persistent moderate dehydration despite treatment,
complications. r Dehydration can cause significant morbidity and
usually related to ongoing losses (eg, vomiting
and/or diarrhea) COMPLICATIONS mortality.
r Electrolyte abnormalities requiring ongoing r Hypernatremia r Clinicians must understand diseases that cause
treatment r Hyponatremia dehydration.
r Moderate or severe dehydration necessitating r Shock r Categorize the severity of dehydration so that
further treatment, including the need for additional r Cerebrovascular accident treatment will be appropriate.
r Lab testing is clinically indicated based on dietary
fluid and electrolyte replacement and monitoring r Shock
r Critical care admission criteria: history or disease or in patients severely dehydrated
Unstable vital signs despite IV hydration or in shock.
r Consider PO, IV, or NG treatment modalities, as each
Severe hypo- or hypernatremia REFERENCES
may be used for specific circumstances.
Discharge Criteria 1. King CK, Glass R, Bresee JS, et al. CDC. Managing
Baseline or near-baseline vital signs and clinical acute gastroenteritis among children: Oral
evidence of adequate hydration (3,5) rehydration, maintenance and nutritional therapy.
Issues for Referral MMWR Recomm Rep. 2003;52(RR-16):116.
Refer to a subspecialist if the dehydration is caused by 2. Gorelick MH, Shaw KN, Murphy KO. Validity and
a subspecialty disease requiring additional evaluation. reliability of clinical signs in the diagnosis of
dehydration in children. Pediatrics. 1997;99(5):e6.
239
DENGUE FEVER
Linda Szema
r In severe dengue, an imbalance of inflammatory PHYSICAL EXAM

BASICS mediators, cytokines, and chemokines occurs, which r Fever
is thought to cause dysfunction of vascular r Rash, typically macular or maculopapular
DESCRIPTION endothelial cells and impaired progenitor cell r Petechiae, ecchymosis, purpura
r Dengue infection is caused by an RNA virus growth: r Mucosal membrane bleeding
transmitted to humans by infected mosquitoes. This causes plasma leakage, hemoconcentration, r Hepatomegaly within a few days of fever onset
r Symptoms vary widely, from subclinical infection to and thrombocytopenia. r In DHF, ascites or pleural effusion
dengue fever (DF) or dengue shock syndrome (DSS). r Hemorrhage may be secondary to
r In DSS, evidence of shock
r Severe infection is categorized as dengue thrombocytopenia, platelet dysfunction, or
hemorrhagic fever (DHF) or DSS. disseminated intravascular coagulation (DIC). DIAGNOSTIC TESTS & INTERPRETATION
r Dengue is one of the viral hemorrhagic fevers Lab
ETIOLOGY
(VHFs), others of which include infections such as Dengue virus (DENV)-1, DENV-2, DENV-3, and Initial Lab Tests
hantavirus, Lassa fever, yellow fever, and Ebola and r CBC:
DENV-4, of the genus Flavivirus
Marburg viruses Leukopenia
EPIDEMIOLOGY Thrombocytopenia
Incidence
DIAGNOSIS Elevated hematocrit
r 50100 million cases of dengue worldwide each Blood smear may show atypical lymphocytes.
HISTORY r Basic metabolic panel:
year; this includes: r Abrupt high-grade fever
r Incubation ranges from 314 days. Electrolyte/Acid-base abnormalities or hypo- or
500,000 DHF cases
hyperglycemia may occur.
22,000 deaths, mostly among children r DF, the acute phase of the illness, is characterized by r LFTs: AST and ALT may be mildly elevated:
r Incidence over the last 50 yr has increased 30-fold.
high fever for 27 days and two or more of the Normal AST is an extremely strong negative
r Following diarrheal diseases and respiratory
following: predictor of DF.
infections, DF/DHF has become a leading cause of Headache r Stool guaiac
hospitalization and death among children in Retro-orbital pain r Urinalysis
Southeast Asia. Myalgia/Arthralgia
r An increasing number of cases in the Caribbean, r Additionally, DIC panel, type and cross-match, blood
Rash
Central America, and Mexico: Leukopenia gas, and blood, urine, and CSF cultures as necessary
r Providers should report cases of patients with
Areas of the U.S. that border these locations as Mild hemorrhagic manifestations
well as cities that receive travelers from these Bleeding of mucous membranes denguelike illness and recent travel to affected areas
locations have an increasing incidence. Petechiae to the local or state health department and send
r Associated symptoms not meeting the definition for specimens for lab testing:
RISK FACTORS Specimens may be submitted directly to CDC
r Traveling to or living in tropical and subtropical DF include:
Fatigue laboratories in San Juan, Puerto Rico.
environments 2 serum specimens should be sent:
r Most U.S. citizens acquire the infection in Puerto Irritability
Acute (drawn prior to day 5 of illness) for
Rico, the U.S. Virgin Islands, Samoa, and Guam, Anorexia
Nausea RT-PCR for dengue virus
which are endemic for the virus. Convalescent (drawn on days 630) for ELISA
r Dengue is present in urban and suburban areas in Abdominal pain
Persistent vomiting for dengue IgM
the Americas, Southeast Asia, Eastern r If the temperature drops to 38 C and the Imaging
Mediterranean, and Western Pacific and in rural r CXR to assess for pleural effusion
areas in Africa. symptoms improve on days 37, then the patient is
said to have nonsevere dengue. r Abdominal sonography as needed to diagnose
r Children <15 yr have increased severe and fatal
r If capillary permeability and hematocrit increase, this ascites
disease.
marks the start of the critical phase and severe Diagnostic Procedures/Other
GENERAL PREVENTION dengue: Tourniquet test: Positive tourniquet testBP cuff is
r Avoid mosquito bites by using repellent, wearing New symptoms at the critical phase may include inflated to midway between systolic and diastolic
clothing to reduce areas of exposed skin, and staying persistent vomiting, severe abdominal pain, and pressure for 5 min, then petechiae are counted
inside air-conditioned or well-screened buildings. difficulty breathing. r If >10 square inches, the test is positive.
r Public health efforts include mosquito population The critical phase lasts for 2448 hr.
control. r DHF characterized by: DIFFERENTIAL DIAGNOSIS
Presence of resolving fever or recent history of Depends on the geographic origin of the patient;
PATHOPHYSIOLOGY includes:
r Dengue virus is a single-stranded RNA virus fever lasting 27 days
Any hemorrhagic manifestation r Influenza
belonging to the genus Flavivirus.
r It is transmitted by infected Aedes mosquitos, Thrombocytopenia (platelet count <100 109 /L) r Chikungunya
Increased vascular permeability evidenced by: r Infectious mononucleosis
primarily Aedes aegypti. >20% rise in hematocrit for age and sex
r Incubation is followed by viremia, causing the acute r HIV
>20% drop in hematocrit following treatment r Measles
phase of the illness. with fluids as compared to baseline
r Dengue cannot be spread directly from person to r Enteroviral infections
Signs of plasma leakage: Hypoproteinemia, r Malaria
person. ascites, or pleural effusion
r Viral clearance occurs with defervescence and is r DSS includes all criteria for DHF plus circulatory r Leptospirosis
accomplished through the generation of antibodies r Typhoid
failure, evidenced by:
and the activation of CD4+ and CD8+ T Rapid and weak pulse and narrow pulse pressure r Rickettsial diseases
lymphocytes. (>20 mm Hg) r VHFs
Age-specific hypotension and cold, clammy skin r Other Flavivirus infections: Yellow fever, St. Louis
and restlessness encephalitis, Japanese encephalitis, West Nile
240
DENGUE FEVER
Second Line COMPLICATIONS

r Rare but can include:
TREATMENT NSAIDs are relatively contraindicated due to the
theoretical potential to exacerbate hemorrhage. Hepatic injury
PRE HOSPITAL Encephalopathy
DISPOSITION
Assess and stabilize airway, breathing, and circulation. Myocarditis
Admission Criteria r Death much more frequently occurs in cases outside
INITIAL STABILIZATION/THERAPY r Abdominal pain or tenderness
r Assess and stabilize airway, breathing, and r Persistent vomiting of the U.S.
circulation. r Ascites
r Supportive treatment is the mainstay of care: r Hemorrhage, spontaneous bleeding ADDITIONAL READING
No antiviral therapy is available. r Lethargy, altered mental status, or restlessness
r Based on extensive experience treating children in r CDC. Dengue. Available at http://www.cdc.gov/
r Rising hematocrit
dengue epidemics in Southeast Asia, the World r Coexisting conditions: Pregnancy, infancy, dengue/. Accessed August 5, 2010.
Health Organization (WHO) advocates a specific r World Health Organization. Dengue: Guidelines for
protocol to treat hypotensive shock:
immunocompromise, diabetes, renal failure
r Critical care admission criteria: diagnosis, treatment, prevention, and control.
Geneva, Switzerland: Author; 2009.
D
Initial bolus of D5 normal saline or Ringer lactate
(20 mL/kg of body weight) infused over 15 min, Signs of shock
Severe bleeding See Also (Topic, Algorithm, Electronic
followed by continuous infusion (1020 mL/kg/hr
Fluid overload Media Element)
depending on the clinical response) until vital
Signs of organ impairment such as hepatic injury, Idiopathic Thrombocytopenic Purpura
signs and urine output normalize
As the patient has clinical improvement, the encephalitis, myocarditis
infusion rate should be slowly reduced until it Discharge Criteria
matches plasma fluid losses. All of the following should be satisfied: CODES
Adequacy of treatment is assessed by BP, pulse, r Vital signs normal or with minimal elevation of heart
hematocrit, and urine output. rate, though fever is not a contraindication for ICD9
r 061 Dengue
If shock persists, use WHO-recommended therapy; discharge
blood or platelet transfusion may also be r Ability to tolerate adequate oral fluids r 065.4 Mosquito-borne hemorrhagic fever
necessary. r Passing of urine at least once q6h
r If no warning signs (see below) are present, oral r No spontaneous bleeding or a rising hematocrit
hydration should be encouraged; if not tolerated, PEARLS AND PITFALLS
give IV fluid therapy for rehydration and then Issues for Referral r The clinical presentation of dengue infection varies
reassess for PO tolerance. Consider transfer to a critical care setting capable of
r If warning signs (see below) are present, fluid managing severe shock. widely.
r A history of recent travel to endemic areas and
therapy with isotonic solution should be initiated
with reassessment of hematocrit and clinical status. denguelike illness should prompt providers to report
r If signs of severe dengue are present, judicious IV FOLLOW-UP to local or state authorities.
r DF can progress to DHF or DSS with severe
fluid resuscitation is necessary, with the goal to FOLLOW-UP RECOMMENDATIONS
improve central and peripheral circulation and hypoperfusion; this will last for 2448 hr.
Discharge instructions and medications: r Vital signs and CBC must be monitored, with
end-organ perfusion. r Take acetaminophen for fever or analgesia.
r Warning signs: r Instructions for immediate return to care if assessment for bleeding, hypoperfusion, and
Abdominal pain or tenderness dehydration.
deterioration or hemorrhage are critical r Give acetaminophen for fever, and avoid NSAIDs
Persistent vomiting
Clinical fluid accumulation Patient Monitoring and aspirin.
Caregivers may monitor for petechiae or hemorrhage. r Overhydration to point of pulmonary edema is a risk
Bleeding
Lethargy, altered mental status, restlessness PROGNOSIS of therapy.
Liver enlargement >2 cm r Varies with severity of illness, particularly degree of r When patients have stable vital signs, normal
Increase in hematocrit concurrent with rapid thrombocytopenia, hemorrhage, and shock hematocrit, and are able to take PO, discontinue IV
decrease in platelet count r Permanent end-organ damage and death may result fluid therapy.
MEDICATION from hemorrhage and/or shock.
First Line
r Threshold for blood or platelet transfusion varies
with institution:
In the setting of hemorrhage, platelet transfusion
if <25 109 /L
If asymptomatic, platelet transfusion if <10
109 /L
241
DEPRESSION
David Chao
Richard J. Scarfone
r School-age children:
BASICS DIAGNOSIS Depressed school-age children are cognitively able
to internalize environmental stressors (including
DESCRIPTION HISTORY family conflict) and display low self-esteem and
r Depression can refer to sadness but also describes a r Diagnostic and Statistical Manual of Mental
guilt.
syndrome with cognitive, physiologic, and affective Disorders (DSM) diagnosis of MDD: Presence of 5 of This inner turmoil is expressed through somatic
components (1). 9 of the following, occurring almost daily for 2 wk: complaints, anxiety, and irritability.
r Childhood depressive disorders include sadness Depressed/Irritable mood (must be present), Key features of childhood depression are
variation, bereavement, sadness problem, diminished interest or pleasure (must be present), dysphoric mood (looking or feeling sad,
adjustment disorder with depressed mood, major psychomotor agitation/retardation, recurrent moodiness/irritability, and crying easily) and
depressive disorder (MDD), dysthymic disorder, and thoughts of death/suicidality, fatigue/energy loss, self-deprecating ideation (low self-esteem,
bipolar disorder (2). weight change, feelings of worthlessness, poor feelings of worthlessness, and suicidality).
concentration (4): Depressed children often present with
EPIDEMIOLOGY DSM criteria were established for adults. Children
r In the U.S., the prevalence of MDD is about 1% of somatization (eg, stomach aches, headaches),
and adolescents with depression may not present school problems (including school phobia), temper
preschoolers, 2% of school-age children, and 58% with these classic symptoms. tantrums, runaway behavior, phobias, separation
of adolescents (2): It is critical to ascertain degree of functional anxiety, and fire setting.
1 in 5 teens has a history of depression at some impairment rather than attempting to fit Because many of these symptoms can be observed
point during adolescence (2). symptoms into a set of diagnostic criteria. in the school setting, teachers should be included
The prevalence of depression appears to be The Diagnostic and Statistical Manual for Primary in the evaluation process.
increasing, with onset at earlier ages (2). Care (DSM-PC), Child and Adolescent Version, r Adolescents:
Gender ratio is equal in prepubertal children and provides a concise guide for diagnosis of pediatric
but there is a 2:1 female predominance in Adolescents undergo a period of biopsychosocial
mental health disorders (5). maturation that is fertile for the development of
adolescents (2). r SIG E CAPS mnemonic (give energy capsules):
r Only 2035% of youth who meet full criteria for depressive symptoms in predisposed individuals.
Sleep, Interest, Guilt, Energy, Concentration, Adolescent depression is similar to adult-onset
depression currently receive treatment (2). Appetite, Psychomotor changes, Suicidality depression.
r The SHADDSSSS mnemonic can also be used to help
RISK FACTORS Red flags include somatization, academic
r Family history of depression address a complete inventory of psychosocial problems, promiscuity, drug/alcohol use,
r Previous depressive episodes functioning, including School, Home, Activities, aggressive behavior, and stealing.
r Family conflict Depression, Drugs/Alcohol, Sexuality, Suicide, Because of their developmental struggle with
r Sexuality conflict Safety, Strengths (1). autonomy from authority figures, it is particularly
r Children and adolescents often present to the important to establish a good rapport with
r Poor academic performance
r Dysthymia, anxiety disorders emergency department setting when symptoms adolescent patients.
have reached a crisis point (eg, suicide attempt).
r Substance abuse disorders (3) r Most children present with nonpsychiatric chief PHYSICAL EXAM
r Evaluation of the childs mental status takes place
PATHOPHYSIOLOGY complaints (eg, somatic symptoms, school problems,
r A multifactorial theory of depression is widely held, throughout the emergency department visit:
behavior problems, irritability).
r Diagnosis is challenging because many psychiatric Features of the mental status examination include
with biologic, environmental, psychological, and orientation, appearance, memory, cognition,
social inputs. illnesses (including psychotic disorders, ADHD, behavior, relatedness, speech, affect, thought
r Monoamine hypothesis: Depression results from anxiety disorders, disruptive behavior disorders content, and insight/judgment.
deficiency or abnormal functioning of serotonin, including oppositional defiant disorder and conduct r A depressed patient may appear withdrawn, lack
epinephrine, and norepinephrine in the CNS: disorder, and substance abuse disorders) present
spontaneous speech, express negativistic thoughts,
Medical therapy is based on this theory (eg, with similar symptoms:
and demonstrate psychomotor retardation and a
selective serotonin reuptake inhibitors). Patients may lack insight into their problems with
limited range of affect.
mood.
ETIOLOGY r The clinician cannot rule out depression based on DIAGNOSTIC TESTS & INTERPRETATION
r It is important to consider organic (nonpsychiatric)
patients rejection of this diagnosis. Lab
causes of depression, which include the following: r A comprehensive history to determine suicidality
r Neurologic: Stroke, subdural hematoma, Initial Lab Tests
should include method and timing, lethality, r Pregnancy test
postconcussive syndrome, brain tumors (especially r An initial presentation of depression may prompt an
circumstances, history of prior attempt(s), level of
frontal), Huntington disease, seizure disorder,
planning, current affect and psychological status, evaluation for organic causes:
syphilis
r Metabolic: Vitamin B deficiency, pellagra (niacin family consistency/dynamics, pharmaceuticals CBC
12 available to patient, history of interpersonal Electrolytes and LFTs
deficiency), hypercalcemia, hyponatremia, conflict/loss, history of substance abuse, history of Thyroid function tests
hypokalemia, Wilson disease psychological disorder or medical problem, history of Vitamin B12 level
r Endocrinologic: Thyroid disease (hypo- or
abuse/neglect/incest, social supports and coping Acetaminophen level if intentional ingestion and
hyperthyroid), adrenal disease (Addison disease, strategies, feelings of regret, or continued desire for possibly other toxicologic screening (2)
Cushing syndrome), diabetes mellitus self-harm (6).
r Medications and toxins: Beta-blockers, r The presentation of depression differs based on Imaging
Consider CT or MRI of brain
anticonvulsants, antipsychotics, corticosteroids, stages of development (2).
estrogens/oral contraceptives, amphetamines, r Infants and preschool-age children: Diagnostic Procedures/Other
stimulants (cocaine, crack), marijuana, alcohol, Manifestations of depression in infancy is typically The Pediatric Symptom Checklist and the Beck
heavy metals the result of loss of the mother and lack of Depression Inventory are widely accepted screening
r Other: Various infections (hepatitis, HIV, Epstein-Barr tools used to detect psychopathology in the pediatric
nurturance.
virus), malignancy, anemia, systemic lupus Symptoms include apathy, listlessness, staring, population (2).
erythematosus hypoactivity, poor feeding/failure to thrive, and
COMMONLY ASSOCIATED CONDITIONS increased rate of infections.
See Risk Factors and Etiology.
242
DEPRESSION
DIFFERENTIAL DIAGNOSIS Discharge Criteria 5. American Academy of Pediatrics. The Classification

r See Etiology. A patient may be discharged to home in the care of of Child and Adolescent Mental Diagnoses in
r Consider factitious disorders. family members if team members feel that he or she is Primary Care: Diagnostic and Statistical Manual for
not at risk for harm to self or others and adequate Primary Care (DSM-PC) Child and Adolescent
outpatient follow-up is arranged. Version. Elk Grove, IL: Author; 1996.
TREATMENT Issues for Referral 6. American Academy of Child and Adolescent
Patients who are determined to have a primary Psychiatry. Practice parameter for the assessment
r The 3 major goals are determining suicidal potential, depressive disorder and/or suicidality should receive and treatment of children and adolescents with
follow-up outpatient psychiatric care. suicidal behavior. J Am Acad Child Adolesc
uncovering acute precipitants, and making the
Psychiatry. 2001;40(7 Suppl):24S51S.
appropriate disposition (1). Additional Therapies
r Ascertain suicidal intent (eg, When you took those St. Johns Wort, omega-3 fatty acids, thyroid extract, 7. Birmaher B, Brent DA; AACAP Work Group on
and combination herbal preparations are sometimes Quality Issues. Practice parameters for the
pills, what did you expect to happen? What did you
used to treat depressive symptoms. assessment and treatment of children and
hope would happen?) (1).
adolescents with depressive disorders. J Am Acad
r Patient should be asked to change into a hospital
Child Adolesc Psychiatry. 2007;46(11):15031526. D
gown, belongings should be secured out of the
patients reach, the patient should be under
FOLLOW-UP 8. Levine LJ, Pletcher JR. Suicide. In Schwartz MW, ed.
The 5-Minute Pediatric Consult. 5th ed.
constant supervision by emergency department FOLLOW-UP RECOMMENDATIONS Philadelphia, PA: Lippincott Williams & Wilkins;
personnel, and the exam room should be free of Patient Monitoring 2008.
objects with which the patient can use to harm him- Outpatients must be monitored closely by family
or herself. members and primary care physicians for suicidal
MEDICATION ideation or self-injurious behavior. CODES
r Agitation:
PROGNOSIS
Agitation or combativeness are less common in r Early recognition and treatment of depressive ICD9
children than adults and infrequently require r 296.20 Major depressive affective disorder, single
disorders improves functioning and prognosis.
chemical restraint/sedation. r Efficacy of pharmacotherapy and psychotherapy episode, unspecified degree
Lorazepam 0.05 mg/kg IV, with a max single dose r 309.0 Adjustment disorder with depressed mood
varies (3).
of 2 mg in adolescents r 311 Depressive disorder, not elsewhere classified
Haloperidol 0.0250.05 mg/kg IV/IM; use a 5-mg COMPLICATIONS
dose in adolescents. r Suicide
r Antidepressants are typically not initiated in the r Self-injury
r Poor social functioning
PEARLS AND PITFALLS
emergency setting:
These medications take weeks to months to begin r Depression may be secondary to a primary
working and should be initiated and monitored by psychiatric disorder or organic pathology.
the patients long-term mental health provider. REFERENCES r Most children with depression present with
nonpsychiatric chief complaints (eg, somatic
ALERT 1. Chun TH, Sargent J, Hodas G. Psychiatric
symptoms, school problems, behavior problems).
Selective serotonin reuptake inhibitors are emergencies. In Fleisher GR, Ludwig S, and r The mnemonic SIG E CAPS (Sleep, Interest, Guilt,
associated with increased suicidality in some Henretig F, et al., eds. Textbook of Pediatric
Emergency Medicine. 5th ed. Philadelphia, PA: Energy, Concentration, Appetite, Psychomotor
patients. These medications should only be changes, Suicidality) is helpful in assessing the key
prescribed in coordination with a mental health Lippincott Williams & Wilkins; 2005.
features of MDD.
professional as part of a comprehensive treatment 2. Son SE, Kirchner JT. Depression in children and r The SHADDSSSS mnemonic can be used to help
plan. adolescents. Am Fam Physician. 2000;62(10):
22972308, 23112312. address a complete inventory of psychosocial
functioning. The components of the history should
3. An update on depression in children and
DISPOSITION include School, Home, Activities, Depression,
adolescents. J Clin Psychiatry. 2008;69(11):
Admission Criteria Drugs/Alcohol, Sexuality, Suicide, Safety, and
r Any patient who is at risk of harm to self or others 18181828.
Strengths.
4. American Psychiatric Association. Diagnostic and r The 3 major goals of managing depression are
but who is medically stable requires inpatient
Statistical Manual of Mental Disorders. 4th ed.,
psychiatric hospitalization. determining suicidal potential, uncovering acute
r Any patient who is unable to attend to self-care and Text Revision. Washington, DC: Author; 2000.
precipitants, and making an appropriate disposition.
whose family is unable to adequately provide care
requires inpatient psychiatric hospitalization.
r An actively suicidal patient should never be
discharged to home.
243
DERMATOMYOSITIS
Vincenzo Maniaci
Imaging
BASICS DIAGNOSIS r No imaging is necessary in the emergency
department.
DESCRIPTION HISTORY r As an outpatient or inpatient, MRI is useful in
r Dermatomyositis is a systemic autoimmune r Insidious vs. acute onset of muscle weakness and
detecting areas of disease activity and localization
vasculopathy primarily affecting the skeletal muscles rash for muscle biopsy (8).
and skin, causing symmetric muscle weakness and a r Muscle weakness may lead to limitations in
characteristic skin rash. performing activities of daily living such as brushing Diagnostic Procedures/Other
r Outpatient referral for electromyography of the
r Characteristic skin rash plus three of the following hair, getting out of bed, rising from a chair, or
climbing stairs. muscles
criteria are necessary for a definitive diagnosis (1,2): r Outpatient referral for muscle biopsy of a clinically
Symmetric proximal muscle weakness r May also complain of:
Elevated muscle enzymes Low-grade fever affected but not atrophied muscle
r Outpatient referral for pulmonary function testing to
Electromyographic changes of myositis Weight loss
Muscle biopsy evidence of myositis and muscle General weakness evaluate the progression of interstitial lung disease
necrosis Arthralgia Pathological Findings
Dysphagia Lymphocytic vasculitis of small arteries and veins of
EPIDEMIOLOGY Abdominal pain muscle, skin, subcutaneous tissue, and GI tract
Incidence Melena
r Peak age is 510 yr. DIFFERENTIAL DIAGNOSIS
r Girls are affected more than boys (ratio 2.3:1). PHYSICAL EXAM r Mixed connective tissue disease, scleroderma,
r Muscle: Symmetric, proximal muscle (deltoid,
r 2.54.1 cases per million children per year systemic lupus erythematosus
r Rates by race (3): quadriceps) weakness r Muscular dystrophy, Becker muscular dystrophy,
r Dermatologic:
3.4 cases per million white non-Hispanic limb-girdle muscular dystrophy, facioscapulohumeral
Heliotrope dermatitis: Reddish-purple rash of the dystrophy, spinal muscle atrophy
3.3 cases per million African American
upper eyelids, usually accompanied with r Myasthenia gravis, amyotrophic lateral sclerosis,
non-Hispanic
periorbital edema poliomyelitis, Guillain-Barre syndrome
2.7 cases per million Hispanic
Gottron papules: Erythematous, violaceous r Drug-induced myositis: Chloroquine, azathioprine,
RISK FACTORS plaques located over the bony prominences of the penicillamine, ipecac, ethanol, corticosteroids
r Strong association with HLA antigens B8/DR3, finger joints, elbows, knees, and ankles r Hypothyroidism, hyperthyroidism, Cushing syndrome
DQA1*0501 (4), HLA-DRB*0301, and DQA1*0301 Nailfold changes: Capillary dilatation and
allele (5) tortuosity
r Polymorphism of the tumor necrosis factor alpha Calcinosis:
Superficial plaques or nodules on the extremities
TREATMENT
and interleukin-1 receptor antagonist (6)
Deep muscle calcification potentially limiting PRE HOSPITAL
PATHOPHYSIOLOGY joint mobility r Assess and stabilize airway, breathing, and
r Involves activation of the cell-mediated and humoral
Linear calcification along myofascial planes circulation.
immune system, resulting in endothelial cell Subcutaneous calcium deposition of the torso r Suctioning of secretions from oral cavity if necessary
damage. The activation of cytotoxic CD8+ T cells, Skin ulceration is generally a sign of significant
macrophages, and autoantibodies against an vasculopathy. INITIAL STABILIZATION/THERAPY
unknown endothelial antigen leads to upregulation r Assess and stabilize airway, breathing, and
of the expression of major histocompatibility DIAGNOSTIC TESTS & INTERPRETATION circulation.
complex class I and II (7). Lab r Intubation and mechanical ventilation for patients
r Immune complexes are deposited, leading to Initial Lab Tests with respiratory failure or inability to protect upper
complement activation and subsequent vascular r Elevated muscle enzymes:
airway
injury and muscle inflammation. Aspartate aminotransferase r Suctioning of the oral cavity in those patients with
Aldolase dysphagia
ETIOLOGY
Creatine phosphokinase r Placement of an NG tube for gastric decompression
Unclear but proposed autoimmune vasculopathy
Lactate dehydrogenase r Intubation and mechanical ventilation for patients
provoked by a possible environmental trigger (group A r Myositis-specific antibodies seen in about 10% of
beta-hemolytic streptococci, coxsackievirus, ECHO with respiratory failure or inability to protect upper
virus, ultraviolet light) in a genetically susceptible patients:
airway
person Antisynthetase autoantibodies
Anti-Mi-2 autoantibodies
Antisignal recognition autoantibodies
r Antinuclear antibody, mainly speckled pattern,
elevated in about half of patients
r Nonspecific lab findings:
ESR may be normal or elevated
Elevated Von Willebrand factor
244
DERMATOMYOSITIS
MEDICATION 5. Mamyrova G, OHanlon TP, Monroe JB, et al.

Institution of medications is usually done in FOLLOW-UP Immunogenetic risk and protective factors for
conjunction with consultation with a rheumatologist. juvenile dermatomyositis in Caucasians. Arthritis
FOLLOW-UP RECOMMENDATIONS Rheum. 2006;54(12):39793987.
First Line Activity:
Corticosteroids are the mainstay for muscle 6. Pachman LM, Liotta-Davis MR, Hong DK, et al. TNF
r Physical activity is encouraged to maintain range of alpha-308A allele in juvenile dermatomyositis:
involvement:
r Prednisone 12 mg/kg/day PO motion and prevent contractures. Association with increased production of tumor
r Avoid ultraviolet exposure with protective clothing necrosis factor alpha, disease duration, and
Second Line and sunscreen. pathologic calcifications. Arthritis Rheum.
Methotrexate 1025 mg/m2 /wk PO or SC, max 40 2000;43(10):23682377.
mg/wk Patient Monitoring
Outpatient monitoring of muscle enzymes and muscle 7. Engel AG, Arahata K, Emslie-Smith A. Immune
SURGERY/OTHER PROCEDURES strength every 36 mo effector mechanisms in inflammatory myopathies.
Surgical excision of areas of calcinosis causing pain or Res Publ Assoc Res Nerv Ment Dis. 1990;68:
DIET 141157.
physical impairment may be done as an outpatient
referral. Supplemental calcium and vitamin D if taking 8. Fraser DD, Frank JA, Dalakas M, et al. Magnetic
D
corticosteroids resonance imaging in the idiopathic inflammatory
DISPOSITION myopathies. J Rheumatol. 1991;18(11):
PROGNOSIS
Admission Criteria r Variable disease progression with 3 distinct clinical 16931700.
courses: 9. Huber AM, Lang B, LeBlanc CM, et al. Medium-
Myocarditis, CHF Monocyclic and long-term functional outcomes in a multicenter
Dysphagia with inability to handle secretions Polycyclic cohort of children with juvenile dermatomyositis.
Respiratory failure secondary to pulmonary fibrosis Chronic continuous (50% developing chronic Arthritis Rheum. 2000;43(3):541549.
or weakness of the diaphragm and intercostal disease within 24 mo of diagnosis) (9)
muscles r 23% mortality
Hemodynamic instability from mucosal ulcerations ADDITIONAL READING
resulting in GI bleeding and bowel wall COMPLICATIONS
perforations r Calcinosis cutis with secondary bacterial infection Woodward AL, Sundel RP. Rheumatologic
Septic shock r Joint contractures from calcinosis or prolonged emergencies. In Fleisher GR, Ludwig S, eds. Textbook
r Inpatient admission criteria: immobility of Pediatric Emergency Medicine. 6th ed. Philadelphia,
Progressive muscle weakness PA: Lippincott Williams & Wilkins; 2010:11271170.
Velopalatine weakness leading to pooling of oral See Also (Topic, Algorithm, Electronic
secretions, nasal voice, and aspiration pneumonia REFERENCES Media Element)
Discharge Criteria 1. Bohan A, Peter JB. Polymyositis and Weakness
Ability to handle oral secretions and resolution of dermatomyositis (first of two parts). N Engl J Med.
respiratory dysfunction 1975;292(7):344347.
Issues for Referral 2. Bohan A, Peter JB. Polymyositis and CODES
Multidisciplinary outpatient approach: dermatomyositis (second of two parts). N Engl J
Rheumatologist, dermatologist, physical therapist, Med. 1975;292(8):403407. ICD9
occupational therapist, speech therapist 3. Mendez EP, Lipton R, Ramsey-Goldman R, et al. US 710.3 Dermatomyositis
Additional Therapies incidence of juvenile dermatomyositis, 19951998:
Physical, occupational, and speech therapy Results from the National Institute of Arthritis and
Musculoskeletal and Skin Diseases Registry.
PEARLS AND PITFALLS
Arthritis Rheum. 2003;49(3):300305. r Dermatomyositis should be considered in patients
4. Reed AM, Pachman L, Ober C. Molecular genetic presenting with rash and muscle weakness.
studies of major histocompatibility complex genes r Delayed recognition and treatment with
in children with juvenile dermatomyositis: Increased corticosteroids results in disease progression and
risk associated with HLA-DQA1 *0501. Hum poor outcome.
Immunol. 1991;32(4):235240.
245
DIABETES INSIPIDUS
Phillip Visser
Peter L. J. Barnett
r Nephrogenic DI: DIAGNOSTIC TESTS & INTERPRETATION

BASICS X-linked recessive inheritance (vasopressin V2 Lab
receptor gene defect) and autosomal recessive Initial Lab Tests
DESCRIPTION inheritance (aquaporin-2 gene defect) r Blood:
r Diabetes insipidus (DI) is defined as the inability to Chronic renal disease Random plasma osmolality
concentrate urine, leading to polyuria and Obstructive uropathy Renal function and electrolytes, calcium,
compensatory polydipsia. Renal dysplasia phosphate
r It can result in severe fluid and electrolyte imbalance. Polycystic kidney disease Random glucose
r Central DI is the failure of adequate antidiuretic Sickle cell disease r Urine:
hormone (ADH) release. Electrolyte disturbances such as hypercalcemia Random urine osmolality
r Nephrogenic DI occurs when the distal tubules of and hypokalemia Urinalysis and microscopy
the nephron do not respond to ADH. Diabetes mellitus is often responsible for r Pregnancy test in females
secondary ADH resistance. r These tests help to establish the diagnosis and
EPIDEMIOLOGY Various drug associations exist: Amphotericin B,
r It is a rare condition with onset in childhood and unmasking possible differential diagnosis.
chlorpromazine, cisplatin, diphenylhydantoin, r Low serum sodium and osmolality suggest primary
early adult years. diuretics, ethanol, foscarnet, lithium, reserpine,
r Development of the condition depends on the polydipsia; in untreated cranial or nephrogenic DI,
rifampicin, and volatile anesthetics.
underlying pathologic process. serum sodium and osmolality are typically in the
normal to high-normal range. Concomitant urine
PATHOPHYSIOLOGY DIAGNOSIS osmolality aids interpretation.
r ADH concentrates urine by binding to the r Renal impairment and hypercalcemia can identify
vasopressin V2 receptor in the distal collecting HISTORY the underlying causes of nephrogenic DI.
tubule of the kidney. It inserts aquaporin 2, a r Patients with complete DI do not voluntarily stop r Elevated random glucose will identify underlying
water-channel protein, into the cell membrane. This drinking for >2 hr, even at night. diabetes mellitus, a cause of polyuria on its own, but
allows passage of water from the lumen of the r Water is the preferred fluid, and children may drink
it can also be responsible for secondary nephrogenic
nephron, along an osmotic gradient, into the cells of it from any available source. DI.
the collecting duct. r Estimate the daily volume of urine and frequency of r Tumor markers:
r Inadequate levels of ADH or decreased effect on
micturition. Alpha-fetoprotein and hCG levels should be
collecting tubules result in loss of water in urine. r New-onset enuresis may be a presenting complaint.
r An intact thirst mechanism results in polydipsia to measured if underlying malignancy is suspected.
r Infants may present with polyuria, irritability, and
compensate for increased water losses. Imaging
r If access to water is unavailable or thirst mechanism failure to thrive. r Brain MRI may show the loss of hyperintense signal
r Breast-feeding infants can present later due to
is absent, severe dehydration ensues. on T1-weighted images of the posterior pituitary in
lower solute load in feeds, and the need for both cranial and nephrogenic DI and identify
ETIOLOGY additional water feeds is often reported in infants. tumors:
r Cranial DI: r Previous episodes of dehydration requiring medical
Serial MRI should be done in idiopathic cranial DI
Head trauma and neurosurgical procedures treatment would suggest previously unrecognized to screen for evolving disease.
Genetic causes include autosomal dominant, illness. r Skeletal survey should be done to identify or rule out
autosomal recessive (very rare), X-linked recessive r Signs and symptoms of cranial tumor:
Langerhans cell histiocytosis as the cause of cranial
(very rare), and DIDMOAD (Diabetes Insipidus Headache DI.
Diabetes Mellitus Optic Atrophy Deafness) Visual disturbance
syndrome. Abnormal weight gain or loss Diagnostic Procedures/Other
Midline brain developmental defects (eg, Hyperpyrexia A water deprivation test can be used to assess the
septo-optic dysplasia) Precocious puberty patients ability to produce ADH in the CNS and the
Craniopharyngioma, pituitary adenoma, r Family history will be important in directing the renal response to it:
germinoma, and optic glioma are common causes. r Requires inpatient admission under close supervision
investigation and to provide genetic counseling.
Meningoencephalitis, tuberculous granulomas, DIFFERENTIAL DIAGNOSIS
congenital cytomegalovirus, and toxoplasmosis PHYSICAL EXAM r Psychogenic polydipsia
r Look for signs of dehydration, deficient nutritional
are infective conditions responsible for DI. r Diabetes mellitus
Langerhans cell histiocytosis is a common status, and trauma.
r Midline anomalies can predispose to DI. r Hypernatremic dehydration
inflammatory cause for DI and less commonly r Primary polydipsia
sarcoid and lymphocytic neurohypophisitis. r Visual field defects and papilledema are early signs
of intracranial tumors; very young patients will r Polyuric renal failure
Hypoxic/Ischemic brain damage can cause
transient or permanent DI. require an ophthalmology consultation. r Hypercalcemia
Very commonly, no apparent cause is found. r Abdominal mass can be present with r Adrenal insufficiency
hydronephrosis or bladder distension associated r Cerebral salt wasting
with DIDMOAD syndrome.
246
DIABETES INSIPIDUS
Discharge Criteria ADDITIONAL READING

TREATMENT An educated patient and caregiver with clear
r Cheetham T, Bayliss PH. Diabetes insipidus in
understanding of follow-up instructions, the ability to
PRE HOSPITAL maintain fluid balance with medication, and with free children: Pathophysiology, diagnosis and
r Assess and stabilize airway, breathing, and access to water can safely be discharged. management. Paediatr Drugs. 2002;4(12):785796.
r Knoers N, Monnens HAL. Nephrogenic diabetes
circulation.
r Manage trauma, if present. insipidus: Clinical symptoms, pathogenesis, genetics
FOLLOW-UP and treatment. Pediatr Nephrol. 1992;6:476482.
INITIAL STABILIZATION/THERAPY r Maghnie M, Cosi G, Genovese E, et al. Central
r Assess and stabilize airway, breathing, and FOLLOW-UP RECOMMENDATIONS
r DI is a complex condition that is usually lifelong and diabetes insipidus in children and young adults.
circulation. N Engl J Med. 2000;343:9891007.
r Manage trauma, if present. will require ongoing follow-up by an r Morello JP, Bichet DG. Nephrogenic diabetes
r Assess the degree of dehydration and hypovolemia; endocrinologist.
r Anterior pituitary hormone deficiency commonly insipidus. Ann Rev Physiol. 2001;63:607630.
sodium >150 mmol/L should be corrected over r Richman RA, Post EM, Notman DN, et al.
48 hr. occurs in patients with cranial DI and should be
actively investigated if suspected. Simplifying the diagnosis of diabetes insipidus in D
ALERT r Discharge instructions and medications: children. Am J Dis Child. 1981;135:839841.
r Wang LC, Cohen ME, Duffner PK. Etiologies of
Correction of hyponatremia that occurs too rapidly Families and patients should be educated in the
may result in central pontine myelinosis and correct use of DDAVP and instructed to present for central diabetes insipidus in children. Ped Neurol.
permanent neurologic injury. assessment if the following develops: 1994;11:273277.
Any sign of dehydration See Also (Topic, Algorithm, Electronic
r Unless a patient is having seizures as a result of Irritability Media Element)
hyponatremia, it is advised to limit hyponatremia Lethargy r Hyponatremia
sodium correction to not more than 10 mmol/L/ Reduced urine output r Polyuria
24 hr. Sudden increase in weight
r Hypotension should be corrected using normal Seizures
saline in 20 mL/kg boluses. Symptoms of urinary tract infections
r Symptomatic or severe hypertonicity should be CODES
Patient Monitoring
corrected to: Weight should be used as a measure of fluid balance
Serum osmolality of 330 mOsm/L ICD9
at home, and abrupt changes should prompt r 253.5 Diabetes insipidus
Serum sodium 155 mmol/L or until asymptomatic reassessment. r 588.1 Nephrogenic diabetes insipidus
MEDICATION DIET
Cranial DI: r Patients on treatment should drink only when thirsty,
r Desmopressin, given as IV, SC, intranasal, or oral provided they have an intact thirst mechanism. PEARLS AND PITFALLS
form r Infants and patients without a thirst mechanism
r Synthetic analogue of ADH (DDAVP) with prolonged r Pearls:
should only be given a carefully calculated fluid
antidiuretic action; available in intranasal, tablet, volume per day. Hyponatremia and fluid overload can be avoided
and parenteral forms in patients on treatment by allowing a period of
r Initiation should typically be on inpatient basis PROGNOSIS permissible polyuria, during which free fluid is
r Usually has a good prognosis cleared before the next dose of DDAVP is given.
under specialist supervision. r It depends on the primary cause whether the r Pitfalls:
DISPOSITION condition is transient or lifelong and if management Patients with psychogenic polydipsia (habitual
Admission Criteria is going to be easy or difficult. drinking) may fail a water deprivation test
r Patients with newly diagnosed DI, as well as any because:
COMPLICATIONS
with dehydration or electrolyte imbalance requiring r Dehydration Prolonged excessive water intake can wash out
correction, should be admitted: r Hypernatremia renal medullary gradient required for
In the presence of severe intercurrent illness such r Hyponatremia concentrating the urine.
as respiratory infections and GI conditions There may have been surreptitious intake of
r Cerebral edema
affecting the administration and absorption of water during the test.
r Seizure
medication, admit for management of fluid Idiopathic DI may be due to a slow-growing tumor
balance. that was not evident on the first MRI, thus further
r Inability to cope with management at home imaging may be indicated later.
warrants admission.
Sodium level <110 or >170 mmol/L
Hyponatremic seizure
247
DIABETIC KETOACIDOSIS
Mia L. Karamatsu
Lilit Minasyan
r Increased glucose production and limited glucose r Useful calculations:

BASICS utilization results in hyperglycemia, osmotic diuresis, Anion gap = Na (Cl + HCO3 ):
electrolyte loss, dehydration, decreased glomerular Normal is 12 +/ 2
DESCRIPTION filtration rate, and hyperosmolarity. Corrected sodium = measured Na + [(glucose
r Diabetic ketoacidosis (DKA) results from a relative or r Lipolysis aids in gluconeogenesis and ketoacidosis, (mg/dL) 100) 0.016]
absolute insulin deficiency associated with generating beta-hydroxybutyrate and acetoacetate. Effective osmolality = 2 [Na + K] + glucose
hyperglycemia, acidosis, and ketosis: r Ketoacidosis, along with lactic acidosis from poor (mg/dL)/18:
Glucose >11 mmol/L (>200 mg/dL) perfusion, results in metabolic acidosis. Frequently between 300 and 350 mOsm/L
Venous pH <7.3 and/or bicarbonate 15 mmol/L r If febrile, send appropriate lab specimens for
Moderate to large ketones in the urine ETIOLOGY analysis or culture.
r Severity of DKA is determined by the degree of r T1DM:
Autoimmune destruction of b-cells Imaging
acidosis (1): r A CT scan of the head should be ordered for the
r T2DM:
Mild: pH <7.3; bicarbonate <15 mmol/L
Heterogeneous glucose disorder associated with a patient with altered level of consciousness and
Moderate: pH <7.2; bicarbonate <10 mmol/L
family history and obesity suspected cerebral edema:
Severe: pH <7.1; bicarbonate <5 mmol/L
It may show focal or diffuse cerebral edema.
EPIDEMIOLOGY However, in patients with cerebral edema, 40% of
Incidence DIAGNOSIS scans are initially normal.
r The overall incidence of type 1 diabetes mellitus r CXR if clinically indicated (for pulmonary edema,
(T1DM) is 15 per 100,000 annually. HISTORY acute respiratory distress syndrome [ARDS])
r Polyuria (including nocturia), polydipsia, polyphagia,
r In the U.S., 2530% patients newly diagnosed
weight loss Diagnostic Procedures/Other
with DM present with DKA: r Nausea, abdominal pain, and vomiting ECG, if indicated
Prevalence of DKA decreases with age. r Possible precipitating event such as concurrent
r In established T1DM, the risk of DKA is 110% per DIFFERENTIAL DIAGNOSIS
febrile illness r Hyperglycemic hyperosmolar nonketotic coma
patient-year. r Infection: Sepsis, acute gastroenteritis
r Up to 9.7% of patients with type 2 diabetes mellitus PHYSICAL EXAM
r Vital signs: r Ingestion or poisonings: Methanol, ethylene glycol,
(T2DM) may present in DKA.
Tachycardia propylene glycol, iron, isoniazid, salicylate, carbon
RISK FACTORS monoxide, cyanide, uremia
r New-onset diabetes: Hypotension
r Acute appendicitis, chronic renal failure
Kussmaul respirations (rapid, deep breaths)
Younger ager (<4 yr old) r Mental status/CNS:
Low socioeconomic status
Fatigue/Lethargy
Limited access to health care
Headache
TREATMENT
Lower parental education level
r Established T1DM: Altered mental status INITIAL STABILIZATION/THERAPY
Insulin omission:
Irritability/Restlessness r Address airway, breathing, circulation, and mental
More common in adolescent girls Focal neurologic deficit status promptly.
Psychosocial reason or psychiatric disorder, Coma r Obtain serum glucose and venous blood gas.
r Signs and symptoms of clinical dehydration:
including eating disorders r Volume expansion with normal saline or lactated
Low socioeconomic status, poor metabolic Dry mucous membranes
Ringer solution 1020 cc/kg over 1 hr.
control: Higher hemoglobin A1c (HbA1c), previous Delayed capillary refill
episodes of DKA Poor skin turgor MEDICATION
Patients with insulin pumps may develop DKA if Most patients have a 510% deficit. First Line
r Cerebral edema may be suggested by r After the initial fluid bolus, start 0.45% saline or
they do not administer additional insulin.
lethargy/coma/depressed level of consciousness or higher tonicity fluid with potassium chloride,
GENERAL PREVENTION irritability/restlessness, focal neurologic signs, potassium acetate, and/or potassium phosphate
r Early recognition and diagnosis of T1DM via
headache, recurrent emesis, elevation of BP, and (total potassium concentration equals 40 mmol/L) at
screening tests and awareness campaigns, inappropriate decrease in heart rate. 1.52 times the maintenance rate:
comprehensive diabetes education programs r Acanthosis nigricans suggests T2DM. Rehydrate evenly over 48 hr. Slow correction with
r Close follow-up care by a diabetes care team and a
isotonic or near-isotonic fluids results in earlier
24-hr helpline DIAGNOSTIC TESTS & INTERPRETATION resolution of acidosis.
r Evaluate and treat the psychosocial reason for Lab r Insulin 0.1 U/kg/hr is the standard:
insulin omission, educate about recognition and Initial Lab Tests Insulin is started after the initial volume expansion
r Bedside serum glucose, urinalysis, and venous blood
treatment of impending DKA, and have a and concurrently with the IV rehydration therapy.
responsible adult supervise insulin administration. gas A bolus of insulin is not routinely recommended,
r CBC, serum electrolytes, BUN, creatinine,
PATHOPHYSIOLOGY but it is acceptable therapy.
magnesium, phosphorus, calcium, urinalysis, HgA1c, Some evidence suggests that bolus insulin may be
Insulin deficiency due to b-cell failure, omission of and beta-hydroxybutyrate:
insulin, or ineffective insulin due to antagonistic effect associated with increased risk of cerebral edema.
Most patients have a total body sodium, Patients without previous diagnosis of DM may be
of counterregulatory hormones and/or physiologic potassium, chloride, phosphorus, and magnesium
stress (eg, sepsis): very sensitive to exogenous insulin. Lower initial
depletion. insulin dosing and careful blood glucose
r The counterregulatory hormones include glucagon,
Leukocytosis is common but does not necessarily monitoring are warranted in these patients.
catecholamines, growth hormone, and cortisol. They indicate a bacterial infection. r If continuous IV insulin is unavailable, administer
help promote glycogenolysis and gluconeogenesis
and limit glucose utilization. fast-acting insulin q12h SC or IM.
248
DIABETIC KETOACIDOSIS
r Dextrose is added to the IV fluid when serum REFERENCES

glucose drops to 17 mmol/L (300 mg/dL): FOLLOW-UP
Usually, 5% dextrose can be added to the IV fluid 1. Dunger DB, Sperling MA, Acerini CL, et al.
to maintain a steady plasma glucose level FOLLOW-UP RECOMMENDATIONS European Society for Paediatric
r Follow up with a pediatric endocrinologist. Endocrinology/Lawson Wilkins Pediatric Endocrine
(100200 mg/dL). However, if the glucose falls
too rapidly (>100 mg/dL/hr), 10% or 12.5% r Fast-acting insulin SC as previously instructed by the Society consensus statement on diabetic
dextrose may be necessary. endocrinologist and/or diabetes team ketoacidosis in children and adolescents. Pediatrics.
r Transition to SC fast-acting insulin and taper off IV 2004;113(2):e133e140.
Patient Monitoring
fluids when the patient can tolerate oral intake, r Continuous cardiopulmonary monitoring 2. Wolfsdorf J, Glaser N, Sperling MA. Diabetic
serum glucose is <200 mg/dL, and the ketoacidosis r Hourly vital signs, fluid input and output, neurologic ketoacidosis in infants, children, and adolescents. A
has resolved (pH >7.3, bicarbonate 18 mmol/L). consensus statement from the American Diabetes
exam for signs and symptoms of cerebral edema, Association. Diabetes Care. 2006;29(5):
Second Line serum glucose, and venous blood gas, especially 11501159.
r Potassium replacement: while receiving continuous insulin therapy
r Repeat serum electrolytes, magnesium, phosphorus, 3. Stewart C. Guidelines for the ED management of
Boluses are not recommended unless the patient
has an arrhythmia secondary to hypokalemia. and calcium q24h for the 1st 8 hr, then q4h.
pediatric diabetic ketoacidosis (DKA). Pediatr D
r The goals are to restore adequate perfusion to Emerg Med Practice. 2006;3(3):116.
Otherwise, give with the start of insulin therapy.
Patients with hyperkalemia should not receive 4. Rewers A, Klingensmith G, Davis C, et al. Presence
tissues and organs, correct dehydration and of diabetic ketoacidosis at diagnosis of diabetes
potassium until urine output has been electrolyte imbalances, improve the glomerular
documented. mellitus in youth: The Search for Diabetes in Youth
filtration rate, clear glucose and ketones from the Study. Pediatrics. 2008;121(5):e1258e1266.
r Phosphate replacement: blood, and avoid complications of treatment such as
Give in the form of potassium phosphate if the 5. Glaser N, Barnett P, McCaslin I, et al. Risk factors
cerebral edema.
level is <1 mg/dL. However, clinical benefit has for cerebral edema in children with diabetic
not been shown in prospective trials. If given, DIET ketoacidosis. N Engl J Med. 2001;344(4):264269.
r NPO during the initial resuscitation
monitor for hypocalcemia. r Diabetic diet (including counting calories):
r Bicarbonate has not been proven to be beneficial in
controlled trials: PO intake should coincide with transition from IV CODES
The use of bicarbonate may cause paradoxical to SC insulin.
CNS acidosis. PROGNOSIS ICD9
r 250.10 Diabetes mellitus with ketoacidosis type ii or
Bicarbonate use has been associated with the Mortality rate of DKA is 0.150.31%.
development of cerebral edema. unspecified type, not stated as uncontrolled
Rapid correction of acidosis results in hypokalemia COMPLICATIONS r 250.11 Diabetes mellitus with ketoacidosis, type I
r Cerebral edema:
and an increased sodium load and hypertonicity. (juvenile type) not stated as uncontrolled
Only give if the patient is severely acidotic, has Symptomatic cerebral edema occurs in 0.31%
cardiac dysfunction, and has life-threatening of all episodes of DKA.
hyperkalemia. Administer 12 mmol/kg cautiously Typically occurs 412 hr after the initiation of PEARLS AND PITFALLS
over 60 min. therapy but can present prior to treatment or
r Antibiotics as needed develop at any time during treatment r Misdiagnosis of gastroenteritis is a risk in children
The leading cause of DKA-related deaths not known to be diabetic whose presentation of
SURGERY/OTHER PROCEDURES Associated with a 2025% mortality rate DKA includes vomiting.
r Once cerebral edema is recognized, it must be Significant morbidity such as pituitary insufficiency r Cerebral edema is the leading cause of death in
treated promptly: in 1026% of patients DKA.
Mannitol 0.251 g/kg IV over 20 min or 3% Pathophysiology may be thought to be due to r The cause of cerebral edema is unknown, but it may
normal saline 510 mL/kg over 30 min cellular swelling; however, it may also be due to be associated with extreme acidosis, extreme
r Intubation to protect the airway and provide vasogenic (or extracellular) edema. hypocapnia, extreme BUN elevation or dehydration,
adequate ventilation: Risk factors include young age, new-onset T1DM, and overly rapid correction of hyperglycemia. There
Hyperventilation is associated with poorer longer duration of symptoms, and more profound may also be an association with the administration
neurologic outcomes. acidosis. of bicarbonate and the development of cerebral
Other factors include higher BUN on initial edema.
DISPOSITION presentation, more severe hypocapnia, and r Patients with T2DM can present in DKA.
Admission Criteria administration of bicarbonate.
r Admit all patients with new-onset T1DM and
Hyponatremia or the lack of a progressive increase
patients with previously diagnosed DM presenting in in sodium with a concomitant fall in glucose
DKA. increases the risk of cerebral edema.
r Critical care admission criteria: r Hypo- or hyperkalemia, arrhythmia, hypoglycemia,
Altered mental status infection, sepsis, ARDS, pulmonary edema,
Moderate to severe dehydration and acidosis (pH pneumomediastinum, CNS hematoma or
<7.2 or bicarbonate <10 mmol/L) thrombosis, and rhabdomyolysis
Specific criteria may be institution dependent,
including age <5 and the need for insulin
infusion.
Discharge Criteria
Patient with known T1DM:
r Ketoacidosis is minimal or resolved, patient is
tolerating oral intake, serum glucose is stable on SC
insulin, patient has adequate supplies, and close
follow-up is arranged
249
DIAPER RASH
Solomon Behar

BASICS r Overhydration of skin r Inflammatory conditions:
r Friction Irritant contact dermatitis
DESCRIPTION r Urine and feces Allergic contact dermatitis
r The most common dermatologic problem in infancy, r Microorganisms Seborrheic dermatitis
diaper rash is a group of inflammatory conditions Psoriasis
leading to red, macerated skin in the groin region. COMMONLY ASSOCIATED CONDITIONS Granuloma gluteale infantum (associated with the
r It is most commonly due to irritation or infection. r Diarrhea
use of high-potency topical steroids)
r Location of erythema, presence of bullae, scales, or r Thrush r Infectious conditions:
satellite lesions aid with distinguishing the Candidiasis
underlying cause. DIAGNOSIS Folliculitis
r Rarely, diaper rash can be a symptom of more Impetigo
serious illness. HISTORY Perianal streptococcal infection
Presence of erythema, pain, or itching in the diaper HSV infection
EPIDEMIOLOGY Scabies
region
Incidence Congenital syphilis
Variable due to regional differences in hygiene, diaper PHYSICAL EXAM r Nutritional (associated with failure to thrive):
r Irritant diaper dermatitis:
use, and toilet training Acrodermatitis enteropathica (zinc deficiency)
Redness, scaling of convex areas of skin
Prevalence Biotin deficiency
(mountain peaks) that come into contact with
Unknown, but widely acknowledged to be the most Kwashiorkor
the diaper
common dermatologic problem of infancy Cystic fibrosis
Usually spares skin folds r Malignancy:
RISK FACTORS r Candida diaper dermatitis:
r Infrequent diaper changing Langerhans cell histiocytosis (associated
Beefy erythema in intertriginous areas (valleys)
r Poor hygiene hepatosplenomegaly, lymphadenopathy,
with papular satellite lesions
r Diarrhea petechiae, erosions, vesicopustules, otorrhea)
May have oral thrush present r Miscellaneous:
r Recent antibiotic use r Bacterial diaper dermatitis: Bullae or impetiginous
Child abuse (immersion burn)
r Thrush lesions (honeycrust)
r Folliculitis: Small red papules and pustules on Kawasaki disease (fever, cervical
r Urinary tract abnormalities lymphadenopathy, conjunctivitis, strawberry
buttocks, thighs, and low abdomen tongue, extremity peeling or swelling)
GENERAL PREVENTION r Herpes simplex virus (HSV): Vesicles or bullae during
r Changing diapers frequently (q34h or ASAP when
1st few weeks of life progressing to punched-out
stool or urine is present) blisters TREATMENT
r Using barrier cream for skin protection (eg, zinc r Jacquet dermatitis: Severe erosions with
oxide, petrolatum) punched-out lesions INITIAL STABILIZATION/THERAPY
r Using nonocclusive diapers r Remove stool/urine-containing diapers.
r Using superabsorbent diapers DIAGNOSTIC TESTS & INTERPRETATION r Cleanse gently with warm water and mild soap with
r Avoiding cloth diapers Diagnostic Procedures/Other a cotton ball or rinse with a squeeze bottle.
r Avoiding scented wipes r If the diagnosis is in question, a skin scraping may r Remove adherent feces with cotton balls and
be performed, which will show pseudohyphae when mineral oil.
PATHOPHYSIOLOGY KOH prep is done in cases of Candida diaper
r Enzymes in stool break down skin dermatitis.
r Alterations in pH from stool and urine r Culture of bullae or lesions may yield a definitive
r Once skin integrity is interrupted from irritation, diagnosis.
fungi and bacteria may invade skin, leading to r In rare cases of refractory dermatitis with other
infection systemic symptoms (eg, chronic otorrhea,
hepatosplenomegaly), biopsy is needed (eg,
histiocytosis).
250
DIAPER RASH
MEDICATION r Railan D, Wilson JK, Feldman SR. Pediatricians who

First Line Issues for Referral prescribe clotrimazole-betamethasone dipropionate
r For fungal dermatitis: Refractory cases of diaper rash not responding to (Lotrisone) often utilize it in inappropriate settings
Topical antifungal: usual therapy should be referred to a dermatologist. regardless of their knowledge of the drugs potency.
Nystatin 100,000 U/g topical b.i.d. 714 days: Dermatol Online J. 2002;9:3.
Additional Therapies r Scheinfeld N. Diaper dermatitis: A review and brief
Cream used for most candidal rashes
Cornstarch powder applied topically to the diaper area
Powder may be used for rashes that are very survey of eruptions of the diaper area. Am J Clin
daily:
moist and macerated. r Helps reduce friction on skin Dermatol. 2005;6(5):273281.
Miconazole 2% cream or lotion topically b.i.d. r Spraker MK. Update: Diapers and diaper dermatitis.
r Useful for contact dermatitis associated with
714 days Pediatr Dermatol. 2000;17:7583.
Apply directly to skin every diaper change prolonged wetness
until clear for up to 7 days.
May add a layer of a barrier cream
FOLLOW-UP CODES
r For contact dermatitis:
Topical barrier paste, ointment or cream (eg, zinc FOLLOW-UP RECOMMENDATIONS ICD9
D
oxide, petrolatum, lanolin); liberally apply every Discharge instructions and medications: r 112.3 Candidiasis of skin and nails
diaper change. r Change diapers q34h, including 1 overnight diaper r 691.0 Diaper or napkin rash
Low-potency steroid cream (hydrocortisone 1%) change.
applied topically b.i.d. for max of 2 wk r Apply topical medication every diaper change until
Stomahesive powder (for severe cases refractory the rash resolves as noted above. PEARLS AND PITFALLS
to steroids/antifungals and barrier creams)
r For bacterial infections: Patient Monitoring r Avoid use of clotrimazole/betamethasone
Topical mupirocin 2% cream t.i.d. until clear for Follow up with the primary care provider in 12 days dipropionate (Lotrisone), a combination
up to 7 days to check healing of lesions. high-potency steroid and antifungal cream. The
Second Line COMPLICATIONS steroid component is too strong for use in infants
For contact dermatitis, may apply all of the following Bacterial superinfection, scarring from delayed and may lead to systemic symptoms of steroid
topically until rash is improved: therapy toxicity.
r Irritant diaper dermatitis present for >3 days usually
r Topical sucralfate
r 2% eosin (aqueous) has a component of Candida infection, even if the
r Topical cholestyramine ointment (in high stool
ADDITIONAL READING typical candidal appearance is not yet present. Treat
r Arad A, Mimouni D, Ben-Amitai D, et al. Efficacy of these cases with an antifungal cream.
output states) r Mupirocin has antifungal properties, so if treating a
topical application of eosin compared with zinc
DISPOSITION presumed bacterial infection, it may alleviate the
oxide paste and corticosteroid cream for diaper
Admission Criteria patient needing to apply an antifungal cream.
dermatitis. Dermatology. 1999;199:319322. r Avoid use of talcum or other powders near an
Diaper rashes generally do not result in hospital r Atherton DJ. The aetiology and management of
admission. infants face, as it is an aspiration risk.
irritant diaper dermatitis. J Eur Acad Dermatol r Do not use allylamine (terbenafine, naftifine) or
r Signs of Kawasaki disease or histiocytosis may Venereol. 2001;15(Suppl 1):14.
warrant admission. r Berg RW, Milligan MC, Straight FC. Association of thiocarbamates (tolnaftate) topical antifungals, as
r Systemic illness from bacterial or fungal sepsis in skin wetness and pH with diaper dermatitis. Pediatr
their activity against Candida albicans is limited.
premature or low-birth-weight infants may require Dermatol. 1994;11:1820.
admission. r De Wet PM, Rode H, van Dyk A. Perianal candiosis:
Discharge Criteria A comparative study with mupirocin and nystatin.
Most diaper rash cases can be discharged safely to Int J Dermatol. 1999;38:618622.
home. r Gupta AK, Skinner AR. Management of diaper
dermatitis. Int J Dermatol. 2004;43:830834.
251
DIARRHEA
Caroline Altergott
r Acute infectiousbacterial:
BASICS Salmonella: Initially fever (<48 hr), abdominal DIAGNOSIS
pain, and green mucoid stool may have blood.
DESCRIPTION Associated with poultry, livestock, and reptiles or HISTORY
r Diarrhea is an alteration in the normal bowel r Focus on signs of dehydration and symptoms of
ingestion of unsafe food. Increased invasive
pattern characterized by increase in water content, disease in children with diarrhea.
volume, or frequency of stools. r Dehydration: Tears, urine output, sticky saliva,
hemoglobinopathies/immune deficiency
r Can be acute (14 days), persistent (>14 and Shigella: 40 serotypes, Shigella sonnei most activity level
<30 days) or chronic (>30 days) common in the U.S. Range: Mild to severe. r Stool symptoms:
Abdominal cramps; high fever; and watery, green Color, consistency, volume, and number
EPIDEMIOLOGY Quantity of associated blood or mucus
diarrhea. 40% with bloody stools. Usually resolves
Incidence in 72 hr. Occasionally is associated with seizures Onset (acute, persistent, chronic)
r 2.6 episodes of diarrhea per year per child <5 yr r Travel history
and hemolytic uremic syndrome (HUS).
r Increased rate in children attending day care r Medications
Campylobacter: Watery diarrhea with abdominal
RISK FACTORS pain and fever; 2/3 with gross blood in stool; r Changes in diet or food intake
Infectious diarrhea: sometimes confused with appendicitis; r Associated symptoms:
r Travel to developing area immunoreactive complications (arthritis, erythema Vomiting (onset, frequency, quantity, quality)
r Ingestion of unsafe foods (raw meats, eggs, nodosum, Guillain-Barre). Abdominal pain (onset, location, degree,
Yersinia enterocolitica: Watery diarrhea usually consistency)
shellfish, unpasteurized milk or juices) mild and self-limited but can also be bloody. Older
r Swimming/Drinking untreated fresh water Systemic signs:
children can have mesenteric adenitis or Rashes, arthralgias with chronic diarrhea:
r Contact with animals known to be carriers
pseudoappendicitis syndrome. Consider IBD.
r Day care or residential facility Clostridium difficile: Pseudomembranous colitis. Dysuria, frequency, urgency: Consider urinary
r Recent antibiotic use Bloody diarrhea is associated with antibiotic use. tract infection.
r Contact with other infected individuals Escherichia coli: Altered sensorium: Severe dehydration or
Enteropathogenic (EPEC): Infantile diarrhea
GENERAL PREVENTION intussusception
Enterotoxigenic (ETEC): Travelers diarrhea
r Hand washing: The most important preventative
Enteroinvasive (EIEC): Similar to Shigella PHYSICAL EXAM
measure Enterohemorrhagic (EHEC 0157:H7): Bloody r Current and previous weight
r Rotavirus vaccine r Elevated temperature: Suspect infectious
diarrhea associated with HUS
r Typhoid vaccine: If traveling to endemic areas Vibrio cholera: Painless, voluminous diarrhea r Assess perfusion: Capillary refill, skin color, and
PATHOPHYSIOLOGY without abdominal cramps or fever. It is warm vs. cold extremities may be helpful.
r Fluid output overwhelms the absorptive capacity of associated with travel to or ingestion of food from r Tachycardia, poor skin turgor and dry mucous
the intestines. Latin America or Asia or eating raw or uncooked membranes indicate severe dehydration:
r Multifactorial: shellfish in Gulf Coast states. Skin turgor may be doughy with hypernatremia
r Parasitic: and therefore a poor marker of degree of
Secretory: Enterotoxins increase the secretion of
fluids and electrolytes from the mucosa. Entamoeba histolytica: Chronic episodic diarrhea; dehydration.
may have constipation episodes r Abdominal exam:
Osmotic: Increase in osmotic load to the bowel
lumen causes increased influx of water to the Giardia: Explosive, watery, foul-smelling stool Mass in the right upper quadrant: Intussusception
bowel lumen. Cryptosporidiosis: Immune-deficient patients with Right lower quadrant pain: Appendicitis
Inflammatory: Decreased absorption in the colon nonbloody diarrhea and abdominal pain Distension, rebound, and guarding: Peritonitis
r Malabsorption: Rectal exam for acute diarrhea:
from direct injury of the mucosa
Food allergy: Milk and soy most common Presence of blood: Food allergy or infection
ETIOLOGY Lactose deficiency: Congenital or acquired (usually Current jelly stools: Intussusception
r Acute Infectious: Viral (7080% of all infectious
after acute enteritis) Mucus in stools: Infection
diarrhea): Antibiotic use Rectal exam for chronic diarrhea:
Rotavirus: Vomiting and low-grade fever precedes Celiac disease: Intolerance to wheat gluten; Anal fistulas: Crohn disease
watery diarrhea; usually affects children 315 mo; failure to thrive with intermittent diarrhea Hard stool in vault: Overflow encopresis
26 day duration; more prevalent in winter Cystic fibrosis: Foamy, bulky, foul-smelling stools Empty vault: Hirschsprung disease
Norwalk: 12 day illness with explosive vomiting, Inflammatory bowel disease (IBD): Ulcerative
watery diarrhea, abdominal pain, and fever; colitis or Crohn disease DIAGNOSTIC TESTS & INTERPRETATION
school age; more prevalent in winter r Structural: Lab
Enterovirus: Fever and vomiting with diarrhea Intussusception Most patients with acute, nonbloody diarrhea, who
lasting days to weeks; more prevalent in summer Hirschsprung disease are well appearing and not dehydrated do not require
Encopresis: Overflow stool past obstruction any lab testing.
Short bowel syndrome
Overfeeding: Common in neonates
r Miscellaneous:
Toxins: Laxative abuse in adolescence
HUS: Several days of diarrhea followed by bloody
stools, hemolysis, and renal insufficiency
252
DIARRHEA
Initial Lab Tests DISPOSITION COMPLICATIONS

r Severe dehydration: Serum electrolytes r Dehydration
Admission Criteria
r Suspected bacteremia/immune-compromised r Critical care admission criteria: r Electrolyte abnormalities
patients: CBC and blood culture Shock refractory to 60 cc/kg IV fluids over 1 hr r Shock from hypovolemia or sepsis
r Consider selectively: Altered mental status r HUS
Standard stool cultures (Salmonella, Shigella, r Inpatient admission criteria:
Campylobacter, and Yersinia species) for acute >1015% dehydration or inability to replace
inflammatory diarrhea, for food handlers, for ongoing losses while in the emergency department ADDITIONAL READING
institutionalized patients, and for those in day care Significant electrolyte abnormalities ( sodium, r Fleisher GR. Diarrhea. In Fleisher GR, Ludwig S, eds.
E. coli 0157:H7 for acute grossly bloody diarrhea sodium, potassium)
or HUS Severe anemia (secondary to hematochezia) Textbook of Pediatric Emergency Medicine. 6th ed.
r C. difficile toxin for diarrhea associated with Acute abdomen: Intussusception, appendicitis Philadelphia, PA: Lippincott Williams & Wilkins;
2010.
antibiotic use Discharge Criteria r Guerrant RL, Van Gilder T, Steiner TS, et al.
r Vibrio parahaemolyticus for those with recent r Corrected dehydration (eg, moist mucous
shellfish ingestion membranes, adequate urine output)
Infectious Diseases Society of America. Practice D
r Testing stool for WBCs in young infants at risk for guidelines for the management of infectious
r Normal mental status
diarrhea. Clin Infect Dis. 2001;32:331351.
Salmonella: r Minimal to absent electrolyte abnormalities r King CK, Glass R, Bresee JS, et al. Managing acute
If positive, send standard stool culture. r Minimal to absent ongoing blood loss gastroenteritis among children. MMWR Recomm
r Testing for ova and parasites, and Giardia lamblia r Caregiver can follow through on appropriate oral Rep. 2003;52(RR-16):116.
antigen testing for chronic diarrhea, travelers, and rehydration therapy r Mann CH. Vomiting and diarrhea. In Barren J,
those in endemic areas
Issues for Referral Rothrock S, Brennan JA, Brown L, eds. Pediatric
Imaging Chronic diarrhea Emergency Medicine. Philadelphia, PA: Saunders;
r Usually not necessary for diarrhea 2008:567575.
r For intussusception, consider a contrast enema (may Additional Therapies r Ramaswamy K, Jacobson K. Infectious diarrhea in
r Controversial efficacy:
therapeutically reduce) or US if indeterminate. children. Gastroenterol Clin North Am.
Lactobacillus 2001;30:611624.
DIFFERENTIAL DIAGNOSIS Absorbents
See Etiology. Zinc supplements
r Not recommended because of significant side
CODES
effects:
TREATMENT Loperamide
Bismuth sulfate ICD9
PRE HOSPITAL r 008.8 Intestinal infection due to other organism, not
r Assess and address the airway, breathing, and
elsewhere classified
circulation. FOLLOW-UP r 009.2 Infectious diarrhea
r Supplement with a balanced commercially available r 787.91 Diarrhea
electrolyte solution. FOLLOW-UP RECOMMENDATIONS
r IV fluid resuscitation for those with severe Discharge instructions and medications:
r Follow-up within 24 hr for moderate to severe
dehydration PEARLS AND PITFALLS
dehydration with patients who meet discharge
INITIAL STABILIZATION/THERAPY criteria. r Changes in BP are a late sign of significant
r Treat dehydration appropriately. Refer to
r Return for worsening dehydration ( urine output, dehydration.
Dehydration topic for specific therapy. r Assess serum glucose immediately in children with
r Other than treatment of dehydration or electrolyte tears, dry mucous membranes, lethargy), blood
to stool, and abdominal pain. depressed mental status and diarrhea.
imbalance, no specific therapy is initially required. r Consider intussusception in a child with diarrhea
DIET
MEDICATION r Commercially available balanced oral rehydration and lethargy.
Use antibiotics, if indicated. However, most infectious solution for ongoing losses
diarrhea resolves without intervention, and antibiotic r Homemade solutions (rice water) are often
treatment may be harmful. See the Gastroenteritis
improperly balanced.
topic for specific antibiotic therapy recommendations. r Restricting to clear liquids alone has no benefit.
r Breast-fed infants should continue feeding;
formula-fed infants should resume their usual
formula upon rehydration.
r Older children should receive semisolid or solid
foods low in simple sugars.
253
DIGOXIN TOXICITY
Amit K. Gupta
Mark Su
r Digoxin increases automaticity and shortens the r Serum electrolytes, magnesium, BUN, creatinine,
BASICS repolarization intervals of the atria and ventricles. glucose
r Virtually any type of dysrhythmia can occur with r Serum potassium is prognostic for dysrhythmia
DESCRIPTION toxicity, with the exception of the rapidly conduced (potassium >5.0 mEq/L).
r Digoxin is the most commonly prescribed r Assess acetaminophen and salicylate levels if
supraventricular tachydysrhythmias.
cardioactive steroid in the U.S. r Hypokalemia inhibits Na+ K+ ATPase activity and suicidal ingestion.
r Other internationally available preparations include r Urine drug screen usually is not indicated unless for
contributes to the toxicity induced by digoxin.
digitoxin, ouabain, lanatoside C, deslanoside, and r Hypomagnesemia also inhibits Na+ K+ ATPase forensic purposes such as suspected malicious intent
gitalin. activity and may result in refractory hypokalemia. or child abuse.
r Most cases of digoxin toxicity are seen in adults;
however, there is still a concern in children due to ETIOLOGY Imaging
The main causes of digoxin toxicity in the pediatric r A CT of the brain should be considered in individuals
the narrow therapeutic index and wide availability.
r Toxicity can be acute or chronic. population are: with altered mentation.
r Erroneous dosing in infants, which is usually r CXR may be performed to assess for pulmonary
r Plant sources of cardioactive steroids include
parenteral and frequently severe edema.
oleander (Nerium oleander), yellow oleander
r Unintentional ingestion in younger children Diagnostic Procedures/Other
(Thevetin peruviana), foxglove (Digitalis species), lily
r Intentional ingestion in older children and young r ECG should be performed. Sinus bradycardia and
of the valley (Convallaria maritime), dogbane
(Apocynum cannabinum), and red squill (Urginea adults, which may be the result of a suicidal attempt 1st-degree or 2nd-degree atrioventricular blocks are
maritime). more common in pediatric patients than in adults,
r Animal sources of cardioactive steroids include the COMMONLY ASSOCIATED CONDITIONS whereas ventricular ectopy is more common in
Congenital heart disease, CHF, cardiac dysrhythmia adults.
cane toad (Bufo marinus); toxicity from ingestion,
r Bidirectional ventricular tachycardia is virtually
instead of intended topical application, of a
purported aphrodisiac derived from the dried DIAGNOSIS pathognomonic for digoxin toxicity.
r Suspect digoxin toxicity with increased automaticity
secretion of this toad has been reported.
HISTORY and depressed conduction.
EPIDEMIOLOGY r Obtain history of exposure, other possible
Incidence coingestants, and events that led to exposure. DIFFERENTIAL DIAGNOSIS
r Ingestion of digoxin is often difficult to establish, r The peak effect with PO dosing is 26 hr, and that r Calcium channel blocker toxicity
and precise numbers of exposure are unknown. r Beta-blocker toxicity
with IV dosing is 530 min.
r The overall mortality rate and rate of response to r Ask parents to bring in pill bottles if possible. r Clonidine toxicity
Fab therapy in children are similar to those in adults. r Nausea and vomiting are common. r Cardiogenic shock
The mortality rate as a direct result of cardiac toxicity r Lethargy or weakness may occur. r Hemorrhagic shock
is 321%. r Visual disturbances can occur: Aberrations of color r Septic shock
r Gastroenteritis
RISK FACTORS vision, such as yellow halos around lights, scotoma,
Coingestants with other cardiotoxic agents such as blurry vision, or decreased visual acuity. r Acute MI
calcium channel blockers, beta-blockers, cyclic
antidepressants, and neuroleptics may exacerbate PHYSICAL EXAM
r Assess vital signs, with attention to cardiovascular TREATMENT
toxicity.
stability.
GENERAL PREVENTION r GI symptoms include anorexia, nausea, vomiting, PRE HOSPITAL
Poison-proofing homes and giving parents poison r Assess and stabilize airway, breathing, and
and nonspecific abdominal pain.
prevention advice is the most effective way to prevent r Lethargy, confusion, and weakness may occur with circulation.
exposure in children. r Supplemental oxygen
acute or chronic toxicity.
r Cardiovascular effects may include bradycardia. r Establishment of an IV line with cardiac monitoring
PATHOPHYSIOLOGY
r Digoxin inhibits sodium-activated and
DIAGNOSTIC TESTS & INTERPRETATION INITIAL STABILIZATION/THERAPY
potassium-activated adenosine triphosphatase r Activated charcoal (1 g/kg) may be given if the
(Na+ K+ ATPase) pump during repolarization. The Lab
Initial Lab Tests patient is protecting the airway.
result is an increase in the intracellular sodium and r Immediately assess capillary blood glucose. r Because of the enterohepatic circulation of digoxin,
calcium concentrations and a decrease in the r Digoxin level: Normal therapeutic range is 0.52.0 multiple-dose charcoal (1 g/kg/day) may be
intracellular potassium concentration. beneficial.
r Improved inotropy is due to an increased ng/mL. Always assure units reported are correct: r Syrup of ipecac is contraindicated.
concentration of cytosolic calcium ions during A 6-hr level postingestion is also recommended
systole, which increases the force of contraction of and is more representative of a postdistribution
the cardiac muscle. concentration.
r Hyperkalemia can occur with acute toxicity due to A digoxin level may be falsely elevated after
digoxin Fab fragment administration.
increased extracellular concentration.
r Digitalis also has a negative chronotropic action,
which is due to the vagal effect on the sinoatrial
node.
254
DIGOXIN TOXICITY
MEDICATION DISPOSITION r Bismuth C, Gaultier M, Conso F, et al. Hyperkalemia

First Line Admission Criteria in acute digitalis poisoning: Prognostic significance
r Atropine 0.02 mg/kg IV (min dose 0.1 mg and max r Consider hospital admission of any patient with a and therapeutic implications. Clin Toxicol. 1973;6:
2 mg) for bradycardia: history of a large ingested dose, especially if 153162.
Atropine may be effective due to enhanced vagal coexisting risk factors increase the patients r Bower JO, Mengle HAK. The additive effects of
tone with digoxin. susceptibility to digoxin toxicity. calcium and digitalis: A warning, with a report of 2
r Digoxin immune Fab fragments are the treatment of r Critical care admission criteria: deaths. JAMA. 1936;106:11511153.
choice for digoxin toxicity: Patients with signs of hemodynamic instability r Hack JB, Lewin NA. Cardioactive Steroids. In
Indications for administration are any potential should be admitted to an ICU setting. Goldfrank LR, Flomenbaum NE, Lewin NA, et al.,
digoxin-related life-threatening dysrhythmia, renal eds. Goldfranks Toxicologic Emergencies. 8th ed.
Discharge Criteria
failure, potassium concentration >5.0 mEq/L in May discharge if the patient remains asymptomatic
Stamford, CT: Appleton & Lange; 2006:971982.
the setting of acute overdose, digoxin serum r Taboulet P, Baud FJ, Bismuth C, et al. Acute digitalis
after observation for 12 hr
concentration 15 ng/mL at any time or intoxication: Is pacing still appropriate? Clin Toxicol.
>10 ng/mL 6 hr post-ingestion.
Digoxin immune Fab fragments may also be FOLLOW-UP
1993;31:261273.
D
beneficial in poisoning by nondigoxin cardioactive
steroid (plant or animal sources). FOLLOW-UP RECOMMENDATIONS Media Element)
r Discharge instructions and medications: r Beta-Blocker Poisoning
1 vial of Digibind neutralizes 0.5 mg of digoxin. r Calcium Channel Blocker Poisoning
Number of vials for digoxin Fab dosing is Follow up with the primary pediatrician.
Return to the emergency department for change r Cardiogenic Shock
calculated using the following equation:
No. of vials = [serum digoxin level (ng/mL) in behavior, alteration in mental status, or if ill r Dysrhythmia, Atrial
patients weight (kg)] 100 appearing. r Dysrhythmia, Ventricular
r Activity:
Empiric therapy for acute poisoning is 1020 vials.
Empiric therapy for chronic poisoning is 24 vials. Normal activity after discharge
r Magnesium and potassium should be supplemented Patient Monitoring CODES
if serum concentrations are low. Patients with intentional overdoses should be
r Calcium administration is contraindicated since this monitored for acts of self-harm. ICD9
may lead to excessive intracellular calcium and PROGNOSIS 972.1 Poisoning by cardiotonic glycosides and drugs
cardiac tetany (stone heart). It is safe to The prognosis is usually good if the diagnosis is of similar action
administer after digoxin Fab fragments have been recognized and digoxin Fab fragments are
given. administered.
Second Line PEARLS AND PITFALLS
In the event that digoxin Fab fragments are not
COMPLICATIONS r Digoxin exerts its ionotropic effects by inhibiting the
r Hyperkalemia
available, the secondary drugs for the management of r Dysrhythmia Na+ K+ ATPase pump during repolarization.
ventricular irritability include IV phenytoin
r Cardiogenic shock r Suspect digoxin toxicity with increased cardiac
(1520 mg/kg, rate <50 mg/min) or IV lidocaine
(1.5 mg/kg). r Death automaticity and depressed conduction.
r A 6-hr post-ingestion digoxin level is more indicative
COMPLEMENTARY & ALTERNATIVE of a post-distribution concentration.
THERAPIES ADDITIONAL READING r The most clinically useful indication for digoxin
r External or transvenous pacing has a limited role for immune FAB fragments is any potentially
r Antman EM, Wenger TL, Butler VP, et al. Treatment
digoxin toxicity since digoxin-specific Fab antibodies life-threatening digoxin-related dysrhythmia.
are widely available. of 150 cases of life-threatening digitalis intoxication
r Transvenous pacing may increase the risk of with digoxin-specific Fab antibody fragments. Final
initiating cardiac dysrhythmias and should be report of a multicenter study. Circulation. 1990;81:
avoided. 17441752.
r Cardiac defibrillation should be reserved for
hemodynamically unstable ventricular tachycardia or
ventricular fibrillation.
255
DIPHTHERIA
James M. Wu
Craig A. McElderry
ETIOLOGY Imaging
BASICS r C. diphtheriae: Gram-positive, aerobic pleomorphic Consider chest radiograph to evaluate for diphtheria
bacillus pneumonia, if indicated depending on the clinical
DESCRIPTION r 4 main toxin-producing strains with slight assessment.
r Diphtheria is an upper respiratory tract illness
differences in growth characteristics and toxin Pathological Findings
characterized by sore throat, low-grade fever, and production: Microscopy of the pseudomembrane will reveal fibrin
an adherent pseudomembrane of the nasopharynx, C. diphtheriae gravis: exudates, neutrophils, and colonies of C. diphtheriae.
oropharynx, and/or larynx. Most rapid growth rate
r Diphtheria can also present as primary cutaneous Most rapid and copious toxin production DIFFERENTIAL DIAGNOSIS
r Respiratory diphtheria: Most of the following can be
disease and, less commonly, vaginal, conjunctival, C. diphtheriae intermedius
and otic disease. C. diphtheriae mitis ruled out with a good clinical history of incomplete
r Disease is caused by Corynebacterium diphtheriae, a C. diphtheriae belfanti immunizations and physical exam findings of
gram-positive, aerobic, pleomorphic bacillus. gray-brown adherent membrane in nasopharynx or
oropharynx:
EPIDEMIOLOGY DIAGNOSIS Exudative pharyngitis (group A beta-hemolytic
Incidence streptococcus, Epstein-Barr virus)
r 05 cases per year in the U.S. HISTORY Acute necrotizing ulcerative gingivitis (Trench
r 0.001 cases per 100,000 in the U.S. since 1980 (1): r Respiratory diphtheria:
mouth, Vincent angina)
No data on cutaneous diphtheria, as it is not Low-grade fever Epiglottitis
reportable Sore throat Herpes simplex virus (HSV)
r Endemic in other countries where the population is Malaise Mucositis
not completely immunized: Serosanguinous nasal discharge Thrush
Recent epidemics in independent nations of the Difficulty swallowing r Cutaneous diphtheria: Lesions are relatively
former Soviet Union Respiratory distress nonspecific, and thus the differential diagnosis may
r Cutaneous diphtheria:
include a broad range of dermatologic diseases:
RISK FACTORS Generally lower extremity lesions Streptococcal or staphylococcal impetigo
Unimmunized or incompletely immunized children or History of skin lesions (eg, eczema, dermatitis), Ecthyma
adults trauma, or bruising Cutaneous TB
GENERAL PREVENTION Pain, tenderness with subsequent anesthesia Pyoderma gangrenosum
r Maintain up-to-date immunizations: (25 wk after infection) Insect bites
Immunization estimated efficacy is 97%. Erythema
Immunized patients have milder disease, but Initial vesicle or pustule with subsequent
immunization does not prevent asymptomatic ulceration and membrane formation TREATMENT
carriage of C. diphtheriae. PHYSICAL EXAM MEDICATION
r Avoid skin contact with cutaneous lesions. r Respiratory diphtheria:
Diphtheria is best treated using a 2-pronged approach
r Avoid contact with respiratory secretions. White to gray-brown membrane in nasopharynx, with antitoxin and antimicrobials (3).
r Avoid travel to endemic areas. oropharynx, tonsils, and/or larynx
r Prevention may be difficult due to asymptomatic Scraping of membrane causes bleeding. First Line
r Antitoxinneutralization of toxins and prevention
carriers. Serosanguineous nasal discharge
Cervical lymphadenitis, soft tissue swelling (bull of secondary effects:
PATHOPHYSIOLOGY neck) Available via the CDC
r Humans are the sole reservoir of C. diphtheriae. Administer as early as possible without waiting for
Low-grade fever
r Organisms are spread via respiratory droplets, direct bacteriologic confirmation.
Tachycardia
contact, and occasionally fomites. Airway obstruction Test for sensitivity to horse serum via cutaneous
r Incubation period is 27 days (2). r Cutaneous diphtheria: and then intradermal testing prior to
r C. diphtheriae colonizes, proliferates, and invades Ulceration with sharply demarcated borders
administration.
Desensitize if patient reacts.
superficial local tissues of the throat and produces Peripheral edema, erythema
Dosage is severity dependent:
exotoxins in low iron conditions. White to gray-brown membrane Cutaneous disease: 2040,000 units IV/IM 1
r Exotoxin causes local necrotic injury of epithelial
DIAGNOSTIC TESTS & INTERPRETATION Pharyngeal/Laryngeal disease <48 hr:
cells by irreversibly inhibiting protein synthesis. 2040,000 units IV/IM 1
r Pseudomembraneswhite to gray-brown adherent Lab
r Culture and PCR of specimens from nose, throat, or Nasopharyngeal disease: 4060,000 units IV/IM
membranes consisting of blood plasma, fibrin, 1
other mucosal or cutaneous lesions
epithelial cells, leukocytes, erythrocytes and r Culture on cystine-tellurite blood agar or modified Extensive disease 3 days or diffuse neck
C. diphtheriae cellsform at the areas of injury. swelling: 80120,000 units IV 1
r Toxin is absorbed and disseminated via lymph and Tinsdale agar
r If C. diphtheriae recovered, test for toxigenicity (Elek
blood, causing degenerative changes to tissues
including heart muscle, nerves, liver, kidneys, and test).
r May measure serum antibodies to diphtheria toxin
adrenals.
r Organisms are present in nasopharyngeal and r Other, if positive test results:
oropharyngeal secretions and skin lesions for Refer close patient contacts for culture and
26 wk after infection (3). treatment with empiric antibiotics.
256
DIPHTHERIA
r Antimicrobialdestruction of organisms: COMPLICATIONS r CDC. Diphtheria. Epidemiology and Prevention of

Erythromycin 4050 mg/kg/day PO or IV divided Most commonly seen complications are cardiac and Vaccine-Preventable Diseases. The Pink Book:
t.i.d. or q.i.d.: neurologic: Course Textbook. 11th ed. Atlanta, GA: Author;
For 14 days for respiratory r Myocarditis, dysrhythmias, cardiac failure: 2009. Available at http://www.cdc.gov/vaccines/
For 10 days for cutaneous 240 days after onset of pharyngitis pubs/pinkbook/downloads/dip.pdf.
Penicillin G 100,000150,000 units/kg/day q6h Poorer prognosis with earlier onset of myocarditis r Norton SA. Chapter 183: Miscellaneous bacterial
IM or IV: r Polyneuropathy: infections with cutaneous manifestations. In Wolff
For 14 days for respiratory K, Goldsmith LA, Katz SI, et al., eds. Fitzpatricks
Paralysis of soft palate, eye muscles, limbs,
For 10 days for cutaneous Dermatology in General Medicine. 7th ed.
diaphragm
Referral for prophylaxis of close contacts: 18 wk after onset of pharyngitis Columbus, OH: McGraw-Hill; 2008. Available at
Erythromycin PO 4050 mg/kg per day for http://www.accessmedicine.com/content.
Usually resolves completely
10 days OR r Renal failure aspx?aID=2995332.
Penicillin G benzathine IM 600,000 units r Pneumonia r Ogle JW, Anderson MS. Chapter 40: Infections:
(<30 kg) and 1.2 million units (>30 kg) Bacterial & spirochetal. In Hay WW Jr., Levin MJ,
Second Line Sondheimer JM, et al., eds. CURRENT Diagnosis & D
Immunization: REFERENCES Treatment: Pediatrics. 19th ed. Columbus, OH:
r Immunize with diphtheria toxoid containing vaccine McGraw-Hill; 2009. Available at http://www.
1. CDC. Diphtheria. Available at http://www.cdc.gov/ accessmedicine.com/content.aspx?aID=3410745.
after resolution of disease, as disease does not r Todar K. Diphtheria. Todars Online Textbook of
ncidod/dbmd/diseaseinfo/diptheria t.htm. Accessed
necessarily confer immunity.
r Refer close contacts for immunization if not fully January 13, 2010. Bacteriology. Available at http://www.
2. CDC. Travelers HealthYellow Book. Available at textbookofbacteriology.net/diphtheria.html.
immunized or if no booster has been received within
http://www.nc.cdc.gov/travel/yellowbook/2010/
5 yr.
chapter-2/diphtheria.aspx. Accessed January 13,
DISPOSITION 2010. CODES
Admission Criteria 3. American Academy of Pediatrics. Red Book: 2009
r Admit all patients with suspected diphtheria for Report of the Committee on Infectious Diseases. ICD9
antitoxin treatment, antimicrobial treatment, and 28th ed. Elk Grove Village, IL: Author; 2009:280. r 032.1 Nasopharyngeal diphtheria
observation for secondary complications. 4. Hadfield TL, McEvoy P, Polotsky Y, et al. The r 032.2 Anterior nasal diphtheria
r Observe contact and respiratory precautions. pathology of diphtheria. J Infect Dis. 2000;181: r 032.9 Diphtheria, unspecified
S116S120.
5. Tiwari T, Clark T. Use of Diphtheria Antitoxin (DAT)
FOLLOW-UP for Suspected Diphtheria Cases. Available at
http://www.cdc.gov/vaccines/vpd-vac/diphtheria/
PEARLS AND PITFALLS
FOLLOW-UP RECOMMENDATIONS r Clinical diagnosis based on:
dat/downloads/protocol 032504.rtf. Accessed
The test of cure 24 hr after antibiotic treatment has
January 13, 2010. History of incomplete immunization
been completed is having 2 negative cultures collected
24 hr apart. Travel to or contact with travelers from endemic
areas
PROGNOSIS ADDITIONAL READING Physical findings of nasopharyngeal,
r Majority of cases resolve with treatment.
r Buescher ES. Diphtheria (Corynebacterium oropharyngeal, and laryngeal pseudomembrane
r Respiratory diphtheria has a 510% case fatality r Antitoxin should be given as early as possible.
diphtheriae). In Kliegman RM, Behrman RE, Jenson
rate (2). r The best way to prevent diphtheria is to maintain
r Primary causes of death are airway obstruction and HB, et al., eds. Nelson Textbook of Pediatrics. 18th
ed. Philadelphia PA: WB Saunders; 2007. proper and complete immunization of patients.
asphyxiation secondary to pseudomembrane
detachment and myocarditis.
257
DISCITIS
Katherine Remick

BASICS r Etiology in children is controversial, although Diagnosis of discitis requires a high index of suspicion.
infectious etiologies must be considered. Lab
DESCRIPTION r Discitis may be due to Staphylococcus aureus in up
r Discitis is infection or inflammation of the Initial Lab Tests
to 60% of cases, but a number of bacteria have The following tests, though nonspecific, should be
intervertebral disc leading to narrowing of the disc been implicated (1,4). considered in patients suspected of having discitis:
space (15). r Cultures from disc space biopsies are positive in
r Infection may extend to or from the adjacent CBC with differential, ESR, C-reactive protein (CRP),
<40% of samples (1). PPD testing, and blood cultures (especially if the
vertebral end plates. r Rare etiologies may include malignancy and patient is febrile):
r It is usually localized to the lumbar region but may
nonstaphylococcal pyogenic infections from r WBC counts are often in the high-normal range.
affect any disc in the thoracic, lumbar, or sacral Streptococcus pneumoniae and Salmonella species r ESR is usually moderately elevated but can be
spine (1,2). as well as TB, fungal infections, and brucellosis
r Discitis is uncommon, and in some cases it may be a normal; mean 42 mm/hr (range 485 mm/hr) (2).
(4,6,8). r CRP is normal in >60% of patients (1).
self-resolving low-grade infection that is r Blood cultures are negative in >80% of patients
underdiagnosed. COMMONLY ASSOCIATED CONDITIONS
r Preceding or concomitant infections such as
r Most commonly affects children <5 yr with a 2nd with isolated discitis (2).
respiratory illness, urinary tract infection, or otitis
smaller peak in early adolescence (2,3) Imaging
media (5) r Plain radiographs:
RISK FACTORS r History of trauma or surgery
r Bacteremia r Vertebral osteomyelitis Disc space narrowing may be seen as early as
r Recent sore throat or upper respiratory tract 12 wk after the onset of symptoms.
Irregularity of the adjacent vertebral end plates is
infection usually not identified until 34 wk after the onset
r Spinal surgery DIAGNOSIS of symptoms (3).
r Trauma r Technetium 99m bone scintigraphy:
r Vertebral osteomyelitis HISTORY
r The onset of discitis is usually insidious, with subtle High sensitivity but low specificity for detecting
PATHOPHYSIOLOGY findings often leading to delay in diagnosis from the discitis (7)
r Trauma, inflammation, and infection have all been onset of symptoms. Changes may be seen as early as 35 days after
r Diagnosis is often delayed until 46 wk after the the onset of symptoms (1,4).
attributed as the etiology of the disease process.
Most authors, however, attribute discitis to onset of symptoms (5,7). Helpful in localizing the affected spinal level(s)
infectious causes (13). r Children present with a variety of symptoms that when the history or physical exam fails to do so (4)
r Disc space infections are caused most commonly by often mimic other disease processes such as If characteristic findings are present, the addition
meningitis, abdominal pathology, or septic arthritis. of plain radiographs is sufficient to make the
hematogenous spread and rarely result from direct
extension (eg, vertebral osteomyelitis) or direct r Diagnosis can be challenging, especially in younger diagnosis (4).
r MRI with gadolinium enhancement:
inoculation (eg, postoperative discitis). children who are unable to provide an accurate
r Pediatric patients are at higher risk of developing history. The gold standard with the ability to differentiate
disc space infections due to the large network of r Symptoms in toddlers often differ from those in discitis from vertebral osteomyelitis, paraspinal
older children (6): abscess, tumors, or other inflammatory conditions
blood vessels that traverse the vertebral end plate
The most common symptoms in toddlers include (2,3,9)
between the vertebral body and the intervertebral
refusal to walk, limp, refusal to bear weight, More sensitive than CT scan, which may only
disc (3,4).
r These blood vessels terminate at the intervertebral abdominal pain, neck pain, irritability, nausea, demonstrate erosion of the vertebral end plates
and vomiting. due to poor soft tissue enhancement
disc. Thus, relative to the adjacent vertebral body, Recommended in children who fail to show
the disc is an avascular space with a limited immune r The most common symptoms in older children
improvement after 23 days of IV antibiotic
response creating a safe haven for bacteria (4,6). include back pain and neck pain or neck stiffness.
r Proliferation of bacteria within the disc space leads r It is important to remember that children may therapy
Recommended as primary imaging modality if:
to degradation of the annulus fibrosis and, present with nonspecific symptoms such as Thoracic spine is involved due to difficulty
subsequently, narrowing of the disc space, as is excessive crying, irritability, or fever. interpreting plain radiographs in this region OR
evident on plain radiographs (4). In children with >7 days of refusal to walk
r In addition, the hyaline cartilage covering the end PHYSICAL EXAM
r Afebrile or low-grade to moderate fever. Recommended in any child with concurrent
plates may become eroded, resulting in destruction r Refusal to bear weight sometimes including refusal neurologic deficits or meningeal signs
and the characteristic saw tooth appearance of
to sit or pain on crawling Diagnostic Procedures/Other
the vertebral end plates (4). r Inability or refusal to flex spine
r Such erosion eventually leads to increased blood The following may be considered as part of the
r Loss of lumbar lordosis inpatient or outpatient evaluation:
flow to the site of infection, which results in either r Gibbus deformity (sharp structural kyphosis in an r Biopsies are not recommended in children due to
resolution of the infection secondary to increased
host defense or progression of the infection to area of vertebral body collapse) the low yield of positive cultures (3560%) and high
r Tenderness to palpation upon palpation of adjacent risk of complications (4,5).
adjacent areas (eg, vertebral osteomyelitis or
spinous processes r Biopsies should be reserved for patients with known
paraspinal abscess) (4).
r In contrast to adults, infants and young children r Toddlers may be unable to localize the spinal level. immunodeficiency states or a lack of response to
have a large network of anastomoses between the r Limp antibiotic therapy (1,4,7).
r Poorly localized hip or leg pain r If indicated, CT-guided needle biopsy is
intraosseous arteries of the vertebral bodies. These
enhance bacterial clearance and decrease the risk of recommended prior to open surgical biopsy.
pyogenic vertebral body infections (4).
r Such anastomoses significantly decrease by 15 yr of
age and disappear by adulthood, likely leading to
the increased risk of vertebral osteomyelitis, rather
than discitis, in older patients (4).
258
DISCITIS
DIFFERENTIAL DIAGNOSIS DISPOSITION 6. Offiah AC. Acute osteomyelitis, septic arthritis and
r Vertebral osteomyelitis discitis: Differences between neonates and older
Admission Criteria
r Septic arthritis of the sacroiliac joint Patients diagnosed with discitis should be managed in children. Eur J Radiol. 2006;60:221232.
r Paraspinal abscess an inpatient setting during the early stages to monitor 7. Karabouta Z, Bisbinas I, Davidson A, et al. Discitis
r Malignancy: Primary or metastatic for response to antimicrobial therapy. in toddlers: A case series and review. Acta
r Tuberculous spondylitis Issues for Referral Paediatr. 2005;94(10):15161518.
r Brucellosis r As inpatient, pediatric orthopedic or neurosurgical 8. Kayser, R, Mahlfield K, Greulich M, et al.
r Spondylolysis/Spondylolisthesis consultation is recommended. Spondylodiscitis in childhood: Results of a
r Transverse myelitis r Particular attention should be paid to evolving long-term study. Spine. 2005;30(3):318323.
r Scheuermann kyphosis neurologic deficits and the possible need for surgical 9. Arthurs OJ, Gomez AC, Set PAK. The toddler
consultation. refusing to bear weight: A revised imaging guide
and case series. Emerg Med J. 2009;26:797801.
TREATMENT Thoracolumbosacral orthosis is recommended if
r A delay in antibiotic therapy may lead to a
imaging reveals extensive bony destruction, sagittal or ADDITIONAL READING D
coronal deformity, or soft tissue involvement (4).
prolonged course, prolonged or recurrent symptoms, Cushing A. Diskitis in children. Clin Infect Dis.
and more severe infections (3,4). 1993;17:16.
r Duration of therapy should be guided by FOLLOW-UP
normalization of ESR with serial measurements,
unrestricted passive spinal mobility, and resolution
Follow up with plain x-rays at regular intervals for CODES
of pain.
r Up to 75% of patients may have an associated 1218 mo to assess return of vertebral height (4).
ICD9
paravertebral inflammatory mass and may suggest PROGNOSIS r 722.90 Other and unspecified disc disorder of
the need for more aggressive or longer duration of r Several studies have shown the prognosis is good
unspecified region
antibiotic therapy (1). regardless of antimicrobial therapy. r 722.91 Other and unspecified disc disorder of
r In children who receive antibiotic therapy, the
cervical region
ALERT majority will have resolution of symptoms within r 722.92 Other and unspecified disc disorder of
Children with disc protrusion causing nerve root 3 wk and fewer long-term complications (3,4).
r Long term, 80% of children in 1 series were thoracic region
entrapment or the presence of paravertebral
abscess require immediate surgical consultation. asymptomatic with full mobility of the spine (8).
r Partial restoration of disc space height may be seen
MEDICATION PEARLS AND PITFALLS
r Antistaphylococcal antibiotics: as early as 23 mo following therapy. However, full
recovery of disc space height may take 13 yr (1). r Discitis is a rare cause of back pain in children but
Cefazolin (methicillin sensitive) 25100 often presents with other nonspecific symptoms.
mg/kg/day IV q6h; adult dose 12 g COMPLICATIONS r Rest and analgesia combined with
Clindamycin (methicillin resistant) 30 mg/kg/day r Chronic low back pain
r Loss of vertebral height, usually recovered within antistaphylococcal antibiotics is the mainstay of
IV q8h, max single dose 900 mg
therapy.
Vancomycin (methicillin resistant) 40 mg/kg/day 12 yr r Discitis should be considered in any child with
IV q6h, max single dose 1 g r Spinal fusion if >50% loss in vertebral height (1)
r If there is a poor response to standard antimicrobial r Limited physical activity refusal to bear weight.
r Any child with neurologic deficits should receive
therapy, further treatment should be guided by
results of PPD testing and/or biopsy (as indicated): immediate orthopedic or neurosurgical consultation.
r Poor response to antimicrobial therapy should raise
Authors vary on duration of antibiotic therapy. REFERENCES
Treatment should begin with IV antibiotics (714 the suspicion for less common infectious etiologies,
days) followed by transition to oral antibiotics 1. Brown R, Hussain M, McHugh K, et al. Discitis in the presence of a paravertebral abscess, or a
(16 mo) once the patient shows evidence of young children. J Bone Joint Surg Br. noninfectious pathology.
clinical and laboratory improvement (4,7,8). 2001;83(1):106111.
Choice of oral antibiotics depends on 2. Fernandez M, Carrol CL, Baker CJ. Discitis and
susceptibilities of the organism. vertebral osteomyelitis in children: 18 year review.
r Analgesia, rest, and immobilization: Pediatrics. 2000;105:12991304.
Acetaminophen 15 mg/kg/dose PO q4h PRN 3. Herman T, Siegel M. Thoracic discitis. Clin Pediatr.
Ibuprofen 10 mg/kg/dose PO q6h PRN 2009;48(1):120123.
Morphine 0.1 mg/kg IV/IM/SC q2h PRN: 4. Early S, Kay R, Tolo V. Childhood diskitis. J Am Acad
Initial morphine dose of 0.1 mg/kg IV/SC may Orthop Surg. 2003;11:413420.
be repeated q1520min until pain is controlled, 5. Garron E, Viehweger E, Launay F, et al.
then q2h PRN. Nontuberculous spondylodiscitis in children.
J Pedatr Orthop. 2002;22:321328.
Surgical debridement is rarely indicated and should
only be performed in patients who fail to respond to
conventional therapy and demonstrate the presence of
an abscess or evolving neurologic deficits (4).
259
DISLOCATION, KNEE
John Munyak
Kristopher Hunt

r Knee dislocation refers to dislocation of the r Conscious patients may relate a history of a fall,
Splint the knee in a position of comfort.
tibiofemoral joint, with a disruption of 3 of the sporting injury, or motor vehicle accident.
stabilizing ligaments. r Knee pain with an associated sensation of INITIAL STABILIZATION/THERAPY
r The direction of dislocation is defined by the r If a sufficient trauma mechanism exists, then primary
immobility or dislocation is common.
direction of tibial movement relative to the femur. r In preverbal patients, inability to bear weight on the attention should be given to ABCs as well as more
r Directions of dislocation include anterior, posterior, affected limb and pain may be the only clues. severe injuries:
Knee dislocations do not directly result in airway,
or lateral when translational forces are applied; PHYSICAL EXAM breathing, or circulation compromise aside from
when rotary forces are involved, directions of r Deformity will be obvious if the joint has not
vascular compromise to the affected limb.
dislocation include anterior, posterior lateral, medial, spontaneously reduced. r The main therapy is reduction of dislocation and
or rotary. r If not spontaneously reduced, the affected knee will
r Knee dislocations represent true orthopedic analgesia.
be grossly deformed, swollen, and immobile.
emergencies, and this injury may be limb threatening r In a spontaneously reduced knee dislocation, the MEDICATION
due to associated neurovascular compromise. examiner will elicit instability in multiple directions. First Line
r If the peroneal nerve is affected, a conscious patient r Analgesics are indicated.
EPIDEMIOLOGY r Opioids:
The majority of knee dislocations are anterior. may relate decreased sensation or numbness in the
1st dorsal web space of the foot with or without Morphine 0.1 mg/kg IV/IM/SC q2h PRN:
RISK FACTORS Initial morphine dose of 0.1 mg/kg IV/SC may
r As with most dislocations, knee dislocations are diminished foot dorsiflexion when compared to the
unaffected, contralateral side. be repeated q1520min until pain is controlled,
more common in males. r Vascular assessment may be accomplished with then q2h PRN.
r Contact sports r NSAIDs:
palpation or the use of duplex Doppler US at the
GENERAL PREVENTION dorsalis pedis, posterior tibial, anterior tibial, and Consider NSAID medication in anticipation of
r Close supervision is an effective means to prevent popliteal arteries. prolonged pain and inflammation.
injury in events such as sporting activities, especially r Despite a present distal pulse, the popliteal artery Ibuprofen 10 mg/kg/dose PO/IV q6h PRN
contact sports where large forces are exerted on the may be injured in 10% of cases. Ketorolac 0.5 mg/kg IV/IM q6h PRN
lower limbs. Naproxen 5 mg/kg PO q8h PRN
r Appropriate use of padding/equipment in contact DIAGNOSTIC TESTS & INTERPRETATION r Moderate sedation may be required to aid with the
sports is necessary to prevent limb injury. Imaging reduction for both anxiolysis and pain reduction.
r Safe driving and appropriate use of child restraints Plain films of the knee should be sufficient to confirm r See the Procedural Sedation and Analgesia topic for
are essential in preventing any potential motor the diagnosis of knee dislocation; however, the detailed information.
vehiclerelated injury. diagnosis may be made from physical exam alone.
Second Line
Diagnostic Procedures/Other Pain medications such as anti-inflammatories and
PATHOPHYSIOLOGY r In a joint that does not appear grossly deformed but
r Most knee dislocations in any direction involve narcotic analgesics used post reduction will likely be
a sufficient mechanism for injury has occurred, a required due to postreduction pain and inflammatory
transmission of large forces to the tibiofemoral joint
high index of suspicion should remain for a knee changes.
after blunt-force trauma; low-energy knee
dislocation that has spontaneously reduced and an
dislocations in pediatric populations are uncommon. SURGERY/OTHER PROCEDURES
r After the force is transmitted, dislocation occurs due appropriate physical exam and diagnostic testing r Early reduction is the hallmark of good therapy.
should ensue.
to tearing and disruption of the majority of the r Significant controversy exists regarding the use of r Reduction is accomplished with in-line longitudinal
ligamentous and soft tissue structures supporting traction and manipulation of the joint back into
emergent arteriography in all cases of knee
the knee. Typically, the anterior cruciate ligament position.
dislocation.
(ACL), posterior cruciate ligament (PCL), and an r Patients without a pulse at any time pre- or post r In the case of an anterior dislocation, for example,
additional collateral ligament are involved. an assistant should apply continuous longitudinal
r Anterior dislocations usually occur due to a reduction require emergent angiography as well as
those with other signs of vascular injury including traction while the femur is lifted anteriorly,
hyperextension mechanism after high-energy maintaining another hand on the tibia for stability.
bruit or distal ischemia.
trauma is sustained to the joint. r Some authors advocate for serial vascular r For posterior dislocation, the knee should be
ETIOLOGY examinations on admission for patients with a promptly immobilized in 15 degrees of flexion so as
r 2/3 of knee dislocations are secondary to motor low-energy mechanism, normal pulses pre- and post to avoid any tension on the popliteal artery.
vehicle collisions. r Arthrotomy may be required if impinging soft tissue
reduction, and normal ankle brachial indices.
r Other etiologies include falls, sporting injuries, and r If any doubt is present, arteriography should be between bony structures will not allow for closed
industrial injuries. ordered because intimal tears in the popliteal artery reduction.
r In pediatric patients where closed reduction is
COMMONLY ASSOCIATED CONDITIONS may not be apparent in some cases for several days.
r High incidences of popliteal artery, peroneal nerve, successful, surgery will likely be required at a later
DIFFERENTIAL DIAGNOSIS time to repair the involved ligaments.
and tibial nerve injuries are associated with knee ACL tear, PCL tear, isolated collateral ligament tear,
dislocations. tibia/fibular fracture, knee fracture, femoral fracture, or
r Most of these associated injuries are due to patellar dislocation
posterior dislocations; popliteal arterial injury occurs
in 50% of such dislocations.
r Knee dislocations are frequently associated with
proximal tibial fractures.
260
DISLOCATION, KNEE
DISPOSITION PROGNOSIS r Steele MT, Glaspy JN. Musculoskeletal disorders in

r Inadequate assessment and treatment of vascular children: Knee Injuries. In Tintinalli JE, Gabor D,
Admission Criteria
r All patients with suspected vascular injury, which injuries within 4 hr can lead to an amputation rate Stapczynski JS, et al., eds. Tintinallis Emergency
includes the vast majority of knee dislocations, of 50%; at 8 hr, this rate increases to 80%. Medicine: Comprehensive Study Guide. 6th ed.
should be admitted for arteriography and/or serial r After reduction with or without surgical ligamentous Columbus, OH: McGraw-Hill; 2003.
exams after successful reduction. repair and arterial repair, the need for a brace for r Tay BKB, Colman WW, Berven S, et al. Orthopedics:
r Critical care admission criteria: strenuous activities may be permanent. Injuries of the knee region, dislocation of the knee
Many patients will have coexisting injuries due to joint. In Doherty GM, Way LW, eds. CURRENT
COMPLICATIONS
the blunt force required to create a knee r Limb loss may result from arterial injury loss of blood Surgical Diagnosis & Treatment. 12th ed. Columbus,
dislocation; the patient with multiple traumatic OH: McGraw-Hill; 2006.
flow to the lower leg.
injuries may require a higher level of care, such as r Other complications include degenerative arthritis, See Also (Topic, Algorithm, Electronic
a surgical ICU setting. Media Element)
limited range of motion, recurrent dislocation, and
Discharge Criteria associated proximal tibial fracture. r Dislocation, Patella
r Patients with conditions other than knee dislocation r Knee, Ligamentous Injury
may be discharged as appropriate.
D
r If the patient with knee dislocation has been ADDITIONAL READING
thoroughly evaluated, deemed to not have vacular r Frassica FJ, Sim FH, Staeheli JW, et al. Dislocation of CODES
compromise, and the orthopedic surgeon
the knee. Clin Orthop. 1991;(263):200205.
recommends discharge, then this is appropriate. r Gutman D, Savitt DL, Storrow AB. Extremity trauma: ICD9
However, this is atypical since most patients with r 836.50 Closed dislocation of knee, unspecified part
knee dislocations have vascular compromise. Knee dislocation. In Knoop KJ, Stack LB, Storrow
AB, eds. Emergency Medicine Atlas. 2nd ed. r 836.51 Anterior dislocation of tibia, proximal end,
Issues for Referral Columbus, OH: McGraw-Hill; 2002. closed
r Emergent orthopedic consultation should be r Jones RE, Smith EC, Bone GE. Vascular and r 836.52 Posterior dislocation of tibia, proximal end,
obtained when a knee dislocation is recognized orthopedic complications of knee dislocation. Surg closed
given the emergent potential for operative reduction Gynecol Obstet. 1979;149(4):554558.
with failed closed reduction. r Kaufman SL, Martin LG. Arterial injuries associated
r Emergent vascular surgical consultation may be PEARLS AND PITFALLS
with complete dislocation of the knee. Radiology.
required in cases where arterial damage is apparent 1992;184(1):153155. r True knee dislocation requires a significant
with physical exam. r Kennedy JC. Complete dislocation of the knee joint.
mechanism.
J Bone Joint Surg. 1963;45(5):889904. r Knee dislocations are orthopedic emergencies and
r McCutchan JD, Gillham NR. Injury to the popliteal
FOLLOW-UP may be vascular emergencies as well due to
artery associated with dislocation of the knee: associated popliteal injury.
FOLLOW-UP RECOMMENDATIONS Palpable distal pulses do not negate the requirement r Palpation and Doppler exam of lower limb arteries
Activity: for arteriography. Injury. 1989;20(5):307310.
r After reduction with or without vascular and r Patterson BM, Agel J, Swiontkowski MF, et al. Knee are insufficient to rule out arterial injury, and either
arteriogram or serial exams must be employed when
ligamentous repair, the affected extremity should be dislocations with vascular injury: Outcomes in the a knee dislocation has been identified.
immobilized from the groin to the toes in a fashion Lower Extremity Assessment Project (LEAP) Study.
allowing for frequent reassessment of the dorsalis J Trauma. 2007;63(4):855858.
pedis pulse. r Seroyer ST, Musahl V, Harner CD. Management of
r The extremity should be immobilized for 8 wk the acute knee dislocation: The Pittsburgh
without weight bearing, after which time a long-leg experience. Injury. 2008;39(7):710718.
brace may be applied at the discretion of the r Smith WR, Agudelo JF, Parekh A, et al.
orthopedist. Musculoskeletal trauma surgery. In Skinner HB, ed.
r After reduction and weeks of immobilization, CURRENT Diagnosis & Treatment in Orthopedics.
intensive quadriceps and hamstring rehabilitation 4th ed. Columbus, OH: McGraw-Hill; 2006.
will be required in order to minimize the functional
loss of the knee joint.
261
DISLOCATION, PATELLA
John Munyak
Kristopher Hunt

r Typically, a history of rotating the knee on a fixed
Patellar dislocation occurs when the patella is Splint the leg in a position of comfort.
displaced either medially or laterally from the patellar lower leg is related.
surface, which is located on the distal femur superior r Patients may describe a sensation of the knee INITIAL STABILIZATION/THERAPY
r If a sufficient trauma mechanism exists, then primary
to and between the lateral and medial femoral popping out of place.
condyles. attention should be given to airway, breathing, and
PHYSICAL EXAM circulation and more severe injuries. Patellar
EPIDEMIOLOGY r If dislocated, a lateral mass may be noted that is
dislocations do not directly result in airway,
Incidence asymmetric to the contralateral leg, and the knee breathing, or circulation compromise.
r The majority of injuries sustained to the pediatric will commonly be held in flexion. r The main goal of therapy is reduction of the
r Positive Fairbank sign, or apprehension test: When
patella are dislocations. dislocation.
r Patellar dislocation is one of the most common the patella is moved laterally, the patient appears r Analgesia should be provided if necessary.
causes of hemarthrosis in children. apprehensive though not typically in pain.
r Often the patella will have reduced spontaneously MEDICATION
RISK FACTORS by patient motion en route. If this is the case, a First Line
Recurrent dislocation is associated with increased hemarthrosis over the medial patellar retinaculum r See the Procedural Sedation and Analgesia topic for
quadriceps angle, generalized ligamentous laxity, may be the only clinical finding. detailed information.
family history, laxity in the medial patellofemoral r A large amount of effusion may be noted if a r Opioids:
ligament, and weakness in the vastus medialis Morphine 0.1 mg/kg IV/IM/SC q2h PRN:
significant amount of time has elapsed prior to
obliquus. Initial morphine dose of 0.1 mg/kg IV/IM may
reduction.
GENERAL PREVENTION r If gross instability of the patella exists, it may be repeated q1520min until pain is controlled,
r Close supervision is an effective means to prevent indicate that the soft tissue disruption to the medial then q2h PRN.
injury in events such as sporting activities, especially aspect of the knee has become extensive. r NSAIDs:
contact sports where large forces are exerted on the Consider NSAID medication in anticipation of
lower limbs. DIAGNOSTIC TESTS & INTERPRETATION prolonged pain and inflammation.
r Appropriate use of padding/equipment in contact Imaging Ibuprofen 10 mg/kg/dose PO/IV q6h PRN
r Reduction need not be delayed for imaging if the
sports is necessary to prevent limb injury. Ketorolac 0.5 mg/kg IV/IM q6h PRN
r In cases of chronic dislocation, operative repair may diagnosis is readily apparent from history and Naproxen 5 mg/kg PO q8h PRN
physical exam.
be required to prevent recurrence. r Plain films are sufficient to confirm the diagnosis of Second Line
PATHOPHYSIOLOGY patellar dislocation if it is not readily apparent from Pain medications including NSAIDs and a short course
r The mechanism for a patellar dislocation is history and physical exam alone. of opiates post reduction should be offered to aid in
commonly a twisting of a planted knee with a lateral r Post reduction plain films should be obtained to the rehabilitation process.
force applied. document successful reduction and examine the SURGERY/OTHER PROCEDURES
r The majority of patellar dislocations occur laterally; lateral femoral condyle as well as the medial patellar Reduction: Extend knee to 180 degrees, as this will
however, horizontal, superior, and intercondylar margin, which are the 2 most common sites of typically force the patella to return to its normal
dislocations do occur. associated fracture. location:
r This may be accompanied by simultaneous pressure
See Pathophysiology. Several bony disruptions may be mistaken for a patellar against the patella, moving it in a lateral to medial
dislocation, which include but are not limited to distal direction.
r Fractures in children may result from direct trauma femoral fracture, quadriceps rupture, patellar tendon
or, more commonly, with a sleeve fracture rupture, patellar fracture, or frank knee dislocation.
mechanism.
r The patellar sleeve fracture takes place when a
forceful contraction of the quadriceps tendon occurs
against a fixed lower leg, separating the distal
patellar sleeve from the body of the patella.
262
DISLOCATION, PATELLA
DISPOSITION ADDITIONAL READING r Nietosvaara Y, Aalto K, Kallio PE. Acute patellar

Admission Criteria dislocation in children: Incidence and associated
r Arendt EA, Fithian DC, Cohen E. Current concepts of
If a significant trauma mechanism exists, other factors osteochondral fractures. J Pediatr Orthop.
may require admission. lateral patella dislocation. Clin Sports Med. 1994;14(4):513515.
2002;21(3):499519. r Smith WR, Agudelo JF, Parekh A, et al.
Discharge Criteria r Atkin DM, Fithian DC, Marangi KS, et al.
Musculoskeletal trauma surgery: Patellar injuries. In
Reduction of dislocation and no other injuries or Characteristics of patients with primary acute lateral Skinner HB, ed. CURRENT Diagnosis & Treatment in
problems that would require admission patellar dislocation and their recovery within the Orthopedics. 4th ed. Columbus, OH: McGraw-Hill;
Issues for Referral first 6 months of injury. Am J Sports Med. 2006.
r Consultation with an orthopedist is recommended in
2000;28(4):472479.
cases of associated fracture/dislocation. r Beasley LS, Vidal AF. Traumatic patellar dislocation See Also (Topic, Algorithm, Electronic
r Early consultation is recommended in cases of a Media Element)
in children and adolescents: Treatment update and r Dislocation, Knee
sleeve fracture, in which case specific therapy is literature review. Curr Opin Pediatr.
based on the degree of displacement. r Knee, Ligamentous Injury
2004;16(1):2936.
r Recurrent episodes require operative repair for r Cash JD, Hughston JC. Treatment of acute patellar D
effective treatment. dislocation. Am J Sports Med. 1988;16(3):244249.
r Colvin AC, West RV. Patellar instability. J Bone Joint CODES
FOLLOW-UP Surg Am. 2008;90(12):27512762.
r Gutman D, Savitt DL, Storrow AB. Extremity trauma: ICD9
PROGNOSIS r 718.36 Recurrent dislocation of lower leg joint
Patellar dislocation. In Knoop KJ, Stack LB, Storrow
Patients with an isolated, primary patellar dislocation r 836.3 Dislocation of patella, closed
AB, eds. Emergency Medicine Atlas. 2nd ed.
have an excellent prognosis with good functional Columbus, OH: McGraw-Hill; 2002.
outcomes. r Hopkins-Mann C, Leader D, Moro-Sutherland D,
COMPLICATIONS et al. Musculoskeletal disorders in children: Knee PEARLS AND PITFALLS
Complications include but are not limited to injuries. In Tintinalli JE, Gabor D, Stapczynski JS, r Patellar dislocation is typically lateral.
degenerative arthritis, patellofemoral syndrome, et al., eds. Tintinallis Emergency Medicine: r Reduction can be accomplished simply by extending
patellar instability, recurrent dislocations, and Comprehensive Study Guide. 6th ed. Columbus, OH:
McGraw-Hill; 2003. the leg and manipulating the patella back between
fractures. the 2 femoral condyles.
r Prereduction films are often unnecessary.
263
DISLOCATION, TEMPOROMANDIBULAR JOINT

Mandisa A. McIver
William I. Krief
Superior dislocations occur after a direct blow to a DIAGNOSTIC TESTS & INTERPRETATION
BASICS partially opened mouth: Imaging
Can result in facial nerve palsy, cerebral r Mandibular series of radiographs
DESCRIPTION contusions, or deafness r Panoramic radiographs
r The temporomandibular joint (TMJ) is comprised of r Once dislocated, the condyle stays out of the r TMJ radiographs
the articular surface lying between the mandibular temporal fossa due to spasms of the lateral r CT of mandible
condyles and the temporal bone. pterygoid and temporal muscles.
r Dislocation is defined as displacement of the Diagnostic Procedures/Other
condyle out of the mandibular fossa. ETIOLOGY Tongue blade test:
r Trauma (4099% of all TMJ dislocations)
r TMJ dislocation can result from both traumatic and r Patient attempts to grasp and hold a tongue blade
r Extreme mouth opening
nontraumatic processes. between the molars while the examiner twists the
r Most dislocations can be managed in the emergency COMMONLY ASSOCIATED CONDITIONS tongue blade to the point of breaking
department with outpatient follow-up. r Bruxism (abnormal grinding of the teeth) r Mandibular fractures can be ruled out (negative
r Anterior dislocation is most common, but posterior, r Malocclusion/Deep overbite predictive value 96%) if performed successfully (1).
lateral, and superior dislocations can also occur. r Lax ligaments r Both sides should be tested.
r Dislocations are classified as acute, chronic r Stress
recurrent, and chronic. r Rheumatoid arthritis r Mandibular fracture
r Osteoarthritis r Maxillary fracture
EPIDEMIOLOGY
r Viral infections (eg, mumps, measles) r Dystonic reaction
Prevalence
r Hypermobility syndromes
TMJ dislocations represent 3% of all dislocated joints
in the body.
TREATMENT
RISK FACTORS
r Shallow mandibular fossa
DIAGNOSIS
r Previous TMJ dislocation or trauma HISTORY r Assess and stabilize airway, breathing, and
r Dystonic reactions r Jaw pain and trismus after extreme mouth opening
circulation.
r Seizures or after trauma to the jaw r Attend to life-threatening conditions 1st:
r Difficulty speaking or swallowing
r Hypermobility syndromes (eg, Marfan, TMJ dislocation is primarily a condition of
r Malocclusion
Ehlers-Danlos) morbidity.
r Prolonged dental procedures r There may be a history of previous dislocations. r Provide adequate analgesia.
r Psychiatric medications r Past medical history may include hypermobility r Reduce dislocation as rapidly as feasible.
syndromes.
GENERAL PREVENTION MEDICATION
PHYSICAL EXAM r Analgesia, sedation, and muscle relaxation may be
Avoid extreme mouth opening. r Must do a thorough exam of the head, neck, and
required for successful reduction:
PATHOPHYSIOLOGY nervous system. Procedural sedation may be necessary if the
r The dislocation is described by the position of the r Examine the oral cavity for any gingival lacerations patient is unable to cooperate.
mandibular condyle in relation to the temporal or extraoral chin lacerations, which may raise r Midazolam 0.1 mg/kg IV (max 2 mg) can be used as
articular groove: suspicion for an open fracture. a muscle relaxant.
Anterior dislocationsmost common: r Unilateral dislocations cause deviation of the jaw r Local injection of lidocaine 2%, 25 mL into the
Following direct trauma to mandible
away from the affected side. TMJ at the site of preauricular depression
Resulting from dystonic reaction or seizure r Bilateral dislocations cause an underbite or r Morphine 0.1 mg/kg IV/IM/SC q2h PRN:
Extreme mouth opening (yawning, lengthy
prognathia with pain over both TMJ areas. Initial morphine dose of 0.1 mg/kg IV/SC may be
dental procedures, general anesthesia, vomiting, r Pay special attention during the neurologic exam to
seizures, laughing, screaming, singing): The repeated q1520min until pain is controlled, then
masseter and temporalis muscles elevate the cranial nerves V and VII. q2h PRN.
r Assess hearing and inspect the external auditory r Ketorolac 0.41 mg/kg IV/IM:
mandible while the lateral pterygoid muscle is
still contracting, pulling the mandibular condyle canal, especially in suspected posterior TMJ Children >16 yr of age can be given 30 mg IV as
anteriorly out of the temporal fossa. dislocations. a single dose.
Posterior dislocations can occur after a direct blow
to the chin and may cause external auditory canal
injury.
Lateral dislocations are frequently associated with
mandibular fractures.
264
DISLOCATION, TEMPOROMANDIBULAR JOINT
SURGERY/OTHER PROCEDURES REFERENCE

r Reduction of anterior TMJ dislocation (following Issues for Referral
radiologic study): Follow-up by specialist (oral maxillofacial surgeon, 1. Schwab RA, Genners K, Robinson WA. Clinical
The patient is seated upright facing the physician otolaryngologist, or dentist) for evaluation of possible predictors of mandibular fractures. Am J Emerg
performing the reduction. complications and ongoing care Med. 1998;16(3):304305.
Stabilize the head posteriorly with head rest or Additional Therapies
assistance. If recurrent dislocation occurs, a bandage can be
Physician should wrap his or her thumbs in gauze ADDITIONAL READING
placed around the head and chin (Barton bandage) for
for protection. several days to limit jaw movement. r Chaudhry M, Rosh AJ. Dislocation, mandible.
Using the thumbs, apply gentle pressure
eMedicine. May 5, 2010. Available at
downward and backward on the occlusal surfaces
http://emedicine.medscape.com/article/823775-
of the patients lower molars: FOLLOW-UP overview.
The downward pressure moves the dislocated r Pratt A, Loiselle J. Reduction of temporomandibular
condyles below the articular eminences. FOLLOW-UP RECOMMENDATIONS
The backward pressure shifts the condyles r Discharge instructions and medications: joint dislocation. In King C, Henretig FM, eds.
Textbook of Pediatric Emergency Procedures. 2nd
D
posteriorly into the mandibular fossa. Avoid extreme mouth opening for at least 6 wk.
This may require a significant amount of The patient should hold the chin against his or her ed. Philadelphia, PA: Lippincott Williams & Wilkins;
strength. It is common that a senior physician chest or hand during yawning to avoid wide 2008.
with experience in the procedure may give mouth opening.
supervision and instruction to a junior clinician Soft diet for 1 wk
with greater strength, such as a resident or Warm compresses CODES
fellow, who actually performs the procedure. NSAIDs
The clinician performing the dislocation may Muscle relaxants ICD9
stand on a chair, stool, or bed to gain additional r Activity: 830.0 Closed dislocation of jaw
force by using body weight in addition to arm As tolerated
strength to lower the jaw.
r Other TMJ dislocations are reduced similarly, with DIET PEARLS AND PITFALLS
Soft diet for 1 wk
adjustments in direction for the 2nd maneuver. r Prior to attempting reduction of TMJ dislocation, a
r TMJ dislocation associated with mandibular PROGNOSIS radiologic study should be performed to exclude any
r Conservative methods provide temporary alleviation
fractures often requires open reduction and internal associated fractures.
fixation. of symptoms with common recurrence. r Delay in reduction of TMJ dislocations further
r Surgical intervention is generally known to be the
DISPOSITION aggravates muscle spasms and makes reduction
more effective definitive treatment. more difficult.
Admission Criteria r Pediatric patients with posttraumatic internal r Bilateral dislocations that are associated with severe
r Failed closed reduction
derangements of the TMJ are prone to retrognathia spasms may require reduction of 1 condyle at a time.
r TMJ dislocation with mandibular fractures requiring
and facial asymmetry years later.
open reduction
COMPLICATIONS
Discharge Criteria r Chronic recurrent dislocations
r Stable respiratory condition r Ischemic necrosis of the condylar head
r Able to tolerate fluids PO r Traumatic damage to the articular disc
r Pain well controlled r Mandibular osteomyelitis
r Appropriate follow-up arranged r Permanent malocclusion (chronic untreated
dislocations)
265
DISORDERS OF ENERGY METABOLISM (MITOCHONDRIAL DISEASE)

Richard G. Boles
Solomon Behar
Derek A. Wong
r Functional disease, such as: Diagnostic Procedures/Other

BASICS Chronic pain syndromes, including migraine Diagnosis may require muscle biopsy and/or
GI dysmotility, including irritable bowel or sophisticated biochemical and molecular testing
DESCRIPTION constipation performed by an expert geneticist or neurologist.
r Mitochondrial disease refers to a group of hundreds Cyclic vomiting
of different inborn errors of metabolism that result DIFFERENTIAL DIAGNOSIS
Chronic fatigue/exercise intolerance r Very broad and dependent on clinical presentation
in pathology due to defective energy metabolism. r Some common presentations include:
r Examples of mitochondrial disease include: r Consider:
Dysautonomia
MELAS (mitochondrial myopathy, encephalopathy, Prader-Willi and Angelman syndromes
Abnormal movements
lactic acidosis, stroke) Zellweger syndrome
Cardiomyopathy
MERRF (myoclonic epilepsy with ragged red fibers) Organic acidemias
Renal tubular dysfunction or acidosis
NARP (neuropathy, ataxia, retinitis pigmentosa) Congenital defects of glycosylation
Stroke (especially basal ganglial and/or thalamic)
Kearns-Sayre syndrome Disorders of creatine metabolism
Acute loss of milestones
Cytochrome C oxidase deficiency Chromosomal copy number variants
Autistic spectrum disorders r Consider a diagnosis of mitochondrial disease when
Most patients do not have one of the named
conditions. PHYSICAL EXAM a patient presents with:
r Often normal Idiopathic disease involving at least 2 systems or
EPIDEMIOLOGY r Myopathy may involve any or all of the following: tissues
Prevalence Skeletal: Hypotonia, decreased bulk, weakness Idiopathic complex neurologic, neuromuscular, or
r Mitochondrial disease as a whole is by far the most Ocular psychiatric disease
common kind of metabolic disorder. Cardiac Intermittent, transient, functional, or
r Common: Some prevalence estimates give a GI dysautonomic disease manifestations
minimal figure as high as 1 in 500. r Encephalopathy (eg, mental retardation) Unexplained GI symptoms
When there is suspicion of fictitious disorder
GENERAL PREVENTION DIAGNOSTIC TESTS & INTERPRETATION
Prenatal diagnosis is feasible in a minority of cases. Lab
r Often normal (especially in the absence of stressors) TREATMENT
PATHOPHYSIOLOGY
r Mitochondrial disease is caused by abnormalities in r Urine ketosis
the ability of cells to make ATP (energy). r Anion gap metabolic acidosis during acute illness or Avoid fasting by administration of calories, including
r As a consequence, those tissues with the highest deterioration fruit juices, chocolate milk, etc.
energy requirements are affected 1st, especially r Fasting hypoglycemia:
nerve and muscle tissues: Rarely postprandial hypoglycemia r IV fluids with 10% dextrose 0.45% normal saline at
Secondary tissues affected include endocrine r Increased transaminases (usually mild) a high rate of 1.52 times maintenance
glands, liver, kidney, and bone marrow. r Renal tubulopathy (especially abnormal urine r If diagnosed disease:
r Clinical manifestations are generally intermittent organic acids when stressed) Consult family to avoid fasting in patient:
and typically occur at times of high-energy demand, r Free carnitine deficiency Age <5 mo: Max fast = 4 hr
including viral infection, fasting, overexercise, r Elevated creatine kinase (CK) when ill Age 511 mo: Max fast = the number of hours
psychological stress, and environmental temperature r Elevated lipase while ill equal to the age of the patient in months
extremes. r Neutropenia in some cases Age 1 yr: Max fast = 12 hr
ETIOLOGY r Lactic acidosis in many cases Consider a recommendation for the patient to
r Mitochondria have their own DNA (mtDNA) that is r Hyperammonemia (occasional, usually <200 start on coenzyme Q10:
10 mg/kg/day, usually divided b.i.d.
maternally inherited from a mother to all of her micromolar) 200 mg/day for older children and adults
children, without recombination: Initial Lab Tests Known side effects are rare and benign.
Mitochondrial disease can be due to mutations in r Chemistry panel, ALT, lipase, CK Can be purchased in many drug stores
mtDNA, which are usually maternally inherited.
r Most proteins in the mitochondria are encoded by CBC with differential Liquid and gel capsules work best.
Urine dipstick Avoid systemic steroids and valproic acid.
the chromosomes and imported into mitochondria: r After initial lab tests above, if mitochondrial disease Referral to a tertiary care facility with an expert in
Mitochondrial disease can be due to mutations in is suspected, consider: mitochondrial disease:
the nuclear genes encoding those imported Urine organic acids: Experts may be neurologists, geneticists, or
proteins; in these cases, inheritance is mendelian Most important test occasionally endocrinologists.
(usually autosomal recessive). Collect the sample and freeze.
Plasma acylcarnitines ALERT
DIAGNOSIS Plasma carnitines Avoid fasting, especially during illness and prior
Plasma lactate and pyruvate to medical/surgical procedures.
HISTORY Blood coenzyme Q10 level r D10 0.45% normal saline at 1.5 times
r Extremely variable Consider mitochondrial DNA screening test. maintenance during the perioperative period is
r Intermittent, protean, and multiple disease generally protective for most procedures.
Imaging
manifestations or symptoms are most common. r Brain MR or CT if stroke is suspected
r Neurologic (including psychiatric) and/or muscular MR spectroscopy may show an increased lactate
disease peak.
r Multisystem failure associated with an acute r Upper GI series with small bowel follow-through to
stressor, such as a viral illness rule out malrotation in cases with severe vomiting
266
DISORDERS OF ENERGY METABOLISM (MITOCHONDRIAL DISEASE)
r Ondansetron for nausea/vomiting at 0.30.4 FOLLOW-UP
mg/kg/dose (adult dose 1216 mg) given by 1. Cohen BH, Shoffner J, DeBoer G. Anesthesia and
standard routes (IV or oral dissolving tablet): FOLLOW-UP RECOMMENDATIONS mitochondrial cytopathies. Available at
r Follow the management plan recommended by the http://www.umdf.org/atf/cf/%7B28038C4C-02EE-
Patients with mitochondrial disease do not
generally respond to the lower doses but generally specialist, including diet, activity, medications, and 4AD0-9DB5-D23E9D9F4D45%7D/mitoane.pdf.
respond to higher doses. cofactors:
r Give L-carnitine by oral or IV route if patient takes Adequate hydration and caloric intake are
this compound: essential. ADDITIONAL READING
r Patient/Family should contact the specialist or his or
Most patients receive 100 mg/kg/day divided r Haas RH, Parikh S, Falk MJ, et al. Mitochondrial
b.i.d. (adult dose 1 g b.i.d.) her office the following day.
r Amitriptyline is frequently used with chronic pain or r Return for: disease: A practical approach for primary care
physicians. Pediatrics. 2007;120:13261333.
other functional symptoms: Altered mental status (eg, lethargy, excessive r Parikh S, Saneto R, Falk MJ, et al. A modern
0.51 mg/kg/day qhs irritability, loss of abilities)
r In critically ill patients, an insulin drip with IV Significant vomiting
approach to the treatment of mitochondrial disease.
Curr Treat Options Neurol. 2009;11:414430.
D
dextrose (generally high concentration of both via Signs of dehydration r Wong LJ, Boles RG. Mitochondrial DNA analysis in
central access) can be lifesaving. Poor enteral intake
r Coenzyme Q10 at 5 mg/kg/dose b.i.d. (adult dose Increased urine ketones not responding to sugar clinical laboratory diagnostics. Clin Chim Acta.
solutions 2005;354:120.
200 mg b.i.d.)
r Riboflavin 100 mg/day or one B100 tablet/day Difficulty breathing
r Many patients take other cofactors including vitamin Increased weakness or pain
Other worrisome findings CODES
C (2501,000 mg/day), other antioxidants, and/or
creatine (140 mg/kg/day or 5 g/day) Patient Monitoring
r Mental status ICD9
r Urine ketones 277.87 Disorders of mitochondrial metabolism
ALERT
r Multiple medications frequently provoke adverse r Serum anion gap, if very ill
reactions in these patients:
PROGNOSIS PEARLS AND PITFALLS
Systemic corticosteroids (if absolutely needed, r Variable but generally good r Pearls:
watch ketones, can counter effect with IV r Mitochondrial disease is a chronic illness.
insulin): Avoid fasting, especially during illness and prior to
Moderate amounts of inhaled steroids are COMPLICATIONS medical/surgical procedures.
r Stroke Adverse reactions to anesthesia and many drugs
usually tolerated.
Oral and injected hormonal contraceptives r Seizures (many potential etiologies) are common.
r Liver failure GERD is very common in patients with
Valproic acid
r Surgery and anesthesia pose special risks in this r Functional bowel disorders mitochondrial disease. Frequently, GERD is
r Chronic pain syndromes misdiagnosed in these patients as asthma or
population (1): chronic sinusitis.
Avoid propofol. r Rhabdomyolysis
Urine ketone dipsticks are often effective for
Dysautonomia is common, including respiratory r Pancreatitis evaluation and monitoring.
arrest with sedative use. r Renal tubular dysfunction/acidosis: r Pitfalls:
Malignant hyperthermia precautions Rarely: Renal failure Lactic acid can be fictitiously elevated by use of a
r Cardiomyopathy tourniquet or improper specimen handling,
DISPOSITION r Apnea/Hypoventilation (especially drug related) especially in infants and toddlers.
Admission Criteria r Pancytopenia, or any element(s) thereof
r Failure to tolerate adequate caloric intake in a
r Chronic variable immunodeficiency:
patient on fasting avoidance (most are):
Especially: Line infections with sepsis
Less than half of the usual caloric intake often r Hypoglycemia
requires admission. r Any endocrinopathy (eg, hypoglycemia, diabetes,
r Serum anion gap 20 mM (sodium minus chloride
minus HCO3 ): hypothyroid, growth hormone deficiency)
r Depression, especially in adolescents
Serum anion gap 1819 is borderline.
r Large urine ketones (>40 mg/dL): r Malignant hyperthermia
r Any dysautonomia, especially tachycardia
Moderate is borderline.
r Loss of abilities, altered mental status (relative to r Multisystem failure
baseline), or new neurologic finding r Sudden death
r Pancreatitis, rhabdomyolysis, apnea, cardiac failure
Discharge Criteria
r Ability to tolerate adequate enteral intake
r Negative urine ketones
r Normal serum anion gap (<14 mM)
267
DISSEMINATED INTRAVASCULAR COAGULATION

Kristin Welch
Adam M. Silverman
r Trauma and tissue injury: PHYSICAL EXAM

BASICS Crush injury r Signs of underlying disease (fever, trauma,
Massive burns pregnancy):
DESCRIPTION Extensive surgery Excessive bleeding
r Disseminated intravascular coagulation (DIC) is a Severe brain injury Petechiae
secondary process caused by systemic activation of Severity of coagulopathy is a predictor of adverse Purpura
coagulation and fibrinolysis by tissue damage from a outcomes. Hemorrhagic bullae
variety of underlying diseases. r Malignancy: Wound, venipuncture site bleeding
r Characterized by coexistent hemorrhage and Rare in acute lymphocytic leukemia but reported Epistaxis
microvascular thrombosis in patients with uncommon translocation t(17;19) Hemoptysis
r Acute DIC occurs when clotting factors are Can present acutely with hemorrhage in patients r Excessive thrombosis:
consumed more rapidly than they be can with acute promyelocytic leukemia due to granules Thrombophlebitis
replaced: within blast cells that contain procoagulants Calf swelling in the case of DVT
Hemorrhage dominates, overshadowing ongoing Chronic disorder of hypercoagulation in patients Chest pain, tachycardia, tachypnea, hypoxemia in
thrombosis. with solid tumors the case of PE
r Chronic DIC is when the body is able to keep up r Severe immunologic reactions: Acral gangrene
with clotting factor consumption: Severe anaphylaxis Thrombotic endocarditis
Thrombosis is predominant clinical feature. Transplant rejection Ischemic infarcts of bowel, CNS, liver, kidneys
Acute hemolytic transfusion reactions r Organ damage or failure:
RISK FACTORS r Kasabach-Merritt syndrome:
r Neonates CNS (altered mental status, coma, focal
r Pregnancy Patients with aggressive giant hemangioma neurologic symptoms)
r Malignancy (kaposiform hemangioendothelioma) in which Kidney (edema)
there is prolonged contact of abnormal endothelial Liver (jaundice, contributes to coagulopathy)
r Sepsis
surface with blood in areas of vascular stasis Lungs (pulmonary hemorrhage/hemoptysis,
r Trauma respiratory distress, respiratory failure)
Platelets, fibrinogen consumed; fibrinolysis
r Congenital deficiency of anticoagulants (eg, enhanced DIAGNOSTIC TESTS & INTERPRETATION
protein C, antithrombin) Usually chronic and compensated but can
transform into acute fulminant disease
Lab
r Exposure of blood to procoagulants: Endothelial Similar phenomenon occurs in: r D-dimer (normal <500 ng/mL):
50% of patients with hereditary hemorrhagic
tissue damage from initiating primary disease Elevated in 90%
telangiectasia
releases procoagulants into the bloodstream. Some patients with large venous malformations Most sensitive lab assay for DIC
r Formation of fibrin in the circulation: Interaction of r CBC with peripheral smear:
r Purpura fulminans:
tissue factor and factor VII leads to thrombin
Hemorrhagic skin necrosis Thrombocytopenia (platelets <100,000/mm3 );
formation, which promotes fibrin formation and due to consumption, platelets often large
Associated with homozygous protein C deficiency
deposition as well as platelet aggregation. Platelet count can be normal due to compensation
r Fibrinolysis: Fibrin formation activates fibrinolysis (neonatal purpura fulminans) or acquired protein
C deficiency (eg, meningococcemia) in chronic DIC.
pathway, producing plasmin that cleaves fibrin and r Heat stroke Microangiopathic hemolytic anemia; due to
fibrinogen into fibrinogen degradation products r Obstetric complications: mechanical shearing of RBCs by intravascular
(FDPs), which interfere with normal fibrin fibrin strands
polymerization and platelet aggregation. Severe preeclampsia: r PT (normal 1012 sec):
r Depletion of clotting factors and platelets: Ongoing HELLP syndrome
Prolonged in 5075%
Amniotic fluid embolism from placental abruption,
activation of the coagulation system and fibrin More likely to be normal in chronic DIC
in which there is leakage of thromboplastin-like r aPTT (normal 2538 sec):
deposition consume clotting factors and platelets,
material into maternal circulation resulting in
leading to bleeding. Prolonged in 5060%
r End-organ damage: Clots cause microvascular and massive hemorrhage
Septic abortion More likely to be normal in chronic DIC
macrovascular thrombosis, leading to tissue r Fibrinogen level: Low due to consumption in
Dead fetus syndrome, in which tissue factor from
ischemia and end-organ damage. retained fetus or placenta enters maternal formation of fibrin (normal 180430 mg/dL)
r Hemolysis: Intravascular fibrin strands cause r FDP (normal 010 g/dL):
circulation and initiates DIC and fibrinolysis
mechanical shearing of RBCs, resulting in Present/Elevated in 85100%
microangiopathic hemolytic anemia. r Electrolytes, BUN, creatinine, glucose:
ETIOLOGY DIAGNOSIS Elevated BUN, creatine due to renal insufficiency
r Precipitated by many disease states r Arterial or venous blood gas:
HISTORY
r Neonates: r Fever Metabolic acidosis
Sepsis r Trauma Increasing Aa gradient
Conditions associated with prematurity such as r Malignancy Imaging
respiratory distress syndrome and necrotizing r Current or recent pregnancy r CXR if respiratory distress or if pneumonia is
enterocolitis r Chest pain in the case of pulmonary embolism (PE) suspected
Perinatal conditions: Fetal anoxia or birth asphyxia r Head CT for altered mental status
r Sepsis: r Leg swelling in the case of deep vein thrombosis
r Other studies as needed for precipitating condition
Variety of gram-negative and gram-positive (DVT)
r Decreased urine output if renal vein thrombosis Pathological Findings
bacteria r Microvascular thrombosis
r Spontaneous bleeding
Also associated with viral, rickettsial, fungal, and r Fibrin deposition within organs
parasitic infections r Recent transfusion
r Microangiopathic hemolytic anemia
268
DISSEMINATED INTRAVASCULAR COAGULATION
DIFFERENTIAL DIAGNOSIS MEDICATION REFERENCES

r Idiopathic thrombocytopenic purpura r Medications are secondary to transfusion of blood
r Hemolytic uremic syndrome products in the treatment of DIC (1,2). 1. Franchini M, Manzato F. Update on treatment of
r Alloimmune neonatal thrombocytopenia r Anticoagulation: disseminated intravascular coagulation.
r Clotting factor deficiencies Heparin (administration of extrinsic Hematology. 2004;9:8185.
r Hepatic failure anticoagulants): 2. Levi M. Disseminated intravascular coagulation.
r Vitamin K deficiency Not indicated in most cases Crit Care Med. 2007;35:21912195.
Use if life threatening or symptomatic thrombi 3. White B, Livingstone W, Murphy C, et al. An open
without active bleeding (eg, purpura fulminans, label study of the role of adjuvant hemostatic
TREATMENT acral gangrene) support with protein C replacement therapy in
May be used to interrupt underlying purpura fulminans-associated meningococcemia.
PRE HOSPITAL coagulopathy Blood. 2000;96:3719.
r Assess and stabilize airway, breathing, and Potential to aggravate bleeding 4. Nadel S, Goldstein B, Williams MD, et al.
circulation. Contraindicated in CNS injury or liver failure REsearching severe Sepsis and Organ dysfunction
r Circulation: Unfractionated heparin 510 U/kg/hr IV for in children: A gLobal perspective (RESOLVE) study D
Apply pressure to control active bleeding. chronic DIC group. Drotrecogin alfa (activated) in children with
Establish IV access. Protein C, antithrombin concentrates (restoration severe sepsis: A multicentre phase III randomized
IV fluids to support BP. of endogenous anticoagulant proteins): controlled trial. Lancet. 2007;369:836843.
Controversial; minimal studies in children
INITIAL STABILIZATION/THERAPY Protein C has been effective in children with See Also (Topic, Algorithm, Electronic
r Assess and stabilize airway, breathing, and Media Element)
purpura fulminans due to congenital r Hemophilia
circulation: homozygous protein C deficiency.
Control bleeding. Mixed results with use of activated protein C in r Hypotension
Establish IV access. sepsis; some evidence that adults with severe r Sepsis
r Restore and maintain circulating blood volume. r Transfusion Reaction
sepsis benefit from administration; study in
r Treatment of precipitating condition: children showed no benefit (3,4).
Antibiotics for sepsis r Inhibition of fibrinolysis:
Debridement of devitalized tissue in trauma -aminocaproic acid (EACA) CODES
Evacuation of uterus if retained fetus Tranexamic acid
Chemotherapy in malignancy Minimal experience in children ICD9
Cooling for heat stroke r 286.6 Defibrination syndrome
r 776.2 Disseminated intravascular coagulation in
ALERT Off-label use of activated factor VII has been used in
r TRANSFUSION OF BLOOD PRODUCTS IS patients with DIC: newborn
r This therapy is associated with significant morbidity
CRITICAL.
r Primary treatment of DIC is treatment of the and mortality in other settings.
r Pending evidence of safety and efficacy in treating PEARLS AND PITFALLS
suspected or known underlying derangement
(1,2). DIC, use is not recommended. r Identification and treatment of the underlying
r Replace depleted blood components: DISPOSITION precipitating condition is the most important part of
Indicated in patients with significant bleeding Admission Criteria management.
r Use clinical conditions (eg, bleeding) to guide
symptoms or those at high risk for bleeding due Critical care admission criteria:
to impending invasive procedure r Severe precipitating illness in combination with DIC replacement therapy rather than lab values alone.
r Goal is to reduce or stop significant bleeding, not r The most common cause of DIC is infection and
requires ICU admission.
necessarily to normalize lab values (1,2): subsequent septic shock. Antibiotics administration
Fresh frozen plasma: is paramount in such a setting.
Provides procoagulant and anticoagulant FOLLOW-UP r In the setting of hemorrhage, if large volumes of
proteins RBCs are transfused without concurrent
For prolonged PT and active bleeding
FOLLOW-UP RECOMMENDATIONS replacement of clotting factors that are not
1015 mL/kg, max 4 units Patient Monitoring contained with packed RBCs, DIC may develop.
Close monitoring of hemodynamic status, mental
Platelets:
If platelets <20,000/mm3 or <50,000/mm3 status, electrolytes, gas exchange, and hematologic
and coagulation abnormalities
with ongoing bleeding
12 units/10 kg, max 6 units PROGNOSIS
r Depends on underlying condition
Cryoprecipitate:
For severe hypofibrinogenemia (<50 mg/dL) r Generally poor, associated with significant morbidity
or fibrinogen <100 mg/dL with active and morality
bleeding COMPLICATIONS
10 mL/kg, max 10 units r Thrombotic or hemorrhagic stroke
r Packed RBC transfusions for significant blood r Digit or limb amputation
loss/anemia r Multiorgan dysfunction
r Death
269
DIZZINESS/VERTIGO
Steven Krebs
Faye E. Doerhoff
r Dizziness: Middle ear disease, dehydration, r History of perinatal infections, especially

BASICS orthostatic hypotension, heat-related illness (heat toxoplasmosis, rubella, cytomegalovirus, herpes
exhaustion, heat stroke), hypoglycemia, anemia, simplex (TORCH), have been associated with
DESCRIPTION arrhythmia, anxiety/panic disorder, hyperventilation, labyrinthitis.
r Vertigo (also called true vertigo) refers to the depression, presyncope, vasovagal episode, r Family history including migraine, epilepsy, hearing
perception of rotation of either the environment intoxication/ingestion loss
around the patient or the patient within the r Thorough review of systems
environment.
r Vertigo is a rare complaint in children: DIAGNOSIS PHYSICAL EXAM
r Nystagmus should be found in almost all truly
The most common forms are associated with
HISTORY vertiginous patients but may not be present at the
migraine or otitis media (OM) r The key historical element differentiating vertigo
Benign paroxysmal positional vertigo (BPPV) is time of exam:
from dizziness is the subjective sense of rotation. Check in all gaze and head positions for
rare in children and, if present, classified as r Nausea and vomiting are commonly associated with
benign paroxysmal vertigo of childhood (BPVC). nystagmus.
No consensus exists as to whether BPPV or BPVC vertigo. Fast component of nystagmus is usually in the
r Timing, pattern, and severity of spells: same direction as perceived rotation.
are separate entities or along the spectrum of
migraine disorders. Sudden onset of persistent vertigo suggests Dix-Hallpike maneuver for BPPV or BPVC:
r Dizziness, or pseudovertigo, is a generic term and trauma, infection, stroke, or ingestion. Rapid transition from sitting to supine position
common complaint in children. Peripheral etiologies typically cause more severe with head turned 45 degrees to 1 side and tilted
r Dizziness is distinguished from vertigo by the vertigo. 20 degrees in extension
Central causes are more commonly recurrent, Typical latency is 510 sec.
absence of a subjective sensation of rotation. Rotary nystagmus indicates a positive test.
chronic, and/or progressive: Migraine, BPPV or
EPIDEMIOLOGY BPVC, seizures, brainstem/cerebellar mass. Fast component of rotary nystagmus is toward
Prevalence If recurrent, identify suspected triggers: affected ear (the one closest to the ground).
Vertigo and dizziness among school-age children has Provocation by changes in head position, r Peripheral vestibular function is evaluated by warm
been reported to be 15% (1). without tinnitus or hearing loss, suggests BPPV or cold calorimetric response testing:
or BPVC. With patient in a 60-degree recumbent position,
RISK FACTORS Provocation by coughing or sneezing may careful irrigation of cold (10 mL ice water or 100
Recent head injury, recurrent or chronic OM, patient or suggest a perilymphatic fistula (causing mL water 7 C below body temperature) or warm
family history of migraine increased perilymphatic drainage). (44 C) water
PATHOPHYSIOLOGY r Details of any headaches or head trauma: Normal response to cold water is slow eye
r Vertigo represents a disturbance in either the Head trauma and headaches are more frequently movement toward stimulus and fast movement
peripheral or central vestibular system. observed in children with vertigo than healthy away.
r The peripheral vestibular system is comprised of the controls (2). Warm water causes the reverse response.
labyrinth (semicircular canals and the vestibule) and Prior head injury suggests possible temporal bone Lack of response indicates peripheral vestibular
the vestibular nerve, and lie in the petrous portion of fracture or concussion syndrome. dysfunction on the affected side.
the temporal bone: Basilar migraine is characterized by throbbing To improve tolerance of the procedure in children,
The semicircular canals are stimulated by, and occipital headache associated with vertigo, ataxia, consider use of warm water or warm/cooled air
responsible for, detection of rotational movement. dysarthria, and/or tinnitus: Up to 1 in 5 children instead of water.
The vestibule contains the utricle and saccule, with migraine may experience vertigo during their r Cerebellar exam including gait, finger-nose, rapid
which detect planar motion and orientation. aura. alternating movements, heel-shin, looking for
Afferent impulses from the labyrinth travel via the r Medication/Drug exposure: ataxia, dysmetria:
vestibular portion of cranial nerve (CN) VIII to Any current/recent medications, especially Unsteady gait may result from both cerebellar and
vestibular nuclei in the brainstem and cerebellum. ototoxic drugs (eg, aminoglycosides) vestibular dysfunction.
r The central vestibular system refers to the cortex, Presence of prescription or over-the-counter If lesion is unilateral, the patient will fall toward
brainstem, and cerebellum: medications in the home and how they are stored the side of the lesion.
Balance and position sensation are supported by Illicit drug use/ingestion, intentional or accidental r Thorough CN assessment to identify palsies (may
cerebellar and vestibulospinal tract efferents going r Details of ear/hearing-related complaints: indicate intracranial process)
to peripheral muscles. Recurrent/Chronic ear infections (increased risk of r Signs of head trauma, especially around the
Oculovestibular reflexes are due to vestibular cholesteatoma, perilymphatic fistula) ear/temporal regions, and basilar skull fracture
nuclei efferent impulses traveling to CNs III, IV, Recent surgical procedures involving ears (Battle sign, raccoon eyes)
and VI. Presence/Absence of associated hearing loss r Basic assessment of hearing including symmetry (eg,
r Lesions in any of these areas or related pathways (central etiologies typically spare hearing) scratch test)
may affect the vestibular system and result in Tinnitus, sensation of ear fullness, and progressive r All aspects of otoscopy are relevant:
vertigo, among other symptoms. hearing loss are typical for Meniere disease (rare External auditory canal inspection: Cerumen
in children). impaction, foreign body, pus (from tympanic
ETIOLOGY r History of recurrent or transient altered mental
r Vertigo: membrane [TM] rupture), herpetic lesions (Ramsay
status (basilar migraine, seizures) Hunt syndrome), blood and/or clear fluid
Peripheral: Labyrinthitis (suppurative or serous), r Recent/Current upper respiratory infections or other
external ear impaction, BPPV or BPVC, (traumatic injury)
febrile illness TM for signs of OM, perforation, effusion, mass
intoxication/ingestion, perilymphatic fistula, r Risk factors for dehydration
cholesteatoma, vestibular neuritis, temporal bone (suggesting cholesteatoma)
r Recurrent/Remitting neurologic complaints may Pneumatic otoscopy beneficial for evaluating TM
fracture, acoustic neuroma, vestibular concussion,
Meniere disease, Ramsay Hunt syndrome suggest MS. mobility (presence of OM): Hennebert
Central: Migraine, tumor, meningitis, motion signepisode of vertigo triggered by change in
sickness, encephalitis, trauma, increased middle ear pressure (perilymphatic fistula)
r Assess for meningeal irritation (nuchal rigidity,
intracranial pressure, seizure, stroke, MS
Kernig and Brudzinski signs).
r Visual acuity and field testing
270
DIZZINESS/VERTIGO
DIAGNOSTIC TESTS & INTERPRETATION Second Line REFERENCES

Diagnostic testing should be guided by historical and r Diazepam: Children 12 yr for severe symptoms,
physical findings. PO 210 mg/dose t.i.d.q.i.d., IM/IV 210 mg/dose 1. Russell G, Abu-Arafeh I. Paroxysmal vertigo in
q34h PRN childrenan epidemiological study. Int J Pediatr
Lab r Steroids (IV or PO) may be of benefit for labyrinthitis, Otorhinolarygol. 1999;49(Suppl 1):105107.
r Other than serum glucose, routine lab testing is not
though clear data on this is lacking. Consider in 2. Niemensivu R, Kentala E, Wiener-Vacher S, et al.
typically necessary.
r Blood glucose conjunction with neurology or ENT consultation for Evaluation of vertiginous children. Eur Arch
r CBC treatment options. Otorhinolaryngol. 2007;264(10):11291135.
r Urine drug screen DISPOSITION
r Serum drug levels (EtOH, acetaminophen, Admission Criteria ADDITIONAL READING
salicylates, tricyclics) r Severe cases refractory to medical treatment
r Fife TD, Tusa RJ, Furman JM, et al. Assessment:
r BUN and creatinine to assess renal function r Unable to tolerate PO therapy due to vomiting
r If meningitis/encephalitis is suspected, lumbar r Significant dehydration unable to tolerate PO Vestibular testing techniques in adults and children.
puncture for CSF studies: rehydration
Report of the Therapeutics and Technology
Assessment Subcommittee of the American
D
Culture and Gram stain r Critical care admission criteria:
Academy of Neurology. Neurology. 2000;55(10):
Cell count, protein, glucose Traumatic head injuries with neurologic findings, 14311441.
Viral studies as indicated (enterovirus, herpes evidence of intracranial injury, or skull fracture r Teach SJ. Dizziness. In Fleisher GR, Ludwig S, eds.
simplex virus) Meningitis/Encephalitis with signs of shock or risk Textbook of Pediatric Emergency Medicine. 6th ed.
Imaging of rapid deterioration Philadelphia, PA: Lippincott Williams & Wilkins;
Brain imaging is indicated in posttraumatic, chronic, or Discharge Criteria 2010.
recurrent vertigo: r Well-appearing patients with good response to
r For posttraumatic vertigo, especially when initial therapy
associated with hearing loss or facial palsy, CT is r Patients with symptoms clearly linked to external or CODES
both fast and reliable for identification of middle ear disease that has resolved or is being
intracranial hemorrhage and should include specific treated ICD9
temporal bone imaging. r 386.11 Benign paroxysmal positional vertigo
r MRI is ideal for imaging of the posterior fossa and
Issues for Referral
r Neurosurgery consultation in the emergency r 780.4 Dizziness and giddiness
brainstem. department: Radiologic evidence of
Diagnostic Procedures/Other intracranial/posterior fossa mass, basilar skull
r Abnormal orthostatic BP changes (reduction of 20 fracture, or intracranial hemorrhage PEARLS AND PITFALLS
or 10 mm Hg in systolic BP or diastolic BP, r Otorhinolaryngology consultation: Evaluation of r Vertigo is often accompanied by nystagmus, nausea,
respectively, from supine to standing) may suggest temporal bone fracture and vomiting.
dehydration causing dizziness. r Otorhinolaryngology referral: Formal auditory testing r Vertigo is most commonly associated with migraine
r EEG if associated with altered or loss of in cases with associated hearing loss, evaluation of or OM.
consciousness perilymphatic fistula, cholesteatoma, r Dizziness is most commonly caused by eustachian
r ECG to evaluate for arrhythmia chronic/complicated OM
r Neurology consultation: Suspected seizure, CNS tube or middle ear disease.
r Complaints of unremitting vertigo or dizziness with
disease or migraine refractory to outpatient therapy,
TREATMENT neurologic signs may signal a CNS lesion, tumor, or
vertiginous patients with other focal neurologic
degenerative process.
findings r Any suspected vestibular or cerebellar findings on
PRE HOSPITAL r Neurology referral: Vertigo not requiring admission
In the setting of recent trauma, cervical spine neurologic exam should warrant evaluation for a
for formal vestibular function testing
stabilization and evaluation of ABCs possible posterior fossa mass.
INITIAL STABILIZATION/THERAPY r Epley maneuvers may be curative for BPPV in adults,
though there is little experience in children.
circulation. r Motion sickness may be treated with simple
r Appropriate immobilization in cases of trauma
behavioral changes (eg, looking outside vehicle
r Crystalloid 20 mL/kg bolus if dehydrated
while traveling).
MEDICATION
First Line
r Dimenhydrinate (Dramamine) 5 mg/kg/day PO
FOLLOW-UP
divided q6h, max single dose 75 mg/day (26 yr) or FOLLOW-UP RECOMMENDATIONS
150 mg/day (612 yr) Discharge instructions and medications:
r Meclizine (Antivert) 25 mg PO q12h for those r Follow up with an appropriate specialist as noted.
12 yr for vertigo; 2550 mg prior to travel for
motion sickness
PROGNOSIS
r Prochlorperazine PO/PR 2.5 mg per dayb.i.d. Good prognosis for common causes of
vertigo/dizziness in children
(1014 kg), 2.5 mg b.i.d.-t.i.d. (1518 kg), 2.5 mg
t.i.d. or 5 mg b.i.d. (1939 kg): IM/IV 0.10.15 mg/
kg/dose, max 40 mg/day for severe nausea/migraine.
Consider coadministration of diphenhydramine
1.25 mg/kg (max single dose 50 mg) to prevent a
dystonic reaction.
r Meningitis: See Meningitis topic.
271
DROWNING
Donna M. Simmons
GENERAL PREVENTION
BASICS r Supervise children at pools and at beaches. DIAGNOSIS
r Educate parents and children.
DESCRIPTION r Use secured fencing and gating around pools. HISTORY
r Drowning is an injury caused by submersion in a r Age and underlying medical problems
r Use appropriate flotation devices.
liquid and resulting in respiratory insufficiency: r Consider the use of drugs and alcohol.
r Avoid alcohol and drugs.
Ultimately, this can lead to significant morbidity or r Suspect head and spine injuries as possible causes
r Swim with a partner.
death (1). of near drowning.
r Near drowning is survival after a submersion injury. PATHOPHYSIOLOGY r Characteristic of the fluid (saltwater, freshwater,
r Secondary drowning is death due to respiratory r Panic leads to a loss of the normal breathing pattern sewage) determines risk of infection and aspiration
failure following a near-drowning event. and breath-holding as one struggles to keep above of sediment.
r Wet drowning is associated with aspiration of water. r Duration of submersion and temperature of fluid:
fluid into the lungs. r Gasping with aspiration and laryngospasm: Hypothermia is neuroprotective, and complete
r Dry drowning is asphyxia due to laryngospasm Loss of protective reflexes results in fluid recovery may occur even with prolonged
that occurs during submersion. aspiration in 85%, while persistent laryngospasm resuscitation.
r The difference between wet and dry drowning is not causes asphyxia without significant aspiration of r Timing of rescue and resuscitation efforts
clinically significant. Management is the same, and fluid in 15%. r Response to resuscitation
r Hypoxemia leads to loss of consciousness, r Associated injuries
this terminology is no longer used.
multiorgan failure, acidosis, and cardiac arrest.
EPIDEMIOLOGY r When the face is suddenly immersed in cold water, PHYSICAL EXAM
r Perform complete physical exam.
Incidence the diving reflex is thought to occur, resulting in
r There were 3,568 unintentional deaths due to r Assess for hypothermia and hypotension.
inhibition of respiration causing apnea;
drowning in the U.S. in 2006 in persons <85 yr: r Arrhythmias may occur:
vasoconstriction of blood vessels to nonessential
Of these deaths, 765 (21.4%) were children systems; and shunting of blood to the lungs, heart, Sinus bradycardia and atrial fibrillation are most
14 yr. and brain: common.
Drowning was the 2nd leading cause of Most pronounced in children relative to adults. Ventricular fibrillation and asystole may also occur.
unintentional injuryrelated death in this age Children have greater chance of surviving r Pulmonary insufficiency or respiratory distress will
group. prolonged submersion in cold water. manifest as shortness of breath or tachypnea,
r For children 4 yr, drowning was the cause of death coughing, nasal flaring, grunting, wheezing, stridor,
Resulting risk for dysrhythmia and neurologic
in 28.4% of the cases of fatal unintentional injuries. injury and/or retractions.
r The highest incidence occurs among children age r Theoretically, saltwater and freshwater drowning r Auscultation may reveal rales and wheezing with
4 yr and teens 1519 yr. will cause changes in serum electrolytes when a bronchospasm.
r Males are more likely to die from unintentional large amount of water is aspirated: r Neurologic signs include altered mental status,
drowning (2). During saltwater drowning, hypertonic saltwater confusion, lethargy, unconsciousness, and seizures.
r Children 14 yr drown most commonly in pools, and draws fluid into the lungs, leading to pulmonary
children 1 yr are more likely to drown in the edema, decreased blood volume, hypertonic
bathtub. serum, hypoxemia, and shock. Lab
r Teen drowning commonly occurs in natural bodies Freshwater drowning causes volume overload as Initial Lab Tests
r CBC, electrolytes, glucose, and renal function tests
of water with associated alcohol use (3). aspirated hypotonic water facilitates the
r Other tests should be performed to assess
r Drowning is most common in blacks (2). movement of water into the intravascular space.
r Near-drowning victims usually do not aspirate a end-organ injury and metabolic status including liver
Prevalence significant amount of fluid and do not have profile, coagulation studies, and lactate level.
The rate of unintentional drowning deaths in 2006 for r Blood gas in symptomatic patients
electrolyte imbalances.
children 14 yr was 1.26 cases per 100,000 r Loss of surfactant occurs with saltwater (dilutes
population (2). Imaging
surfactant) or freshwater (destroys surfactant): r CXR for symptomatic patients:
RISK FACTORS The resulting atelectasis and decreased lung May initially be normal or show pulmonary edema
r Children who are inadequately supervised compliance leads to V/Q mismatching, or atelectasis
r Lack of barriers around pools intrapulmonary shunting, and hypoxemia. r Consider CT scans for patients with altered mental
r Overestimating of capability to swim or inability to r Inflammatory mediators are released and may cause status or head and neck injuries.
swim pulmonary HTN and edema and result in the
r Hypothermia: Diagnostic Procedures/Other
development of acute respiratory distress syndrome r Continuous pulse oximetry
Can cause disorientation, early muscle fatigue, or (ARDS). r ECG to look for dysrhythmia
cardiac arrhythmias r CNS hypoxia and neuronal injury leads to cerebral
r Hyperventilating prior to a shallow dive lowers edema and elevated intracranial pressure (ICP), loss DIFFERENTIAL DIAGNOSIS
PaCO2 , as swimming uses oxygen and lowers PaO2. of autoregulation, and seizures. Consider other medical conditions, which may be the
The slow increase in PaCO2 delays the stimulus to r Autonomic instability may lead to HTN, tachycardia, initial inciting factor:
breathe, resulting in hypoxia, seizure, or loss of diaphoresis, agitation, muscle rigidity, r CNS injuries, cardiac arrhythmias, MI, complications
consciousness. rhabdomyolysis, and myoglobinuria. of diabetes, syncope, closed head injury, spinal cord
r Risk-taking behavior in adolescents r Cardiac dysrhythmia can develop secondary to injury, or seizures
r Impaired judgment due to drugs or alcohol hypoxia or hypothermia. Acidosis can result in
r Water sports myocardial dysfunction:
r Unexpected changes in the currents of the water, Tako-tsubo cardiomyopathy has been associated
such as rip currents in the ocean with near drowning (4).
r Underlying medical conditions: r Acute tubular necrosis from renal hypoxemia and
Cardiac arrhythmias such as congenital long QT or myoglobinuria may lead to renal failure.
familial polymorphic VT
MI, trauma
Seizures, syncope
Diabetes mellitus and hypoglycemia
Depression
272
DROWNING
Discharge Criteria REFERENCES

r Patients remaining asymptomatic after 8 hr of
TREATMENT
observation may be discharged. 1. Van Beeck EF, Branche CM, Szpilman D, et al. A
PRE HOSPITAL r Mildly symptomatic patients who have normal pulse new definition of drowning towards documentation
r Assess and stabilize airway, breathing, and oximetry, CXR, and arterial blood gas and who and prevention of a global-public health problem.
circulation: improve after a prolonged observation may be Bull World Health Organ. 2005;83(11):853856.
Provide supplemental oxygen and support discharged. 2. CDC. Injury Prevention & Control: Data & Statistics
breathing. Issues for Referral (WISQARS). Available at http://www.cdc.gov/
Provide cervical spine immobilization when Rehabilitation injury/wisqars/index.html.
cervical spine injury is suspected. 3. Brenner RA; American Academy of Pediatrics
r Assess pulse before beginning CPR, as sinus Additional Therapies Committee on Injury, Violence, and Poison
r Extracorporeal membrane oxygenation for persistent
bradycardia and atrial fibrillation do not require Prevention. Prevention of drowning in infants,
treatment initially in hypothermic patients. respiratory failure despite intubation/ventilation and children, and adolescents. Pediatrics. 2003;112:
r Prevent cooling: with rewarming 440445.
Remove wet clothing and cover with blankets.
r Bronchoscopy and bronchoalveolar washings
4. Citro R, Previtali M, Bossone E. Tako-tsubo D
Minimize movement in patients with severe cardiomyopathy and drowning syndrome: Is there a
hypothermia with temperature <30 C due to risk FOLLOW-UP link? Chest. 2008;134(2):469.
of development of ventricular fibrillation. 5. Orlowski J. Prognostic factors in pediatric cases of
Begin rewarming hypothermic patients with FOLLOW-UP RECOMMENDATIONS drowning and near-drowning. Ann Emerg Med.
temperature <33 C according to hypothermia Return for development of respiratory symptoms, fever, 1979;8:176179.
protocols. or other signs of ill appearance. 6. Habib DM, Tecklenburg FW, Webb SA, et al.
With profound hypothermia, CPR should be Predictions of childhood drowning and
Patient Monitoring
performed if ventricular fibrillation develops. near-drowning morbidity and mortality. Pediatr
Follow pulmonary function with blood gas, cardiac
INITIAL STABILIZATION/THERAPY monitoring for dysrhythmias and myocardial Emerg Care. 1996;12(4):255258.
r Perform ABCDEs as per Advanced Trauma Life dysfunction, electrolyte abnormalities, renal function, See Also (Topic, Algorithm, Electronic
Support (ATLS) and Pediatric Advanced Life Support and neurologic status. Media Element)
(PALS) guidelines: r Aspiration
PROGNOSIS
Support respirations and intubate if there are r Varies with length of submersion, time to r Hypothermia
signs of respiratory failure (PaO2 <60 with high
resuscitation, and severity of concomitant medical
oxygen supplementation) or neurologic
conditions
deterioration. Use of BiPAP/CPAP may correct r Neurologic recovery is possible after prolonged
hypoxemia in awake patients:
CODES
Bronchodilators for bronchospasm submersion, especially cold water submersion.
r Poor outcomes are associated with: ICD9
Avoid excessive hyperventilation, maintain
PaCO2 at 3035 mm Hg, and elevate the head Submersion >5 min (5) 994.1 Drowning and nonfatal submersion
to lower ICP. Time to resuscitation >10 min (5)
Remove wet clothing and rewarm to 32 C if Coma on arrival to emergency department (5)
hypothermic, as continued hypothermia has not Age <3 yr or pH <7.1 (5) PEARLS AND PITFALLS
been shown to improve outcome. Arrest on arrival to emergency department (6) r Pearls:
Hypotension is treated with fluid replacement and Fixed/Dilated pupils or posturing (6)
Survival and neurologic recovery are possible after
inotropic support. Warm water submersion (6)
prolonged submersion in cold water, and
r Manage head, spinal, chest, and abdominal injuries COMPLICATIONS exhaustive attempts at resuscitation are
appropriately. r Respiratory failure warranted in such cases.
r Seizures should be treated to prevent increased r ARDS Manage hypothermia.
metabolic demand. r Electrolyte abnormality r Pitfalls:
r Prophylactic antibiotics are not indicated unless r End-organ injury: Need to properly manage hypothermia
there is aspiration of grossly contaminated water. Permanent neurologic injury Not recognizing concomitant injuries head, spinal,
r Maintain normoglycemia, and correct electrolyte Hepatic injury chest, and abdomen or treating underlying
abnormalities. Renal injury conditions
r MI
DISPOSITION
r Death
Admission Criteria
r Admit patients with respiratory compromise,
abnormal CXR, concerning blood gas, or abnormal
vital signs, such as pulse oximetry.
r Admit patients requiring treatment of concomitant
injuries, especially those with underlying medical
problems that may complicate their course.
Patients requiring intubation and those with
severe neurologic dysfunction or multiorgan
system failure require ICU care.
273
DUCTAL-DEPENDENT CARDIAC EMERGENCIES

Kumarie Etwaru
Kristy Bunagan
Robert J. Hoffman
ETIOLOGY r Hypercyanotic spells are usually the presenting

BASICS 3 types of ductal-dependent lesions: symptom in an infant with TOF. During a spell,
r Lung-dependent CHDs are pulmonary atresia, intense cyanosis and hyperpnea present rapidly
DESCRIPTION pulmonary stenosis, tricuspid atresia, truncus while the murmur decreases in intensity.
r The ductus arteriosus is a vascular connection r Signs of heart failure soon develop when the
arteriosus, Ebstein anomaly, and TOF.
between the main pulmonary artery and aorta. r Systemic circulationdependent CHDs are pulmonary vascular resistance begins to fall:
r It shunts fetal blood away from the lungs and closes Tachypnea, tachycardia, sweating, gallop rhythm,
coarctation of the aorta, severe aortic stenosis, and
within the 1st few days after birth. Infants with hypoplastic left heart syndrome. and hepatomegaly.
ductal-dependent critical congenital heart diseases r Transposition of the great arteries (TGA) depends on r With systemic circulationdependent CHDs, the
will present in extremis when the duct begins the patent duct for mixing of systemic and presentation may be similar to sepsis. These patients
closing. pulmonary blood flow. experience tachypnea, mottled gray skin, and poor
r Ductal-dependent lesions are congenital heart perfusion with decreased peripheral and central
diseases that need the ductus arteriosus to remain COMMONLY ASSOCIATED CONDITIONS pulses.
r Ebstein anomaly is associated with
open after birth in order to supply blood to the lungs
and systemic circulation or for mixing of systemic Wolff-Parkinson-White syndrome. DIAGNOSTIC TESTS & INTERPRETATION
and pulmonary blood. r Truncus arteriosus and TOF are associated with Lab
DiGeorge syndrome (22q11 microdeletion). Initial Lab Tests
EPIDEMIOLOGY r Coarctation of the aorta is associated with with r Assess bedside glucose for hypoglycemia.
Prevalence per 10,000 births based on the r Blood gas analysis with lactate measurement to
Turner syndrome.
Metropolitan Atlanta Congenital Defect Program: r Pulmonary stenosis is associated with with Noonan assess oxygenation, ventilation, and perfusion
r Pulmonary atresia 0.8, pulmonary stenosis 6.3, r CBC with differential count, C-reactive protein:
syndrome.
tricuspid atresia 0.5, truncus arteriosus 1.0, Ebstein Anemia, heart failure, sepsis, or shock may be
anomaly 0.6, tetralogy of Fallot (TOF) 6.1, clinically similar presentations.
coarctation of the aorta 4.7, aortic stenosis 1.6, DIAGNOSIS r Comprehensive chemistry (CHEM 20):
hypoplastic left heart 3.3, transposition of great Various abnormalities may be present.
arteries 4.0 HISTORY Low bicarbonate, elevation of BUN/creatinine, and
r The presence of other heart defects, the timing of
RISK FACTORS elevations of AST/ALT may occur due to
closure of the ductus arteriosus, and the degree of
Some factors are associated with an increased hypovolemia or poor perfusion.
pulmonary vascular resistance determine the onset r Consider blood culture, urinalysis, urine culture, and
incidence of ductal-dependent lesions: and severity of symptoms.
r Genetic or chromosomal abnormalities r In the 1st days to weeks of life, the presence of CSF analysis/culture if considering sepsis as causal
r Maternal diabetes or phenylketonuria of symptoms.
critical CHD is herald by increasing cyanosis in a
r Use of medications such as lithium or phenytoin patient who may not be in respiratory distress. Imaging
during pregnancy r Depending on the lesion, those affected may r CXR:
develop symptoms of heart failure such as poor Radiographic findings include cardiomegaly with
PATHOPHYSIOLOGY increase vascular marking:
r In the fetus, the right ventricle handles 60% of the feeding, sweating while feeding, and/or tachypnea.
r Other patients may present with acute signs and In a cyanotic neonate, this should prompt
total cardiac output. consideration of ductal-dependent lesions.
r The pulmonary circulation has a high vascular symptoms of shock with ductal closure.
Pulmonary atresia: Boot-shaped heart with absent
resistance while the systemic vascular resistance is PHYSICAL EXAM main pulmonary shadow
low, which facilitates blood flow from the right r Assess vital signs, with focus on cardiopulmonary
Pulmonary stenosis: Prominent main pulmonary
ventricle to the descending aorta through the ductus and pulse oximetry parameters. artery
arteriosus. r Severe cyanosis occurs early in infants with TGA, TOF: Boot-shaped heart, with right-sided aortic
r After birth, with the onset of breathing, the lungs
Ebstein anomaly, and pulmonary atresia once the arch in 2650% of cases
expand and systemic oxygen saturation rises. This ductus arteriosus closes. Truncus arteriosus: Right-sided aortic arch and
causes pulmonary vasodilation and a decrease in r Aortic coarctation: Arterial HTN in the right arm with prominent vascular markings
pulmonary vascular resistance. Simultaneously, lower to normal BP in the lower extremities is the TGA may demonstrate the egg on a string
when the placenta is removed, systemic vascular classic finding. If the coarctation is located before appearance in 1/3 of patients.
resistance rises, leading to reversal of blood flow in the subclavian artery, a pressure difference between r Transthoracic echo with cross-sectional and Doppler
the ductus arteriosus from left to right. the right and left arm exists. flow analysis is the diagnostic modality of choice.
r The ductus arteriosus remains open when there is r Auscultatory clues are helpful to early diagnosis:
prostaglandin E2 and low arterial oxygen. Diagnostic Procedures/Other
Single S2 for truncus arteriosus, tricuspid atresia, r ECG:
r Any anatomic abnormality in the fetal heart affects
TGA, and hypoplastic left heart Lung-dependent CHDs have right atrial
normal cardiovascular circulation. Aortic ejection click for truncus arteriosus
r In lung-dependent coronary heart diseases (CHDs), enlargement or right ventricular hypertrophy
Single and loud S2 and hyperactive precordium on (RVH).
deoxygenated blood cannot pass through to the palpation for critical coarctation of the aorta, With coarctation of the aorta and severe aortic
lungs to be oxygenated due to lack of opening in severe aortic valve stenosis, and hypoplastic left stenosis, left ventricular hypertrophy is observed.
the right side of the heart. heart syndrome With TGA, right axis deviation and RVH are also
r In systemic circulationdependent CHDs, If ventricular septal defect, a loud holosystolic evident plus an upright T wave in V1, which may
oxygenated blood cannot reach vital organs due to murmur at the left lower sternal border may be be the only abnormality present.
constriction of the left side of the heart. present.
r The patent ductus is the only means for oxygenated Systolic ejection murmurs at the upper sternal
blood to reach the systemic circulation. border for coarctation of the aorta and aortic
stenosis are present.
274
DUCTAL-DEPENDENT CARDIAC EMERGENCIES
r Hyperoxia test: r Palliative systemic to pulmonary artery shunts (eg, COMPLICATIONS

Used to differentiate between cardiac and Blalock-Taussig shunt): For TOF, hypoplastic left r CHF
pulmonary cause of hypoxia/cyanosis heart, tricuspid atresia, pulmonary stenosis: r Failure to thrive
A cardiac cause (right to left shunt) is suspected Increases pulmonary blood flow by shunting blood r Shock
when the PaO2 is <100 mm Hg after 100% from the systemic circulation r Multiorgan system failure
oxygen is administered for 1015 min. r Fontan procedure: For heart lesions with a single r Death
Pulse oximetry reading may be used in lieu of ventricle like tricuspid atresia and hypoplastic left
repeated blood gas measurements. heart:
DIFFERENTIAL DIAGNOSIS A connection between the superior vena cava ADDITIONAL READING
r Cyanotic heart disease not involving ductal with the right pulmonary artery plus a connection
r Doyle T, Kavanaugh-McHugh A, Graham T, et al.
dependence between right atria and inferior vena cava to
r CHF pulmonary arteries are created. Clinical manifestations and diagnosis of patent
Separates the systemic and pulmonary circuits ductus arteriosus. September 2010. UpToDate.
r Pneumonia
r Norwood procedure: For hypoplastic left heart Available at http://www.uptodate.com/patients/
r Infections: Sepsis, meningitis
r Persistent pulmonary HTN syndrome. There are 2 stages: content/topic.do?topicKey=rFjXi1HGQtKmgs. D
1st stage creates a connection between main Accessed December 15, 2010.
r Methemoglobinemia r Fleisher G, Ludwig S, Henretig F. Textbook of
pulmonary arteryaorta, and Blalock-Taussig
shunt provides pulmonary blood flow. Pediatric Emergency Medicine. 5th ed. Philadelphia,
The 2nd stage is a bidirectional Glenn shunt to PA: Lippincott Williams & Wilkins; 2006:727728.
TREATMENT decrease blood flow to the right ventricle and a r Kliegman RM, Behrman RE, Jenson HB, et al. Nelson
modified Fontan procedure. Textbook of Pediatrics. 18th ed. Philadelphia, PA:
PRE HOSPITAL r Ross procedure: For aortic or pulmonary stenosis; WB Saunders; 2007:18551857, 18911893,
Assess and stabilize airway, breathing, and 19001903, 19061928.
circulation. replacement of the aortic valve with the autologous
pulmonary valve or vice versa r Mejia R, Greenwald B, Fields A, et al. Pediatric
INITIAL STABILIZATION/THERAPY Fundamental Critical Care Support. Mount Prospect,
r Assess and stabilize airway, breathing, and DISPOSITION IL: Society of Critical Care Medicine; 2008:
circulation. Admission Criteria 18.118.11.
r Administer supplemental oxygen. r Select stable patients may be considered for floor
r If there is strong suspicion of a ductal-dependent admission. See Also (Topic, Algorithm, Electronic
r Condition requiring surgery within 48 hr Media Element)
lesion, titrate oxygen to maintain saturation to 85% r Critical care admission criteria: Cyanotic Heart Disease
and start prostaglandin infusion.
r Infants with respiratory failure should be intubated Newly diagnosed patients generally should be
and have an orogastric tube inserted. admitted to an ICU, even if stable, for rapid
r If perfusion is poor and shock is evident, administer detection and management of deterioration. CODES
Unstable vital signs
1020 mL/kg of normal saline IV bolus rapidly.
r Antibiotic prophylaxis should be initiated in patients Prostaglandin needed in the emergency ICD9
department or required in hospital r 746.1 Tricuspid atresia and stenosis, congenital
who presents in shock. r 746.02 Stenosis of pulmonary valve, congenital
r Cardiology consultation Discharge Criteria
r 747.3 Congenital anomalies of pulmonary artery
Unless previously diagnosed and under cardiology
MEDICATION care, these patients are not discharged from the
Prostaglandin E1 infusion (alprostadil): emergency department:
r Rapid administration is needed to keep the ductus r Selective discharge from the emergency department PEARLS AND PITFALLS
arteriosus open; this is lifesaving. rarely is possible under cardiology recommendations. r Mild hypoxia or cyanosis may be the presenting
r Start with 0.050.1 g/kg/min and titrate up as
Issues for Referral symptom of an infant with serious congenital heart
needed (to 0.2 g/kg/min if needed). disease.
r Continuous vital sign monitoring is needed. Follow up with cardiology, cardiothoracic surgery, and
primary care physicians. r Poor feeding or tiring/sweating while feeding may
r Side effects include hypotension, apnea, fever and
be a symptom of heart failure due to congenital
flushing. heart disease.
r Be prepared to support ventilation, perform FOLLOW-UP r Prostaglandin E1 infusion is lifesaving for neonates
endotracheal intubation, and administer fluids and with ductal-dependent lesions.
inotropic support: FOLLOW-UP RECOMMENDATIONS
Some prefer to perform endotracheal intubation Discharge instructions and medications:
r These patients are admitted to the hospital.
electively under controlled conditions prior to
prostaglandin infusion. Patient Monitoring
SURGERY/OTHER PROCEDURES Caregivers must closely monitor for any deterioration
r Cardiac catheterization: and have ability to immediately return to the
Routine catheterization is not necessary. 2D-echo emergency department if needed.
can detect anatomic abnormalities and assess PROGNOSIS
blood flow patterns. Catheterization only is r Depends on the specific congenital heart lesion and
essential when discrepancies are seen or is type of intervention
necessary for surgical management. r Morbidity, mortality, and long-term survival have
r Surgical repair procedure depends on the specific
increased, with patients reaching adulthood.
heart lesion.
r Atrial septostomy:
Sometimes performed urgently or emergently
For TGA and tricuspid atresia; creates atrial septal
defect tp allow blood mixing (oxygenated and
deoxygenated) between atria.
275
DYSRYTHMIA, ATRIAL
Ameer P. Mody
Tommy Y. Kim
In antidromic AVRT, impulses are conducted Imaging

BASICS antegrade down the accessory pathway, then r Consider a chest radiograph to evaluate for
retrograde up the AV node and back down the potential causes or consequences of dysrhythmia.
DESCRIPTION accessory pathway: Cardiomegaly: Myocarditis or cardiomyopathy
r Atrial dysrhythmia is defined as a cardiac rhythm This circuit results in a wide complex r Once stable, patients with new-onset atrial
disturbance generated from above the tachycardia. dysrhythmia should have an echo to assess cardiac
atrioventricular (AV) node. During sinus rhythm, if the electrical impulse is anatomy and function.
r Frequently results in tachycardia conducted antegrade down the accessory
r Premature atrial contractions (PACs)/atrial Diagnostic Procedures/Other
pathway, then the impulse arrives at the ventricle
ECG characteristics in different forms of atrial
extrasystoles are an early occurrence of P waves rapidly, without delay at the AV node, which
tachyarrhythmias will often provide the diagnosis:
followed by a normal or widened QRS. causes pre-excitation: r PAC: Isolated early P wave followed by a normal
r Supraventricular tachycardia (SVT), or paroxysmal The finding on ECG during sinus rhythm consists
of a short PR interval, a widened QRS with a QRS, a block at the AV node, or a block in the
SVT, is the most common pathologic dysrhythmia in
delta wave. bundle branch showing a RSR pattern
children. Can be atrioventricular reentrant r SVT (AVNRT): Heart rate >180 bpm, often >220
tachycardia (AVRT) (75%), including This phenomenon is referred to as a WPW
Wolff-Parkinson-White (WPW) syndrome, pattern. bpm in infants with no beat-to-beat variability, P
r AVNRT has 2 conducting pathways within the AV wave within or after the QRS complex, narrow QRS
atrioventricular nodal reentrant tachycardia (AVNRT)
(13%), or primary atrial tachycardia (14%) (1). node that are designed fast and slow: complex
r Atrial flutter is a rapid, uniform atrial dysrhythmia r SVT (AVRT): Heart rate >180 bpm, often >220
These pathways allow for a reentrant loop utilizing
with an atrial rate between 240 and 450 bpm. the 1st pathway antegrade and 2nd pathway bpm in infants with no beat-to-beat variability, no
r Atrial fibrillation is a chaotic, multifocal atrial retrograde: visible P wave:
This circuit results in a narrow complex Narrow QRS complex in orthodromic
depolarization with a variable resultant ventricular
tachycardia. Wide QRS complex in antidromic SVT has an ECG
tachycardia.
appearance similar to ventricular tachycardia.
EPIDEMIOLOGY ETIOLOGY r Atrial flutter: Saw-tooth flutter waves that are best
r Idiopathic
Incidence r Accessory pathways viewed in leads II, III, and V1, typical atrial rates of
r SVT is the most common cardiac dysrhythmia in 300 bpm, accompanied typically by AV conduction
r WPW syndrome
children (24): of 2:1 to 4:1
r Myocarditis and cardiomyopathies r Atrial fibrillation: Atrial rates of 300600 bpm with
89,000 new cases reported per year
2 cases per 1,000 people r Sick sinus syndrome variable ventricular response to atrial impulses
r Atrial flutter and fibrillation are uncommon in resulting in irregularly irregular heart rates. Irregular
children without a history of cardiac surgery. P waves are best viewed on lead V1.
r 5% of patients who have undergone a Fontan DIAGNOSIS r With significant tachycardia, slow down the ECG
operation will have a cardiac dysrhythmia, most HISTORY paper speed to evaluate for the presence of P waves.
commonly atrial flutter. r Infants can be asymptomatic or present with
RISK FACTORS irritability and/or poor feeding. r Sinus tachycardia secondary to fever, anemia, sepsis,
r Congenital heart disorders r Older children may present with the sensation of a hypovolemia, thyrotoxicosis, medications, illicit drug
r Stimulant medications (eg, beta-agonists, caffeine, racing heart, chest pain, palpitations, use, or shock
anticholinergics, cocaine) light-headedness, fatigue, or syncope. r Ventricular tachycardia
r Myocarditis and cardiomyopathies r Inquire about a history of previous episodes, cardiac r Junctional ectopic tachycardia
r Hyperthyroidism disease, cardiac surgery, medication use, and family
r Pericarditis history.
r Electrolyte disturbances PHYSICAL EXAM
TREATMENT
r Metabolic acidosis r The initial goal of examination is to determine the
PRE HOSPITAL
r Surgically corrected structural heart disease childs hemodynamic stability: Assess and stabilize airway, breathing, and
r Neuromuscular disease Assess for tachycardia and hypotension. circulation.
r Signs consistent with hemodynamic compromise
PATHOPHYSIOLOGY include respiratory distress, pallor, cyanosis, cool INITIAL STABILIZATION/THERAPY
r The normal electrical impulse of the heart is initiated r Cardiac monitoring with rhythm strip analysis should
extremities, prolonged capillary refill, weakened
at the sinoatrial node near the right atrium, to the peripheral pulses, and altered mental status. be initiated immediately.
AV node, to the bundle of His, which divides to the r Other findings consistent with cardiac dysfunction r Most children tolerate atrial dysrhythmias without
right and left bundle branches to the Purkinje fibers include hepatomegaly, edema, and extra heartbeats. significant hemodynamic compromise.
of the ventricular myocardium. r The 1st priority is to differentiate sinus tachycardia
r Atrial dysrhythmias are caused by alternative nodes DIAGNOSTIC TESTS & INTERPRETATION from an atrial dysrhythmia.
of conduction in the atria or disordered conduction Lab r Vagal maneuvers may be attempted for awake
within the atria. Initial Lab Tests patients in SVT (2,3,5):
r AVRT requires an accessory pathway connecting the r Assessment of hemodynamic status takes priority
Hold a bag of ice water slurry to the face of an
atrium and ventricle: above any diagnostic evaluation. infant for 2530 sec to elicit a diving reflex;
r Blood gas analysis with electrolyte values (if
In orthodromic AVRT, impulses are conducted successful in 3060% of cases (6):
antegrade down the AV node to the ventricle, available) may reveal underlying acidosis or Immersion of the head in cold water is
then retrograde up the accessory pathway and metabolic disturbance. dangerous and not recommended.
back down the AV node: r Metabolic panel inclusive of calcium and Valsalva maneuver for children and adolescents:
This circuit results in a narrow complex magnesium (as hypocalcemia or hypomagnesemia Bearing down, blowing into a straw
tachycardia. can be arrhythmogenic) Avoid carotid massage and ocular pressure.
r Thyroid function tests
276
DYSRYTHMIA, ATRIAL
r If hemodynamic compromise is present for SVT, Discharge Criteria 5. Sreeram N, Wren C. Supraventricular tachycardia
atrial flutter, or atrial fibrillation, proceed to r Simple, isolated PACs in asymptomatic patients with in infants: Response to initial treatment. Arch Dis
synchronized cardioversion (4): no risk factors require no additional intervention. Child. 1990;65:127129.
Synchronized cardioversion 0.51 J/kg r Patients with a known history of SVT, without 6. Kugler JD, Danford DA. Management of infants,
2 J/kg for subsequent attempts hemodynamic compromise, and structurally normal children, and adolescents with paroxysmal
Intubation/Airway protection may be required. hearts may be discharged home safely after supraventricular tachycardia. J Pediatr.
Sedation/Analgesia should be provided to awake adequate response to medical or vagal cardioversion 1996;129:324.
patients: and a period of observation: 7. Manole MD, Saladino RA. Emergency department
Decision to initiate anticoagulation prior to Discharge in consultation with a cardiologist. management of the pediatric patient with
cardioversion or after cardioversion of atrial supraventricular tachycardia. Pediatr Emerg Care.
fibrillation is best made in conjunction with a 2007;23:176118.
pediatric cardiologist. FOLLOW-UP 8. Dixon J, Foster K, Wyllie J, et al. Guidelines and
MEDICATION FOLLOW-UP RECOMMENDATIONS adenosine dosing in supraventricular tachycardia.
Arch Dis Child. 2005;90(11):11901191.
First Line
For stable SVT, adenosine is preferred (2,4,7,8):
Follow up with a pediatric cardiologist.
9. Kirk CR, Gibbs JL, Thomas R, et al. Cardiovascular
D
PROGNOSIS
r Adenosine 0.1 mg/kg (up to 6 mg) IV rapid push r 38% of children <4 mo of age and 19% of children collapse after verapamil in supraventricular
tachycardia. Arch Dis Child. 1987;62:12651266.
over 12 sec followed by a rapid 5 cc saline flush >4 mo of age initially present in heart failure (10).
r Repeat dose 0.2 mg/kg (up to 12 mg) if no response r Sudden death from SVT is uncommon in patients 10. Garson A Jr., Gillette PC, McNamara DG.
Supraventricular tachycardia in children: Clinical
to the 1st dose after 12 min; may repeat a 3rd dose with a normal structural heart.
r Use an antecubital vein or central line. r Increased risk of sudden death in patients with features, response to treatment, and long-term
r Transient asystole may occur. follow-up in 217 patients. J Pediatr. 1981;98:875.
WPW, 2.3% with a catastrophic event at 11. Russell MW, Dorostkar PC, Dick M II. Incidence of
r Contraindications to adenosine use include a presentation (11)
r The prognosis of atrial fibrillation and atrial flutter catastrophic events associated with the
deinnervated heart (eg, heart transplant), 2nd- or Wolff-Parkinson-White syndrome in young
3rd-degree heart block. depends on the underlying cardiac defect. patients: Diagnostic and therapeutic dilemma
Second Line COMPLICATIONS (abstract). Circulation. 1993;88:II484.
r In a hemodynamically stable patient with SVT who is r Atrial flutter and fibrillation can lead to atrial
unresponsive to adenosine or where adenosine is thrombus formation and subsequent risk of embolic
contraindicated: phenomena. CODES
Amiodarone 5 mg/kg IV (max 300 mg/dose) over r Untreated SVT can lead to heart failure.
2060 min, followed by a continuous infusion of r Adenosine can rarely precipitate a prolonged ICD9
10 mg/kg/day (3) OR r 427.9 Cardiac dysrhythmia, unspecified
asystole, ventricular tachycardia, atrial fibrillation,
Procainamide 15 mg/kg IV (max 100 mg/dose) and/or apnea. r 427.61 Supraventricular premature beats
over 3060 min; in children <1 yr of age, r 427.89 Other specified cardiac dysrhythmias
10 mg/kg. Follow with a continuous infusion of
50 g/kg/min (3). REFERENCES
May consider a beta-blocker such as propranolol
or esmolol in consultation with a cardiologist 1. Ko JK, Deal BJ, Strasburger JF, et al. PEARLS AND PITFALLS
Verapamil is contraindicated in infants and Supraventricular tachycardia mechanisms and r Pediatric patients can tolerate tachycardia for many
children <1 yr of age due to risk of shock and their age distribution in pediatric patients. Am J hours to days but should be treated promptly due to
cardiac arrest (9). Cardiol. 1992;69:1028. the risk of decompensation.
r If pharmacologic treatment fails, radiofrequency 2. Losek JD, Endom E, Dietrich A, et al. Adenosine r A 20 mL/kg bolus of normal saline may help
catheter ablation may be necessary. and pediatric supraventricular tachycardia in the differentiate sinus tachycardia from SVT.
emergency department: Multicenter study and r Preparation for emergent cardioversion should be
SURGERY/OTHER PROCEDURES review. Ann Emerg Med. 1999;33:185191.
For AVNRT or WPW, the accessory pathway can be made prior to administration of adenosine:
3. The International Liaison Committee on Use the largest pads or paddles that can fit on the
ablated by radiofrequency catheter.
Resuscitation (ILCOR) consensus on science with chest wall without the pads touching to minimize
DISPOSITION treatment recommendations for pediatric and transthoracic impedance.
Admission Criteria neonatal patients: Pediatric basic and advanced r Adenosine failure may be related to inadequate IV
Critical care admission criteria: life support. Pediatrics. 2006;117(5):e955e977. access, insufficient rapidity of administration, or use
r Most patients with an atrial dysrhythmia should be 4. 2005 American Heart Association (AHA) of caffeine or theophylline.
admitted to a monitored pediatric unit, preferably a guidelines for CPR and emergency cardiovascular r Consultation with a pediatric cardiologist is advised
pediatric ICU, for observation and cardiology care (ECC) of pediatric and neonatal patients: for all cases of atrial dysrhythmia.
consultation. Pediatric advanced life support. Pediatrics.
2006;117:e1005.
277
DYSRYTHMIA, VENTRICULAR
Tommy Y. Kim

DESCRIPTION HISTORY
r Obtain a history for heart disease, metabolic ALERT
Ventricular dysrythmia is defined as a wide complex
(prolonged QRS duration) tachycardia beyond the disease, medication use, drug exposure, family VF is an unstable rhythm that should be treated
upper limit of normal for the patients age. history of sudden cardiac death, or electrical burns. immediately with unsynchronized defibrillation. If
r Premature ventricular contractions (PVCs) are r Most children present with vague, nonspecific this rhythm is not converted, progression to asystole
frequent in children. symptoms. and inability to resuscitate is likely.
r Ventricular tachycardia (VT) consists of 3 r Infants can present with fussiness and difficulty
feeding but may not show signs until significantly PRE HOSPITAL
consecutive PVCs. r Maintain airway, breathing, and circulation.
r Ventricular fibrillation (VF) is a form of pulseless impaired cardiac output develops. r CPR for nonperfusing rhythms
r Older children can present with chest pain,
arrest. The heart has no organized rhythm, but r Apply an automated external defibrillator (AED) for
instead the myocardium quivers and does not pump palpitations, light-headedness, dizziness, fatigue or
syncope. children >1 yr, if indicated (7).
blood.
r Pulseless VT is treated the same as VF. PHYSICAL EXAM INITIAL STABILIZATION/THERAPY
r Torsades de pointes is a distinctive form of r The initial goal of the physical exam is to determine r The hemodynamic status drives the decision-making
polymorphic VT, which can be seen in conditions the childs hemodynamic stability. process for a child with ventricular dysrhythmias.
such as long QT syndrome, hypomagnesemia, r Signs consistent with hemodynamic compromise Children may be hemodynamically stable during the
antiarrhythmic drug toxicity, or other drug toxicities. include respiratory distress, cool extremities, initial assessment, but VT can quickly decompensate
prolonged capillary refill, weak peripheral pulses, to hemodynamic compromise:
EPIDEMIOLOGY Stable VT with pulse: Consider antiarrhythmic
r VF/VT occurs in up to 19% of out-of-hospital and altered mental status.
r Other findings consistent with cardiac dysfunction drugs.
cardiac arrest and up to 27% of in-hospital cardiac Unstable VT with pulse: Requires synchronized
arrest (1,2). include hepatomegaly, peripheral edema, and/or a
cardioversion 0.51 J/kg and 2 J/kg for
r The incidence increases with age, and up to 50% of cardiac gallop.
subsequent attempts (8,9)
patients have an underlying cardiac etiology (36). DIAGNOSTIC TESTS & INTERPRETATION In adolescents and adults, synchronized
RISK FACTORS Lab cardioversion should be performed with 100 J
r Congenital heart disorders Initial Lab Tests initially and 200 J for subsequent shocks.
r Myocarditis r Assessment of hemodynamic status takes priority r Pulseless VT/VF is a nonperfusing rhythm; CPR
r Cardiomyopathies above any diagnostic evaluation. should be initiated immediately and followed by
r The basic metabolic panel may reveal metabolic defibrillation 2 J/kg and 4 J/kg for subsequent
r Surgically corrected heart disorders
causes of dysrhythmia such as hypokalemia or shocks (8,9):
r Long QT syndrome
hyperkalemia. In adolescents and adults, defibrillation should be
r Family history of sudden death r Calcium and magnesium levels may reveal performed with 200 J initially and 360 J for
PATHOPHYSIOLOGY hypocalcemia or hypomagnesemia, which has been subsequent shocks.
r The normal electrical impulse of the heart is initiated r Numerous toxins, such as beta-blockers, calcium
associated with ventricular dysrhythmias.
at the sinoatrial node near the right atrium, to the r Blood gas analysis may reveal potential reversible channel blockers, cocaine, digoxin, TCAs, and others,
atrioventricular node, to the bundle of His, which causes of ventricular dysrhythmias such as severe may require treatment by Toxicologic-Oriented
divides to the right and left bundle branches to the metabolic acidosis. Advanced Cardiac Life Support (TOX-ACLS) protocols
Purkinje fibers of the ventricular myocardium. that differ from standard Pediatric Advanced Life
r Ventricular dysrhythmias are caused by disturbances Imaging Support (PALS) or ACLS protocols (10).
r Obtain a chest radiograph to evaluate for potential
in impulse formation or conduction. causes of dysrhythmias: MEDICATION
ETIOLOGY Cardiomegaly: Myocarditis or cardiomyopathy First Line
r Severe electrolyte disturbances (eg, hyperkalemia, Free air: Pneumothorax r If defibrillation is unsuccessful, administer
hypokalemia, hypocalcemia, hypomagnesemia) r Once stable, all patients with significant ventricular epinephrine 0.01 mg/kg, 1:10,000 solution, and
r Metabolic abnormalities (hypoglycemia, metabolic dysrhythmias should have an echo to evaluate continue CPR.
cardiac anatomy and function. This may be done in r If stable VT with a pulse, then consider
acidosis)
r Congenital heart disorders the emergency department or during the admission. antiarrhythmic drugs:
r Drug toxicity (eg, tricyclic antidepressants [TCAs], Diagnostic Procedures/Other Amiodarone 5 mg/kg IV (max 300 mg/dose) over
cocaine, antiarrhythmic drugs, macrolide antibiotics, Obtaining an appropriate 12- or 15-lead ECG is critical 2060 min (8) OR
antihistamines) for diagnosis. The ECG shows a rapid, wide QRS Procainamide 15 mg/kg IV (max 100 mg/dose)
r Myocarditis and cardiomyopathies complex: over 3060 min (8)
r If pulseless VT or VF is refractory to defibrillation and
r Cardiac tamponade r QRS complexes are often >0.14 sec.
r Tension pneumothorax r QRS complexes can be monomorphic or epinephrine, then consider antiarrhythmic drugs:
Amiodarone 5 mg/kg rapid IV bolus (max 300
r Inherited disorders of cardiac conduction (long QT polymorphic. mg/dose) (9) OR
syndrome) DIFFERENTIAL DIAGNOSIS Procainamide 15 mg/kg rapid IV bolus (max 100
r Electrical burns mg/dose, not to exceed 50 mg/min) (9)
Sinus tachycardia, supraventricular tachycardia,
r Hypothermia Because amiodarone and procainamide prolong
junctional ectopic tachycardia, pre-existing bundle
branch block, supraventricular tachycardia with the QT interval, they should not be given together.
aberrancy, antidromic supraventricular tachycardia
278
DYSRYTHMIA, VENTRICULAR
r In the presence of polymorphic VT secondary to REFERENCES ADDITIONAL READING

prolonged QT syndrome, use of amiodarone is
1. Mogayzel C, Quan I, Graves JR, et al. r Atkins DL, Hartley LL, York DK. Accurate recognition
contraindicated, as it may exacerbate the arrhythmia
(11). Out-of-hospital ventricular fibrillation in children and effective treatment of ventricular fibrillation by
r Polymorphic VT secondary to long QT syndrome: and adolescents: Causes and outcome. Ann automated external defibrillators in adolescents.
Administer magnesium sulfate 2050 mg/kg IV Emerg Med. 1995;25:484491. Pediatrics. 1998;101:393397.
2. Topjian AA, Berg RA, Nadkarni VM. Pediatric r Jones P, Lode N. Ventricular fibrillation and
(max 12 g/dose), but doses of 2.312 mg/kg have
been found to be effective (12,13). cardiopulmonary resuscitation: Advances in defibrillation. Arch Dis Child. 2007;92:916921.
r VT secondary to TCA toxicity: Administer sodium science, techniques, and outcomes. Pediatrics. r Markenson D, Pyles L, Neish S; Committee on
bicarbonate 12 meq/kg IV bolus (14): 2008;122:10861098. Pediatric Emergency Medicine and Section on
Give to max of 50 meq/dose while monitoring for 3. Atkins DL, Everson-Stewart S, Sears GK, et al. Cardiology and Cardiac Surgery. Ventricular
narrowing of QRS complexes, followed by a Epidemiology and outcomes from out-of-hospital fibrillation and the use of automated external
continuous drip. cardiac arrest in children: The ROC Epistry-Cardiac defibrillators on children. Pediatrics. 2007;
Arrest. Circulation. 2009;119:14841491. 120:e1368e1379.
Second Line
Lidocaine 1 mg/kg IV (max 100 mg/dose) if first-line
4. Young KD, Gausche-Hill M, McClung CD, et al. A r Pediatric Advanced Life Support, Provider Manual, D
prospective, population-based study of the copyright American Heart Association, 2006.
medications are not immediately available or if r Samson RA, Atkins DL. Tachyarrhythmias and
epidemiology and outcome of out-of-hospital
amiodarone or procainamide are contraindicated
pediatric cardiopulmonary arrest. Pediatrics. defibrillation. Pediatr Clin North Am. 2008;55:
DISPOSITION 2004;114:157164. 887907.
Admission Criteria 5. Samson RA, Nadkarni VM, Meaney PA, et al. r Young KD, Seidel JS. Pediatric cardiopulmonary
All patients with a ventricular dysrhythmia should be Outcomes of in-hospital ventricular fibrillation in resuscitation: A collective review. Ann Emerg Med.
admitted to a monitored pediatric unit, preferably a children. N Eng J Med. 2006;354(22):23282339. 1999;33:195199.
pediatric ICU, for observation and cardiology 6. Alexander ME, Berul CI. Ventricular arrhythmias:
consultation. When to worry. Pediatr Cardiol. 2000;21:
Discharge Criteria 532541. CODES
r In asymptomatic patients who present with isolated 7. Samson R, Berg R, Bingham R, et al. Use of
PVCs with no risk factors, no treatment is necessary. automated external defibrillators for children: An ICD9
r Any symptomatic patient or asymptomatic patients update. An advisory statement from the Pediatric r 427.1 Paroxysmal ventricular tachycardia
who have couplets, multiform PVCs, or frequent Advanced Life Support Task Force, International r 427.41 Ventricular fibrillation
PVCs, consultation with a cardiologist is warranted Liaison Committee on Resuscitation. r 427.89 Other specified cardiac dysrhythmias
prior to discharge. Resuscitation. 2003;57:237243.
8. The International Liaison Committee on
Resuscitation (ILCOR) consensus on science with PEARLS AND PITFALLS
FOLLOW-UP treatment recommendations for pediatric and
neonatal patients: Pediatric basic and advanced r Children may tolerate rapid ventricular rates for
FOLLOW-UP RECOMMENDATIONS life support. Pediatrics. 2006;117(5):e955e977. many hours but should be treated promptly due to
All patients with a verified ventricular dysrhythmia will risk of hypotension and degeneration into VF.
9. 2005 American Heart Association (AHA)
need follow-up with a cardiologist. r When preparing for defibrillation, use the largest
guidelines for cardiopulmonary resuscitation
PROGNOSIS (CPR) and emergency cardiovascular care (ECC) of pads or paddles that can be placed on the childs
r Better outcome exists with patients who experience pediatric and neonatal patients: Pediatric chest wall without the pads touching to minimize
VT/VF as the initial rhythm (35% survival) compared advanced life support. Pediatrics. 2006;117: transthoracic impedance.
to those who develop VT/VF during the course of e1005. r Defibrillation success is improved if effective chest
resuscitation (11%) (5). 10. Albertson TE, Dawson A, De Latorre F, et al. compressions are provided.
r Survival to discharge is better for those with an initial TOX-ACLS: Toxicologic-oriented advanced cardiac r Consultation with a cardiologist is advised for all
rhythm of VF/VT (2030%) compared to those with life support. Ann Emerg Med. 2001;37:S78S90. cases of ventricular dysrhythmias.
asystole or pulseless electrical activity (5%) (3,5). 11. Fishberger SB, Hannan RL, Welch EM, et al.
r Witnessed arrest has been found to be statistically Amiodarone for pediatric resuscitation: A word of
associated with improved survival in children with caution. Pediatr Cardiol. 2009;30(7):10061008.
VT/VF (3). 12. Hoshino K, Ogawa K, Hishitani T, et al. Optimal
COMPLICATIONS administration dosage of magnesium sulfate for
Of those who survive cardiac arrest secondary to torsades de pointes in children with long QT
VT/VF, up to 34% survive with good neurologic syndrome. J Am Coll Nutr. 2004;23(5):
outcome (5). 497S500S.
13. Hoshino K, Ogawa K, Hishitani T, et al. Successful
uses of magnesium sulfate for torsades de pointes
in children with long QT syndrome. Pediatr Int.
2006;48(2):112117.
14. Brown TCK, Barker GA, Dunlop ME, et al. The use
of sodium bicarbonate in the treatment of tricyclic
antidepressant-induced arrhythmias. Anaesth
Intensive Care. 1973;1:203210.
279
DYSTONIA
Katherine Remick
Patricia Padlipsky
r However, the specific pathophysiology likely varies Medication use

BASICS between the various subtypes of primary dystonia: Headaches or signs of increased intracranial
To date, more than 16 genetic forms have been pressure
DESCRIPTION described (6). Exposure to drugs or toxins
r Dystonia is involuntary, patterned muscle r Dopa-responsive dystonia usually arises from
contractions that result in twisting movements or PHYSICAL EXAM
enzymatic defects in dopamine or serotonin r Involuntary twisting or sustained contraction of
abnormal postures. synthesis.
r The onset, duration, severity, and clinical features r Secondary dystonia develops following any variety muscle groups, may involve laryngeal muscles:
Physicians should have a heightened awareness
are highly variable. of environmental insults (eg, perinatal trauma or
r Dystonia is further classified according to age of for acute laryngeal dystonia (particularly following
CNS infection) and is often associated with other use of phenothiazines).
onset (early or late), anatomic distribution (focal, neurologic signs and symptoms. r Opisthotonus
segmental, or generalized), and/or etiology (primary r Additionally, a number of neurodegenerative r Complete neurologic exam including motor and
or secondary). diseases (eg, metabolic disorders) can cause
r Few are true emergencies: Acute laryngeal dystonia, sensory evaluation. Evidence of gross sensory loss is
secondary dystonia. The dystonic symptoms may uncommon in primary dystonia and should prompt a
oculogyric crisis, and dystonic storm (continuous vary from a minor complication to one of the further workup.
unremitting generalized dystonic spasms [1]). primary manifestations of the disease. r Mental status exam: Alterations in mental status
r Dystonia can occur in any age group from childhood r Acute dystonic reactions are usually caused by
should lead the clinician to consider alternative
to adulthood. medications that interfere with central dopamine
r Childhood-onset dystonia is more likely to affect the etiologies (eg, seizures, toxins, infections).
receptors. r Ophthalmologic exam to evaluate for symptoms of
limbs and become generalized, whereas adult-onset
ETIOLOGY increased intracranial pressure or signs of a primary
dystonia is more likely to affect the neck or face and r Primary dystonia: Any of a variety of genetic etiology (eg, Wilson disease)
remain localized.
mutations or deletions; 16 molecular subtypes
EPIDEMIOLOGY described (6) r Diagnosis of dystonia is based primarily upon
Studies have demonstrated a wide range in the r Secondary dystonia: Perinatal cerebral injury,
physical findings.
incidence and prevalence of dystonia depending upon infectious or postinfectious encephalopathies, r Lab testing is generally not helpful in the diagnosis
the populations assessed, but in all accounts, dystonia trauma, toxins, medication induced, brain tumors,
is a rare condition. of primary dystonia.
neurosyphilis, and cerebrovascular disease r The evaluation of a patient with secondary dystonia
r Heredodegenerative dystonia: Homocystinuria,
Incidence can be extensive to try and determine the underlying
r Focal dystonia is thought to be 10 times more glutaric acidemia, lysosomal storage diseases,
cause.
common than generalized dystonia, with an ataxia-telangiectasia, Rett syndrome, methylmalonic
estimated incidence of 2 vs. 24 cases per million aciduria, mitochondrial diseases, neurodegeneration Lab
population per year (2). with brain iron accumulation, Fahr disease, Hartnup Initial Lab Tests
r Incidence of oculogyric crisis in patients treated with disease, juvenile parkinsonism, Huntington disease, Secondary dystonia:
Wilson disease, Pelizaeus-Merzbacher disease r The history and physical exam should be used to
chronic neuroleptics may be as high as 10% (3).
r Acute exposure to haloperidol may lead to r Acute dystonic reactions including acute laryngeal guide lab testing.
dystonia and oculogyric crisis: Common offending r Initial studies may include CBC, electrolytes, renal
development of an oculogyric crisis in as many as
58% (14/24) of children (4). agents include antiemetics, levodopa, and hepatic function, ESR, and serum creatinine
antipsychotics, ergotamines, and anticonvulsants. kinase (if there is concern for rhabdomyolysis).
Prevalence r Acute laryngeal dystonia: Phenothiazines r Further tests might include antinuclear antibody,
r Best estimates suggest primary, early-onset dystonia
r Dystonic storm: Patients often have an underlying serum ceruloplasmin, copper levels, and rapid
to have a prevalence of 250 cases per million (5).
r All races and genders can be affected; however, history of dystonia. The storm is often triggered by plasma reagin.
illness, dehydration, and/or hyperthermia. Imaging
certain populations have a higher frequency of
genetic subtypes, which may lead to disease COMMONLY ASSOCIATED CONDITIONS Physical findings consistent with focal neurologic
expression (eg, DYT1 mutation is more common in r Cerebral palsy deficits or concern for neurodegenerative disease
Ashkenazi Jews and leads to a 5-fold increase in r Neurodegenerative disorders should lead to further evaluation with neuroimaging
disease frequency) (6). r Psychiatric illness treated with antipsychotics (head CT or MRI).
RISK FACTORS Diagnostic Procedures/Other
r Family history Any patient with an affected relative should be
r Underlying medical disorder DIAGNOSIS referred to a genetic specialist to undergo further
r Use of dopamine-receptor blocking drugs HISTORY genetic testing.
r History of cerebral injury or insult r History is the most important tool in the diagnosis Pathological Findings
r Previous dystonic reaction and evaluation of dystonia. No specific neuropathologic findings have been
r Neurosyphilis r Ask about history of involuntary movements: Onset, identified. However, in the case of neurodegenerative
timing, severity, duration, location, radiation, and disease, calcifications or other abnormalities may be
GENERAL PREVENTION frequency. seen within the basal ganglia and associated
Avoidance of neuroleptics, antiemetics, and other r In addition, any associated activities, current structures.
dopamine receptorblocking medications. medications, recent illnesses, drug use or abuse, and DIFFERENTIAL DIAGNOSIS
PATHOPHYSIOLOGY additional symptoms should be discussed. r Torticollis (infectious or noninfectious)
r Not well understood r Past medical history (including birth history, growth r Sandifer syndrome
r Primarily attributed to basal ganglia corticostriatal- and development, and mental health) r Musculoskeletal disorder
thalamocortical motor circuit dysfunction r Family history of neurodegenerative diseases and/or r Posterior fossa mass
r Studies have also shown that cerebellar stimulation movement disorders r Soft tissue neck mass
r For acute dystonic reactions, ask about possible
can lead to dystonic movements (7). r Tetanus
r In primary dystonia, coexisting subclinical precipitants such as: r Atlantoaxial rotary subluxation
abnormalities in perception and sensory processing Trauma (Any history of trauma should prompt the r Psychogenic or pseudodystonia
may be present (8). clinician to consider other causes such as
r Seizure
atlantoaxial rotary subluxation.)
280
DYSTONIA
r Patients in dystonic storms should be managed in a 1. Poston KL, Frucht SJ. Movement disorder
r The primary goals of treatment are aimed at pediatric ICU. emergencies. J Neurol. 2008;255(S4):213.
decreasing abnormal postures, decreasing pain, and r Patients with acute laryngeal dystonia should be 2. Nutt JG, Muenter MD, Aronson A, et al.
limiting contracture formation. admitted for monitoring. Epidemiology of focal and generalized dystonia in
r Primary and secondary dystonia may require chronic Rochester, Minnesota. Mov Disord.
Issues for Referral 1988;3(3):188194.
palliative management. r Any child who presents with primary or secondary
r In the case of acute dystonic reactions, the risks and 3. Sachdev P. Tardive and chronically recurrent
dystonia should be referred to a neurologist or oculogyric crises. Mov Disord. 1993;8:9397.
benefits of stopping all suspicious medications movement disorder specialist.
should be strongly considered. r Secondary causes of dystonia (eg, Wilson disease) 4. Yoshida I, Sakaguchi Y, Matsuishi T, et al. Acute
accidental overdosage of haloperidol in children.
MEDICATION may require referral to additional subspecialists Acta Paediatr. 1993;82:877880.
First Line depending upon the underlying diagnosis. 5. Defazio G, Abbruzzese G, Livrea P, et al.
r Acute dystonic reactions: Following initial treatment r A neurologist should be consulted in the emergency
Epidemiology of primary dystonia. Lancet Neurol. D
with one of the medications listed below, oral department if the etiology or diagnosis of dystonia 2004;3:673678.
anticholinergic therapy should be continued for remains unclear. 6. Schwarz CS, Bressman SB. Genetics and treatment
2 wk (especially if long-acting dopamine Additional Therapies of dystonia. Neurol Clin. 2009;27:697718.
receptorblocking agents had been used) (9): r Deep brain stimulation may be considered in cases
7. Shanker V, Bressman SB. Whats new in dystonia?
Anticholinergic agents: A prompt response to of generalized primary dystonia refractory to medical Curr Neur Neurosci Rep. 2009;9:278284.
anticholinergic medications helps to confirm the management (11): 8. Tinazzi M, Fiorio M, Fiaschi A, et al. Sensory
diagnosis: Approved for use in children 7 yr old functions in dystonia: Insights from behavioral
Trihexyphenidyl PO dosing is not well A relatively new technology that requires further studies. Mov Disord. 2009;24(10):14271436.
established in pediatrics (antiparkinsonian use to assess target populations
r Physical therapy: To help prevent the development 9. Rodnitzky, RL. Drug-induced movement disorders
medication of the antimuscarinic class).
Benztropine 0.020.05 mg/kg/dose IV or IM per in children and adolescents. Expert Opin Drug Saf.
of contractures (12) 2005;4(1):91102.
day b.i.d. r Speech and language therapy
Diphenhydramine 12 mg/kg IV or IM q6h 10. Albright AL, Ferson SS. Intraventricular baclofen
r Occupational therapy
Benzodiazepines: Diazepam and clonazepam have for dystonia: Techniques and outcomes. J
r Transcutaneous electrical nerve stimulation (TENS) Neurosurg Peds. 2009;3:1114.
been used when anticholinergic agents fail to r Sensory and motor training
provide an immediate response. 11. Marks WA, Honeycutt J, Acosta F, et al. Deep
Carbidopa/Levodopa: Treatment is initiated at a brain stimulation for pediatric movement
low-dose, 1/2 tablet (25/100 mg) b.i.d. and disorders. Semin Pediatr Neurol. 2009;16:9098.
gradually titrated to effectiveness.
FOLLOW-UP 12. Delnooz CC, Horstink MW, Tijssen MA, et al.
Botulinum neurotoxin injection: Treatment of FOLLOW-UP RECOMMENDATIONS Paramedical treatment in primary dystonia: A
choice in focal dystonia (7) r Patients who develop acute laryngeal dystonia systematic review. Mov Disord. 2009;24(15):
Baclofen: Intrathecal or intraventricular (10) should be monitored closely for recurrence. 21872198.
r Acute laryngeal dystonia: Immediate treatment with r The family should be educated regarding future
IV diphenhydramine: avoidance of offending agents if known.
Botulinum toxin injection of the vocal chords has r Movement disorder specialists should be directly ADDITIONAL READING
been used in chronic cases (1). involved in the ongoing treatment of any patient Vidailhet M, Grabli D, Roze E. Pathophysiology of
r Oculogyric dystonia: IM or IV anticholinergics. Oral
with chronic dystonia. dystonia. Curr Opin Neurol. 2009;22:406413.
clonazepam may be effective for chronic oculogyric
crises resistant to anticholinergics. PROGNOSIS
r Dystonic storm: May be resistant to all of the above r The prognosis for patients with acute dystonic
reactions is excellent if treated promptly. Immediate CODES
listed medicines
r Focal or generalized dystonia: use of anticholinergics and/or botulinum toxin
injection is lifesaving in acute laryngeal dystonia. ICD9
Anticholinergics at high doses (trihexyphenidyl) r Patients with dopa-responsive dystonia show r 333.89 Other fragments of torsion dystonia
alone or with baclofen r 333.90 Unspecified extrapyramidal disease and
r Trial with L-dopa (up to 10 mg/kg/day for 3 mo) is marked improvement following treatment with
carbidopa/levodopa. Additionally, other primary abnormal movement disorder
the 1st choice in all patients with early-onset
dystonias may also respond to treatment with r 781.0 Abnormal involuntary movements
dystonia:
levodopa.
This may also be considered in any patient with r Primary dystonias are highly variable with respect to
focal or generalized dystonia of unknown etiology,
to evaluate for dopa-responsive dystonia. treatment response and prognosis. PEARLS AND PITFALLS
r If a secondary cause of dystonia can be identified, r The prognosis of secondary dystonia varies greatly
r The onset and presentation of dystonia is highly
treatment should be directed toward the underlying depending upon the primary disease process.
variable.
disease. COMPLICATIONS r The ability to recognize acute laryngeal dystonia can
r Rhabdomyolysis be lifesaving.
r Compression of the spinal cord, plexus, and r Patients who present in dystonic storms should be
It is best to avoid all antihistamines in pregnancy,
especially during the 1st trimester. peripheral nerves. managed in an intensive care setting with careful
r Scoliosis attention to the development of rhabdomyolysis.
Second Line r Limited physical function r Anticholinergics and benzodiazepines are
The combination of benzhexol, tetrabenazine, and r Medical treatment may lead to sedation, confusion, considered first-line therapy for dystonia.
pimozide has been proven effective in refractory r Consider the use of botulinum toxin, baclofen, or
dystonic storms. In severe cases, patients may require and decreased memory function.
r Deep brain stimulation with electrode placement antiparkinsonian medication early.
sedation and paralysis (1). r In refractory cases a child may benefit from sedation
can be complicated by hemorrhage, stroke,
migration, infection, and electrode malfunctions. and paralysis.
r The etiologies of secondary dystonia are diverse, and
treatment should be directed at the primary disease.
281
LWBK822-driver-E LWBK822-Hoffman ch140.xml April 15, 2011 13:7
EATING DISORDERS
Kalyani Samudra
Charles W. Pruitt

BASICS Starvation leads to hypoglycemia, protein and r Look for signs of the eating disorder itself as well as
vitamin deficiencies, hypercortisolemia, and endorphin its medical complications.
DESCRIPTION release. r The physical exam can be entirely normal, especially
r Anorexia nervosa (AN) is an eating disorder
ETIOLOGY early in the course of illness.
characterized by: r General: Cachexia
Weight loss to <85% of expected body weight or Multidimensional model:
r A person with risk factors begins dieting, bingeing, r HEENT: Sunken eyes, gingivitis, dental caries, eroded
failure to make expected weight gains dental enamel, enlarged parotids
Amenorrhea (absence of 3 consecutive or compensatory behaviors. r Pulmonary: Wasting of respiratory muscles
menstrual cycles) if postmenarchal r Physical changes associated with dieting include
r Cardiovascular: Bradycardia, orthostatic
Distorted body image increased secretion of corticotropin-releasing
Intense fear of weight gain despite being hormone, which has anorectic effects. hypotension, arrhythmias, acrocyanosis, midsystolic
underweight r Exercising causes norepinephrine and endorphin click of mitral valve prolapse; signs of
Restricting subtype: Self-induced starvation is the release, which creates a sense of well-being, which cardiomyopathy from ipecac abuse (Direct
main method of weight loss. reinforces exercising. cardiotoxicity may cause tachycardia, ECG changes,
Binge-eating/Purging subtype: Regular r Psychological reinforcers can include compliments CHF, hypotension, or shock.)
r GI: Abdominal distention with meals, abnormal
bingeing/purging received from others for weight loss or anxiety relief
r Bulimia nervosa (BN) is characterized by: experienced after bingeing/purging. bowel sounds, acute gastric distention:
Recurrent binge-eating episodes followed by r Thus, the patients fasting, bingeing, or purging Rare: Signs of gastritis, esophagitis, Mallory-Weiss
compensatory behaviors (purging, fasting, tears, pancreatitis, and colonic dysmotility
continues. r Skeletal: Short stature, arrested skeletal growth (in
excessive exercise) aimed at purging calories and
preventing weight gain: COMMONLY ASSOCIATED CONDITIONS severe illness)
r Substance abuse disorders are common in patients r Skin: Marks/Scars from self-injury; lanugo,
Compensatory behaviors occur, on average,
twice a week for 3 mo. with BN, binge eating disorder, and in the binge petechiae, conjunctival hemorrhage after vomiting;
Purging subtype: Regular self-induced vomiting or eating/purging type of BN. scars or callouses on the dorsum of dominant hand,
r Mood, anxiety, and personality disorders poor turgor, pitting edema
laxative, diuretic, ipecac, or enema use
r AN: Social phobia and obsessive compulsive r Hematologic: Easy bruising/bleeding
Nonpurging type: Compensatory behaviors
(fasting, excessive exercise) without purging disorder (OCD) r Endocrine/Metabolic: Hypothermia
behavior r BN: Social phobia, OCD, posttraumatic stress r Reproductive: Arrested sexual development
r Eating disorder not otherwise specified (EDNOS) is a disorder, and simple phobia (2) r Psychiatric/Neurologic: Anxiety, depression,
diagnosis given to patients with disordered eating irritability, seizures (27)
behaviors that do not meet full criteria for either AN
or BN. This category includes patients with: DIAGNOSIS DIAGNOSTIC TESTS & INTERPRETATION
Binge eating disorder: Recurrent bingeing without Lab
HISTORY r Most test results will be normal.
compensatory behaviors r Eating disorder patients often deny the seriousness
All symptoms of AN but normal weight or normal r Initial labs: Comprehensive chemistry panel, CBC
of their condition.
menses r AN often presents with extreme weight loss, failure with differential, urinalysis, hCG:
Purging after eating small amounts of food Blood chemistries: Hypokalemia (diuretic and
to gain weight, food refusal, and dehydration.
Criteria for BN but less frequent compensatory r Ask about current dietary practices including fasting; laxative use), hyponatremia due to water loading,
behaviors hypomagnesemia, hypophosphatemia,
A mix of AN and BN symptoms highest and lowest weight; exercise habits; binge hypochloremic alkalosis due to purging, increased
Patients who chew and spit out large amounts of eating; self-induced vomiting; and use of diet pills, BUN due to dehydration, hypocalcemia
food without swallowing (1) ipecac, laxatives, and diuretics. CBC and differential: Anemia, mild leukopenia,
r Ask about use of diet pills, energy pills/drinks, and
thrombocytopenia; increased hemoglobin
EPIDEMIOLOGY herbal teas for weight loss (which can contain hCG: Pregnancy is in the differential diagnosis for
Prevalence ephedra or other stimulants). amenorrhea and vomiting.
r Most common in adolescents/young adults r Psychiatric history: Depression, anxiety,
Thyroid function tests, LFTs
r Male to female ratio is between 1:6 and 1:10. suicidal/self-injurious thoughts/behaviors; past r Urinalysis to screen for renal disease, dehydration,
r AN: Lifetime prevalence in women ranges from mental health treatment and water loading
0.33.7% (depending on the definition). r Family history: Obesity, eating disorder, depression, r If there is concern for suicidality or ingestion, order
r BN: Lifetime prevalence in women has ranged from substance abuse urine and/or serum toxicology screens for illicit
14%. r Menstrual history: Age at menarche, last menstrual
drugs, acetaminophen, salicylates, or tricyclics.
r EDNOS: >50% of patients with eating disorders period, cycle regularity
r Substance abuse history, sexual history, past Diagnostic Procedures/Other
who present to outpatient settings
r Subsyndromal eating disorder symptoms, which ECG for patients who are severely symptomatic,
physical/sexual abuse
r Review of systems: malnourished, have metabolic abnormalities, or have
often do not rise to the level of a disorder according a history of ipecac abuse:
to the Diagnostic and Statistical Manual of Mental General: Light-headedness, fatigue, weakness r Bradycardia is the most common abnormality.
Disorders, 4th ed., are also quite common. Oropharyngeal: Dental decay, swollen cheeks r Prolonged QTc is a rare complication.
r Eating disorders are more common in Hispanic, Pulmonary: Shortness of breath
r ST depression if electrolyte abnormalities
Native American, and Caucasian women than in Cardiovascular: Palpitations, chest pain
GI: Abdominal pain, heartburn, hematemesis, r Dysrhythmias include supraventricular beats and
African American and Asian women (2).
vomiting, diarrhea, constipation, bloating ventricular tachycardia.
Reproductive: Regression of secondary sex r Ischemic changes in ipecac cardiotoxicity (2,6,7)
characteristics; menstrual irregularities
Urinary: Decreased urinary volume
Metabolic: Weight fluctuations, muscle cramping;
cold intolerance
Skeletal: Bone pain with exercise
Hematologic: Pallor, easy bruising/bleeding (24)
282
EATING DISORDERS
DIFFERENTIAL DIAGNOSIS Discharge Criteria r Seizures, death

r Medical illness can mimic eating disorders: r Medically stable, not needing NG feeds, IV fluids, or r A potentially life-threatening refeeding syndrome
CNS or other malignancy multiple daily lab tests can occur when very low weight patients (<70% of
GI: Inflammatory bowel disease, celiac disease, r Weight must be >85% of ideal body weight, but ideal body weight) are fed too rapidly:
malabsorption syndromes weight should never be the sole criterion. Consider Consists of fluid retention, hypocalcemia,
Endocrine disorders: Diabetes mellitus, discharge for patients 7585% of ideal body weight. hypomagnesemia, hypophosphatemia
hyperthyroidism, hypopituitarism, Addison disease r Consider ability to control restricting/compensatory Delirium and cardiac failure can occur.
Pregnancy behaviors, supervision level needed during and after Syndrome is prevented by slow refeeding and
r Psychiatric: Depressive disorders, OCD, meals, and suicidality (2). phosphorus supplementation (2,4,6).
schizophrenia
Issues for Referral
Consult the psychiatrist in the emergency department REFERENCES
TREATMENT for suicidal, psychotic, agitated, or assaultive patients.
1. American Psychiatric Association. Diagnostic and
PRE HOSPITAL Statistical Manual of Mental Disorders. 4th ed.
Stabilize ABCs per Pediatric Advanced Life Support Washington, DC: Author; 1994:539550.
FOLLOW-UP 2. American Psychiatric Association. Practice
(PALS) protocol.
FOLLOW-UP RECOMMENDATIONS Guidelines for the Treatment of Patients with
INITIAL STABILIZATION/THERAPY r Discharge instructions: Eating Disorders. 3rd ed. Washington, DC: Author;
r Correct volume depletion and metabolic
abnormalities with appropriate IV fluid replacement. Any patient who is discharged will need follow-up
within 1 wk.
2006:10971231.
3. Rome ES, Ammerman S, Rosen DS, et al. Children
E
r Diagnose and treat medical complications of eating
Primary care provider should monitor weight and adolescents with eating disorders: The state of
disorders (see Admission Criteria). the art. Pediatrics. 2003;111:e98e108.
r Multimodal treatment (medications, 13 times per wk. Also monitor urine specific
gravity, orthostatic vital signs, oral temperature, 4. American Academy of Pediatrics, Committee on
individual/group/family therapy, nutritional and electrolytes. Adolescence. Identifying and treating eating
counseling, and frequent medical evaluations) Primary care provider should establish a target disorders. Pediatrics. 2003;111:204211.
MEDICATION weight and realistic rate of weight gain (usually 5. Golden NH, Katzman DK, Kriepe RE, et al. Eating
In general, a psychiatrist should prescribe psychotropic 0.52 pounds per week for outpatients). disorders in adolescents: Position paper for the
medications if necessary. Dietician can develop meal plan, help patient Society for Adolescent Medicine. J Adolesc Health.
choose meals, and widen food choices (2). 2003;33:496503.
DISPOSITION
r Once medically stabilized, treatment for eating PROGNOSIS 6. Rome ES, Ammerman S. Medical complications of
r AN: eating disorders: An update. J Adolesc Health.
disorders can take place in a variety of settings,
ranging from outpatient programs, partial hospital 5070% of teens with AN recover. 2003;33:418426.
programs, residential programs, and inpatient 20% improve but have residual symptoms. 7. Schneider DJ, Perez A, Knilans TE, et al. Clinical and
programs (either medical or psychiatric). 1020% develop chronic AN. pathologic aspects of cardiomyopathy from ipecac
r Most patients presenting to the emergency Mortality rates for AN are high. administration in Munchausen syndrome by proxy.
department will be appropriate for outpatient care or Better prognosis if younger age of onset, shorter Pediatrics. 1996;97:902906.
intermediate levels of care (such as partial hospital). illness duration
Worse prognosis if lower initial weight, vomiting,
Admission Criteria binge eating, chronicity of illness, repeated CODES
r Weight <75% of ideal body weight or acute weight
hospitalizations, and obsessive-compulsive
loss with food refusal, intractable vomiting. personality symptoms
Consider admission for patients 7585% of ideal
ICD9
r BN: r 307.1 Anorexia nervosa
body weight. r 307.50 Eating disorder, unspecified
r Medical instability: Prognosis, if untreated, is poor.
Long-term outcome is good in 60%, r 307.51 Bulimia nervosa
Heart rate <50 bpm or arrhythmia intermediate in 30%, and poor in 10%.
BP <80/50 mm Hg Better prognosis if adolescent onset
Orthostatic change in pulse or BP Worse prognosis if comorbid OCD, longer illness
Hypokalemia, hypophosphatemia, PEARLS AND PITFALLS
duration
hypomagnesemia Comorbid substance abuse increases risk of r Males with eating disorders are not rare:
Need for IV fluid/NG tube feeds suicidal behaviors. Higher rates of substance abuse than females
Temperature <97 F or <36.1 C r EDNOS: Little is known about prognosis (2,3). Males commonly present with drive to increase
r Suicidality or comorbid psychiatric conditions
upper torso muscle mass rather than fear of
requiring admission COMPLICATIONS becoming obese
r Consider admission if the patient: r Severe electrolyte abnormalities
r Caffeine, over-the-counter or herbal stimulants
r ECG abnormalities, life-threatening arrhythmias,
Is uncooperative with less intensive treatment (ma huang/ephedra), or thyroid supplements are
Is preoccupied with intrusive thoughts cardiomyopathy (from ipecac abuse) sometimes abused for weight loss.
Is very unmotivated or lacks family support r Mallory-Weiss tears, gastric or esophageal rupture,
Needs supervision during and after all meals superior mesenteric artery syndrome, pancreatitis
Has multiple daily episodes of purging r Renal stones, renal failure
Has failed less intensive treatment programs r Aspiration pneumonia
r When deciding whether to admit to a psychiatric or r Dental caries and loss of dental enamel
general medical unit, consider the patients medical
condition, the skills of the pediatric or psychiatric
staff, and whether a specialized program for eating
disorders is available (25).
283
ECTOPIC PREGNANCY
Ilene Claudius
ETIOLOGY Imaging
BASICS Anything that delays movement of the blastocyst r Endovaginal US: Absence of gestational sac with
through the fallopian tube, allowing implantation -hCG >1,500 mIU/mL (generally 5.5 wk estimated
DESCRIPTION outside of an appropriate location in the uterus; can gestational age) indicates probable ectopic
r Ectopic pregnancy is implantation and maturation of be due to scarring or anomaly of the fallopian tube pregnancy.
the conceptus outside of the endometrial cavity. r Other US findings include free fluid (25%),
9597% are found in the fallopian tubes, while the COMMONLY ASSOCIATED CONDITIONS
1/10,0001/30,000 heterotopic pregnancies pseudogestational sac (20%), or adnexal mass.
remaining are accounted for by pregnancies in the
cornea of the uterus, ovary, cervix, and abdomen (1). (increases to 1% with fertility drug use) Diagnostic Procedures/Other
r Laparoscopy
r Rupture of ectopic pregnancy leads to internal
r Negative uterine curettage
bleeding: DIAGNOSIS r Culdocentesis yielding nonclotting blood is
Current mortality is 0.05%.
Remains a leading cause of pregnancy related HISTORY suggestive of a ruptured ectopic pregnancy.
death in the 1st trimester, accounting for 10% of r Classic triad: Abdominal pain, amenorrhea, and Pathological Findings
all pregnancy-related deaths (2) vaginal bleeding r Products of conception: Extrauterine gestational sac,
Death rates are highest in girls 1519 yr old (3). r May or may not be aware of or disclose knowledge yolk sac, or fetal parts
of pregnancy r If a dilation and curettage is performed to assist
EPIDEMIOLOGY r Typically occurs 58 wk after the last menstrual with diagnosis, frozen sections are 93% sensitive for
Incidence
period presence of chorionic villi if pregnancy is intrauterine.
100,000 cases per year r Abdominal/pelvic pain
Prevalence r 50% have a history of vaginal bleeding DIFFERENTIAL DIAGNOSIS
r Early normal intrauterine pregnancy
2% of all live pregnancies r Miscarriage
PHYSICAL EXAM
RISK FACTORS r Abdominal/pelvic tenderness (8097% of cases) r Early abnormal intrauterine pregnancy (eg, blighted
r Previous ectopic pregnancy (number 1 risk factor)
r Peritoneal signs if ruptured (tenderness, Cullen sign, ovum)
r History of pelvic inflammatory disease
r Tubal ligation or surgery etc.)
r Adnexal tenderness (7598% of cases)
r Intrauterine device use (at time of conception) r Abdominal mass (50% of cases) TREATMENT
r Congenital abnormalities r Closed cervical os on speculum exam
r Fallopian tube tumors PRE HOSPITAL
r Material passing through os, if present, will not r Address any issues related to ABCs.
r Advanced maternal age r Administer oxygen and IV fluid as needed.
contain products of conception.
r Smoking r May have paradoxical bradycardia/lack of
r In utero exposure to diethylstilbestrol INITIAL STABILIZATION/THERAPY
compensatory tachycardia if the ectopic pregnancy r Oxygen
r History of infertility increases ectopic rate ruptures and results in intraperitoneal blood r If hypovolemic due to hemorrhage, support BP with
GENERAL PREVENTION DIAGNOSTIC TESTS & INTERPRETATION normal saline or blood transfusion if necessary.
Education on STI prevention Lab
MEDICATION
r Urine -hCG (frequently positive) First Line
Conceptus implants and grows in the fallopian tube,
r Quantitative serum -hCG (rises more slowly than Analgesics if indicated
abdomen, ovary, cervix, or abdomen. As it grows, it
may present as a nonruptured mass or as a tubal intrauterine pregnancy) Second Line
r Rh type r Methotrexate (50 mg/m2 IM) can be used after
rupture.
r CBC obstetric consultation in select patients for
r Progesterone level alone is not a reliable marker of termination (5).
r Rh (D) immune globulin (RhoGAM) in Rh-negative
ectopic pregnancies. o
r Type and cross if hemodynamically unstable women: If <12 wk pregnant, 50 g IM; if 13 wk
r Check CBC, LFTs, and creatinine if methotrexate is pregnant, 300 g IM. Administer within 72 hr of
hemorrhage.
planned (4).
284
ECTOPIC PREGNANCY
SURGERY/OTHER PROCEDURES Patient Monitoring 3. Mukul LV, Teal SB. Current management of ectopic
Laparoscopy/laparotomy for ruptured ectopic Return for severe abdominal pain, signs of pregnancy. Obstet Gynecol Clin North Am. 2007;
pregnancies or those who are not candidates for hemodynamic instability 34(3):403419.
methotrexate 4. Practice Committee of the American Society for
DIET
DISPOSITION If medically treated with methotrexate, avoid folic Reproductive Medicine. Medical treatment of
acidcontaining foods (eg, folate-fortified foods; ectopic pregnancy. Fertil Steril. 2008;90(Suppl 3):
Admission Criteria S206S212.
r Critical care admission criteria: green leafy vegetables; many beans, peas, and lentils;
beets; fruits such as oranges, bananas, strawberries). 5. McWilliams GD, Hill MJ, Dietrich CS. Gynecologic
Hemodynamic instability unresolved with
emergencies. Surg Clin North Am. 2008;88(2):
transfusion and/or surgery PROGNOSIS
r Other indications for floor admission: 265283.
r Risk of future ectopic pregnancies is increased by
6. Helmy S, Sawyer E, Ofili-Yebovi D, et al. Fertility
Need for surgical intervention (severe pain, 1025%. outcomes following expectant management of
hemodynamic instability, evidence of rupture, not r Chances of normal pregnancy are dependent on
tubal ectopic pregnancy. Ultrasound Obstet
eligible for medical therapy) what abnormalities contributed to the ectopic, Gynecol. 2007;30(7):988993.
Inability to ensure follow-up in candidate whether advanced maternal age or fertility issues
otherwise eligible for medical therapy existed, and the management. 1 large study showed See Also (Topic, Algorithm, Electronic
Discharge Criteria subsequent fertility rates of 83% in a group of Media Element)
r Follow-up ensured women managed expectantly and 64% in those Vaginal Bleeding During Pregnancy (<20 week
r Candidate for either medical treatment or needing managed surgically (5). gestation)
further workup
r No severe pain or evidence of rupture
COMPLICATIONS E
r Rupture leading to hemodynamic instability and/or
r Hemodynamic stability death
CODES
r Failure of medical management with methotrexate
Issues for Referral ICD9
r Patients in whom diagnosis is unclear due to a (10% risk for single-dose protocol) r 633.00 Abdominal pregnancy without intrauterine
quantitative -hCG <1,000 mIU/mL and no r Transient abdominal separation pain 37 days
pregnancy
intrauterine gestational sac should be followed in after methotrexate use, which is thought to be due r 633.10 Tubal pregnancy without intrauterine
2 days for repeat testing by an obstetrician to assess to an expanding hematoma within the fallopian
pregnancy
doubling time of -hCG. tube and is self-limited r 633.20 Ovarian pregnancy without intrauterine
r Patients receiving medical therapy with r Failure of surgical management to remove ectopic
pregnancy
methotrexate need 2-day follow-up to assess need pregnancy (520% risk with laparoscopic
for subsequent doses. salpingostomy)
PEARLS AND PITFALLS
FOLLOW-UP REFERENCES r 50% of ectopic pregnancies are missed at initial
FOLLOW-UP RECOMMENDATIONS 1. Ferentz KS, Nesbitt LS. Common problems and visit.
r Discharge instructions and medications: emergencies in the obstetric patient. Prim Care. r Not all patients with ruptured ectopic pregnancies
Follow-up within 2 days for either serial -hCG 2006;33(3):727750. have tachycardia or peritoneal signs.
testing or assessment of methotrexate 2. Chandrasekhar C. Ectopic pregnancy: A pictorial r Dont forget to administer RhoGAM if the patient is
effectiveness. review. Clin Imaging. 2008;32:468473. Rh negative.
Counsel regarding side effects of methotrexate, if
used: Nausea, stomatitis, dizziness, alopecia,
neutropenia, pneumonitis, vaginal bleeding,
increase in abdominal pain.
r Activity:
No heavy lifting
No sexual intercourse until -hCG is undetectable
No breast-feeding if methotrexate used
285
ECZEMA HERPETICUM
Kyle A. Nelson
ETIOLOGY r Polymerase chain reaction for HSV deoxyribonucleic

BASICS r HSV 1 and HSV 2 can cause EH (1,2,6). acid or direct fluorescent antibody tests:
r Other viruses have been associated with KVE, More sensitive and specific than Tzanck test but
DESCRIPTION including Coxsackie, Varicella, and Vaccinia (1,2). results not readily available (1,4)
r Eczema herpeticum (EH) is an acute skin infection r Most children with EH have primary HSV 1 r Viral culture:
caused by herpes simplex virus (HSV) in patients infections; adults may have primary or recurrent Send in Hanks media.
with atopic dermatitis (AD). infections (4,5). May take >24 hr (1,4)
r It has potential to be severe, disseminated, and life r Serologic testing is less specific (1).
threatening (1,2). COMMONLY ASSOCIATED CONDITIONS r HSV IgM may be positive without IgG or initially
r Kaposi varicelliform eruption (KVE) is another term r HSV skin infections have been associated with other
skin disorders including irritant contact dermatitis, negative with subsequent seroconversion.
for skin infections by HSV or similar viruses; some r Consider other lab tests based on clinical
use KVE and EH interchangeably. Darier disease, psoriasis, pemphigus vulgaris, and
burn injuries (1,5). scenario:
r EH is more frequently used to specifically describe
r As immunodeficiency may be associated with EH, CBC, C-reactive protein, blood culture, wound
such an infection with AD (1,2). cultures (4)
consider possible comorbidities.
EPIDEMIOLOGY Diagnostic Procedures/Other
r Prevalence and incidence are not accurately known Skin biopsy is rarely performed (1).
but appear to be rising (1). DIAGNOSIS
r It is debated whether rising HSV incidence is Pathological Findings
HISTORY Microscopy characteristically shows ground glass
resulting in higher EH incidence (1,3,4). r Sine quo non skin rash: appearance and/or eosinophilic inclusions of nuclei,
r No gender or racial predilection
Typical rash is painful and pruritic. multiinucleated and/or necrotic cells, pallor or
r Can affect any age group r Often begins as sudden worsening of AD with crops ballooning of keratinocytes, acantholytic or necrotic
r Recent studies report higher incidence in teenagers epithelium, and intraepidermal blistering (10).
of typical lesions (5,8)
and young adults (3,4). r Typically begins at sites of pre-existing AD may
r No significant seasonality (4,5). DIFFERENTIAL DIAGNOSIS
rapidly disseminate (5,8) r Impetigo
r Patients may report lesions of different stages, r Contact dermatitis
RISK FACTORS
r Occurs predominantly in patients with pre-existing similar to varicella (5). r Shingles (varicella zoster)
skin disorders such as AD (1,2) r Skin eruptions may continue for 710 days. r Chickenpox (varicella) if more disseminated
r Close contact with persons having cold sores r Fever, chills, malaise, and lymphadenopathy are
(herpes labialis) is common (5). frequent accompanying complaints (1,8).
r Elevated IgE levels may be associated (4,5). r Inquire about recurrent herpes labialis and recent TREATMENT
r Reduced cell-mediated and humoral immunity are exposures (8).
thought to be risk factors (5): INITIAL STABILIZATION/THERAPY
PHYSICAL EXAM Depending on disease severity, some patients may
Reduced natural killer cell activity in AD is thought r Typical EH lesions are umbilicated vesicles or
to allow HSV infections that suppress immune show signs of toxicity and should be rapidly stabilized
vesicopustules, but papules may occur (1,5). and treated accordingly.
function (5). r Lesions rupture, spontaneously or from excoriation,
HSV-specific T-cell immunity appears unimpaired MEDICATION
leaving punched-out lesions that may be
in children with EH (5). First Line
r Asthma or hay fever are not risk factors (4). hemorrhagic and painful (5).
r Lesions may occur in crops or be widespread r Acyclovir has traditionally been the preferred
r Corticosteroids as risk factor is debated (4,5). antiviral therapy (1,4,5):
r Pimecrolimus, a topical calcineurin inhibitor, has (disseminated) and may be at different stages (5).
r Pustules or purulent drainage suggest bacterial IV route preferred as initial treatment for
been associated with EH (7). superinfection (5). ill-appearing patients or disseminated EH
r Eye involvement is an ophthalmologic emergency Typical dose: 1530 mg/kg/day IV divided into
GENERAL PREVENTION 3 doses 57 days; transition to PO after
r Exposure to persons with active herpes labialis (1). Assess visual acuity and corneal staining with
improvement
lesions should be avoided. fluorescein.
r Early treatment of EH may limit severity of disease r Viremia may occur and rarely may result in fulminant Oral treatment may be used in well-appearing
patients with limited skin involvement.
and prevent morbidity/mortality (5). disease with signs of toxicity and multiple organ Typical dose: 4080 mg/kg/day PO divided into
system abnormalities (5). 35 doses 710 days
PATHOPHYSIOLOGY
r Viral infection from inoculation of skin; either DIAGNOSTIC TESTS & INTERPRETATION PO dosing frequently given as adult dosing:
autoinoculation in patients with latent or active Diagnosis is usually made clinically, as EH has such 200400 mg 5 times per day 10 days
infections (eg, herpes labialis) or exposure to an characteristic features (1,4). r Valacyclovir:
infected individual (1) Lab Pharmacologically equivalent to acyclovir
r Impaired immunity purported to play role in EH r Vesicular fluid may be sent for testing: Dosing and compliance easier
pathophysiology (4); antibodies against HSV appear r Tzanck test, which examines for multinucleated Typical dose: 20 mg/kg PO q8h 5 days, max
to limit spread and severity. 1,000 mg/dose
r Lesions are pruritic; autoinoculation of eczematous giant cells
Higher cost
May be done rapidly but is not sensitive or specific r Famciclovir:
and noneczematous skin may occur (8,9). for HSV (1,4)
r Lesions may coalesce, forming large denuded areas While also pharmacologically equivalent to
that become superinfected with bacteria (1,5). acyclovir, pediatric dosing has not been
established.
286
ECZEMA HERPETICUM
r Topical acyclovir (Zovirax) may be considered: Second Line

r Acyclovir resistance:
REFERENCES
Apply to affected area 56 times per day
7 days. In cases of acyclovir resistance, valacyclovir, 1. Olson J, Robles DT, Kirby P, et al. Kaposi
r Systemic antibiotics if suspected bacterial cellulitis: famciclovir, and penciclovir will be ineffective. varicelliform eruption (eczema herpticum).
Staphylococcus species most common Administration of foscarnet or vidarabine or Dermatol Online J. 2008;14(2):18.
Streptococcus and Pseudomonas species possible cidofivir may be indicated in such circumstances. 2. Nikkels AF, Pierard GE. Treatment of
(1,5) Dermatology and/or infectious disease mucocutaneous presentations of herpes simplex
Consider treatment for MRSA as indicated consultation should be considered in such cases to virus infections. Am J Clin Dermatol. 2002;3(7):
Cephalexin 25100 mg/kg/day PO q612h assist with management. 475487.
Augmentin: <40 kg, 2545 mg/kg/day PO q12h; r Foscarnet: 3. Bork K, Brauninger W. Increasing evidence of
>40 kg, 250500 mg/dose PO q8h Typical dose: >12 yr, 40 mg/kg IV q812h for eczema herpeticum: Analysis of seventy-five
Clindamycin: IV, 1540 mg/kg/day q68h; PO, 23 wk; dosing <12 yr not established cases. J Am Acad Dermatol. 1988;19:10241029.
3040 mg/kg/day q68h r Vidarabine IV dosing for pediatrics is not 4. Wollenberg A, Zoch C, Wetzel S, et al.
r Antiviral and antibacterial treatment should not be established. Predisposing factors and clinical features of
delayed or withheld pending confirmatory lab test Vidarabine topical for ocular HSV: Apply 0.5-inch eczema herpeticum: A retrospective analysis of
results if high clinical suspicion (1). ribbon to lower conjunctival sac 3 times per day 100 cases. J Am Acad Dermatol. 2003;49:
r For analgesia, consider NSAIDs, acetaminophen, or r Cidofivir dosing for pediatrics is not established. 198205.
opioids. 5. Goodyear HM. Eczema herpeticum. In Harper J,
r Pain and inflammation may be prolonged. SURGERY/OTHER PROCEDURES
Oranje A, Prose N, eds. Textbook of Pediatric
r NSAIDs: Wound care for denuded skin (5)
Dermatology. 2nd ed. Halden, MA: Blackwell E
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN DISPOSITION Publishing; 2006:291295.
Ketorolac 0.5 mg/kg IV/IM q6h PRN Admission Criteria 6. Peng WM, Jenneck C, Bussmann C, et al. Risk
Naproxen 5 mg/kg PO q8h PRN Extensive skin involvement, significant bacterial factors of atopic dermatitis patients for eczema
Some clinicians may avoid due to theoretical superinfection, signs of dehydration, or signs of sepsis herpeticum. J Invest Dermatol. 2007;127:
concern of effect on coagulation and callus or multiple organ system involvement 12611263.
formation. Discharge Criteria 7. Wahn U, Bos JD, Goodfield M, et al. Efficacy and
r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN safety of pimecrolimus cream in the long-term
Well-appearing patients with limited skin involvement,
r Opioids: appropriate wound care, and access to follow-up for management of atopic dermatitis in children.
Morphine 0.1 mg/kg IV/IM/SC q2h PRN: re-evaluation Pediatrics. 2002;110(1 Pt 1):e2.
Initial dose of 0.1 mg/kg IV/SC may be repeated Issues for Referral 8. Menni S, Gualandri L, Boccardi D, et al. Kaposi
q1520min until pain controlled, then q2h PRN. If diagnosis is uncertain, dermatology consultation varicelliform eruption in an infant. J Pediatr.
Fentanyl 12 g/kg IV q2h PRN: may be necessary. 2005;146:432.
Initial dose of 1 g/kg IV may be repeated 9. Amatsu A, Yoshida M. Detection of herpes simplex
q1520min until pain controlled, then q2h PRN. ALERT virus DNA in non-herpetic areas of patients with
Codeine or codeine/acetaminophen dosed as To prevent autoinoculation of eye or other body eczema herpeticum. Dermatology. 2000;200:
0.51 mg/kg of codeine component PO q4h PRN areas, it is critical to educate patient and control 104107.
Hydrocodone or hydrocodone/acetaminophen pruritus; in young children, trim fingernails short 10. Leinweber B, Kerl H, Cerroni L. Histopathologic
dosed as 0.1 mg/kg of hydrocodone component and consider mitten use. features of cutaneous herpes virus infections
PO q46h PRN (herpes simplex/herpes varicella/zoster): A broad
r Antipruritics may prevent autoinoculation and spectrum of presentations with common pseudo-
bacterial superinfection. FOLLOW-UP lymphomatous aspects. Am J Surg Pathol. 2006;
r 1st-generation antihistamine agents can be 30:5058.
sedating; consider for use at night or in regimen FOLLOW-UP RECOMMENDATIONS
with nonsedating antihistamine agents: Patient Monitoring
Diphenhydramine: PO, IM, IV, 5 mg/kg/day divided r Follow-up should occur within a few days to assess CODES
q68h clinical status and discern need for additional
Hydroxyzine: PO, 24 mg/kg/day divided q68h; treatment (eg, antibacterials). ICD9
IM, 0.51 mg/kg/dose q46h as needed r If good response to medications and no 054.0 Eczema herpeticum
r Standard dose of a 2nd- or 3rd-generation H1 complications, follow-up may be unnecessary.
antihistamine agent: r Patients should be considered contagious until all
Less commonly available; more expensive lesions have scabbed over. PEARLS AND PITFALLS
Less sedating than traditional 1st-generation r EH treatment should not be delayed to await
antihistamines; only penetrate blood-brain barrier
PROGNOSIS
r Most children heal without complications (5). confirmatory lab test results.
to slight extent r Lesions usually heal within 26 wk (4). r EH diagnosis should be considered in patients with
Cetirizine: 510 mg/day in adults and children
r Mortality rate is <10% with appropriate treatment acutely severe and rapid worsening AD.
12 yr of age; 2.5 mg (1/2 teaspoon) to 5 mg r EH around eye and varicella zoster virus infection of
(1 tsp) once daily in children 25 yr; 2.5 mg and is associated with delayed presentation and
(1/2 teaspoon) once daily in children 623 mo treatment (5). the trigeminal nerve may be confused. Varicella
Desloratadine: 5 mg once daily in adults and r 20% of children will have recurrent HSV infections zoster virus infections are characterized by
children 12 yr of age; 2.5 mg once daily in (5). periorbital, forehead, and nasal vesicles that do not
children 611 yr; 1/2 teaspoon (1.25 mg in cross midline.
COMPLICATIONS
2.5 mL) once daily in children 12 mo to 5 yr; 2 mL r Scarring
(1.0 mg) once daily in children 611 mo r Autoinoculation to eyes, mouth, genitals
r Topical corticosteroids, pimecrolimus, and tacrolimus
r Cellulitis
are often discontinued during active infections due r Sepsis
to concern of association with viral infection in r Multiorgan failure
patients with AD (1,5).
r Shock
r Death
287
EDEMA
David J. Mathison
Dewesh Agrawal
r Decreased capillary oncotic pressure generally r Growth parameters:

BASICS results in anasarca. Examples include: When possible, quantify trends in weight vs.
Decreased protein synthesis: trends in height.
DESCRIPTION Malnutrition (eg, kwashiorkor) Growth failure can be seen in chronic liver or
Alterations in capillary hemodynamics can lead to Liver failure kidney diseases.
increases in interstitial fluid volume, manifesting as Increased protein excretion: Acute weight gain is characteristic of fluid
tissue swelling, or edema. This can be either localized Proteinuria (eg, nephrotic syndrome) retention and acute nephropathy.
or generalized (anasarca). Protein-losing enteropathy (eg, celiac disease, r Auscultation:
PATHOPHYSIOLOGY milk protein enterocolitis, inflammatory bowel S3 gallopheart failure
r 65% of body water is intracellular while 35% of disease, right heart dysfunction, post-Fontan Crackles/Rales, asymmetrypulmonary
body water is extracellular, divided between the cardiac procedure) effusion/edema
r Increased capillary permeability occurs from: r Abdominal exam:
vascular space (1/4) and interstitium (3/4).
r Edema results when fluid shifts from the vascular Burns HepatomegalyCHF, intrinsic hepatic disease,
space to the interstitium. This shift occurs secondary Sepsis/Infection portal HTN
to the following mechanisms: Trauma Isolated ascites is characteristic of portal HTN.
Increased capillary hydrostatic pressure. Anaphylaxis Look for fluid wave, shifting dullness, and
Hydrostatic pressure is most affected by changes Hereditary angioedema abdominal distention.
r Evaluate for signs of intravascular volume depletion
in capillary volumes. In states of generalized fluid
overload, increases in venous fluid volume lead to (eg, tachycardia, pallor, delayed capillary refill).
DIAGNOSIS r Assess for localized vs. generalized edema:
pressure increases in the venules, which are
transmitted to the capillary bed. The resultant HISTORY Extremity edema can be generalized and
pressure gradient increases the transcapillary r Acute or chronic (duration of symptoms) positional (eg, after standing).
movement of fluid into the interstitial space. r Age of onset When localized, look for other signs such as pain,
Decreased capillary oncotic pressure: r Recent illness: erythema, ecchymoses, and blistering to
Since the concentrations of electrolytes in A recent streptococcal infection might be distinguish cellulitis, venous clot, tumor, burn, and
plasma and the interstitium are relatively equal, suggestive of an acute postinfectious trauma.
osmotic force is governed by charged protein glomerulonephritis. Facial (periorbital) edema is often associated with
molecules (colloids), predominantly albumin. r Systemic symptoms: Arthritis, rash, dyspnea, fevers, nephrotic syndrome in children.
Hypoalbuminemia results in decreased capillary r Assess for pitting edema: The tissue swelling from
exercise intolerance, diarrhea, etc.
oncotic pressure, favoring the movement of fluid r Quantify weight gain: This is sometimes qualified by lymphedema classically does not cause pitting.
from the vascular to interstitial compartment to r Look for scrotal/labial edema.
parents using rapid changes in clothing rather than r Look for dysmorphic features.
equilibrate the oncotic (or osmotic) pressures.
quantified by changes in body mass.
Increased capillary permeability. Cytokine release r Quantify urine output and qualify urine consistency r Look for signs of systemic or multisystem illness
and inflammatory mediators can influence (eg, clubbing, rash, joint swelling, signs of
endothelial leak (eg, permeability), leading to fluid and color:
Oliguria can be a sign of hypovolemia or renal malnourishment or vitamin deficiency).
shifts.
insufficiency. DIAGNOSTIC TESTS & INTERPRETATION
ETIOLOGY Frothy urine suggests proteinuria.
r Generalized increases in hydrostatic pressure occur Lab
Hematuria raises concern for acute Initial Lab Tests
from increased salt and water retention, such as in glomerulonephritis.
r Family history: Urinalysis with microscopy:
CHF, renal insufficiency, and glomerulonephritis.
r Localized increases in hydrostatic pressure occur r 3+ protein (300 mg/dL) is suggestive of
Nephropathy
from venous obstruction. Examples include: proteinuria.
Hereditary angioedema r Urinalysis protein may appear falsely elevated with
Malignancy r Allergies
Deep vein thrombosis (DVT) r Medical history alkaline urine, in concentrated specimens, or with
Vasculitis r Recent exposures gross hematuria.
Venous catheters r Microscopy evaluates for urine sediment associated
Portal HTN (eg, hepatic cirrhosis) PHYSICAL EXAM with renal disease.
r Vital signs:
Secondary Lab Tests
Tachypnea, hypoxemiapulmonary edema r Urine protein/creatinine ratio using spot (random)
Tachycardiaheart failure urine protein and urine creatinine levels to quantify
HTNsalt retention/volume overload the degree of proteinuria:
Feversepsis, infection >0.2 is abnormal.
>3.5 is indicative of nephrotic range proteinuria
(1); best evaluated by the first morning sample (2).
r Renal function panel (electrolytes, BUN/creatinine,
albumin level) to evaluate for renal insufficiency and
hypoalbuminemia
r Complement levels (C3, C4, total complement) to
evaluate for glomerulonephritis, vasculitis, or acute
inflammatory disease:
Complement levels are usually normal in nephrotic
syndrome.
288
EDEMA
C3 is low in cirrhosis, postinfectious r Inpatient admission criteria:

glomerulonephritis, and sepsis. TREATMENT Respiratory distress
When C3 and C4 are both low in the presence of Significant HTN, azotemia, or oliguria
kidney disease, it is suggestive of INITIAL STABILIZATION/THERAPY Severe infection (eg, peritonitis)
membranoproliferative or lupus nephritis. r Address any issues related to ABCs. Need for further diagnostic or therapeutic
r Liver panel (AST, ALT, bilirubin, total protein) to r Further therapy depends on the etiology. procedures
evaluate for hepatic inflammatory disease Initiation of heparin
r PT to evaluate for signs of liver dysfunction MEDICATION Significant burn care
r Generalized edema:
r Coagulation studies to evaluate for Postanaphylaxis observation
Avoid excess sodium:
hypercoagulability (see Deep Vein Thrombosis topic) Goal daily sodium intakes = 23 mEq/day
r Consider the following under the appropriate
Avoid saline boluses unless for resuscitation of FOLLOW-UP
circumstances: hypovolemic shock.
Antinuclear antibody, hepatitis B and C titers, and Fluid restriction FOLLOW-UP RECOMMENDATIONS
HIV ELISA to evaluate for potential causes of renal Diuretic therapy: Consultation with a specialist is essential for
insufficiency and systemic inflammatory disease Diuretics are effective in conditions of salt/water underlying disease management.
Consider lipid panel (total cholesterol, retention and increased intravascular volumes
triglycerides), which may support a diagnosis of (eg, heart failure), but use is controversial in
nephrotic syndrome. REFERENCES
conditions of decreased oncotic pressure (eg,
Consider antistreptococcal titers (antistreptolysin
O, anti-DNase-B) to evaluate for antecedent
nephrotic syndrome) and intravascular volume
depletion.
1. Ginsberg JM, Chang BS, Matarese RA, et al. Use of
single voided urine samples to estimate
E
streptococcal infections in the presence of Furosemide is first line: Watch for hypokalemia quantitative proteinuria. N Engl J Med. 1983;309:
suspected postinfectious glomerulonephritis. (dosing: 12 mg/kg IV/IM, max 40 mg, can 15431546.
Vitamin panel to evaluate for vitamin deficiencies repeat every 2 hr if needed). 2. Hogg RJ, Portman RJ, Milliner D, et al. Evaluation
in the presence of malnutrition Spironolactone can be an effective alternative to and management of proteinuria and nephrotic
C1q, C4, C2, and C1 inhibitor to evaluate for furosemide. Spironolactone can be used in syndrome in children: Recommendations from a
inherited or acquired C1 inhibitor deficiency. patients with cirrhosis (spares alkalosis) and pediatric nephrology panel established at the
Stool for alpha-1 antitrypsin to evaluate for congenital heart disease (spares hypokalemia National Kidney Foundation conference on
protein-losing enteropathy (associated with levels and may be cardioprotective by inhibiting proteinuria, albuminuria, risk, assessment,
>2.0 mg/g). fibrosis in the myocardium [3]). Watch for detection, and elimination (PARADE). Pediatrics.
Stool for leukocytes (and eosinophils) to evaluate hyperkalemia (dosing: 13 mg/kg/day PO 2000;105(6):12421249.
for enterocolitis such as from infection, divided b.i.d.q.i.d., max dose 200 mg/day). 3. Kasama S, Toyama T, Kumakura H, et al. Effect of
inflammatory disease, or milk protein allergy. Bumetanide is a loop diuretic that can be used spironolactone on cardiac sympathetic nerve
Tissue transglutaminase antibody (tTG), in recalcitrant edema poorly responding to activity and left ventricular remodeling in patients
endomysial antibody, antigliadin antibody, and furosemide (dosing: 0.020.1 mg/kg IV, max with dilated cardiomyopathy. J Am Coll Cardiol.
serum total IgA level to evaluate for celiac dose 0.35 mg/kg/day). 2003;41:574581.
enteropathy (see Celiac Disease topic). Excess intravascular volume depletion can lead
4. Kher K, Schnaper HW, Makker SP. Clinical Pediatric
Imaging to shock or acute renal failure. Nephrology. 2nd ed. Abingdon, England: Informa
Imaging based on the clinical presentation as Albumin: Use of albumin is controversial and Healthcare; 2006:172.
indicated: reserved for severe anasarca with signs of
r Chest radiograph (if patient has respiratory distress) intravascular volume depletion or
to evaluate for pulmonary edema, effusions, or signs diuretic-resistant anasarca. Albumin infusions ADDITIONAL READING
of cardiopulmonary disease carry a risk for a sudden mobilization of fluid into
r Renal US to evaluate for acute obstruction the intravascular compartment, which can worsen Hisano S, Hahn S, Kuemmerle NB, et al. Edema in
pulmonary edema or CHF. Increasing serum childhood. Kidney Int Suppl. 1997;59:S100S104.
(hydronephrosis), intrinsic disease (cysts, kidney
size), and congenital anomalies (eg, hypoplasia, albumin levels to 2.8 g/dL is adequate to restore
horseshoe kidney, etc.) intravascular oncotic pressures (4). Albumin
r Liver US with Doppler to evaluate for parenchymal (0.51 g/kg 20 or 25% salt-poor human albumin CODES
IV) should be given over 4 hr and immediately
liver disease and portal obstruction
r Extremity US with Doppler to evaluate for DVT followed by furosemide (12 mg/kg IV). ICD9
Corticosteroids: Consider use of IV 782.3 Edema
Diagnostic Procedures/Other methylprednisolone or PO prednisone for
r Echo to evaluate for left ventricular outflow idiopathic nephrotic syndrome or systemic
obstruction, cardiac function, and pericardial inflammatory disease. Dosing and use varies and PEARLS AND PITFALLS
effusion if suspected should be made in consultation with a pediatric
r Renal biopsy should be considered in r Generalized edema (particularly in the face) without
nephrologist or rheumatologist.
steroid-resistant nephrotic syndrome, chronic r Localized edema (depends on cause): other systemic symptoms is suggestive of the
nephropathies, and acute renal insufficiency. Anaphylaxis: See Anaphylaxis topic. idiopathic nephrotic syndrome of childhood.
r If a patient has anasarca of unknown origin and the
Burns: Debridement as necessary, topical
antibiotics/dressing urinalysis is negative for protein, send serum tests
Thrombosis: See Deep Venous Thrombosis topic (including albumin) and consider causes such as
for specifics of antithrombotic therapy with liver failure, protein-losing enteropathy,
unfractionated or low-molecular-weight heparin. malnutrition, and cardiopulmonary disease.
r Edema of the hands and feet in a newborn girl is
DISPOSITION suggestive of Turner syndrome.
Admission Criteria
Ventilator support
Severely depressed cardiac function
Encephalopathy from renal/liver failure
Hemodynamic instability
Sepsis
289
ELECTRICAL INJURY
Tzvi Aaron
Nikhil B. Shah
Conversion of electrical energy into thermal r Musculoskeletal:

BASICS energy as current passes through body tissues: Palpate the extremities and perform a complete
Ohm law: Voltage = current x resistance neurovascular exam:
DESCRIPTION This varies depending on the individual tissue Monitor for compartment syndrome.
Electrical injury is caused by electrical shock from resistance. Generally, the greater the resistance, Long bone, scapular, and vertebral compression
either alternating current (AC) or direct current (DC): the more conversion to heat: fractures may result from secondary blunt
r Commonly occurs from lightning or electrical supply Blood and nerves are least resistant. trauma or intense tetanic contraction.
in homes as well as from electricity supplied from Fat and bone are most resistant. r Ocular:
batteries, generators, power lines, and other Secondary effects or injury: Delayed cataract formation in 6%
high-voltage supplies From falls or getting thrown Ocular burns, uveitis, and hemorrhage
r Wide range of presentation from minimal injury to
severe organ involvement and death
DIAGNOSIS Lab
EPIDEMIOLOGY Initial Lab Tests
Incidence HISTORY r Urinalysis:
r Electrical injuries result in >3,000 admissions r Mechanism determines severity of injury:
Specific gravity, pH, hematuria, and urine
annually to specialized burn units. Type of current: AC is significantly worse than DC. myoglobin if urinalysis is positive for hemoglobin
r Results in 1,300 deaths per year Type of voltage: High voltage (>1,000 V) is Monitor urine output if there are concerns of
r Bimodal pediatric distribution: Toddlers and associated with greater morbidity and mortality. acute renal failure.
Current pathway: Transcranial and transthoracic r Other tests:
adolescents: currents are more commonly fatal.
Household appliancerelated injury predominates For normal household currents, no other tests are
Current intensity: Currents >2050 mA may needed.
in children <12 yr. cause respiratory and cardiac arrest.
High-voltage electrical injury is more common in High-voltage injury or symptomatic patients
Duration of contact require further evaluation, including:
older children due to risk-taking behavior. Tissue resistance (eg, wet skin worse than dry)
r 2 to 1 male:female overall incidence CBC
Type of contact surface Serum electrolytes and creatinine (Severe
r Circumstances surrounding the incident
RISK FACTORS rhabdomyolysis may lead to renal failure.)
r Exposed electrical outlets, cords, or devices r Secondary injury from trauma Check serum myoglobin if urine is positive for
r Adolescents engaged in risk-taking behavior, such myoglobin.
PHYSICAL EXAM
as trespassing in transformer substations or on r Respiratory: Creatine kinase (CK) levels in cases with severe
subways/trains or climbing trees and utility poles Chest wall muscle paralysis from tetanic rhabdomyolysis from high-voltage injuries may
contraction may lead to respiratory arrest. help predict which patients could benefit from
GENERAL PREVENTION
r Proper adult supervision of children r Cardiac: Asystole or dysrhythmia early fasciotomy to prevent amputation (2).
r Education about childproofing, outlet covers, r Skin: Cardiac enzymes for patients with chest pain,
an abnormal ECG or dysrythmia, or a
extension cord and overhead power line dangers, Burns:
Superficial injury may appear minor despite high-voltage injury
and appliance safety (eg, keeping hair dryers away Blood gas analysis for patients needing
from bathtubs) significant deep tissue injury.
r Avoid areas of destruction after storms such as Conversely, the presence of surface burns does ventilator support or requiring urinary
alkalinization for rhabdomyolysis
hurricanes or tornadoes to prevent contact with not accurately predict the extent of possible
fallen high-voltage lines internal injuries (1). Imaging
r Targeted education to adolescents and young adults Type of burn influences severity and extent of r Imaging should be done as clinically indicated for
in construction, public utility, and railway tissue damage. concerns of associated fractures.
Ferning is a specific pattern of burn seen after r Echo if abnormal ECG
transportation trades
lighting strike with a fernlike pattern seen on Diagnostic Procedures/Other
PATHOPHYSIOLOGY skin. r Fasciotomy or escharotomy may be required in
r Electrical current will follow the path of least r Oral burns:
resistance. If this path is through the body or tissue, high-voltage or prolonged low-voltage injuries.
Children, usually <6 yr, who bite or suck on r Obtain early surgical consultation since early
significant injury may occur. household electrical cords
r Electrical injuries result from: fasciotomy may prevent subsequent amputation.
Cosmetic deformity of the lips may occur.
Direct effects of current: Delayed labial artery bleeding (in 23 wk) Pathological Findings
Tissue destruction r CNS: Histologic exam reveals coagulative necrosis of the
Muscle contraction and tetany: epidermis in high-voltage injury.
Transient confusion, amnesia, impaired recall of
Supraphysiologic muscle contraction can lead
events, and loss of consciousness (LOC) DIFFERENTIAL DIAGNOSIS
to chest wall paralysis. Seizure
Cardiac dysrhythmia Most cases have a known etiology, but other
Late paralysis (from direct spinal cord injury), diagnoses to consider include:
transverse myelitis, or transection r Chemical, ocular, or thermal burns
Cervical spine (C-spine) immobilization is r Intracranial hemorrhage
indicated unless patient is completely lucid. r Status epilepticus
r Syncope or arrhythmia
r Toxic ingestion or rhabdomyolysis
r Respiratory arrest
290
ELECTRICAL INJURY
DISPOSITION PROGNOSIS
TREATMENT Admission Criteria Patients with exposure to low voltage and without
r Inpatient care is required for all patients with major electrical events, prolonged unconsciousness, or
PRE HOSPITAL anything other than minor low-voltage injuries: cardiac arrest have excellent outcomes (5).
r For high-voltage incidents, the source voltage LOC or neurologic insult COMPLICATIONS
should be turned off before rescue attempt. Dysrhythmias or myocardial insult r Delayed labial artery hemorrhage
r Separate victim from source. Rhabdomyolysis/myoglobinuria or acidosis r Amputation (high-voltage injuries)
r Rescuers should be aware of scene safety and threat Trauma necessitating admission r Infection/sepsis in deep tissue injury
to bystanders or responders. Concerns of deep tissue damage or internal organ r Acute renal failure
r Approach victims of electrical injuries as both injury
r Neurologic sequelae including loss of sensation,
trauma and cardiac patients: Major burns
r Early initiation of burn and trauma care, preferably myelopathy, paraplegialike syndrome and
C-spine immobilization prior to movement
at a specialized center, is recommended. neurapraxia
Cardiopulmonary monitoring
r Assess and stabilize airway, breathing, and r Critical care admission criteria:
circulation. Patients with cardiac or respiratory arrest, LOC, REFERENCES
abnormal ECG, hypoxia or respiratory distress,
INITIAL STABILIZATION/THERAPY chest pain, myoglobinuria, acidosis, or significant 1. Wright RK, Davis JH. The investigation of electrical
burns or traumatic injuries should be admitted to deaths: A report of 200 fatalities. J Forensic Sci.
circulation. the ICU. 1980;25:514.
r Electrical injuries are more similar to a crush injury
Discharge Criteria 2. Kopp J, Loos B, Spilker G, et al. Correlation E
rather than a thermal injury due to potentially r Healthy children with household current exposures between serum creatinine kinase levels and extent
extensive deep tissue damage in the absence of of muscle damage in electrical burns. Burns.
significant cutaneous injury. who are asymptomatic can be safely discharged
r Resuscitation as per Advanced Trauma Life Support after 4 hr of observation (3). 2004;30(7):680683.
r Minor burns (including oral burns) or patients with 3. Chen EH, Sareen A. Do children require ECG
(ATLS) and Pediatric Advanced Life Support (PALS) evaluation and inpatient telemetry after household
protocols: mild symptoms can be observed for several hours
and discharged if symptoms resolve and there is no electrical exposures? Ann Emerg Med. 2007;49(1):
Cardiopulmonary monitoring: 6467.
Cardiac medications as needed for arrhythmias elevation in CK or myoglobinuria.
4. Pizano LR, Corallo JP, Davies J. Nonoperative
IV hydration with normal saline or lactated Issues for Referral
r Consider additional consultations with management of pediatric burn injuries. J Craniofac
Ringer:
Reduces morbidity in severe burns Surg. 2008;19(4):877881.
trauma/critical care, orthopedics, plastic surgery,
Prevents renal failure ophthalmology, and general surgery, depending on 5. Garcia CT, Smith GA, Cohen DM, et al. Electrical
Large volumes may be required due to the type and severity of traumatic injuries. injuries in a pediatric emergency department. Ann
significant 3rd spacing r Oral or plastic surgeons should evaluate children Emerg Med. 1995;26(5):604608.
Sodium bicarbonate 50 mEq/L (1 ampule per with oral burns. 6. Gronert GA. Succinylcholine-induced hyperkalemia
liter) to alkalinize the urine (pH 7.5) to increase and beyond. Anesthesiology. 2009;111(6):
rate of myoglobin clearance COMPLEMENTARY & ALTERNATIVE 13721377.
Adequate tissue perfusion, vital signs, and urine THERAPIES
r Burn care should include tetanus immunization as
output should guide fluid resuscitation.
Place Foley catheter and maintain urine output indicated. ADDITIONAL READING
r Prophylactic antibiotics are not routinely
0.52 mL/kg/hr, depending on degree of Bailey B, Gaudreault P, Thivierge RL. Experience with
myoglobinuria. recommended (4).
r Oral burns can be splinted to prevent microstomia guidelines for cardiac monitoring after electrical
Immobilize fractures and dislocations. injuries in children. Am J Emerg Med. 2000;18:
Hourly vascular checks for palpable or audible and hold commissure at constant tension. 671675.
Doppler pulses for extremity burns r Splint injured extremities in functional position as
r Adequate pain control indicated.
r Essential tests: r Physical and occupational therapy should be CODES
Cardiopulmonary monitoring: instituted early.
Arrhythmia after electrical injury ranges from ICD9
benign (15%) to fatal. r 994.0 Effects of lightning
Most common fatal arrhythmia is ventricular FOLLOW-UP r 994.8 Electrocution and nonfatal effects of electric
fibrillation (from AC); asystole (from FOLLOW-UP RECOMMENDATIONS current
high-voltage or DC) may also occur r Discharged patients should follow up with a primary
MEDICATION care physician in 2448 hr.
r Discharge instructions and medications: PEARLS AND PITFALLS
First Line
r Morphine 0.1 mg/kg IV/IM/SC q2h PRN: Continue hydration and monitor urine output. r Succcinylcholine is contraindicated in electrical injury
Initial morphine dose of 0.1 mg/kg IV/SC may be Observe for any new bleeding with oral burns.
Analgesics due to risk of hyperkalemia (6).
repeated q1520min until pain is controlled, then r Extensive deep tissue damage may be present
q2h PRN. Awareness of possible long-term neurologic or
r Fentanyl 12 g/kg IV q2h PRN: ocular effects. Follow up as indicated. despite minimal cutaneous injury.
r Severe morbidity is possible after initial period with
Initial dose of 1 g/kg IV may be repeated Physical and occupational therapy as needed
Appropriate follow-up with specialists minimal or no symptoms.
q1520min until pain controlled, then q2h PRN
r Codeine/acetaminophen dosed as 0.51 mg/kg of Patient Monitoring
codeine component PO q4h PRN Immediate re-evaluation is necessary for:
r Tetanus prophylaxis r Decreased urine output
r Change in mental status
Second Line
Furosemide (0.5 mg/kg IV) or mannitol r Chest pain or palpitations
(0.250.5 mg/kg IV) for myoglobin clearance r Bleeding or neurologic deficits
r Respiratory distress
291
EMERGENCY CONTRACEPTION
Janet Semple-Hess
ETIOLOGY
BASICS r Vaginal intercourse without contraception
r Failure of contraception:
TREATMENT
DESCRIPTION Condom breakage PRE HOSPITAL
r Emergency contraception is the use of either
Displacement of diaphragm, hormone patch, or Stabilization of injuries or bleeding for the sexual
combination oral contraceptives (COC), copper IUD assault patient
progestin-only pills, or an intrauterine device (copper Missed OCP for 3 days
IUD) postcoitally to prevent pregnancy. INITIAL STABILIZATION/THERAPY
Being 2 wk late for Depo-Provera injection
r Although levonorgestrel (Plan B) is the simplest and Stabilize injuries/bleeding for sexual assault patient
is well tolerated, 20 other brands of oral COMMONLY ASSOCIATED CONDITIONS
MEDICATION
contraceptives are approved for use for emergency Sexually transmitted infections
First Line
contraception. r Levonorgestrel comes in 2 dose regimens:
r Use of emergency contraception may reduce the risk
DIAGNOSIS Plan B: 1.5 mg single dose within 3 days of coitus
of pregnancy by: Levonorgestrel (generic): 0.75 mg, 2 pills once
7589% with oral contraceptive pills (OCPs) (1) HISTORY only, given within 72 hr of coitus (some authors
99% with a copper IUD (2) r Identify time of unprotected coitus.
extend to 120 hr)
r Background: r Date of last menstrual period Antiemetics are generally not needed with
Median age of first intercourse in the U.S. is 16 yr. r Confirm consensual nature of coitus or levonorgestrel.
900,000 girls and women ages 1219 yr will circumstances of sexual assault. If patient vomits within 1 hr of dose, this is
become pregnant each year in the U.S. r Inquire about other symptoms. considered a missed dose. Administer antiemetic
90% of adolescent pregnancies are unintended: and readminister dose.
35% end in abortion. PHYSICAL EXAM r Numerous other contraceptive pills may be used.
r Pelvic exam for STIs or for injuries if sexually
The following is a partial list of medications for this
ALERT assaulted
r Pelvic exam and Pap smear are not required prior to purpose; 2 doses 12 hr apart are necessary:
Contraception counseling should include a
Alesse: 5 pink pills
discussion of safe sex, future contraception, and STI emergency contraception use. Cryselle: 4 white pills
and HIV prevention. r Pelvic exam is required for copper IUD placement.
Enpresse: 4 orange pills
r Copper IUD as emergency contraception may be Jolessa: 4 pink pills
PATHOPHYSIOLOGY contraindicated if concurrent STI is suspected. Levlen: 4 light orange pills
The exact mechanism of action of the Yuzpe method, Levora: 4 white pills
first described in 1974 (then with ethinyl DIAGNOSTIC TESTS & INTERPRETATION
Lo/Ovral: 4 white pills
estradiol/levonorgestrel) is unknown and may depend Lab Low-Ogestrel: 4 white pills
r Pregnancy testing is typically obtained in all cases. If
upon the stage of the menstrual cycle at the time Nordette: 4 light orange pills
given: the patient is pregnant, no emergency contraception
Ogestrel: 2 white pills
r May inhibit ovulation, interfere with fertilization, or is used.
Ovral: 2 white pills
r Pregnancy test is required prior to copper IUD
prevent implantation Ovrette: 20 yellow pills
r Emergency contraception with OCPs does not insertion. Quasense: 4 white pills
r STI screening, HIV testing, and hepatitis B testing,
terminate an implanted fertilized ovum or fetus. Seasonique: 4 blue-green pills
r Copper IUD interferes with implantation, which especially if sexual assault has occurred, are Tri-Levlen: 4 yellow pills
preferred but not required to give OCPs as Triphasil: 4 yellow pills
occurs between days 6 and12 after ovulation.
emergency contraception.
292
EMERGENCY CONTRACEPTION
r Antiemetics generally are not needed with

Second Line ADDITIONAL READING
Antiemetics may be necessary: levonorgestrel but may be prescribed for use in case
r Metoclopramide 10 mg PO/IV/IM: of vomiting or if other medication is used for r Committee on Adolescence. Emergency
If metoclopramide given IV, administer as postcoital contraception. contraception. Pediatrics. 2005;116:10261035.
r Follow up with a health care provider to discuss r Gold MA, Sucato GS, Conard LA, et al. Society for
piggyback with normal saline over >30 min to
prevent akathisia. long-term contraception within 2 wk. Adolescent Medicine. Provision of emergency
r Ondansetron 48 mg PO/IV given 3060 min prior r Obtain follow-up pregnancy test if next menses is contraception to adolescents. J Adolesc Health.
to contraceptive >1 wk late. 2004;35:6670.
r Greydanus DE, Rimsza ME. Contraception for
SURGERY/OTHER PROCEDURES PROGNOSIS college students. Pediatr Clin North Am. 2005;
Copper IUD should be placed within 5 days of r Levonorgestrelif given:
52:135157.
unprotected coitus. It can be removed with the next Within 1 day of unprotected intercourse: 1/1,000 r Zite NB, Shulman LP. New options in contraception
menstrual cycle or for left in for up to 10 yr. chance of pregnancy
for teenagers. Curr Opin Obstet Gynecol. 2003;15:
Within 2 days: 1/120
Pregnancy Considerations 385389.
r Emergency contraception (COC or progestin-only) Within 3 days: 1/54
r Copper IUD: 1/100 chance of pregnancy
pills are safe to use if pregnant.
r Copper IUD placement should not be used if the COMPLICATIONS CODES
r Nausea/Vomiting (rare with progestin-only pill)
patient could be pregnant.
r Pregnancy (no greater risk for ectopic pregnancy) ICD9
DISPOSITION r Emergency contraception will not disrupt an already V25.03 Encounter for emergency contraceptive E
Discharge Criteria implanted pregnancy nor cause birth defects. counseling and prescription
Patient has tolerated OCP without vomiting r Bleeding, pain, cramping with copper IUD insertion
Issues for Referral
OB/GYN or primary care provider to discuss long-term PEARLS AND PITFALLS
contraception REFERENCES r Pitfalls:
1. Trussell J, Rodriguez G, Ellertson C. Updated Failure to obtain pregnancy test
FOLLOW-UP estimates of the effectiveness of the Yuzpe regimen Placing copper IUD in pregnant patient
of emergency contraception. Contraception. Not ensuring appropriate follow-up
FOLLOW-UP RECOMMENDATIONS 1999;59:147151. Patient fails to tolerate medication due to emesis
Discharge instructions and medications: 2. Zhou L, Xiao B. Emergency contraception with and does not have timely access to repeat dose
r Consider long-term prescription of OCPs for rest of r Pearls:
Multiload Cu-375 SL IUD: A multicenter clinical
the cycle. trial. Contraception. 2001;64:107. A minors right to access contraceptive services
r Advise the patient that pregnancy may occur with without parental consent varies from state to
subsequent coitus. state. Know your states law.
r Consider a 2nd back-up prescription in case Currently, only 9 states allow females <17 yr of
age to obtain emergency contraception in
patient vomits.
r Encourage condom use for STI protection. pharmacies without a prescription.
293
EMPYEMA
Todd P. Chang
r Rare pathogens: Imaging

BASICS Streptococcus pyogenes r CXR: Upright PA and lateral if possible:
Pseudomonas aeruginosa Compensatory scoliosis can be seen if splinting is
DESCRIPTION Mycobacterium tuberculosis (especially in present.
r An empyema is a fibrinopurulent entity in the pleural developing countries) r Lateral decubitus x-ray to evaluate layering of the
space. This develops from complicated Mycoplasma species pleural fluid
parapneumonic or pleural effusions. Haemophilus influenzae type b (post-Hib vaccine) r US:
r Direct extension of pneumonia is the most common Actinomyces US may locate the extent of fluid collection or
cause, though extension from retropharyngeal, Coccidiomycosis, blastomycosis, histoplasmosis presence of loculations.
mediastinal, subdiaphragmatic, or paravertebral It is also useful to guide the needle during
infections are possible. r Pneumonia thoracentesis in a cooperative or sedated patient.
r Empyemas should be considered in the differential r Chest CT is the imaging modality of choice:
r Parapneumonic effusion
diagnosis in a patient with prolonged fever and Loculations and effusions can be clearly seen.
pneumonialike symptoms and signs. CT is especially useful if the fluid collection is
EPIDEMIOLOGY DIAGNOSIS heterogeneous and is often used for preoperative
planning.
Incidence HISTORY
Current rates range from 114 per 100,000 children. r Most children have fever for several days. Diagnostic Procedures/Other
r Diagnosis of empyema is confirmed if there is:
The rate of MRSA empyema has been increasing from r Cough, difficulty breathing, respiratory distress, and
the turn of the 21st century (1). Turbid or purulent pleural fluid
tachypnea are often present
r Older children may report pleuritic chest pain. A positive Gram stain or pleural culture
RISK FACTORS A relatively high WBC with neutrophil
r Pneumonia, particularly with bacteria associated
PHYSICAL EXAM predominance in the pleural fluid
with suppuration r Fever, tachycardia, tachypnea r Because obtaining pleural fluid is invasive, it should
r Anaerobic empyemas are associated with aspiration
r Respiratory distress, retractions, splinting not be done without considering other diagnoses,
pneumonias and lung abscesses. r Dullness to percussion on affected hemithorax considering antibiotic-only therapy, or considering
r Empyemas have been associated with lack of
r Decreased or absent breath sounds, with egophany operative treatment.
antibiotic treatment, age >2 yr, longer preadmission r Concurrent pneumonia can produce crackles or rales. r If tuberculous empyema is suspected, an intradermal
fever duration, and ibuprofen use (2).
r A tension empyema can deviate the trachea to PPD placement should be done, though a negative
GENERAL PREVENTION the opposite hemithorax. These patients pose a PPD does not rule out TB.
r Some pneumococcal infections may be prevented by
significant risk for airway compromise. DIFFERENTIAL DIAGNOSIS
vaccination. r Minimal signs likely indicate a viral or Pleural effusions without infection can have the same
r Hand washing and precautions to limit spread of
parapneumonic effusion instead of empyema. clinical and CXR findings. The differential therefore
MRSA and other nosocomial infections can includes nonpurulent pleural effusions:
theoretically lower empyema risk. DIAGNOSTIC TESTS & INTERPRETATION r CHF
Lab r Nephrotic syndrome
PATHOPHYSIOLOGY
r Stage I (exudative) days 13: Initial Lab Tests r Acute chest syndrome with sickle cell disease
r CBC, C-reactive protein (CRP), and ESR for baseline
Pneumonia or other thoracic infection leads to r Serositis from vasculitis (eg, systemic lupus
inflammatory measurement and to track future daily
local pleural inflammation. erythematosus or connective tissue disorders)
trends
A transudative pleural effusion forms. r Blood culture: r Pulmonary extension of ascites
r Stage II (fibrinopurulent) days 414:
Up to 25% of children with empyema have r Intrapleural central line placement
Infectious pathogens enter pleural space. r Sepsis and acute respiratory distress syndrome
positive, concordant blood cultures (3).
WBCs enter the pleural space with a large r Blood gas if in respiratory distress r Effusion with WBCs can also be a marker for
inflammatory response.
r Pleural fluid testing from thoracentesis or chest tube lymphoma.
Fibroblasts follow, creating a fibropurulent pleural
placement: r Chylothorax
mass with beginning loculations.
r Stage III (organizing) 2 wk: Cell count and differential. Neutrophils almost r Hemothorax from trauma or vascular malformation
The empyema organizes and forms a cortex or always predominate.
rind. Pleural fluid culture and Gram stain:
Fibrin deposits on both pleural surfaces can
A positive Gram stain and culture confirms the TREATMENT
restrict lung movement and may lead to restrictive diagnosis of empyema even with minimal WBCs
in the cell count. PRE HOSPITAL
lung disease. Assess and stabilize airway, breathing, and circulation.
Acid fast bacilli stain and culture
ETIOLOGY r PT, INR, PTT prior to fibrinolytic therapy INITIAL STABILIZATION/THERAPY
r Common pathogens: r Assess and stabilize airway, breathing, and
Staphylococcus aureus, including MRSA, is most circulation.
common. r Airway: Intubate if the patient has a compromised
Streptococcus pneumoniae airway or is in respiratory failure.
Bacterioides species with aspiration pneumonia r Breathing: Maintain oxygenation and allow the
patient to be in a comfortable position, usually
sitting upright.
r Circulation: Maintain adequate circulatory volume:
Drops in BP may be seen if a large amount of
pleural fluid is drained and intrathoracic pressure
is thus relieved.
294
EMPYEMA
r In patients suspected of having TB empyema, such r It is unclear if thoracotomy should be the initial REFERENCES
as recent immigrants or those with recent travel to therapy or if surgical treatment should be reserved
an endemic area, appropriate airborne precautions for children for whom medical management has 1. Buckingham SC, King MD, Miller ML. Incidence and
should also be taken. failed. etiologies of complicated parapneumonic effusions
r Open thoracotomy: Now relatively rare in children, 1996 to 2001. Pediatr Infect Dis J.
MEDICATION r Video-assisted thorascopic surgery (VATS): 2003;22(6):499504.
r Parenteral antibiotic therapy should be started as
VATS has better postoperative and cosmetic 2. Clark JE. Empyema. In Finn A, Curtis N, Pollard AJ,
soon as possible, although in stable patients this eds. Hot Topics in Infection and Immunity in
may be delayed if pleural fluid will be procured. results than open thoracotomy.
r Intrapleural fibrinolytic therapy: Children V. Vol. 634. New York, NY: Springer;
Doing so can increase the yield on pleural cultures. 2009.
r S. aureus and S. pneumoniae are the most common Tissue plasminogen activator, streptokinase, or
urokinase may be infused into the chest tube to 3. Brook I. Microbiology of empyema in children and
pathogens. However, coverage of MRSA and adolescents. Pediatrics. 1990;85:722726.
Gram-negative species is recommended: disrupt the fibrinopurulent mass.
r Fibrinolytics may prevent operative therapy, though 4. Cameron R, Davies HR. Intra-pleural fibrinolytic
Vancomycin 1015 mg/kg/dose IV q6h (adult max
operative therapy may still be required after therapy versus conservative management in the
1,000 mg/dose) PLUS
intrapleural fibrinolytics. treatment of pediatric pleural effusions and
Ceftriaxone 50 mg/kg/dose IV q8h (adult max
2,000 mg/dose) r Antibiotic-only therapy empyema. Cochrane Database Syst Rev. 2008;(2):
r If anaerobes or P. aeruginosa are suspected due to cd002312.
DISPOSITION 5. Coote N. Surgical versus non-surgical management
lung abscess or aspiration pneumonia:
Admission Criteria of pleural empyema. Cochrane Database Syst Rev.
SUBSTITUTE ceftriaxone with
piperacillin/tazobactam 100 mg/kg/dose IV q8h
r A child in no distress with a small empyema may not 2005;(2):cd001956. E
need admission if follow-up is assured within 12
(adult max 3,000 mg/dose)
days. Otherwise, most patients with empyema are
Consider an aminoglycoside to broaden coverage ADDITIONAL READING
admitted.
for P. aeruginosa. r The admitting hospital should have a surgery team
r For penicillin/cephalosporin allergy: Vancomycin plus r Baldwin S, Terndrup TE. Thoracostomy and related
comfortable with pediatric empyema.
meropenem 20 mg/kg/dose IV q8h (adult max r Critical care admission criteria: procedures. In King C, Henretig FM, eds. Textbook
1,000 mg/dose) of Pediatric Emergency Procedures. 2nd ed.
r If TB is suspected, contact your local infectious Sepsis, unstable vital signs, mechanically Philadelphia, PA: Lippincott Williams & Wilkins;
ventilated patients, and other severely ill patients 2008.
disease authority or the Centers for Disease Control
and Prevention prior to triple therapy:
should be admitted to an ICU. r Wheeler JG, Jacobs RF. Pleural effusions and
Isoniazid 1015 mg/kg/dose PO qd (adult max Discharge Criteria empyema. In Feigin RD, Cherry JD, Demmler GJ,
300 mg/dose) PLUS r Generally, patients with empyema are admitted and et al., eds. Textbook of Pediatric Infectious Diseases.
Rifampin 1020 mg/kg/dose PO qd (adult max not discharged from the emergency department. 5th ed. Philadelphia, PA: Saunders; 2004.
600 mg/dose) PLUS r However, a very small empyema may be observed as
Pyrazinamide 2040 mg/kg/dose PO qd (adult an outpatient in a select few stable patients.
max 2,000 mg/dose) CODES
SURGERY/OTHER PROCEDURES FOLLOW-UP
r No one treatment modality is universally superior to ICD9
any other treatment (4,5). FOLLOW-UP RECOMMENDATIONS 510.9 Empyema without mention of fistula
r Thoracentesis: r Parenteral antibiotics should be continued even with
This procedure can be recommended for patients surgical intervention.
with stage I parapneumonic effusions for r The patient should be followed for any worsening of PEARLS AND PITFALLS
symptomatic relief and diagnosis. the empyema. r Consider empyema in a patient with signs and
Repeated thoracenteses may be required. Patient Monitoring symptoms of pneumonia
r Chest tube thoracotomy: r Fevers >72 hr in duration with appropriate r Consider empyema if a large pneumonia
This may be performed in the emergency antibiotic treatment warrant surgical drainage. r Consider the airway when sedating a child for
department to drain a stage I or II empyema. r Serial CXRs empyema drainage
It should be considered for patients with r Serial CBC, CRP, and ESR r Large empyema or loculated empyema warrants
significant respiratory distress or significant
more aggressive management.
amount of effusion on imaging studies. PROGNOSIS
Because the drainage for empyema is likely Patients who have early recognition and treatment for
viscous, empyema chest tube sizes should be of empyema do well, and the majority will return to
adequate caliber. normal function.
COMPLICATIONS
r Restrictive lung disease
Age Weight Tube Size (French)
r Airway compromise
Neonate <5 kg 812 r Thoracentesis and chest tube complications include
01 yr 510 kg 1014
pneumothorax, hemothorax, infection, or damage to
12 yr 1015 kg 1420 mediastinal structures.
25 yr 1520 kg 2024 r Fibrinolytic complications involve bleeding either
510 yr 2030 kg 2028 locally or elsewhere in the thorax.
r Operative complications can also occur with both
>10 yr 3050 kg 2840
Adult >50 kg 3240 VATS and open thoracotomy.
Adapted from King C, Henretig FM, eds. Textbook of Pediatric

Emergency Procedures. 2nd ed. Philadelphia, PA: Lippincott
Williams & Williams; 2008.
295
ENCEPHALITIS
Todd P. Chang
r Common viruses: DIAGNOSTIC TESTS & INTERPRETATION

BASICS Epstein-Barr virus Lab
HSV Initial Lab Tests
DESCRIPTION Varicella zoster virus r Lumbar puncture (LP) is the mainstay of diagnosis:
r Encephalitis is a usually infectious inflammation of Cytomegalovirus (CMV) CSF WBC >8 cells/mm3 , especially with monocyte
brain parenchyma. Enterovirus or lymphocyte predominance, is concerning for
r Diagnosis requires 1 of 2 manifestations: Influenza possible encephalitis, though most are
Altered mental status Adenovirus <500/mm3 .
Focal neurologic findings Arboviruses (eastern equine, western equine, CSF opening pressure (abnormal if >28 mm Hg)
r This is distinct from meningitis, which is meningeal Japanese, St. Louis, California, West Nile) CSF Gram stain and culture
inflammation without parenchymal involvement. r Uncommon viruses include HIV, rabies, lymphocytic HSV polymerase chain reaction (PCR)
However, both may occur concurrently. choriomeningitis virus, measles, mumps, rubella, Enterovirus PCR
polio, and human herpesvirus (HHV 6 or HHV 7). Consider other assays in consultation with
EPIDEMIOLOGY r Nonviral infectious causes include Mycoplasma infectious disease specialists.
Incidence pneumoniae, Toxoplasma gondii, Rickettsia Consultation with public health authorities may be
r 1,0002,000 viral encephalitides are reported to the
rickettsii, Mycobacterium tuberculosis, Borrelia necessary to obtain lab assays for specific viruses.
Centers for Disease Control and Prevention annually. burgdorferi, histoplasmosis, blastomycosis, r Viral samples may be procured from other body
r The most common age for postnatal herpes simplex
coccidiomycosis, leptospirosis, neurosyphilis, fluids, such as blood or nasal secretions.
virus (HSV) encephalitis is between 11 and 17 days Cryptococcus species, and cerebral malaria (usually r CBC as a baseline immunocompetency screen:
of age (1). (See Herpes Simplex Virus topic.) Plasmodium falciparum). Neutropenia or lymphopenia may suggest an
RISK FACTORS opportunistic pathogen.
r Unimmunized children are at higher risk of Blast cells suggest CNS lymphoma or leukemia.
encephalitis from measles, mumps, rubella, varicella, DIAGNOSIS r Blood culture may yield a bacterial cause, especially
polio, or influenza. HISTORY if CSF cultures are negative.
r Maternal herpes infection r Fever or previous flulike symptoms r Electrolytes, especially sodium levels:
r Travel to endemic areas for arboviruses r Headache, neck pain, altered mental status, Low serum sodium (Na+ <135) may indicate
irritability, poor feeding, lethargy, hallucinations, cerebral salt wasting or SIADH
GENERAL PREVENTION
r Meticulous hand washing seizure, or coma: High serum sodium (Na+ >145) may indicate
r Droplet precautions for most viral and nonviral Headaches may improve when upright. diabetes insipidus.
r Vomiting r Other tests to discern alternative causes of altered
causes
r Airborne precautions for TB, measles, or varicella r Significant travel to countries with TB, measles, and mental status:
r Vector avoidance or mosquito repellants in endemic malaria endemics Serum glucose level: Low or high
r Exposure to mosquitoes or swampy areas BUN and creatinine level (uremia): High
areas Ammonia level: High
r Vaccination may prevent encephalitis: r Exposure to bats in North America increases
Bilirubin level (kernicterus): High
Varicella suspicion of rabies.
r Other medical history or exposure history may Ethanol level: High
Measles Toxicology screen: Positive
Polio explain the altered mental status. Serum osmolarity: Higher than calculated
Influenza PHYSICAL EXAM osmolarity
Japanese encephalitis r A careful neurologic and mental status exam may Consultation with a toxicologist and focused
Yellow fever show focal or general abnormalities: toxicology screening if appropriate
Rabies Altered mental status Imaging
PATHOPHYSIOLOGY Cranial nerve palsies r CT brain without contrast is indicated to evaluate for
r Infectious encephalitis is spread to the CNS: Motor and sensory abnormalities, tremor trauma, cerebral edema, or intracranial hemorrhage:
Via hematogenous routes OR Ataxia and gait abnormalities CT brain is also used to rule out evidence of a
Via neural/axonal spread (HSV, varicella, polio, r Seizures, particularly focal seizures in infants, should mass, which may cause increased ICP, which is a
rabies) prompt testing for HSV. relative contraindication to performing an LP.
r Cell-to-cell infection occurs rapidly and leads to r Meningismus and signs of meningitis such as Physical signs suggestive of intracranial lesion or
cellular dysfunction or cell death. photophobia, headache, and neck stiffness may also increased ICP include:
be present. Significant altered mental status
ETIOLOGY r Papilledema may be seen in those with increased Papilledema
r Viral causes are most common, though an etiology
intracranial pressure (ICP). Focal neurologic finding
is not found in most cases. r A skin exam may show rashes or bite marks, Cerebral edema or focal attenuation on CT may be
r Arboviruses and enterovirus are more common
suggesting a vectorborne disease. consistent with encephalitis.
during the North American summer months, r Systemic signs, such as effusions in large joints (eg,
whereas influenza is a winter pathogen.
knees, elbows), hepatosplenomegaly, or
cardiopulmonary failure suggest a systemic infection
or autoimmune process.
296
ENCEPHALITIS
r CT brain with contrast is recommended if brain Second Line COMPLICATIONS

abscesses are suspected, and it has a higher r Seizure control: r Neurocognitive deficits
detection rate than without contrast (3). If no IV access: r Sensorimotor deficits
r MRI is recommended during admission if a causative Diazepam 0.5 mg/kg (25 yr) PR r Seizure disorder
agent cannot be found. Diffusion-weighted imaging Diazepam 0.3 mg/kg (611 yr) PR r Diabetes insipidus or SIADH
and T2-weighted imaging are more likely to detect Diazepam 0.2 mg/kg (12 yr) PR
early viral encephalitides than other MR studies (4): Midazolam 0.1 mg/kg IM
MRI may show temporal lobe hypodensity in HSV With IV access: REFERENCES
encephalitis. Lorazepam 0.1 mg/kg IV, max dose 2 mg; may
repeat 2, q35min 1. Kimberlin DW, Lin CY, Jacobs RF, et al. Natural
DIFFERENTIAL DIAGNOSIS Phenobarbital 20 mg/kg IV load history of neonatal herpes simplex virus infections
r Meningitis
Fosphenytoin 20 mg/kg IV load in the acyclovir era. Pediatrics. 2001;108:223229.
r Postinfectious encephalitis
If seizures still persist despite these treatments, 2. Caviness AC, Demmler GJ, Almendarez Y, et al. The
r Acute demyelinating encephalomyelitis prevalence of neonatal herpes simplex virus
secure the airway in conjunction with
r Brain abscess administering more potent anticonvulsants: infection compared to serious bacterial illness in
r Neurocysticercosis Pentobarbital coma: 1015 mg/kg IV over 1 hr, hospitalized neonates. J Pediatr. 2008;153(2):
r Sepsis/Septic shock then 1 mg/kg/hr; max 3 mg/kg/hr 164169.
r Seizure disorder and postictal period Propofol 2 mg/kg IV, then 200 g/kg/hr 3. Fitzpatrick MO, Gan P. Lesson of the week:
r Hemorrhagic or ischemic stroke r Cerebral edema control: Contrast enhanced computed tomography in the
r Traumatic brain injury or concussion Mannitol 0.251 g/kg slow push over 5 min; may early diagnosis of cerebral abscess. BMJ. 1999;
319(7204):239240.
E
r Subarachnoid hemorrhage repeat q5min; max dose 2 g/kg over 6 hr
r Encephalopathy: 3% hypertonic saline 6 mL/kg IV to raise Na+ by 4. Kastrup O, Wanke I, Maschke M. Neuroimaging of
5 mEq/L, target 150160 mEq/L infections. NeuroRx. 2005;2(2):324332.
Diabetic ketoacidosis Dexamethasone 12 mg/kg IV bolus, then 0.25
Electrolyte abnormalities (Na+ , Ca2+ , Mg2+ ) 5. Kimberlin DW, Lin CY, Jacobs RF, et al. Safety and
mg/kg IV q4h (max 16 mg/day) and taper efficacy of high-dose intravenous acyclovir in the
Hyperammonemia from hepatic failure or Hyperventilation to reach a pCO2 of 3035 mm
metabolic disorder (eg, propionic acidemia) management of neonatal herpes simplex virus
Hg. This should not be continued for more than a infections. Pediatrics. 2001;108(2):230238.
Hypoglycemia few minutes.
Uremia Cerebral edema interventions should prompt an
Multifocal leukoencephalopathy immediate CT brain and neurosurgical consult. ADDITIONAL READING
r Primary or metastatic neoplasm
r CNS leukemia DISPOSITION r Kimberlin DW, Whitley RJ. Viral encephalitis. Pediatr
r Thyroid storm Admission Criteria Rev. 1999;20:192198.
r Lupus cerebritis Critical care admission criteria: r Kumar G, Kalita J, Misra UK. Raised intracranial
r Prion disease (eg, Creutzfeldt-Jacob) r Sepsis or patients with unstable vital signs despite pressure in acute viral encephalitis. Clin Neurol
r Toxins and drugs intervention should be admitted to an ICU. Neurosurg. 2009;111:399406.
r All other patients with encephalitis should be
admitted to an inpatient floor with neurologic
TREATMENT monitoring. CODES
Discharge Criteria
PRE HOSPITAL Children with encephalitis should not be routinely ICD9
r Maintain airway control. r 054.3 Herpetic meningoencephalitis
r Establish IV access. discharged from the emergency department.
r 072.2 Mumps encephalitis
r Seizure control (See Medication, Second Line.) r 323.9 Unspecified cause of encephalitis, myelitis,
FOLLOW-UP and encephalomyelitis
r Airway: Intubate if Glasgow Coma Scale is <8.
r Breathing: For inadequate respiratory effort, r Household contacts with fevers, chills, and flulike
consider empiric administration of naloxone. symptoms should be monitored closely for signs of PEARLS AND PITFALLS
r Support oxygenation. encephalitis. r Encephalitis usually features altered mental status
r IV access r Reporting is required for certain confirmed cases of
or focal neurologic signs.
r Obtain bedside glucose level. epidemic encephalitides, such as West Nile virus. r Other diagnoses with encephalopathy should be
r Minimize cerebral edema: ruled out.
PROGNOSIS
Elevate the head of the bed to 30 degrees. r Prognosis following encephalitis depends on the r Maintain a high suspicion for HSV encephalitis, and
Avoid hypotonic IV solutions. causative agent, degree of neuroinvasion, timeliness consider empiric treatment.
Perform frequent neurologic exams. of available treatment, and ICP/cerebral perfusion
r Seizure control (See Medication, Second Line.) pressure.
r Isolation precautions for the patient and staff r Despite prompt treatment, HSV encephalitis can
MEDICATION cause neurologic sequelae or death, though the risk
is significantly lower with antiviral treatment.
First Line r Seizures can occur for months to years following
r Acyclovir for suspected HSV encephalitis:
recovery from encephalitis.
Neonates (28 days): 20 mg/kg IV q8h (5)
Children and adults: 10 mg/kg IV q8h
r Ganciclovir for suspected CMV encephalitis:
5 mg/kg IV q12h
297
ENDOMETRIOSIS
Jeranil Nunez
ETIOLOGY r More recent studies investigating less invasive

BASICS Theories include altered immune surveillance in the methods of diagnosing endometriosis include:
presence of either (4): The presence of serum autoantibodies to
DESCRIPTION r Retrograde menstruation Thomsen-Friedenreich antigen (elevated in women
r Endometriosis is ectopic, estrogen-dependent r Hematogenous dissemination with endometriosis) (6)
endometrial-like tissue located outside of the uterus. r Metaplastic differentiation of coelomic epithelium Elevated levels of inflammatory markers in the
r Most often located in the pelvis, the tissue can also serum of women with endometriosis such as
r Rarely, direct transplantation of endometrial tissue
be found nearly anywhere in the body (1): tumor necrosis factor-a, C-reactive protein, or
after pelvic or abdominal surgery (eg, C-section) CCR1 (transmembrane chemokine receptor)
Serosa of the uterus
Posterior cul-de-sac COMMONLY ASSOCIATED CONDITIONS mRNA expression on the surface of peripheral
Uterosacral ligaments r Infertility blood leukocytes (7)
Ovaries r Endometriosis is found in higher frequency in
Imaging
Fallopian tubes women with hypothyroidism, fibromyalgia, chronic US (transvaginal), CT, and MRI have limited diagnostic
Abdominal cavity fatigue syndrome, and certain ovarian malignancies value but can aid in the diagnosis of an ovarian
Rarely in the lungs, diaphragm, skin, or CNS (endometrioid carcinoma, clear cell and mixed endometrioma and help map the extent of disease in
r It is seen almost exclusively in women of subtypes of ovarian cancer). the presence of deeply infiltrating endometriosis
reproductive age; rare cases have been described in involving the bladder or bowel.
pre- or postmenarchal women.
r Endometriosis causes cyclic pain that is exacerbated DIAGNOSIS Diagnostic Procedures/Other
Direct visualization of endometrial lesions and biopsy
during menstrual periods. HISTORY
r The most concerning presentation of endometriosis via laparoscopy (preferred), or laparotomy, is the gold
r Variable presentation often leads to delayed standard for the diagnosis of endometriosis:
is a ruptured endometrioma, a cystlike implant on diagnosis. Symptoms do not correlate with severity r Disease is staged according to anatomic location of
ovaries that contains blood, fluid, and menstrual of disease. the lesions and severity of involvement.
tissue. Patients with a ruptured endometrioma r Chronic pelvic or back pain, often cyclic, increased r Negative histology does not exclude disease.
present with acute abdominal pain and a surgical during menses
abdomen on exam. Pain control, fluid resuscitation, r Dysmenorrhea, usually severe Pathological Findings
and expedient surgical consultation are r Peritoneal implants have variable appearance:
r Deep dyspareunia
recommended. r Cyclic bladder or bowel symptoms: Nausea, Raised reddish, powder-burn, blue-black, white, or
EPIDEMIOLOGY yellowish-brown irregularly shaped patches, with
vomiting, bloating, diarrhea, urinary frequency scarred or inflamed peritoneal surface adhesions
Incidence r Dyschezia r Ovarian endometriosis are superficial implants as
r True incidence is unknown r Dysuria
r Increased incidence seen in relatives of affected described above or cystlike structures
r Chronic fatigue
(endometriomas) containing blood, fluid, and
women r Infertility menstrual tissue chocolate cysts.
Prevalence r Histologically: Similar to endometrial tissue with
r Affects 510% of women of reproductive age in PHYSICAL EXAM
r Abdomen: Tenderness; peritoneal signs (guarding, endometrial-like glands and stroma
the U.S. (2)
r Present in 1235% of women of reproductive age rebound tenderness) in the presence of a ruptured DIFFERENTIAL DIAGNOSIS
endometrioma r Appendicitis
and as many as 40% of adolescents undergoing r Pelvic: Nonspecific findings related to the site of r Ovarian cysts
laparoscopy for evaluation of chronic pelvic pain or
endometrial implants such as: r Ovarian torsion
dysmenorrhea (3)
Pelvic tenderness r Ectopic pregnancy
RISK FACTORS Adnexal mass/tenderness r Pelvic inflammatory disease
r Early menarche Uterosacral ligament nodularity or tenderness r Inflammatory bowel disease
r Nulliparity (diagnosed on rectovaginal exam) r Irritable bowel syndrome
r Frequent or prolonged menses Visible cervical or vaginal lesions: Reddish,
r Urinary tract infection
reddish-blue, blue-black patchy lesions
PATHOPHYSIOLOGY r Mittelschmerz
r Hormonally responsive ectopic endometrial tissue DIAGNOSTIC TESTS & INTERPRETATION r Gastroenteritis
spreads locally and hematogenously. Lab r Diverticulosis
r Behaves similarly to endometrial tissue with cyclic Initial Lab Tests
proliferation and secretory and sloughing phases in r Pregnancy test to exclude pregnancy
response to hormonal fluctuations r Serum CA-125 level is elevated in severe disease TREATMENT
Induces an inflammatory response with activation and is a nonspecific marker. Also elevated in other
of macrophages and increased cytokine gynecologic disorders. CA-125 levels >30 IU/mL are PRE HOSPITAL
production leading to surrounding fibrosis and suspicious for gynecologic disease (5). r Pain control as needed
formation of adhesions r If a ruptured endometrioma is suspected, IV
crystalloid fluid resuscitation should be initiated.
r Other life-threatening emergencies should be ruled
out first (eg, appendicitis, ectopic pregnancy,
ruptured endometrioma, or hemorrhagic ovarian
cyst).
r Hydration with IV crystalloid fluids may be necessary
if the patient is unable to tolerate oral fluids or
medications.
r Adequate analgesia with either PO or IV medications
298
ENDOMETRIOSIS

First Line FOLLOW-UP r Nisolle M, Donnez J. Peritoneal, Ovarian and
r Acetaminophen 6501,000 mg PO q4h PRN
r NSAIDs: FOLLOW-UP RECOMMENDATIONS Recto-vaginal Endometriosis: The Identification of
Ibuprofen 400600 mg PO q6h PRN Discharge instructions and medications: Three Separate Diseases. Abingdon, England:
r Outpatient pain management regimen Informa Healthcare; 1996.
Ketorolac 1530 mg IV or IM q6h PRN r Ozkan S, Arici A. Advances in treatment options of
r Morphine 0.1 mg/kg IV/IM/SC q2h PRN: r Trial of hormonal therapy, if necessary, after
Initial morphine dose of 0.1 mg/kg IV/SC may be gynecologic consultation endometriosis. Gynecol Obstet Invest. 2009;67:
repeated q1520min until pain is controlled, then r Gynecologic referral 8191.
r Thach AM, Young GP. Pelvic pain. In Rosen P, Barkin
q2h PRN. Patient Monitoring
r Potential side effects of long-term use of analgesics R, eds. Emergency Medicine: Concepts and Clinical
Second Line Practice. 4th ed. St. Louis, MO: MosbyYear Book;
A trial of hormonal drug therapy for 3 mo may be and hormonal therapy
1998:22932304.
started in consultation with the primary care physician r Careful histories and annual physical exams are
r Valle RF, Sciarra JJ. Endometriosis: Treatment
or gynecologist (8): recommended.
strategies. Ann N Y Acad Sci. 2003;997:229239.
r Combination oral contraceptives such as:
PROGNOSIS
Lo/Ovral: 1 pill PO per day Some patients may exhibit persistent chronic pelvic
Ortho-Novum: 1 pill PO per day pain and/or infertility despite maximal medical CODES
r Androgens:
treatment and surgical excision of lesions.
Danazol 600800 mg PO per day
r Progestogens: COMPLICATIONS ICD9 E
r Morbidity and mortality is associated with multiple r 617.0 Endometriosis of uterus
Medroxyprogesterone 1020 mg PO per day r 617.1 Endometriosis of ovary
r Gonadotropin-releasing hormone analogs: surgical interventions in patients with progressive,
refractory symptoms: r 617.2 Endometriosis of fallopian tube
Leuprolide 3.57.5 mg IM per day
Scarring
SURGERY/OTHER PROCEDURES Formation or progression of abdominal and/or
r Surgical excision or ablation of ectopic endometrial pelvic adhesions PEARLS AND PITFALLS
lesions is curative in some cases of pelvic pain Ureteral or bowel obstruction
r Endometriosis should always be considered in the
refractory to medical management. Bowel perforation
r Lesions can recur. r Chronic pelvic pain differential diagnosis of chronic pelvic pain or
r Ruptured cysts infertility in girls and women of reproductive age.
DISPOSITION r Diagnosis is made with surgical exploration and
Admission Criteria biopsy.
r Critical care admission criteria: r Other causes for chronic pelvic pain should be ruled
REFERENCES
Hemodynamic instability unresponsive to fluid out.
administration requiring vasopressor infusions 1. Giudice LC, Kao LC. Endometriosis. Lancet. 2004; r A significant percentage of women with
Acute surgical abdomen from ruptured ovarian 364(9447):17891799. endometriosis will have symptoms refractory to
endometrioma: Critical care or inpatient medical 2. Olive DL, Schwartz LB. Endometriosis. N Engl J medical and/or surgical management.
ward admission at the discretion of surgical Med. 1993;328:1759. r Certain cancers and other disorders have been seen
consult 3. Vercellini P, Fedele L, Arcaini L, et al. Laparoscopy in women with endometriosis. Annual physical
r Inpatient medical ward admission: in the diagnosis of chronic pelvic pain in adolescent exams are recommended in all women with
Refractory pain women. J Reprod Med. 1989;34(10):827830. endometriosis.
Need for further observation or evaluation 4. Donnez J, Van Langendonckt A, Casanas-Roux F,
Exploratory surgery for unclear diagnosis et al. Current thinking on the pathogenesis of
Discharge Criteria endometriosis. Gynecol Obstet Invest. 2002;
r Pain well controlled 54(Suppl 1):5262.
r History and physical exam most consistent with a 5. Bast RC Jr., Badgwell D, Lu Z, et al. New tumor
diagnosis of endometriosis exacerbation markers: CA125 and beyond. Int J Gynecol Cancer.
r Gynecologic follow-up ensured 2005;15 (Suppl 3):274281.
6. Yeaman GR, Collins JE, Lang GA. Autoantibody
Issues for Referral responses to carbohydrate epitopes in endometri-
Referral to an OB/GYN specialist for further evaluation osis. Ann N Y Acad Sci. 2002;955:174182.
and management is recommended in all cases of
7. Agic A, Xu H, Finas D, et al. Is endometriosis
endometriosis, especially if the following signs or
associated with systemic subclinical inflammation?
symptoms are present:
Gynecol Obstet Invest. 2006;62:139147.
r Chronic pelvic pain
8. Kennedy S, Bergqvist A, Chapron C, et al. ESHRE
r Infertility
guideline for the diagnosis and treatment of
r Suspicion for malignancy endometriosis. Hum Reprod. 2005;20(10):
COMPLEMENTARY & ALTERNATIVE 26982704.
THERAPIES
Complementary therapies such as herbal treatments,
acupuncture, reflexology, and homeopathy have been
reported to reduce pain symptoms in some women
with endometriosis:
r There are no randomized controlled trials supporting
these treatments in endometriosis.
299
ENVENOMATION, INSECT BITES AND STINGS

Mohan Punja
Robert J. Hoffman
PATHOPHYSIOLOGY COMMONLY ASSOCIATED CONDITIONS

BASICS r Hymenoptera: Bees, yellow jackets, wasps, hornets, r Viral encephalitides: Eastern equine encephalitis,
and ants: West Nile virus/western equine encephalitis,
DESCRIPTION Hymenoptera venom contains a mix of peptides Japanese encephalitis
r Insects are a class of animals within the largest and including histamine and melittin, which cause cell r Papular urticaria is a delayed hypersensitivity
most diverse phylumArthropoda. damage and degranulation of basophils and mast reaction to bites/stings manifested by crops of
r Relevant insects can be divided into the major cells. erythematous papules.
orders of Hymenoptera (ants, bees, wasps, and Anaphylaxis usually occurs within 1530 min and r Worldwide, the following conditions cause
hornets), Diptera (mosquitoes, deerflies), Hemiptera is mediated by IgE; cross-reactivity occurs among substantial morbidity and mortality and in North
(bed bugs), Lepidoptera (caterpillars), Siphonaptera vespid venoms. America may be seen in the returning traveler:
(fleas), and Anoplura (lice). Bees are known to be docile and can only sting Malaria, dengue fever, leishmaniasis, lymphatic
r Though generally thought of as pests, insects play once before dying. filariasis, Chagas disease/trypanosomiasis, yellow
the vital role in our ecosystem of recycling organic African honeybees are an aggressive hybrid fever.
compounds. spreading across the southeastern U.S. and are
r The role of insects in medicine is related to their known for being aggressive and responding to
transmission of pathogens, immune system response perceived threats in large swarms. DIAGNOSIS
to venom, or cutaneous and respiratory system Fire ants, especially imported fire ants, infest the
HISTORY
irritation from body parts or secretions. southern U.S. and are more aggressive; their r The patient may be able to identify the specific
unique alkaloid venom tends to cause more pain.
EPIDEMIOLOGY organism after an obvious bite or sting.
r Hymenoptera stings cause more deaths (4050) Alarm pheromones alert colonies of insects to r Patients often report immediate local effects such as
swarm and attack potential threats, resulting in
annually than any other envenomation in the U.S. numerous stings. stinging, paresthesias, and exquisite pain.
r There are reported to be between 6 million and r Patients with anaphylaxis may complain of
Systemic toxicity generally occurs with anaphylaxis
12 million infestations of lice yearly. (not dose dependent) or with large numbers of light-headedness or syncope or may arrive in cardiac
r Bed bugs are an increasing problem, especially in stings. arrest.
urban cities: r Several varieties of butterflies and moths contain
PHYSICAL EXAM
There are likely millions of unreported insect stings urticating hairs that cause stinging and pruritus from r Insect bites are usually associated with localized
or bites annually. a mechanical irritation; stinging caterpillars have erythema, swelling, and vesicles or pustules.
Bed bug infestation is epidemic in the U.S., with spines containing venom typically causing burning r Mosquito bites have an appearance of urticaria,
particularly heavy infestation in New York City. pain, edema, and blistering. characteristically with a central puncture, papule, or
r Blister beetles (also known as the Spanish Fly)
RISK FACTORS vesicle.
Outdoor activities contain Cantharidin, a vesicant that can cause r Bed bug bites are dark red on fair-skinned
topical irritation and blistering and if ingested can individuals and often appear in linear clusters.
GENERAL PREVENTION cause vomiting, GI mucosal sloughing with r With stinging caterpillars, the classic gridlike
r Protective clothing including long-sleeve shirts and
hematemesis and bloody diarrhea, and hematuria. pattern may appear 23 hr after a sting.
long pants Touching ones eye after touching the toxin may r Stings to the oral mucosa or tongue from swallowed
r Insect repellent
cause keratoconjunctivitis or anterior uveitis.
r Many baby soaps and oils contain fragrances that insects may produce edema that compromises the
Generally, children who eat beetles should be less
airway.
may attract insects. symptomatic than those ingesting the concentrated r Stings to loose skin with great capacity to swell,
r Traveling abroad: preparation.
r Lice include the pubic louse (also known as crabs), such as the periorbital area or scrotum, often
Appropriate vaccination (eg, Yellow fever) and
develop an appearance that is difficult to distinguish
chemoprophylaxis as per CDC guidelines head louse, and body louse.
r Appropriate mosquito avoidance (mosquito nets, r Bed bugs are difficult to eradicate insects of the from cellulitis.
r Inflammation from a bite or sting and inflammation
insect repellent, close doors/windows): Cimex genus that infest furniture and bedding,
with cellulitis may both be erythematous, warm, and
Insect repellent with <10% DEET is generally feeding usually at night on human blood via
swollen. Pruritus is suggestive of a bite or sting;
considered safe. painless bites that cause urticarial eruptions.
pain is suggestive of cellulitis.
ETIOLOGY r Suspect anaphylaxis in patients appearing pale with
See Pathophysiology. wheezing, hoarse voice, or stridor with or without
urticaria.
r Consider anaphylactic shock in young patients with
sudden cardiovascular collapse or altered mental
status.
300
ENVENOMATION, INSECT BITES AND STINGS
DIAGNOSTIC TESTS & INTERPRETATION r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN COMPLICATIONS
r 1:1,000 epinephrine for anaphylaxis dosed at r Cellulitis, impetigo
Lab
Initial Lab Tests 0.01 mg/kg (max 0.3 mg/dose) IM repeated q5min r Corneal abrasions
r There are no routinely indicated lab tests. PRN for anaphylaxis r Patients with comorbidities are at risk for
r Serum tryptase levels may be helpful in follow-up in r Prednisone 12 mg/kg PO/IM/IV per day uncommon sequelae (ie, patients with coronary
diagnosing allergic reactions when there is r Dexamethasone 0.150.5 mg/kg IV/SC/PO, max artery disease are at increased for MI) such as MI,
uncertainty. single dose 10 mg acute tubular necrosis, or multiorgan failure.
r Albuterol 0.1 mg/kg up to 2.5 mg/dose in 3 mL r Anaphylactic reactions may result in shock,
r Food/Environmental allergy, food syndrome (eg, saline by nebulizer q15min multisystem organ failure, or death.
scombroid) trauma from sharp objects, and insect or Second Line
other bite/sting r For refractory hypotension during anaphylaxis,
r Altered mental status: Head trauma, CNS infection,
ADDITIONAL READING
titrate IV epinephrine 1:10,000 to appropriate BP
hypoglycemia, metabolic or electrolyte disturbance r Consider glucagon (2030 g/kg bolus, then r Hahn IH, Lewin NA. Arthropods. In Goldfrank LR,
515 g/min) for epinephrine-resistant Flomenbaum NE, Lewin NA, et al., eds. Goldfranks
hypotension. Toxicologic Emergencies. 8th ed. Stamford, CT:
TREATMENT Appleton & Lange; 2006:16291642.
DISPOSITION r Moffitt JE. Allergic reactions to insect stings and
PRE HOSPITAL Admission Criteria bites. South Med J. 2003;96(11):1073.
Assess and stabilize airway, breathing, and r Consider admission for patients with anaphylactic
circulation: reactions that are severe, even if symptoms are See Also (Topic, Algorithm, Electronic E
r If anaphylactic reaction, administer epinephrine controlled with medications in the emergency Media Element)
department. r Anaphylaxis
and/or albuterol as per local protocol.
r Critical care admission criteria: r Cellulitis
INITIAL STABILIZATION/THERAPY Persistence of unstable vital signs, anaphylaxis r Rash, Urticaria
requiring epinephrine infusion, or airway
circulation. compromise
r Pain control and local wound care are the mainstays
Discharge Criteria CODES
of treatment. r Most patients may be discharged home.
r Retained stingers (eg, honey bees) or embedded
r Patients with generalized symptoms that resolve ICD9
hairs should be removed.
r Treatment of anaphylaxis and severe systemic should always be observed for 46 hr in the 989.5 Toxic effect of venom
toxicity are similar. emergency department:
Patients presenting with respiratory distress or
MEDICATION anaphylaxis should be admitted. PEARLS AND PITFALLS
First Line Issues for Referral r Avoid granuloma formation by considering stingers
r Itching: r Allergist: Patients with anaphylaxis or generalized as foreign bodies that must be removed.
Diphenhydramine 1 mg/kg PO/IM/IV q6h PRN reactions for further testing and immunotherapy r Children will often scratch injuries, which may lead
Nonsedating antihistamines such as loratadine r Ophthalmologist: Patients with eye complaints to bacterial infections; consider topical antibiotic
510 mg per day. These are less sedating but also prophylaxis with diffuse stings, or at the very least,
less effective than diphenhydramine. schedule follow-up with a pediatrician.
Topical anesthetic lotions may contain a variety of FOLLOW-UP r It is a common pitfall to underestimate the severity
substances, such as benzocaine, ammonia, baking
FOLLOW-UP RECOMMENDATIONS of an anaphylactic reaction. Carefully assess the
soda, and essential oils.
r Topical steroids: Discharge instructions and medications: airway and cardiovascular status, give IM
r Patients with anaphylaxis should be provided with epinephrine early, and reassess the patient
Hydrocortisone 12.5% cream/ointment topical frequently.
b.i.d.q.i.d. appropriately dosed epinephrine autoinjectors in r Failure to provide an epi-pen is a frequent source of
Triamcinolone 0.1% cream topical b.i.d. addition to 35 days of oral steroids and
litigation.
Mometasone 0.1% cream/ointment topical per antihistamines.
day
r Analgesia: PROGNOSIS
Most patients recover without complications within
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN days.
301
ENVENOMATION, MARINE
Mohan Punja
Robert J. Hoffman
Catfish: Dorsal and pectoral fins contain spines r Tiny spicules may be visible within an abrasion.
BASICS causing self-limited local irritation and pain, r Linear papules or beaded streaks in a whip mark
typically to patients attempting to handle without pattern may be seen with the Portuguese
DESCRIPTION gloves. Man-of-War.
r Marine creatures may cause injury by envenomation, Exotic fish: r Pruritic lesions occurring under clothing in the
trauma, or ingestion. Stone fish: Native Australian fish kept as pets. distribution of swimming trunks or clothes are seen
r Injury by envenomation is extremely common, Highly toxic venom causes smooth and skeletal with sea bathers eruption.
especially in coastal areas and specific parts of the muscle paralysis. Locate antivenin (1 vial/sting)
world (eg, Australia); organisms found in and via a poison control center. DIAGNOSTIC TESTS & INTERPRETATION
around North America are generally less toxic. Lion fish: An exotic, colorful pet fish commonly Lab
r Children may be unable to describe the specific causing mild, self-limited but painful Initial Lab Tests
envenomation by heat-labile toxin. r There are no routinely indicated lab tests.
offending organism, increasing the difficulty of
directing treatment. r Echinoderms: Sea urchins or starfish have hard, r CBC, basic metabolic panel, LFTs, and coagulation
r Dead organisms washed ashore may cause injury to brittle spines filled with venom that may break off studies in patients who appear systemically ill
children playing in sand. and lodge in skin. The animal is not itself venomous, Imaging
but the spines may be coated with a heat-labile r Plain films are indicated in evaluating for
EPIDEMIOLOGY toxin. radiopaque retained foreign bodies such as the barb
Incidence r Sponges: Stationary animals attached to the
of a stingray.
Injuries are extremely common, and the incidence seafloor or coral; they penetrate the skin with tiny r Advanced imaging (or surgical exploration) for
varies widely depending on location: spicules to cause a contact dermatitis and a delayed
r Cnidarians, which include jellyfish and fire coral, are penetrating trauma
irritant dermatitis.
responsible for most envenomations. r Coral, particularly fire coral, may cause a very DIFFERENTIAL DIAGNOSIS
r 2008 poison center data reported 785 jellyfish painful sting. This is distinct from a cut or abrasion, Sunburn, trauma from sharp objects, insect or other
stings, 1/2 of which occurred in patients <19 yr of which often will become infected and ulcerate bite/sting
age. The numbers of unreported envenomations are within days of the injury.
likely dramatically higher.
ETIOLOGY TREATMENT
RISK FACTORS See Pathophysiology.
Injuries are concentrated during warm months; PRE HOSPITAL
occasionally, mass numbers of injuries may occur at a Decontamination: The patient should be separated
single location. DIAGNOSIS from the offending organism, and the area should be
irrigated with saline or saltwater:
GENERAL PREVENTION HISTORY r Vinegar or 5% acetic acid can be doused on the
r Children should wear protective footwear at the r The patient may be able to identify the specific
beach and protective clothes/wetsuits. organism after an obvious bite or sting. wound, or compresses soaked in a solution can be
r Parents should be aware of posted warnings r Patients may report reaching into an aquarium or applied.
r Hot water is known to deactivate specific venoms
concerning infestations or local wildlife. attempting to handle pet fish, etc.
r Patients often report immediate local effects such as (scorpion fish, lionfish, stonefish, sea urchins or sea
PATHOPHYSIOLOGY stars, stingrays and skates). Water must be around
r The mechanism of injury varies widely depending on stinging, itching, paresthesias, and exquisite pain.
r Large numbers of patients from the same location 45 C, and the involved area should be immersed for
the organism involved. 3060 min. Take care not to scald patients.
r Jellyfish (including the Portuguese Man-of-War): may be due to an infestation of jellyfish. r Urinating on the wound for the purpose of applying
r Intensely pruritic lesions occurring diffusely under
Tentacles of jellyfish have stinging cells that inject warm liquid against the skin is an unproven folk
venom that may be myotoxic, neurotoxic, or even clothing may be sea bathers eruption, a remedy to treat heat-labile toxins:
cardiotoxic. Local adverse reactions are common; hypersensitivity reaction to the larval form of thimble We do not recommend such use, but it may be an
anaphylaxis is rare. jellyfish. option if no medical care or source of hot water is
r Fish: r Nausea, vomiting, and abdominal pain may be from
available to irrigate the wound.
Stingrays or skates: Tail contains a barb that can the systemic effects of venom. r Generally, animals causing puncture wounds are
cause significant penetrating trauma in addition to r Stridor, syncope, and difficulty breathing may signal
treated with hot water, while those causing urticaria
significant localized pain and mild systemic anaphylaxis. and vesicular eruptions are treated with vinegar.
toxicity from venom, which is heat labile. PHYSICAL EXAM r Use a flexible straight edge, such as a credit card or
These organisms typically must be directly stepped r Erythema, blistering, vesicles, and urticaria often driving license, to scrape adherent tentacles from
on to cause injury to a human. appear at the site of contact with the offending the skin.
organism. r Antibiotics for patients presenting with signs and
r Generalized edema of the affected extremity symptoms of infection from injuries in salt or
r In the case of stingrays, a visible barb may be brackish water should cover gram-negative rods
present in addition to gaping lacerations or only a such as Vibrio vulnificus.
small puncture wound. r Patients with nonhealing lesions or granulomas may
need extended therapy for Mycobacterium marinum
infection.
302
ENVENOMATION, MARINE
INITIAL STABILIZATION/THERAPY DISPOSITION ADDITIONAL READING

r Pain control, tetanus prophylaxis, and local wound
Discharge Criteria
care are the mainstays of treatment. r Auerbach PS. Marine envenomations. N Eng J Med.
The vast majority of patients may be discharged
r Oral antihistamines, occasionally with topical or oral home: 1991;325(7):486493.
steroids, are indicated for local urticarial lesions. r Patients presenting with respiratory distress or r Brush DE. Marine envenomations. In Goldfrank LR,
r Removal of spines or barbs lodged in skin; for Flomenbaum NE, Lewin NA, et al., eds. Goldfranks
anaphylaxis should be admitted.
sponges, remove spicules with adhesive tape; for r Observation in the emergency department is Toxicologic Emergencies. 8th ed. Stamford, CT:
jellyfish or sea urchins, use forceps or gloved hands. prudent in patients with progressive symptoms or Appleton & Lange; 2006:16291642.
r Antibiotic prophylaxis for open wounds in r Currie BJ. Marine antivenoms. Clin Toxicol. 2003;
neurologic deficits.
immunocompromised patients 41(3):301308.
r Address airway, breathing, and circulation in Issues for Referral r Kizer KW. Marine envenomations. Clin Toxicol.
Contact a local poison control center or medical 1983;21:527555.
patients presenting with severe systemic toxicity.
toxicologist for advice as needed.
MEDICATION
First Line CODES
r Consider NSAID medication in anticipation of FOLLOW-UP
prolonged pain and inflammation: FOLLOW-UP RECOMMENDATIONS ICD9
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN Discharge instructions and medications: 989.5 Toxic effect of venom
Ketorolac 0.5 mg/kg IV/IM q6h PRN r Patients with anaphylaxis should be provided with
r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN appropriately dosed epinephrine autoinjectors. E
r Recommend follow-up in the emergency PEARLS AND PITFALLS
r Opioids:
department or with plastic surgery for open wounds r Envenomations and stings in North America
Morphine 0.1 mg/kg IV/IM/SC q2h PRN: left to close by secondary intention or with a
Initial morphine dose of 0.1 mg/kg IV/SC may generally cause self-limited symptoms such as pain
possible retained foreign body. and often do not require emergency care in the
be repeated q1520 min until pain is controlled, r Plastic surgery follow-up for disfiguring injuries
then q2h PRN. emergency department.
r Consider antibiotics for immunocompromised r Home aquariums may contain exotic animals with
dosed as 0.1 mg/kg of hydrocodone component patients or patients with devitalized tissue or unique toxicities. Consult the regional poison control
PO q46h PRN puncture wounds. center for direction or to obtain antivenom.
r 1:1,000 epinephrine for anaphylaxis dosed at PROGNOSIS r Envenomations known to cause significant
0.01 mg/kg IM to a max of 0.3 mg/dose repeated r Most marine envenomations in North America morbidity or death such as sea snakes, Irukandji
q5min PRN for anaphylaxis resolve after only minor irritation. syndrome from certain box jellyfish, and stonefish,
r Normal saline bolus 20 cc/kg for anaphylaxis r The need for hospitalization is rare, as is systemic are extremely uncommon in North America.
r Diphenhydramine 1 mg/kg up to 50 mg PO/IM/IV illness. r Barbs from stingrays should be treated like
q6h PRN r In other areas, particularly the West Pacific and penetrating trauma; do not remove a barb that
r Prednisone 12 mg/kg PO/IM/IV per day Australia, marine envenomations may be lethal. could be lodged in a vital structure. The venom
injected can cause pain for up to 48 hr.
Second Line COMPLICATIONS r Irrigate and explore wounds to ensure removal of
Hypotension: Vasopressors such as dopamine or r Local skin infection may occur; this is particularly
foreign bodies.
norepinephrine: common with coral injuries, which may even lead to
r Antivenoms generally do not exist for North skin necrosis and ulceration.
r Anaphylaxis may occur to any of these poisons,
American envenomations (there is antivenom for
Australian wildlife such as stonefish). though it appears most common with jellyfish.
r Spines from sea urchins, as well as barbs from
SURGERY/OTHER PROCEDURES stingrays, may break off in the skin and remain as a
r Surgical removal of barbs with transfer to trauma
foreign body.
center if necessary r Severe envenomation may rarely result in shock or
r Orthopedic surgery for injuries involving the joint
r Plastic surgery for disfiguring/facial injuries death in patients who are particularly sensitive to
the toxin or in patients with an extremely high dose
of venom injected.
303
ENVENOMATION, SCORPION
Frank LoVecchio
r Somatic effects
BASICS DIAGNOSIS Involuntary muscle contractions
Restlessness
DESCRIPTION HISTORY r Cranial nerve effects:
r Scorpion venom is neurotoxic. r Usually a history of scorpion exposure and sting are
Roving eye movements
r Autonomic, somatic, and cranial nerve excitation readily available. Blurred vision
r Particularly in toddlers or nonverbal children, history
occurs. Nystagmus
r Symptoms begin within minutes of sting. of exposure might not be known. Tongue fasciculations
r Symptoms persist 172 hr. r These cases may be particularly difficult.
Loss of pharyngeal muscle control
r Local effects: r Grading of envenomation exists:
EPIDEMIOLOGY Pain Grade I: Local pain and/or paresthesias at site
Incidence Hyperesthesia Grade II: Local pain and pain and/or paresthesias
In 2007, 5,629 scorpion stings in patients <19 yr of r Systemic effects: at a remote site
age were reported in the U.S.: Coughing or dyspnea Grade III: Either cranial/autonomic or somatic
r Including 1 fatality in a 2-yr-old child Neurologic: skeletal neuromuscular dysfunction
Altered mental status Grade IV: Both cranial/autonomic and somatic
PATHOPHYSIOLOGY Agitation
r Scorpion venom is neurotoxic. skeletal muscle dysfunction
r Autonomic, somatic, and cranial nerve excitation Involuntary muscle contractions
Blurred vision DIAGNOSTIC TESTS & INTERPRETATION
occurs. Seizure Lab
r The mechanism of action is caused by prolonged
Agitation Initial Lab Tests
opening of sodium channels. Hypersalivation r Grade I and II envenomations:
r In children, envenomation may result in severe None
illness, with altered behavior, excitation, and PHYSICAL EXAM r Grade III and IV envenomations:
r Assess vital signs.
seizures. BUN, creatinine
r Onset occurs within minutes and progresses to r A variety of abnormalities may result:
Electrolytes
maximum severity in about 12 hr but may persist Tachycardia is typical, but bradycardia may occur. Urinalysis
for up to 4872 hr. HTN initially but hypotension later during severe CBC
toxicity r Severely agitated patients:
ETIOLOGY Hyperthermia
r Centruroides sculpturatus, or bark scorpion: r Local tissue effects: Creatine kinase
Urine myoglobin
The only toxic scorpion species in the U.S. Lack of erythema r Severe respiratory distress:
Found in the southern U.S., Mexico, Central Pain
America, and the Caribbean Blood gas analysis
Hyperesthesia
r Many other species in Asia, Africa, Israel, South r Autonomic effects: Imaging
America, and the Middle East r Chest radiograph for respiratory symptoms
Sympathetic symptoms:
Pulmonary edema r ECG for tachycardia
Agitation Diagnostic Procedures/Other
Perspiration ECG in grade II and greater
Parasympathetic effects:
Hypersalivation DIFFERENTIAL DIAGNOSIS
r Snake, spider, insect envenomation
r Tetanus
r Diphtheria
r Botulism
r Overdose, dystonic reaction
r Seizures
r Infections
304
ENVENOMATION, SCORPION
r Local anesthetic: COMPLICATIONS

r Respiratory arrest
TREATMENT Nerve blockade with long-acting local anesthetic
r Seizure
may provide significant analgesia and reduce
PRE HOSPITAL opioid requirement. r Shock
r Assess and stabilize airway, breathing, and Lidocaine, maximum single dose 5 mg/kg r Cardiac arrest
circulation. r Sedative/Anticonvulsant: r Death
r Obtain vascular access. Midazolam: 0.1 mg/kg IV/IM:
Very short acting, so redosing may be necessary
r Assess and stabilize airway, breathing, and Lorazepam 0.05 mg/kg IV ADDITIONAL READING
r Cardiovascular:
circulation. r Boyer LV, Theodorou AA, Berg RA, et al. Antivenom
r Begin IV fluid administration. Labetalol: 0.31 mg/kg/dose IV q10min PRN
Dopamine: 25 g/kg/min IV; increase for critically ill children with neurotoxicity from
r Supportive care as follows scorpion stings. N Engl J Med. 2009;360(20):
510 mcg/kg/min as needed
r Mild envenomationsgrades I and II: r Tetanus toxoid: 0.5 mL IM 20902098.
Oral analgesics r LoVecchio F, McBride C. Scorpion envenomations in
Tetanus prophylaxis Second Line young children in central Arizona. J Toxicol Clin
r Severe envenomationsgrades III and IV: Antivenom: Current trial for new Fab product Toxicol. 2003;41(7):937940.
Antivenom (no longer available in the U.S. but is DISPOSITION r Sofer S. Scorpion envenomation. Intens Care Med.
available in Mexico) Admission Criteria 1995;21(8):626628.
Fab antivenom is undergoing trials in the U.S. and Critical care admission criteria: r Walter GE, Bilden EF, Gibly RL. Envenomations. Crit E
is available at participating institutions. r Grade III and IV envenomations require admission to Care Clin. 1999;15(2):353386.
Tetanus prophylaxis an ICU.
Hypertensive urgencies/emergencies: See Also (Topic, Algorithm, Electronic
r If antivenom is given with resolution of symptoms,
Standard therapy such as labetalol Media Element)
observe for 12 hr if asymptomatic. r Botulism
Hypotension:
IV fluid resuscitation and pressor therapy with r Rhabdomyolysis
Discharge Criteria
dopamine r Grade I and II envenomations: Discharge after a r Seizure
Severe agitation: short observation period (12 hr after sting r Tetanus
Benzodiazepine occurred) for progression of symptoms.
Treatment for rhabdomyolysis, if present r Grade III and IV envenomations given antivenom
MEDICATION with resolution of symptoms can be discharged after CODES
1 hr of observation.
First Line
r NSAIDs: Issues for Referral ICD9
Consulting a medical toxicologist or local poison 989.5 Toxic effect of venom
prolonged pain and inflammation: control center may be very useful.
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN PEARLS AND PITFALLS
Ketorolac 0.5 mg/kg IV/SC q6h PRN
Naproxen 5 mg/kg PO q8h PRN FOLLOW-UP r Maintain a high index of suspicion for scorpion
r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN FOLLOW-UP RECOMMENDATIONS stings in endemic areas when patients present with
r Opioids: Discharge instructions and medications: typical symptoms.
Morphine 0.1 mg/kg IV/IM/SC q2h PRN: r If patient received antivenom, discuss signs and r Younger children are more likely to experience
Initial morphine dose of 0.1 mg/kg IV/SC may symptoms of delayed serum sickness. severe illness.
be repeated q1520min until pain is controlled, r Discuss possibility of persistence of pain and
then q2h PRN. paresthesias at site.
Fentanyl 12 g/kg IV q2h PRN: r Encourage patient to return if there is progression of
Initial dose of 1 g/kg IV may be repeated
symptoms.
q1520min until pain is controlled, then q2h
PRN. PROGNOSIS
Codeine or codeine/acetaminophen dosed as r Most cases resolve without sequelae.
0.51 mg/kg of codeine component PO q4h PRN r Younger children are more likely to experience
Hydrocodone or hydrocodone/acetaminophen severe illness, including airway and respiratory
dosed as 0.1 mg/kg of hydrocodone component compromise, shock, and death.
PO q46h PRN
305
ENVENOMATION, SNAKE
Dean Olsen
r Crotaline snakes: PHYSICAL EXAM

BASICS Fangs are located in front of jaw; envenomation r Crotaline bites result in local, systemic, and lab
from bite is more likely than from elapid snakes. effects:
DESCRIPTION Hemotoxic and myotoxic venom causing Vital sign changes include hypotension and
This topic will be a brief review of snakebites resulting coagulopathy and tissue destruction tachycardia.
from indigenous snakes of the U.S. These include: Venom is usually injected subcutaneously, Puncture wounds may be visualized. With
r Crotaline subfamily (pit vipers): resulting in tissue damage that progresses significant envenomation, swelling with skin
Rattlesnakes proximally up the extremity over minutes to hours. discoloration or ecchymosis is apparent.
Copperhead Rattlesnake bites may result in severe toxicity or Hemorrhage from the fang wound or elsewhere is
Cottonmouth death; copperhead and cottonmouth bites cause possible.
r Elapid family: mild toxicity with virtually no reported deaths. Myalgias may result, as can compartment
r Elapid snakes: syndrome, with associated pain, paresthesia, and
Coral snakes
Fangs are located in rear of jaw. The only North pulselessness. Pallor may or may not be present
EPIDEMIOLOGY American elapid, coral snakes strike and chew to due to tissue injury and ecchymosis.
Each year, 3,000 envenomations are reported to advance teeth for fang contact with prey. Obvious necrotic tissue damage at the site of the
poison centers in the U.S. Many are unreported: Much more frequently have a bite with no fang fang wound or extending proximally is possible,
r 9095% are Crotaline with significant swelling.
contact and no envenomation
r 13% are Elapid Venom is much more potent than that of crotalid. r Elapid bites result in neurotoxicity that may be
r Remainder are exotic snakes. Neurotoxic venom that causes progressive delayed:
r 20% of reported snakebites are in pediatric weakness that can progress to respiratory paralysis Slurred speech, paresthesia, fasciculation,
patients. weakness, paralysis, ptosis, diplopia, dysphasia,
ETIOLOGY
r Crotaline snakes: stridor, and respiratory paralysis
RISK FACTORS
r Unsupervised outdoor activity where venomous Crotalus species: Eastern and western DIAGNOSTIC TESTS & INTERPRETATION
snakes are prevalent diamondback, sidewinder, numerous other species Lab
r Playing near woodpiles, heavy brush, or anywhere across Midwest and Southwest U.S. as well as Initial Lab Tests
snakes are known to be present Mexico Crotaline snakebite may cause:
r Keeping venomous snakes as pets or intentionally Sistrurus species: Massasauga and pygmy r Elevated PT/INR
handling venomous snakes rattlesnakes r Thrombocytopenia
Agkistrodon species: Cottonmouth and r Low fibrinogen and increased fibrin split products
GENERAL PREVENTION copperhead
r Avoidance of areas know to contain venomous r Elapid snakes: r Elevated creatine phosphokinase
snakes r Disseminated intravascular coagulation is rare.
Micrurus species: Coral snake
r Some studies suggest that wearing pants made of Micruroides species: Western and Sonoran coral Diagnostic Procedures/Other
thick material, such as jeans, can decrease the snakes Obtain ECG in all patients.
amount of venom delivery if bitten. r Exotic snakes are not indigenous to the U.S. but are
Imaging
PATHOPHYSIOLOGY imported here for use in zoos or illegally to keep as X-rays should be obtained of the bite site to assess for
r Snake venom is a complex mixture of proteins, pets. fangs that may be retained in the skin.
peptides, and enzymes. The exact composition may COMMONLY ASSOCIATED CONDITIONS
vary, but there is significant cross reactivity between DIFFERENTIAL DIAGNOSIS
Alcohol intoxication Nonvenomous snakebites
species.
r Venom is injected from fangs after a strike.
r Based on bite location and depth, it is possible to DIAGNOSIS TREATMENT
have a direct intravascular injection of venom. This HISTORY
may result in rapid onset of much more severe r History of a bite from a snake with local signs and PRE HOSPITAL
toxicity than intramuscular injection. r Assess and stabilize airway, breathing, and
symptoms of venom effect is strongly suggestive of
r Some bites are dry, meaning no venom was circulation.
crotaline snakebite. r Crotaline snakebites: A lymphatic constriction band
excreted or injected: r Some patients may not get an accurate
Due to coral snake fang location, up to 50% are identification of the snake. may be placed proximal to the bite site to retard
dry bites. r Crotaline bites result in pain and swelling that venom absorption and distribution to the systemic
Percentage of crotalid bites that are dry varies circulation.
progresses over minutes to hours: r Coal snakebites: A compression bandage with an
with species but ranges from 1015%. Nausea, vomiting, and a metallic taste in the
It is impossible to initially know if a bite was with mouth may ensue. ACE wrap may be placed on the effected extremity.
or without venom injection. r Elapid snakebites may be asymptomatic initially with r Transport to a center with antivenom is preferable.
rapid onset of symptoms delayed many hours. INITIAL STABILIZATION/THERAPY
r Slurred speech, paresthesias, weakness, cranial r Assess and stabilize airway, breathing, and
nerve palsy, and paralysis may ensue. circulation.
r In crotaline envenomations, treatment is largely
based on symptoms.
r Elapid snakebites are treated empirically even if no
symptoms are present. Elapid bites are diagnosed
with confirmed coral snake exposure and evidence
of skin penetration.
306
ENVENOMATION, SNAKE
MEDICATION Second Line

r Tetanus toxoid is given to all patients with snakebite
ADDITIONAL READING
First Line r Caravati EM. Copperhead bites and Crotalidae
r CroFab, crotalin venom antibody, dose 46 vials if tetanus booster is needed.
over 1 hr: r Prophylactic antibiotics are usually not necessary. polyvalent immune fab (ovine): Routine use requires
This is a cleaved antibody; it does not result in evidence of improved outcomes. Ann Emerg Med.
serum sickness or severe allergic reactions as r Fasciotomy may be indicated for confirmed r Goto CS, Feng SY. Crotalidae polyvalent immune fab
previous crotalid/rattlesnake antivenom.
compartment syndrome secondary to a snakebite. for the treatment of pediatric crotaline
Redosing may be necessary: r Most cases of compartment syndrome respond to
The patient is reassessed after completion of the envenomation. Pediatr Emerg Care. 2009;25:273.
infusion for evidence of continued swelling or antivenom. r Johnson PN, McGoodwin L, Banner W Jr. Utilisation
coagulopathy; if present, an additional 46 vials DISPOSITION of Crotalidae polyvalent immune fab (ovine) for
in adults or in children are administered. Admission Criteria Viperidae envenomations in children. Emerg Med J.
This is repeated until symptoms are controlled. Critical care admission criteria: 2008;25:793.
Control is generally considered cessation of r All patients with significant envenomation or r LoVecchio F, Klemens J, Welch S, et al. Antibiotics
progression of swelling and systemic symptoms after rattlesnake envenomation. J Emerg Med.
receiving antivenom should be admitted to a critical
in addition to trend toward normal coagulation 2002;23:327.
care unit. r Rieley B, Pizon A, Ruha A. Snakes and other reptiles.
time and correction of thrombocytopenia.
Once control is achieved, maintenance doses Discharge Criteria In Goldfrank LR, Flomenbaum NE, Lewin NA, et al.,
r Patients may be discharged after antivenom
are given as 2 vials q6h for 3 doses, a total of 6 eds. Goldfranks Toxicologic Emergencies. 8th ed.
additional vials. administration and improvement of condition.
r Asymptomatic crotaline snakebites should be
Stamford, CT: Appleton & Lange; 2006. E
For Crotalinae envenomations, antivenom should
be considered as first-line therapy for those observed in a monitored setting for 8 hr: See Also (Topic, Algorithm, Electronic
patients with moderate to severe envenomations. If no venom effect is noted, the patient may be Media Element)
All bites with progression of symptoms are treated discharged. Call (800) 222-1222 to contact a local poison control
with Crotaline Fab. center in the U.S.
Issues for Referral
While each case must be individualized, in the Consider consultation with a poison control center,
vast majority of patients who have a moderate or medical toxicologist, or other clinician with experience
severe envenomation, the benefits of antivenom CODES
managing venomous snakebites.
therapy will outweigh the potential risks.
Antivenom given in a timely manner can reverse ICD9
the coagulopathy and thrombocytopenia and halt FOLLOW-UP 989.5 Toxic effect of venom
progression of local swelling.
r Wyeth antivenom: FOLLOW-UP RECOMMENDATIONS
No longer recommended Discharge instructions and medications: PEARLS AND PITFALLS
Derived from horse serum, is uncleaved antibody r Follow up with primary care physician in 2 days. r Snakebites may be dry bites with no venom
with high incidence of allergic reactions and Patient Monitoring injected, but it is impossible to differentiate between
serum sickness The patient should return to the emergency a dry and venomous bite initially.
r Coral snake antivenom: r Crotalid bites (rattlesnake, copperhead,
department if symptoms recur.
Dose is between 1 and 5 vials in children; 35 cottonmouth) have toxin that is hemotoxic and
vials in confirmed bite, even if no symptoms PROGNOSIS
r Most patients do well after treatment with myotoxic.
This is derived from horse serum and is not a Fab r Rattlesnake bites can be deadly, copperhead and
antivenom. Severe allergic reaction, anaphylaxis, antivenom.
r Crotaline snakebites result in low morbidity and cottonmouth bites usually results in milder toxicity
and serum sickness are possible. without fatality
No longer produced in the U.S., but hospitals mortality. r Some bites, particularly elapid (coral snake), may
continue to stock expired antivenom. COMPLICATIONS
r Crotalid (rattlesnake): result in severe toxicity with no apparent fang
The U.S. FDA has approved extension of the
puncture marks.
expiration date of certain antivenom: Coagulopathy r Coral snake toxicity is delayed after the bite and is
It is recommended for hospitals to maintain Rhabdomyolysis
coral snake antivenom, even if expired. severe. If antivenom is available, empiric treatment
Tissue necrosis based solely on the history of the bite is warranted.
Use of any expired medication is an Compartment syndrome
extraordinary measure taken when no other Dysrhythmia
option is available. Multisystem organ failure
Obtain consent from the patient and/or family Shock
prior to using expired antivenom. Death
Exotic snake antivenom: r Elapid (coral snake):
To treat exotic snakebite, such as cobra, adder,
Paralysis
or mamba, a regional zoo or herpetarium is a Respiratory insufficiency
good resource for antivenom. Shock
They often stock antivenom to treat employees
Death
in the event one is bitten from their own exotic
venomous snakes.
307
ENVENOMATION, SPIDER
Sophia Sheikh
Brent W. Morgan
PATHOPHYSIOLOGY Other symptoms include HTN, CNS effects

BASICS r All spiders produce some degree of venom to (seizures, psychosis, hallucinations, etc.), and
paralyze their prey. cholinergic excess (lacrimation, diarrhea,
DESCRIPTION r They release their venom through hollow fangs. bronchorrhea, increased secretions,
r Spider envenomations discussed here include mydriasis/miosis, etc.).
Most do not possess fangs long or sturdy enough to
Latrodectus mactans (black widow) species, pierce human skin. Thus, only a few species are able Caution should be taken in the elderly and very
Loxosceles reclusa (brown recluse), and tarantulas. to poison humans through their bite. young, as respiratory arrest and severe HTN can
r Mature female L. mactans spiders typically are r The venom produced from spiders is more potent occur.
12 cm in size, shiny black with a red hourglass than venom from most snakes; however, the amount r L. reclusa possible symptoms:
shape on their ventral abdomen. Immature females injected during a bite is much less. It is important to Usually within minutes, pain and burning develops
are brown, and their hourglass color can vary. The take into account the bite victims size: at the bite site.
males are also brown but usually much smaller than L. mactans venom contains alpha-latrotoxin, A bulls-eye lesion can develop within 12 hr. It
females. which opens presynaptic cation channels leading is characterized as 15 cm in diameter with a
r L. reclusa are usually 13 cm, dark brown, and have to the release of norepinephrine, acetylcholine, central blister encircled by a red erythematous ring
a characteristic violin (or fiddle) shape. Other species dopamine, and GABA. This explains the that is further enclosed by a white blanched ring.
of spiders can have a similar fiddle shape on their autonomic and neurologic dysfunction manifested Over the next 13 days, the blister can open and
cephalothorax. However, none of these other by the bitten patient. become necrotic, spreading to the underlying
species will have 6 eyes. Thus, spiders with 3 pairs of L. reclusa venom is cytotoxic and composed of tissue.
eyes and a fiddle shape will be brown recluses. hyaluronidase and sphingomyelinase D. They can Systemic signs occur within 2 days of the bite and
r Tarantulas (family Theraphosidae) range from produce a constellation of symptoms known as include nausea, vomiting, fever, chills, myalgias,
2.510 cm, usually are reddish brown to black, and loxoscelism, which can either be cutaneous or and rarely hemolysis.
are covered in hair. systemic. Most bites do not produce skin r Bites from tarantulas do not cause systemic signs but
ulceration, and even less will manifest systemic can produce pain and inadvertently lead to intense
EPIDEMIOLOGY
r Spiders are ubiquitous throughout the world. Only a symptoms. Many alleged spider biteinduced skin itching from hair that falls within the bite wound:
ulcerations are actually other disease processes Tarantula hairs are especially irritating to the
few spider species in the U.S. have fangs that can
including MRSA infections and not spider respiratory tract, skin, and eyes. This local
pierce the human skin and cause significant health
envenomation. inflammatory response can produce itching that
effects.
r Brown recluse spiders are native to the central U.S., Tarantula venom can paralyze its prey but rarely lasts for weeks.
causes problems in humans. It mainly consists of
from the Gulf of Mexico states of Mississippi, DIAGNOSTIC TESTS & INTERPRETATION
digestive enzymes. The symptoms associated from
Alabama, Louisiana, and Texas east to the Western a tarantula bite, besides pain, are mostly allergic Lab
Georgia region, and north to Kentucky: r L. mactans: Electrolytes, creatine phosphokinase,
reactions from urticating hair embedded in the
They are not native to Florida or any state that bite wound. calcium, glucose, and possibly an ECG for those
borders the Atlantic Ocean other than Georgia. complaining of chest pain
They are not native to any area west of Central r L. reclusa: CBC and chemistry for renal function. If
Texas or north of Nebraska. DIAGNOSIS concern for hemolysis, obtain a disseminated
Generally, this means they are not native to intravascular coagulation panel, haptoglobin, and
Florida, the Atlantic Coast, the Northeast U.S., HISTORY
r Bites usually occur when humans invade the spiders urinalysis looking for hematuria.
and the entire Western U.S., nor Alaska or Hawaii.
It is theoretically possible for a brown recluse to habitat (ie, while cleaning out attics or garages, DIFFERENTIAL DIAGNOSIS
disturbing woodpiles, soil, etc.). r Other spiders and insects can produce similar local
be transported to a nonnative state, though
r Often with necrotizing bites, such as that of a brown symptoms (pain, erythema, swelling, itching, and
reports of this are lacking.
r Black widow spiders are native to nearly the entire recluse, there will be no specific history of bite: ulceration) as those seen from the brown recluse
and black widows.
continental U.S., with various species sometimes PHYSICAL EXAM r Bacterial infections (such as MRSA) and certain
being specific for a geographic region, such as the r Bite marks from black widows and brown recluse
southern black widow. dermatologic or vascular conditions can produce
spiders typically are too small to easily identify.
Black widow spiders are native to all inhabited necrotic skin lesions that may wrongly be attributed
However, those from the tarantula family usually can
continents of the world. to brown recluse bites.
easily be located.
r In 2008, according to the American Association of r L. mactans possible symptoms:
Poison Control Centers (AAPCC), there were a total Local erythema (target lesion with central
of 4,191 spider bites and/or envenomations. Of blanching) and pain that can be delayed
these exposures, 2,524 were from black widow Within hours, muscle spasms and fasciculations
spiders, 1,564 were from brown recluses, and 103 can develop in the bitten extremity and spread
were from tarantulas. centrally. Spasms can be severe enough to mimic
a rigid abdomen or an MI:
308
ENVENOMATION, SPIDER
Its indications include failure to control severe

TREATMENT pain despite liberal use of first-line therapy; FOLLOW-UP
uncontrolled severe HTN; and respiratory distress
PRE HOSPITAL in the elderly, pediatric, or severely ill. FOLLOW-UP RECOMMENDATIONS
r Clean the wound. r Discharge the patient with prescriptions for
The antivenin is administered as 12 vials diluted
r Cool compresses or intermittent use of ice packs to in 50100 mL of 5% dextrose or 0.9% sodium adequate analgesia in cases of black widow spider
limit swelling and pain chloride solution, infused over an hour. bites:
It should not be given to those who are allergic to Provide medication for both pain and muscle
INITIAL STABILIZATION/THERAPY horse serum products. spasms.
Assess and stabilize airway, breathing, and Skin testing is usually not recommended since it is r For brown recluse bites, the patient should be
circulation. neither sensitive nor specific in predicting who will instructed on standard wound care, and follow-up
MEDICATION have an adverse effect. should be ensured prior to discharge.
r Tetanus immunization status should be documented Some authorities recommend pretreatment with
PROGNOSIS
and updated as needed. antihistamines and having epinephrine infusion r Fatalities from spider bites in the U.S. are extremely
r Antibiotics should be given if an infection is readily available.
rare. Most patients recover without serious
suspected (prophylaxis is not recommended). COMPLEMENTARY & ALTERNATIVE complications.
r Black widow: THERAPIES r Brown recluse bites have a variable prognosis, with
Benzodiazepines: Act as muscle relaxant: Brown recluse: some severe envenomations resulting in badly
Lorazepam 0.05 mg/kg IV/PO q6h PRN, max r Anecdotal therapies such as dapsone, erythromycin, necrotizing lesions.
single dose 2 mg and hyperbaric oxygen treatment lack scientific COMPLICATIONS
E
Most effective when combined with an opioid evidence to routinely recommend their use. r Brown recluse bites may result in significant tissue
Opioids: For analgesia and to potentiate
benzodiazepine muscle relaxation: SURGERY/OTHER PROCEDURES loss and badly ulcerated lesions.
r General wound care practices should be sufficient r Infection can develop if wounds are not properly
Initial morphine dose of 0.1 mg/kg IV/SC may for most cases of brown recluse bites. Occasionally, cleaned and managed.
large or slow-healing wounds may require surgical r Black widow bites may rarely result in death.
be repeated q1520min until pain is
controlled, then q2h PRN. wound debridement or skin grafting.
r Brown recluse: r For tarantula hair embedded in the eye, irrigation
First-line therapy includes wound care and pain and surgical removal by an ophthalmologist may be REFERENCE
control. needed. 1. Clark RF, Wethern-Kester S, Vance MV, et al.
NSAIDs: DISPOSITION Clinical presentation and treatment of black widow
Consider NSAID medication in anticipation of spider envenomation: A review of 163 cases. Ann
Admission Criteria
prolonged pain and inflammation. r Admit patients with systemic signs, renal failure, Emerg Med. 1992;21(7):782787.
Ketorolac 0.5 mg/kg IV/IM q6h PRN uncontrolled pain, and those who receive the
Naproxen 5 mg/kg PO q8h PRN antivenin.
r For brown recluse bites, monitor for hemolysis. ADDITIONAL READING
r The urticarial response from tarantula hair can be
r Goldfrank LR, Flomenbaum NE, Lewin NA, et al.,
treated using antihistamines and steroids: Discharge Criteria
Diphenhydramine 1.25 mg/kg/dose PO/IV/SC/IM Monitor the patient for 68 hr. If no systemic eds. Goldfranks Toxicologic Emergencies. 8th ed.
q6h PRN for itching, max dose 50 mg symptoms develop and pain is adequately controlled Stamford, CT: Appleton & Lange; 2006:15621569.
without the use of antivenin, then the patient can be r Olson KR. Poisoning and Drug Overdose. 5th ed.
Prednisone 12 mg/kg PO divided b.i.d. per day
for 25 days, max single dose 60 mg/day discharged with appropriate follow-up. New York, NY: McGraw-Hill; 2006:347350.
Dexamethasone 0.2 mg/kg IV/IM/PO per day Issues for Referral
12 days, max single dose 10 mg The ulcer that forms from brown recluse bites typically
Second Line is limited and heals quickly; rarely it can take several
CODES
Black widow: weeks to heal. So it is important that these patients
r Second-line therapy should be the horse-derived L. are adequately followed as an outpatient to ensure ICD9
healing and no further complications arise. 989.5 Toxic effect of venom
mactans antivenin:
Since it is horse derived, there is a small risk of
anaphylaxis. PEARLS AND PITFALLS
In a review of 163 patients with black widow
spider envenomations, there was 1 documented r Black widow bites can usually be managed with
case of anaphylaxis and death after administration parenteral opioids and benzodiazepines alone.
of antivenin (1). Judicious use of antivenin is recommended.
r Most skin lesions diagnosed as necrotizing spider
bite secondary to brown recluse are not the result of
a spider bite at all. Overdiagnoses is extremely
common, even in areas where brown recluse are not
native.
309
EPIDIDYMITIS AND ORCHITIS

Kajal Khanna
Deborah R. Liu
r Adolescents: PHYSICAL EXAM

BASICS Usually STI (Chlamydia trachomatis, Neisseria r In differentiating epididymitis from testicular torsion,
gonorrhoeae, coliform bacteria) each of the following have been found to be
DESCRIPTION r Various Brucella species may cause brucellosis that statistically significant (3):
r Epididymitis is an inflammatory reaction or infection Normal testicular lie
commonly presents as epididymo-orchitis in any age
of the epididymis, the tubular structure attached to group: Tender epididymis
the upper posterior part of each testicle that collects The bacteria are contracted through ingestion of Intact cremasteric reflex
and stores sperm. unpasteurized dairy products or other animal Scrotal erythema usually present (though not
Orchitis is an inflammation or acute infection of products. statistically significant)
the testicle. r In boys with underlying structural or neurologic r Prehn sign:
Epididymo-orchitis involves infection spreading abnormalities of the genitourinary tract: Alleviation of pain with elevation of scrotum in
from the epididymis to include the testicle. Enterobacteriaceae, Pseudomonas aeruginosa epididymitis
r In young adult males, epididymitis accounts for r Other causes: Trauma, systemic disease such as May worsen pain in testicular torsion
more days lost from service in the military than any Henoch-Schonlein purpura Not consistent in children
other disease. r Bacterial orchitis: Note presence and location of tenderness:
EPIDEMIOLOGY Results from extension of infection or Epididymis vs. testicle
Incidence inflammation from the epididymis (E. coli, DIAGNOSTIC TESTS & INTERPRETATION
r 1.2 per 1,000 prepubertal boys yearly P. aeruginosa, Klebsiella species) Lab
r Peaks for hospital admissions occur in the summer From hematogenous seeding from another source) r Urine testing should be obtained:
r Viral orchitis: Mumps, enterovirus, adenovirus,
and winter (1). Urinalysis shows pyuria
varicella, plus others: Bacterial organisms responsible for infectious
RISK FACTORS Mumps:
r Obstructive anatomic abnormalities epididymitis may be isolated from urine or urethral
Orchitis occurs in 30% of patients. specimens.
r Genitourinary abnormalities (ureteral or vasal Occurs typically 46 days after the onset of 4084% of cultures from boys (typically
ectopia, bladder exstrophy) parotitis prepubertal) diagnosed with epididymitis have no
r Anorectal malformations Possible increased risk of infertility identifiable organism (4).
r Indwelling urethral catheters
Young boys and infants are more likely to have
r Recent urinary tract instrumentation pyuria or bacteruria.
r Uncircumcised boys: 3 times more common DIAGNOSIS Semen sample may be obtained in sexually mature
HISTORY males, though this is not commonly done in the
PATHOPHYSIOLOGY r Can be difficult to differentiate between other acute emergency department setting.
Occurs as an inflammatory and usually postinfectious r Optional: CBC or C-reactive protein may
reaction to a bacterial or viral pathogen or as a scrotal complaints
r Scrotal pain: demonstrate inflammatory changes.
complication of an urethral infection caused by the
following: Gradual in onset Imaging
r Sexually transmitted pathogens Mild to moderate severity US should be obtained in cases indeterminant for
r Genitourinary pathogens Compared to acute pain of testicular torsion epididymo-orchitis and is the gold standard imaging
r Progressive scrotal swelling test:
r Hematogenous spread to the epididymis from a
r Commonly associated symptoms: r May show enlarged epididymis of mixed
primary focus of infection (1,2)
Dysuria echogenicity surrounded by reactive fluid
ETIOLOGY Urinary frequency r Color flow Doppler US usually shows increased
r Neonatal epididymitis: Fever testicular or epididymal venous flow.
Result of ascending urinary tract bacterial r Rarely associated symptoms: r 78.6% sensitivity, 96.9% specificity in detecting
infection (Escherichia coli, Enterococcus faecalis) Nausea testicular torsion and decreased blood flow (5)
Hematogenous spread from primary focus Vomiting r Limitations: Blood flow may not be detected in a
(Haemophilus influenzae type b, Streptococcus r Longer duration of symptoms before seeking
normal prepubertal testis because of smaller
pneumoniae, Neisseria meningitidis, Salmonella medical attention in comparison to testicular torsion testicular size, typically in patients <8 yr (5).
species)
r Prepubescent boys: DIFFERENTIAL DIAGNOSIS
Typically culture negative, thought to be of r Testicular torsion
postinfectious etiology (elevated titers for r Testicular tumor
enterovirus and adenovirus seen in boys with r Torsion of testicular appendages
epididymitis) r Scrotal hematoma/contusion/trauma
r Inguinal hernia
r Hydrocele
310
EPIDIDYMITIS AND ORCHITIS
SURGERY/OTHER PROCEDURES 4. Knight PJ, Vassey LE. The diagnosis and treatment
TREATMENT Surgical indications: of the acute scrotum in children and adolescents.
r Scrotal abscess Ann Surg. 1984;200:664673.
INITIAL STABILIZATION/THERAPY r Inability to exclude testicular torsion 5. Nussbaum Blask AR, Bulas D, Shalaby-Rana E,
IV access and fluids if systemically ill r Suspected or proven ischemia caused by severe et al. Color Doppler sonography and scintigraphy of
epididymitis the testis: A prospective, comparative analysis in
MEDICATION
r Neonatal epididymitis: children with acute scrotal pain. Pediatr Emerg
DISPOSITION Care. 2002;18:6771.
Initial antimicrobial therapy directed against
Admission Criteria 6. Yin S, Trainor JL. Diagnosis and management of
uropathogens such as E. coli, E. faecalis: r Toxic appearance
If Gram stain suggests E. coli, consider testicular torsion, torsion of the appendix testis, and
r Scrotal abscess epididymitis. Clin Pediatr Emerg Med. 2009;10:
3rd-generation cephalosporin such as r Infectious epididymo-orchitis that is severe or
cefotaxime (50 mg/kg/dose IV q8h) 3844.
If Gram stain suggests E. faecalis, consider requires systemic antibiotics, such as brucellosis 7. Al-Taheini KM, Pike J, Leonard M. Acute
ampicillin (50 mg/kg/dose IV q6h) plus Discharge Criteria epididymitis in children: The role of radiologic
aminoglycoside, such as gentamicin r Ability to take oral antibiotics studies. Urology. 2008;71:826829.
(2.5 mg/kg/dose IV q8h) r Well-appearing without scrotal abscess
r Nonbacterial epididymitis in prepubertal boys
(culture negative):
ADDITIONAL READING
FOLLOW-UP r Berger RE. Acute epididymitis. In Holmes KK, Mardh
prolonged pain and inflammation PA, Sparling PF, eds. Sexually Transmitted Diseases.
E
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN FOLLOW-UP RECOMMENDATIONS
r Bed rest: 2nd ed. New York, NY: McGraw-Hill. 1990:
Ketorolac 0.5 mg/kg IV/IM q6h PRN 641651.
Naproxen 5 mg/kg PO q8h PRN Scrotal support with elevation r Shortliffe LM. Infection and inflammation of the
Morphine 0.1 mg/kg IV/IM/SC q2h PRN: Follow up with urology.
r Failure of symptoms to improve within 3 days pediatric genitourinary tract. In Wein AJ, Kavoussi
Initial morphine dose of 0.1 mg/kg IV/SC may LR, Novick AC, et al., eds. Campbell-Walsh Urology.
be repeated q1520min until pain is controlled, requires re-evaluation and possible hospitalization.
9th ed. Philadelphia, PA: Saunders; 2007.
then q2h PRN. Patient Monitoring
Codeine or codeine/acetaminophen dosed as r Follow up with urology for adjunctive imaging: See Also (Topic, Algorithm, Electronic
0.51 mg/kg of codeine component PO q4h PRN Renal and bladder US and voiding cystourethrogram Media Element)
r Epididymitis in prepubertal boys (urinalysis positive): r Scrotal Pain
(VCUG).
r Neonates and infants diagnosed with epididymitis r Scrotal Swelling
Specific antimicrobial agents are dependent on
regional susceptibilities: r Testicular Torsion
have a higher rate of anatomic abnormalities (6).
Cephalexin 2550 mg/kg/day PO divided r Given the low yield of abnormal findings in older
q6hours 10 days patients with a 1st episode of culture-negative
Sulfamethoxazole/Trimethoprim (based on epididymitis, consider selective use of VCUG CODES
612 mg/kg trimethoprim component) divided evaluation after US (7).
q12h 10 days ICD9
Amoxicillin and clavulanic acid 2040 mg/kg PROGNOSIS r 604.90 Orchitis and epididymitis, unspecified
divided q8h 10 days Complications such as scrotal abscess or orchiectomy r 604.91 Orchitis and epididymitis in diseases
r Epididymitis in adolescents (STI pathogens): are seldom seen with directed therapy and close
classified elsewhere
Ceftriaxone 250 mg IM 1 PLUS follow-up of epididymitis. r 604.99 Other orchitis, epididymitis, and
Doxycycline 100 mg PO b.i.d. 10 days COMPLICATIONS epididymo-orchitis, without mention of abscess
r Epididymitis/epididymo-orchitis (due to systemic r Scrotal abscess
infection): r Chronic epididymitis
Antimicrobial therapy, 3rd-generation r Testicular infarction PEARLS AND PITFALLS
cephalosporins, directed against the suspected or r Infertility
r It may be difficult to differentiate testicular torsion
isolated pathogens (typically H. influenzae type b,
Salmonella species, S. pneumoniae, from epididymitis based on history and physical
Mycobacterium tuberculosis, or Brucella species), REFERENCES exam.
r Color Doppler US and testicular scintigraphy are
typically hematogenous spread from primary
focus: 1. Somekh E, Gorenstein A, Serour F. Acute both highly specific in detecting testicular torsion
Ceftriaxone 50 mg/kg/day IV for hematogenous epididymitis in boys: Evidence of a post-infectious but may miss the diagnosis of early or intermittent
spread etiology. J Urol. 2004;171:391394. torsion if blood flow is still present.
Ceftriaxone is not first-line therapy for 2. Gislason T, Noronha RFX, Gregory JG. Acute r Urology evaluation may be critical.
brucellosis; consider gentamicin 5 mg/kg IV/IM epididymitis in boys: A 5 year retrospective study.
per day 7 days plus doxycycline as dosing J Urol. 1990;14:533534.
above. 3. Kadish H, Bolte R. A retrospective review of
r Orchitis: Management of viral orchitis is supportive. pediatric patients with epididymitis, testicular
r Epididymo-orchitis is treated with antimicrobial torsion, and torsion of testicular appendages.
therapy if the urinalysis is suspicious for a bacterial J Pediatr. 1998;102:7376.
pathogen. Please refer to the antibiotics discussion
above.
311
EPIDURAL HEMATOMA
Kara E. Hennelly
Lois K. Lee
r Children more commonly sustain EDH in the frontal, PHYSICAL EXAM

BASICS parieto-occipital, or posterior fossa regions, in r Assess vital signs, especially noting evidence of the
contrast to adults who more typically sustain EDH Cushing triad: Bradycardia, HTN, and irregular
DESCRIPTION around the temporal bone with middle meningeal respirations, which indicate elevated ICP and
r An epidural hematoma (EDH) is a collection of blood artery shearing. impending herniation.
between the skull and the dura mater (outermost r Children less commonly sustain EDH in the temporal r A complete neurologic exam, including Glasgow
layer of the brain). region because the middle meningeal artery is not Coma Scale (GCS) score, thorough motor exam to
r Prompt identification of EDHs in patients with head yet indented into the temporal bone, as in adult evaluate for possible hemiparesis or hemiplegia, and
injury is critical, as they are life threatening yet are patients. cerebellar function, should be performed.
treatable with surgical intervention. r As bleeding continues, mass effect takes place and r Pupillary exam noting reactivity to light and
r EDH should be considered in any patient with head signs of increased intracranial pressure (ICP) occur as extraocular movements. With a dilated pupil, the
trauma and altered mental status. the expanding hematoma displaces CSF, intracranial hematoma is on the same side about 90% of the
r They are typically associated with a blunt impact to venous blood, and finally brain parenchyma within time (3).
the head, although children may have seemingly the fixed cranial space. If untreated, brain herniation r Palpate the scalp for hematomas and step-offs in
minor mechanisms. 50% of children who sustain may occur and result in death. the skull.
an EDH fall from a height of 5 feet. r Infants and young toddlers may tolerate elevations in r Anterior fontanelle should be assessed for fullness
r EDHs are associated with skull fractures in 4080% ICP better than adults. This is because their sutures or bulging in infants.
of pediatric patients, although less commonly in may remain open up to 18 mo of age, and they have
children >2 yr of age. larger subarachnoid and extracellular spaces. DIAGNOSTIC TESTS & INTERPRETATION
r Anemia from hemorrhage may precede signs of Lab
EPIDEMIOLOGY Lab tests are secondary to imaging tests:
increased ICP in these young children.
Incidence r CBC and type and screen may be considered to
r Epidural hematomas account for 13% of closed ETIOLOGY assess for anemia and as part of the preoperative
head injury admissions in pediatrics. EDHs are typically sustained from trauma, including a evaluation.
r Male to female predominance of 22.5:1 direct blow to the head, falls, and abusive head r Blood glucose may be useful, as hyperglycemia is
r Mortality rates from EDH range from 010%. trauma.
associated with poor prognosis with severe
RISK FACTORS COMMONLY ASSOCIATED CONDITIONS traumatic brain injury (4).
r Significant falls An underlying skull fracture, if present, may be r PT, PTT, and INR should be sent to assess for
r Head trauma while not wearing a helmet when associated with an EDH. coagulopathy and as part of the potential
biking, snowboarding, playing baseball, etc. preoperative evaluation.
r Being in a motor vehicle accident without using the DIAGNOSIS Imaging
appropriate car seat/seat belt. Motor vehicle crashes r A noncontrast head CT scan should be obtained in
are the most common cause of EDH in adolescents. HISTORY patients with suspicion for EDH.
r Newborns delivered by vacuum or forceps extraction r Concerning mechanisms should prompt an
The CT appearance of EDH is classically a
evaluation for EDH: hyperdense egg-shaped biconvexity that does not
GENERAL PREVENTION Fall from significant height (>5 feet) cross suture lines.
r Appropriate adult supervision to prevent falls in
Motor vehicle crash Other important findings include mass effect
infants and toddlers Direct blow to the temporal region causing midline shift, ventricular compression,
r Window guards on windows above the 1st floor Suspicion for abusive head trauma gyral effacement, loss of graywhite matter
r Age-appropriate motor vehicle restraints r The classic history for an EDH is an initial loss of differentiation (indicative of cerebral edema), and
r Wearing helmets when appropriate consciousness (LOC) with the impact followed by a transtentorial herniation.
lucid interval of minutes to hours where the child is r Skull films may be helpful in children <2 yr for
PATHOPHYSIOLOGY relatively asymptomatic. As the hematoma expands,
r An EDH occurs when there is: identifying a fracture, which would prompt a CT
mass effect causes clinical deterioration, including scan to evaluate for possible intracranial
A laceration of the vessels from an underlying
headache, vomiting, and altered mental status. hemorrhage. However, absence of a skull fracture
fracture OR
The classic history is less common in children, does not rule out intracranial hemorrhage.
A shearing force to the epidural arteries or veins
r Younger children typically sustain hemorrhage from occurring in 3070% of patients (2).
r Pediatric patients more commonly experience DIFFERENTIAL DIAGNOSIS
dural venous disruption as opposed to vessel r Concussion
headache, vomiting, and lethargy than the classic r Subdural hematoma
laceration.
r Older children and adolescents more commonly symptoms of EDH.
r Patients with small EDHs may be asymptomatic. r Subarachnoid hemorrhage
have lacerated meningeal arteries as the source of r Seizures occur in <10% of cases. r Diffuse axonal injury
bleeding. r Infants with EDHs may present with lethargy, r Scalp hematoma (in isolation)
r 1836% of patients have an arterial source of r Skull fracture (in isolation)
bleeding identified in the operating room. An irritability, repeated vomiting, or not acting like
additional 1020% are found to have a venous him- or herself after a history of head trauma.
source (meningeal veins, emissary veins, diploic
veins, or dural sinuses). The remaining 3040%
have no source identified and are thought to have
oozing from dural venous sites (1).
312
EPIDURAL HEMATOMA
r The admitting hospital should have emergency 4. Young KD, Okada PJ, Sokolove PE, et al. A
TREATMENT access to head CT scanning, an appropriate randomized, double-blinded, placebo-controlled
operating room if needed, and experienced trial of phenytoin for the prevention of early
PRE HOSPITAL personnel who are able to monitor for neurologic posttraumatic seizures in children with moderate to
r Prehospital care includes airway management based changes in pediatric patients. severe blunt head injury. Ann Emerg Med. 2004;
upon the skill level of the prehospital care providers. r Criteria for transfer to a pediatric trauma center 43(4):435446.
r Cervical spine immobilization must be maintained if after stabilization include: 5. Schutzman SA, Barnes PD, Mantello M, et al.
there is suspicion of C-spine injury. GCS 12 in the field Epidural hematomas in children. Ann Emerg Med.
r If the history is concerning by mechanism or Pediatric trauma score 8 1993;22(3):535541.
symptoms for EDH but the initial neurologic exam is Discharge Criteria
normal, serial neurologic exams must be performed. r Patients should be observed for at least 2448 hr
after the injury or evacuation of EDH to evaluate for
ADDITIONAL READING
r The initial management of any patient with closed signs of hematoma expansion. Greenes D. Neurotrauma. In Fleisher GR, Ludwig S,
r Repeat CT scan is recommended prior to discharge eds. Textbook of Pediatric Emergency Medicine. 6th
head injury should include a basic ABCs approach.
r Oxygen should be administered to keep oxygen to evaluate for a potentially expanding hematoma. ed. Philadelphia, PA: Lippincott Williams & Wilkins;
saturation >95%. Issues for Referral 2010.
r Endotracheal intubation is required to maximize If a pediatric neurosurgeon is not available,
oxygenation and ventilation and protect against endotracheal intubation should be performed to
CODES
possible aspiration in the following situations:
Depressed mental status (GCS <9)
secure the airway in any patient with depressed GCS,
neurologic abnormality, or concerning radiologic
E
Rapidly deteriorating mental status findings (temporal location, >10 mm in size). ICD9
r 852.40 Extradural hemorrhage following injury,
Pupillary abnormalities
Respiratory distress without mention of open intracranial wound, with
Hemodynamic instability FOLLOW-UP state of consciousness unspecified
r In patients who are endotracheally intubated, r 852.50 Extradural hemorrhage following injury, with
FOLLOW-UP RECOMMENDATIONS open intracranial wound, with state of
hyperventilation should be avoided unless there are r Resuming activity is at the discretion of the
signs of impending herniation. PaCO2 should be consciousness unspecified
neurosurgeon and depends on the age of the child
maintained between 35 and 40 mm Hg to prevent and extent of associated bony injury.
cerebral ischemia. r Pediatric patients with severe traumatic brain injury
r Patients with hypotension should receive fluid PEARLS AND PITFALLS
may require ongoing neurorehabilitation.
resuscitation (normal saline boluses of 20 mL/kg) to r Early consultation with a neurosurgeon is necessary,
maintain cerebral perfusion pressure (CPP). Patient Monitoring
Patients typically are reimaged in 46 wk to confirm as patients may rapidly deteriorate as the EDH
MEDICATION there is no recurrent hemorrhage. expands.
r Infants with open sutures may initially have a better
First Line
PROGNOSIS tolerance for an expanding EDH. Anemia from blood
Mannitol (0.51 g/kg over 20 min) should be given for r Better neurologic outcomes are obtained in patients
patients with impending herniation. loss into the EDH may present before signs of
who undergo rapid diagnosis by CT scan and increased ICP.
Second Line surgical intervention, if indicated. r Children more commonly sustain EDH in the frontal,
Loading with antiepileptic medication (eg, r The most important factor in determining outcome
parieto-occipital, or posterior fossa regions, in
fosphenytoin) is controversial. The rate of early in patients with EDH is their neurologic status prior contrast to adults who more typically sustain EDH
posttraumatic seizures in patients with moderate to to surgery. around the temporal bone with middle meningeal
severe head injury is low (57%), and fosphenytoin r Neurologic sequelae such as seizures, hemiplegia, or
artery shearing.
minimally affects this rate (5). The risks and benefits of cranial nerve abnormalities are more likely with r Posterior fossa EDH occurs after a fall onto the
antiepileptic drugs must be carefully considered. acute deterioration, neurologic abnormalities, or occiput and is usually associated with a skull
COMPLEMENTARY & ALTERNATIVE altered LOC. fracture. Children may present with LOC, headache,
THERAPIES r 85% of patients with EDH have a good neurologic
and vomiting as well as dizziness, stiff neck, or
Elevate the head of the bed 1530 degrees. This mild outcome. cerebellar signs. They may have a subacute
elevation may lower ICP without adversely affecting COMPLICATIONS presentation but can deteriorate quickly due to
CPP. Delayed diagnosis can result in permanent neurologic brainstem compression.
SURGERY/OTHER PROCEDURES sequelae such as seizures, hemiplegia, cranial nerve
r Surgical craniotomy with hematoma evacuation and abnormalities, or death.
vessel repair is the standard treatment.
r Emergent craniotomy is indicated for EDH with:
REFERENCES
Deterioration of mental status, evidence of
elevated ICP, pupillary changes, hemiparesis, other 1. Choux M, Grisoli F, Peragut JC. Extradural
focal neurologic findings, or cerebellar signs hematomas in children. 104 cases. Childs Brain.
Radiologic findings on CT: Temporal location, 1975;1(6):337347.
large size (thickness >10 mm), and midline shift 2. Pillay R, Peter JC. Extradural haematomas in
r Nonoperative management with close observation is children. S Afr Med J. 1995;85(7):672674.
an option with neurosurgical agreement in patients 3. Chiaretti A, Piastra M, Pulitano S, et al. Prognostic
with normal neurologic exams and CT findings of factors and outcome of children with severe head
small EDH (usually <30 mL and <10 mm thickness). injury: An 8-year experience. Childs Nerv Syst.
DISPOSITION 2002;18(34):129136.
Admission Criteria
r All patients with a diagnosis of EDH should be
admitted to the hospital for close observation for at
least 2448 hr, especially postoperatively. Patients
with a known epidural hematoma should be
admitted to an ICU for close neurologic exam
monitoring.
313
EPIGLOTTITIS/SUPRAGLOTTITIS
Rachel Gallagher
Joshua Nagler
ETIOLOGY r Vital signs:

BASICS r In unvaccinated patients or patients with failed Hib Fever, often reaching 3940 C (102.2104 F)
vaccination, Hib continues to be the primary cause Tachypnea and tachycardia are common.
DESCRIPTION of supraglottitis. 1/3 of Hib supraglottitis is due to Hypoxemia may be present in severe cases.
r Epiglottitis is an acute inflammation of the epiglottis confirmed vaccine failure (4). r Oropharynx:
that can rapidly progress to severe, life-threatening r Other bacterial causes include group A beta- To avoid agitation, defer exam of the mouth and
airway compromise. hemolytic streptococcus, Streptococcus pneumoniae, throat in young children.
r Inflammation may not be limited to the epiglottis Staphylococcus aureus, Klebsiella pneumoniae, The posterior oropharynx is minimally inflamed
but can also include the arytenoid cartilages, Pseudomonas aeruginosa, Haemophilus despite severe dysphagia.
aryepiglottic folds, false cords, posterior tongue, and parainfluenzae, and nontypeable H. influenzae. Drooling may be noted.
the uvula and therefore is more accurately termed r Fungal causes: Candida is rare, but infection can r Respiratory exam:
supraglottitis. occur in immunocompromised hosts. Distress is common.
r The vast majority of cases of supraglottitis are r Viral: Herpes simplex virus type 1, varicella, and Stridor increases with progressive disease.
secondary to acute infection. parainfluenza have all been isolated from confirmed Stridor will be absent in complete airway
r Noninfectious etiologies of supraglottitis also exist, cases. obstruction.
including direct trauma and thermal injury. r Trauma: Post-laryngoscopy or secondary to foreign Lower lung fields are typically clear.
r Goals of therapy include maintenance of a patent bodies DIAGNOSTIC TESTS & INTERPRETATION
airway, commonly with controlled intubation, and r Inhalation injury from smoke, steam, or chemical r Supraglottitis is diagnosed clinically, often with
antimicrobial therapy. fumes confirmation of etiology by culture.
r Mucosal injury from ingestion of hot foods/liquids or r Delay phlebotomy until the airway has been secured
EPIDEMIOLOGY
Incidence contact with caustic substances or the patients respiratory status is stable.
r Dramatic decline since widespread Haemophilus
COMMONLY ASSOCIATED CONDITIONS Lab
influenzae type b (Hib) vaccination began in the late r Patients with varicella or other herpesviruses are at CBC, C-reactive protein (CRP), blood culture, and
1980s increased risk of group A beta-hemolytic supraglottic culture for bacterial etiology and
r The incidence of supraglottitis in children is streptococcus infection. sensitivities should be obtained after the airway is
0.31.8 cases/10,000 admissions (1). r Invasive H. influenzae results from hematogenous secure.
r Peak incidence is 25 yrs of age. spread and therefore can be associated with r CBC may have elevated WBCs with left shift, though
r Recent increase in mean age of presentation, with meningitis and pneumonia. findings are nonspecific.
higher incidence in older children and adolescents r CRP may be elevated, though findings are
(2) nonspecific.
DIAGNOSIS
RISK FACTORS Imaging
r Unimmunized patients or patients with vaccine HISTORY r X-rays:
failure are at increased risk of supraglottitis caused r A typical history includes the acute onset of fever,
Lateral neck radiographs are not routinely used for
by Hib. Vaccine failure occurs more commonly in sore throat, and respiratory distress. diagnosis (5). When obtained:
premature children and those with developmental r Symptoms are typically present for <24 hr: Epiglottis appears thick and round, known as
delay, Down syndrome, neutropenia, and 75% of patients present within 12 hr of onset thumb sign.
immunologic dysfunction (3). of symptoms. Aryepiglottic folds are thickened.
r Immunocompromised patients are at higher risk of r Additional symptoms include: Vallecular space is obliterated.
less common pathogens including Candida and Drooling Chest radiographs should be obtained only to
herpes-family viruses. Difficulty swallowing assess for alternative etiologies of symptoms.
Difficulty speaking, or muffled voice r CT scan:
GENERAL PREVENTION
Distress/Anxiety Rarely required
Routine vaccination r Postvaccination era supraglottitis may present May identify other airway abnormalities including
PATHOPHYSIOLOGY differently: epiglottic or retropharyngeal abscess or foreign
r Hib infection most commonly occurs from body
Patients are often adolescents or adults.
bacteremic spread and seeding at the epiglottis. Predominant symptom is frequently severe
r Most other pathogens cause local infection after Diagnostic Procedures/Other
pharyngitis rather than respiratory distress. r Laryngoscopy:
penetration of the mucosal surface of supraglottic Onset is frequently more insidious. Direct laryngoscopy is the gold standard for
structures. evaluation of the supraglottis.
r Loosely attached submucosal tissue is easily PHYSICAL EXAM
r Exam should be limited to avoid agitating a child, Airway evaluation is most safely performed in the
distensible and allows rapid swelling. which may worsen airway obstruction. operating room, when possible.
r Inflammation and swelling of the epiglottis and r General appearance: r Fiberoptic nasopharyngoscopy is an alternative
surrounding structures lead to obstruction of the Often toxic appearing, anxious, or irritable means for visualization of the supraglottic structures
upper airway. Respiratory distress is common in a stable patient without significant respiratory
r Early disease may present with partial airway
Tripod positioning: Sitting upright and leaning distress.
obstruction. forward with the neck extended
r Progression can lead to complete airway obstruction Pathological Findings
Inflamed, erythematous, edematous epiglottis,
causing respiratory arrest. arytenoids, and aryepiglottic folds with pooled airway
secretions on direct laryngoscopy
314
EPIGLOTTITIS/SUPRAGLOTTITIS
DIFFERENTIAL DIAGNOSIS SURGERY/OTHER PROCEDURES 4. McEwan J, Giridharan W, Clarke RW, et al.

r Croup (laryngotracheitis) r Nasopharyngoscopy is used diagnostically in stable Paediatric acute epiglottitis: Not a disappearing
r Foreign body aspiration patients at low risk. entity. Int J Pediatr Otorhinolaryngol. 2003;67(4):
r Bacterial tracheitis r Direct laryngoscopy in a controlled setting is the 317321.
r Peritonsillar abscess gold standard for diagnosis and is most commonly 5. Stankiewicz JA, Bowes AK. Croup and epiglottitis:
r Retropharyngeal abscess followed by endotracheal intubation to maintain the A radiologic study. Laryngoscope. 1985;95(10):
r Ludwig angina airway. 11591160.
r Emergent cricothyrotomy or tracheostomy may be
r Pertussis 6. Galvis AG. Pulmonary edema complicating relief of
r Pharyngitis required if: upper airway obstruction. Am J Emerg Med. 1987;
r Anaphylaxis/Angioedema A patient cannot be successfully intubated OR 5(4):294297.
A patient presents with complete airway
obstruction
r Although rare in children, drainage of epiglottic ADDITIONAL READING
TREATMENT
abscesses may be required. r Harper MB, Fleisher GF. Infectious diseases
PRE HOSPITAL DISPOSITION emergencies. In Fleisher GR, Ludwig S, eds.
If concern for supraglottitis: Critical care admission criteria: Textbook of Pediatric Emergency Medicine. 6th ed.
r Minimize evaluation of the airway. r All patients should be admitted to the ICU for Philadelphia, PA: Lippincott Williams & Wilkins;
r Communicate with medical control regarding the 2010.
continued airway management.
r Shah S, Sharieff GQ. Pediatric respiratory infections.
pending airway emergency and need to mobilize
operating room resources.
Issues for Referral Emerg Med Clin North Am. 2007;25:961979.
E
r Ideally, pediatric intensivists, otolaryngologists, and
r Avoid attempts at prehospital intubation if possible.
anesthesiologists co-manage patients with See Also (Topic, Algorithm, Electronic
r Provide nonpharmacologic anxiolysis.
supraglottitis. Media Element)
r Interhospital transfer is best performed by a critical r Croup
r Initial stabilization focuses on maintaining a patent care transport team when available. r Upper Airway Obstruction
airway.
r Patients with stridor or progressive respiratory
distress are at high risk for complete airway
FOLLOW-UP CODES
obstruction and require rapid airway management: FOLLOW-UP RECOMMENDATIONS
Endotracheal intubation should be performed in Patient Monitoring ICD9
the operating room whenever possible. r 464.30 Acute epiglottitis without mention of
Continuous cardiorespiratory monitoring until the
Inhaled anesthetic induction allows the patient to patients status has improved obstruction
maintain airway tone and spontaneous respiratory r 464.31 Acute epiglottitis with obstruction
effort until adequately sedated. DIET r 464.50 Supraglottitis, without mention of
An endotracheal tube 1 size smaller than indicated NPO during acute illness obstruction
by the patients age/size is recommended. PROGNOSIS
Skilled anesthesiologists and surgical staff should In the absence of hypoxic events or associated illness,
be present. patients generally recover completely within 12 wks. PEARLS AND PITFALLS
r Patients with insidious onset of symptoms
concerning for supraglottitis and with minimal COMPLICATIONS r Consider supraglottis in any child with fever and
r Inability to safely manage the airway can lead to
respiratory distress are at lower risk for complete stridor.
airway obstruction: hypoxemia or respiratory arrest and may require r Avoid any agitation in the patient with possible
If a patient is low risk and cooperative, initiate emergent cricothyrotomy or tracheostomy. impending airway obstruction.
supplemental oxygen. r Hematogenous spread, particularly with Hib, can r Mobilize resources to expedite controlled intubation
Obtain portable airway films, or have skilled result in meningitis or sepsis. in the operating room as early as possible.
airway providers accompany the patient to the r Postobstructive pulmonary edema occurs in <10% r Initiate broad-spectrum antibiotics as soon as access
radiology suite. of cases (6). is obtained.
Consider nasopharyngoscopy. r Abscess formation on the lingual surface of the r Older patients tend to have a more insidious
Administer broad-spectrum antibiotics. epiglottis is a rare complication, seen primarily in presentation and are less likely to require
MEDICATION older patients. endotracheal intubation.
First Line r Stable patients at low risk for supraglottitis can
Broad-spectrum antibiotics including: REFERENCES undergo evaluation with radiography and possibly
r Ceftriaxone 50 mg/kg IV q24h OR direct or indirect visualization of glottic structures.
r Ampicillin/sulbactam 50 mg/kg IV q6h 1. Heath PT, Booy R, Azzopardi HJ, et al. Antibody r Patients with high suspicion for disease are best
concentration and clinical protection after Hib managed with controlled intubation in the operating
Second Line conjugate vaccination in the United Kingdom. room.
r For possible MRSA: Vancomycin IV 4060 mg/kg/
JAMA. 2000;284(18):23342340.
day divided q68h 2. Tanner K, Fitzsimmons G, Carrol ED, et al.
r For suspected Candida: Fluconazole IV 6 mg/kg/day
Haemophilus influenzae type b epiglottitis as a
r Duration of antibiotic therapy is 710 days.
cause of acute upper airway obstruction in children.
r Steroids are not routinely indicated in the BMJ. 2002;325(7372):10991100.
management of supraglottitis. 3. Shah RK, Roberson DW, Jones DT. Epiglottitis in the
Haemophilus influenzae type B vaccine era:
Changing trends. Laryngoscope. 2004;114(3):
557560.
315
EPISTAXIS
Audrey Le
Sandip Godambe
ETIOLOGY r Visualization may be enhanced with application of a

BASICS r In children, the most common cause of epistaxis is topical vasoconstrictive medication such as
local trauma from nose picking or local mucosal phenylephrine. This may be applied by nasal spray or
DESCRIPTION irritation with upper respiratory tract infections, gauze/cotton soaked in the solution.
Epistaxis is bleeding originating from the naris or both rhinitis, or sinusitis. r If no anterior source is identified, nasal endoscopy
nares. r Direct facial trauma or a foreign body in the naris may be necessary to identify the source of active
EPIDEMIOLOGY can also cause bleeding. bleeding and will likely require consultation with an
r Improper application of intranasal corticosteroids otorhinolaryngologist.
Incidence
r In a seminal early study, epistaxis occurred in 30% can lead to nosebleeds. DIAGNOSTIC TESTS & INTERPRETATION
r Sniffing cocaine, heroin, or glue can cause epistaxis.
of children <5 yr of age and 56% of children Lab
r Nasal neoplasms are rare but are suggested by
610 yr of age (1). Initial Lab Tests
r The estimated annual incidence in those <2 yr of recurrent persistent unilateral bleeding and nasal r Lab studies are usually not indicated in easily
age is 19 per 100,000 (2). obstruction. controlled, simple anterior nosebleeds.
r Incidence is higher during winter months secondary r The history and physical exam may direct the
to low humidity. r Systemic diseases including liver diseases affecting clinician to evaluate hematologic, coagulation,
RISK FACTORS the synthesis of factors in the coagulation pathway, hepatic, or renal function problems:
r Nosebleeds occur in children of all ages, but those renal failure, hematologic malignancies, or CBC, PT, and PTT should be obtained on patients
between the ages of 2 and 10 yr have more idiopathic thrombocytopenia can be associated with with significant bleeding.
frequent occurrences. epistaxis. Patients on anticoagulation medications may
r Concurrent upper respiratory infections predispose r Congenital coagulopathies, such as hemophilia and require a coagulation panel.
to more friable nasal mucosa. von Willebrand disease, or acquired coagulopathies Imaging
r Allergic rhinitis from heparin, enoxaprin, or warfarin can increase CT scanning may be indicated for patients with
the risk of nosebleeds. significant facial trauma or when there is suspicion of
GENERAL PREVENTION r Aspirin and NSAIDs alter platelet function. a tumor in those with recurrent or recalcitrant
r Limiting local trauma by avoiding nose picking and r Garlic, ginkgo, and ginseng are alternative nosebleeds.
vigorous nose blowing medications that inhibit platelet function.
r Hydrating the local nasal mucosa can reduce r Osler-Weber-Rendu disease, or hereditary Diagnostic Procedures/Other
Patients with recurrent nasal bleeding, particularly
mucosal irritation and prevent nosebleeds: hemorrhagic telangiectasia, is characterized by unilateral, may need to be assessed for an occult nasal
Saline sprays or drops fragile telangiectasias and arteriovenous foreign body or tumor by nasal endoscopy.
Ointments such as petroleum jelly malformations that can lead to significant bleeding.
Augmenting the humidity of the environment with r HTN, though not independently associated with DIFFERENTIAL DIAGNOSIS
a cool mist vaporizer or humidifier nosebleeds, can make them more difficult to control. See Etiology and Commonly Associated Conditions
r Patients who use intranasal medications can be sections.
instructed to point the spray laterally.
PATHOPHYSIOLOGY
DIAGNOSIS TREATMENT
r The internal and external carotid arteries supply
HISTORY
blood to the nasal cavity and end in multiple r Origin of the nosebleed (bilateral or unilateral) INITIAL STABILIZATION/THERAPY
anastamoses, the most important of which is the r Duration and severity of the bleed r Keep the head elevated but not hyperextended, as
Kiesselbach plexus: r Associated nasal obstruction the latter will cause the flow of blood backward into
The Kiesselbach plexus (Little area) is a venous r History of nasal or facial trauma the pharynx:
vascular formation that is firmly adherent to the r History of possible foreign body This may trigger a gag response and vomiting or
anterior nasal septal cartilage. The mucosa can result in aspiration of blood.
r Pre-existing medical conditions, medications, or r Most minor epistaxis will cease with 520 min of
overlying this plexus is thin, fragile, and prone to
injury. Anterior bleeds resulting from insult to this drugs of abuse direct continuous pressure.
r Personal or family history of easy bruising or r An ice pack placed over the dorsum of the nose can
area account for 90% of epistaxis.
The Kiesselbach plexus is supplied by the bleeding may suggest an underlying coagulopathy. induce vasoconstriction and aid hemostasis.
anastomoses of 4 arteries: Anterior ethmoid PHYSICAL EXAM r A gauze roll placed between upper lip and gums
artery, great palatine artery, sphenopalatine r The nasal cavity should be viewed using a good light may help compress superior labial artery.
artery, and superior labial artery. source and a nasal speculum for optimal
r Bleeding originating from the posterior aspect of the
visualization of any source of bleeding. Clots
nasal cavity from insult to the sphenopalatine artery, preventing adequate visualization should be cleared
though less common, tends to bleed more profusely. gently.
316
EPISTAXIS
MEDICATION DISPOSITION 6. Ruddy J, Proops DW, Pearman K, et al.

First Line Admission Criteria Management of epistaxis in children. Int J Pediatr
r Inserting a piece of gauze soaked with a nasal r Most patients with uncomplicated anterior Otorhinolaryngol. 1991;21(2):139142.
decongestant spray, oxymetazoline, or 1:10,000 nosebleeds responsive to simple first-line measures 7. Badran K, Malik TH, Belloso A, et al. Randomized
epinephrine or phenylephrine into the naris over the may safely be discharged home. controlled trial comparing Merocel and
anterior nasal septum for 510 min can induce local r Admission is advisable for: RapidRhino packing in the management of
vasoconstriction and stop bleeding (3,4). Any bleed significant enough to lower the anterior epistaxis. Clin Otolaryngol. 2005;30(4):
r Daily application of antiseptic cream hemoglobin level 333337.
(chlorhexidine/neomycin) to the nostrils can prevent Any bleed leading to aspiration. This is seen more 8. Singer AJ, Blanda M, Cronin K, et al. Comparison
recurrence (5,6). commonly with posterior nosebleeds. of nasal tampons for the treatment of epistaxis in
Patients with posterior packing since they can the emergency department: A randomized
Second Line
r Other medications such as aminocaproic acid, factor have apnea and hypoxia controlled trial. Ann Emerg Med. 2005;45(2):
r Critical care admission criteria: 134139.
supplement, or vitamin K to reverse anticoagulation
should be guided by the history. The risks for Any bleed significant enough to cause 9. Derkey CS, Hirsch BE, Johnson JT, et al. Posterior
thrombosis must be weighed against the risk of hemodynamic instability nasal packing: Are intravenous antibiotics really
excessive bleeding: Any bleed leading to airway compromise necessary? Arch Otolaryngol Head Neck Surg.
Aminocaproic acid 100200 mg/kg IV/PO, max 1989;115:439441.
30 g/day 10. Herzon FS. Bacteremia and local infections with
FOLLOW-UP nasal packing. Arch Otolaryngol. 1971;94:317.
Factor VIII: 50 units/kg raises factor to 100%
Factor IX: 50 units/kg raises factor to 50% FOLLOW-UP RECOMMENDATIONS 11. Feusi B, Holzmann D, Steurer J. Posterior epistaxis: E
Vitamin K 0.55 mg PO/SC/IM r All patients should be given instructions on simple Systematic review on the effectiveness of surgical
r Empiric antibiotic therapy should be considered first-line measures for control of nosebleeds as well therapies. Rhinology. 2005;43(4):300304.
when nasal packing is required. If prescribed, as general preventative measures:
antibiotics should be taken until the packing is Use a humidifier in the room to increase ambient
removed (see below): humidity.
ADDITIONAL READING
Cephalexin 2550 mg/kg/day divided q.i.d. Keep the nasal mucosa hydrated with saline r Bernius M, Perlin D. Pediatric ear, nose, and throat
Amoxicillin/Clavulanic acid: 2545 mg/kg/day washes or gels applied 3 or 4 times daily. emergencies. Pediatr Clin North Am. 2006;53:
divided b.i.d. If a nosebleed occurs at home, apply continuous 195214.
Clindamycin 1030 mg/kg/day divided t.i.d. pressure by firmly squeezing the soft part of the r Leong SCL, Karkanevatos A. No frills management
Trimethoprim/Sulfamethoxazole 510 mg/kg/day nose for 1015 min while leaning forward. of epistaxis. Emerg Med J. 2005;22:470472.
divided b.i.d. r Patients with nasal packing should follow up within
SURGERY/OTHER PROCEDURES 12 days. They may require antibiotics with
r If active anterior bleeding is identified, cautery using coverage for staphylococcal and streptococcal CODES
silver nitrate sticks or thermal cautery after organisms while the packing remains in place.
r Based upon the history and severity of the
application of local anesthesia can be effective ICD9
treatments. This should be limited to 1 side of the nosebleeds, patients may require follow-up with an
784.7 Epistaxis
nasal septum to avoid perforation. otorhinolaryngologist for further evaluation.
r Nasal packing with either a commercial product that
COMPLICATIONS
expands when wet or with petroleum gauze strips r Nasal packing may be complicated by sinusitis, PEARLS AND PITFALLS
may be required in nosebleeds impervious to other ulcerations, or perforation of the nasal septum. r Pearls:
treatments (7,8): r Dislodgement of nasal packing into the oropharynx
Packing can be removed after 1530 min for The ABCs remain the 1st priority.
may result in aspiration. Getting a thorough history is essential in
re-evaluation or left in place to be removed at r Infection from nasal packing
follow-up visit. identifying any associated or predisposing
r Septal perforation from cauterization
Although uncommon, patients with bleeding after conditions.
r Pitfalls:
packing removal may require specialist
consultation for repacking left in place for up to Not looking carefully for a potential source of
REFERENCES unilateral bleeding may result in failure to
3 days.
r Prophylactic antibiotics may be considered in 1. Petruson B. Epistaxis in childhood. Rhinology. diagnose a nasal foreign body or tumor.
children with nasal packing to reduce the risk of 1979;17:83. Failure to hold pressure on anterior nares long
toxic shock syndrome and sinusitis (4,9,10). See 2. Paranjothy S, Fone D, Mann N, et al. The enough is a common cause of treatment failure.
Medication section. incidence and aetiology of epistaxis in infants: A
r In rarer cases when cessation of bleeding is not population based study. Arch Dis Child. 2009;
achieved with cautery or packing, the 94(6):421424.
otorhinolaryngologist may need to surgically ligate 3. Douglas R, Wormald PJ. Update on epistaxis. Curr
the bleeding vessels (11). Opin Otolaryngol Head Neck Surg. 2007;
r Posterior nosebleeds are more refractory to simple 15:180183.
measures and usually require the attention of an 4. Gifford TO, Orlandi RR. Epistaxis. Otolaryngol Clin
otorhinolaryngologist for posterior nasal packing, North Am. 2008;41:525536.
endoscopic cauterization, or surgical ligation of the 5. Murthy P, Nilssen EL, Rao S, et al. A randomised
vessel. clinical trial of antiseptic nasal carrier cream and
silver nitrate cautery in the treatment of recurrent
anterior epistaxis. Clin Otolaryngol Allied Sci.
1999;24(3):228231.
317
ERYTHEMA INFECTIOSUM
Craig A. McElderry
COMMONLY ASSOCIATED CONDITIONS DIAGNOSTIC TESTS & INTERPRETATION

BASICS Several other conditions may be caused by parvovirus r Diagnosis of erythema infectiosum is usually made
B19: on the basis of the characteristic features.
DESCRIPTION r Hydrops fetalis r The slapped cheek appearance and lacy, reticulate
r Erythema infectiosum (5th disease) is a common r Transient aplastic crisis rash are almost pathognomonic for erythema
childhood exanthem caused by parvovirus B19. r Polyarthropathy syndrome infectiosum.
r Infection with parvovirus is ubiquitous and occurs
r Chronic red cell aplasia Lab
worldwide. r Papular, purpuric eruptions on the hand and feet r Usually, no lab tests are necessary.
r Infection appears to occur mostly in late winter or
(gloves and socks syndrome) r CBC if concern for aplastic crisis
early spring (1). r In select cases of aplastic crisis or possible
It is relatively common and mildly contagious.
It occurs sporadically or in epidemics. pregnancy exposure, confirmation can be made
DIAGNOSIS through various advanced lab methods:
EPIDEMIOLOGY Anti-B19 IgM antibody capture radioimmunoassay
HISTORY
Incidence r The prodrome, which occurs after a 318-day is considered the best method for confirming
70% of cases occur in children between 5 and 15 yr incubation period, consists of mild symptoms such parvovirus B19 infection, but it is not readily
of age. as fever, malaise, coryza, headache, and nausea. available.
r The prodrome may be absent. Highly sensitive (up to 97%) ELISA is commercially
Prevalence
r Infected persons experience 3 overlapping stages of available, but false positives have been reported
Prevalence of immunity to parvovirus rises with age
due to other viruses or rheumatoid factor.
and is more than 60% in adults (1). rash: Dot-blot hybridization and polymerase chain
RISK FACTORS 1st stage: Slapped-cheek facial rash: reaction testing are also used.
r Exposure to infected individuals Occurs 37 days after the prodrome
r The transmission rate is 50% for those living with Bright erythematous facial exanthem (See Pathological Findings
Physical Exam.) Giant pronormoblasts on a peripheral blood smear or
infected persons and 2030% for susceptible in a bone marrow aspirate are suggestive of
Exacerbated by sunlight
teachers and day care workers who are exposed to parvovirus B19 infection but are not diagnostic.
More common in children
infected children (2).
Fades in 24 days DIFFERENTIAL DIAGNOSIS
GENERAL PREVENTION 2nd stage: Lacy or reticular body rash: r Scarlet fever
r Good hand washing Occurs 14 days after the facial exanthem r Rubella
r Avoidance of known infected individuals Erythematous rash on the trunk, buttocks, r Exanthems caused by enteroviruses
r A vaccine is in development. and/or extremities r Drug eruptions
May be the only manifestation of disease
PATHOPHYSIOLOGY r Sunburn
r Respiratory spread is the most common route of Fades in 12 wk
r Collagen vascular diseases
3rd stage: Evanescence/recrudescence rash:
transmission. Lasts 13 wk r Allergic reactions
r Transplacental, nosocomial, and blood product r Consider measles, rubeola, roseola infantum, and
Exanthem fades and reappears in previously
transmission can also occur. affected sites. erysipelas
r The virus selectively infects human erythroid Varies in relation to factors such as heat,
progenitor cells, with the globoside or P blood group
emotional upset, and sunlight exposure r Pregnancy does not alter parvovirus B19 infection in
antigen as the cellular receptor for the virus. Fades without scarring
r The disease is contagious during the week before r Adolescents in particular may develop arthralgia or the mother. However:
the rash appears. The fetal liver and heart may become infected.
arthritis
r Persons with parvovirus B19 infection are no longer r Patients with sickle cell disease are at risk for Infants may develop anemia from the already
contagious when the rash appears because the shortened RBC life span.
aplastic crisis.
viremia has cleared by this point. Infants may develop myocarditis from direct
r Most symptoms occur secondary to immune PHYSICAL EXAM infection of the heart.
r 1st-stage slapped-cheek facial rash: Anemia and myocarditis can cause CHF and
complex formation (2).
Red papules on cheeks rapidly coalesce in hours to hydrops fetalis.
ETIOLOGY form red, slightly edematous, warm, erysipelaslike r The estimated risk of transplacental infection is
r Parvovirus B19 is a nonenveloped, single-stranded plaques symmetrically on both cheeks. 30%.
DNA virus. Spares perioral areas and nasal bridge r Many fetuses are born without symptoms, but there
r Parvovirus B19 is the only member of the r 2nd-stage rash:
is a 26% risk of fetal loss (2).
Parvoviridae family that causes disease in humans. Erythematous maculopapular rash on trunk, r 2nd-trimester pregnancies are the most vulnerable
extending to buttocks and extremities
Central clearing of rash results in characteristic because of increased hematopoiesis in the liver.
reticular pattern r Although the placenta has an abundance of P
Proximal extremity emphasis and dorsal ventral antigen receptors for the virus, 1st-trimester
spread pregnancies have the lowest risk because of the
r 3rd-stage rash: Rash is the same as in 2nd stage but fetal inability to produce IgM and the difficulty of
comes and goes as described in the History section. antibody transfer across the placenta.
318
ERYTHEMA INFECTIOSUM
r If a pregnant woman is exposed to parvovirus B19, REFERENCES

acute infection should be confirmed. (See Lab FOLLOW-UP
section.) 1. Vafaie J, Schwartz RA. Erythema infectiosum.
r If acute infection is confirmed, serial US (weekly or FOLLOW-UP RECOMMENDATIONS J Cutan Med Surg. 2005;9(4):159161.
Discharge instructions and medications: 2. Servey JT, Reamy BV, Hodge J. Clinical
biweekly) should be performed for 1012 wk after r As noted above presentations of parvovirus B19 infection. Am Fam
initial infection to prevent hydrops fetalis.
r The risk virtually disappears after 12 wk. Physician. 2007;75(3):373376.
COMPLICATIONS
r If hydrops occurs, fetal blood sampling and possible r Hydrops fetalis
transfusion are necessary. r Transient aplastic crisis: More common in patients
r Routine testing for parvovirus is not indicated in with a shortened RBC life span, such as patients
CODES
pregnant women. with the following conditions:
Sickle cell anemia ICD9
Hereditary spherocytosis 057.0 Erythema infectiosum (fifth disease)
TREATMENT Thalassemia
G6PD deficiency PEARLS AND PITFALLS
Generally, erythema infectiosum is benign and Pyruvate kinase deficiency
Autoimmune hemolytic anemia r Erythema infectiosum is a self-limited childhood
self-limited. Treatment is symptomatic. For patients r Polyarthropathy syndrome
with fever, arthralgias, or pruritis (rare), relief can be exanthem that resolves without complications in the
r Chronic red cell aplasia
obtained using oral antipyretics, analgesics, or
antihistamines. r Other potential illnesses that occasionally may be
classic cutaneous form.
r Since children with erythema infectiosum are E
linked to or triggered by parvovirus B19 include the contagious only during the asymptomatic viremic
MEDICATION period (occurring 1 wk before rash appears),
r Acetaminophen 1015 mg/kg/dose PO q46h as following:
Viral-associated hemocytophagia restricting them from attending school is not
needed necessary by the time the clinical diagnosis is made.
r Ibuprofen 510 mg/kg/dose PO q68h as needed Rheumatoid arthritis
Systemic sclerosis r Parvovirus B19 infection in a pregnant patient may
r Diphenhydramine 0.51 mg/kg/dose PO q6h
Systemic lupus erythematosus have devastating effects on the fetus. Recognition of
r Treatment with IV immunoglobulin has been used in
Autoimmunelike pulmonary disease exposure or infection in a pregnant patient or
immunocompromised patients. Idiopathic thrombocytopenic purpura contact is critical.
DISPOSITION Diamond-Blackfanlike anemia
Acute vasculitic syndromes
Admission Criteria
r Aplastic crisis Myocarditis
r Toxic appearance Hepatitis
r Severe arthritis Uveitis
Seizures, encephalitis, and other neurologic
Discharge Criteria manifestations
r Nearly all patients with erythema infectiosum can be Glomerulonephritis/Nephrotic syndrome
discharged to home.
r Most health departments do not recommend
exclusion from school for children with erythema
infectiosum once classic cutaneous features have
manifested, because carriers are no longer
infectious.
Issues for Referral
See Complications.
319
ERYTHEMA MULTIFORME
Cynthia Lodding
Garth Meckler
r EM also has a well-established association with PHYSICAL EXAM

BASICS HSV-1. HSV was detected in 2/3 of patients with EM Skin:
who underwent skin biopsy in 1 study (3). The r Rash usually is symmetric, spreads centripetally, and
DESCRIPTION pathophysiology of HSV-associated EM is thought to has a predilection for extensor surfaces. May
r Erythema multiforme (EM) is a rash with abrupt be mediated by CD34 cells (Langerhans cell coalesce and become generalized but involves
onset thought to result from an immune-mediated precursors). <10% BSA (1).
hypersensitivity reaction. r Though less common than infectious causes, r Typical target lesions are <3 cm in diameter,
r Though once considered on the spectrum of more reaction to drugs and chemicals can lead to EM regular, round with well-defined borders, and at
severe conditions such as Stevens-Johnson through immunologic mechanisms related to CD8+ least 3 zones: 2 concentric rings (1 with palpable
syndrome (SJS) and toxic epidermal necrolysis (TEN), T cells. edema), around a central disc (1).
it is currently classified as a self-limited r Atypical targets are round, edematous, palpable
nonlife-threatening hypersensitivity reaction (1,2). ETIOLOGY
r HSV types 1 and 2 are the most commonly lesions with poorly defined borders and only 2 zones.
r EM is characterized by a classic, generalized r Often begins on extremities and may spread to the
associated conditions now known to cause EM.
erythematous maculopapular rash with dusky r Other infectious etiologies include: trunk, face, and neck over 72 hours
central clearing called target lesions (1) (See r Oral involvement usually limited to lips and anterior
Physical Exam below.) Viral agents (Epstein-Barr, cytomegalovirus,
r EM is often divided into minor (EMm) and major varicella zoster, adenovirus, enterovirus, hepatitis, mucosa and is rare in EM. Bullous oral lesions often
parvovirus) break shortly after formation with resultant swelling
(EMM) forms: and crusting of lips and painful erosions of buccal
Bacterial agents (Mycoplasma pneumoniae,
EMm: Typical lesions distributed acrally involving mucosa and tongue (2).
Streptococcus pneumoniae, Borrelia burgdorferi,
<10% body surface area (BSA), with a r Ocular involvement with symmetric purulent
Salmonella species, Yersinia species,
predilection for extensor surfaces
Mycobacterium tuberculosis) conjunctivitis may be seen in EMM.
EMM: Typical cutaneous lesions with involvement
Fungal agents (Histoplasma capsulatum,
of 2 mucosal sites (usually oral mucosa, with DIAGNOSTIC TESTS & INTERPRETATION
Coccidioides immitis)
ocular and genital lesions less common) involving Lab
Parasites (Trichomonas species, Toxoplasma
<10% total BSA Initial Lab Tests
species) r None necessary
EPIDEMIOLOGY r Drugs (antibiotics, anticonvulsants, NSAIDs,
r If obtained:
Incidence antifungals)
r EM occurs at any age but is most frequently seen in CBC may demonstrate leukocytosis with atypical
COMMONLY ASSOCIATED CONDITIONS lymphocytosis or eosinophilia.
young adults, with 20% of cases occurring in HSV-1 and HSV-2
children. ESR may be elevated but is nonspecific.
r Estimated incidence is 0.011% annually. Diagnostic Procedures/Other
DIAGNOSIS Skin biopsy is indicated only for ambiguous cases:
RISK FACTORS r Skin biopsy with polymerase chain reaction testing
r Herpes simplex virus (HSV): HSV-1 and HSV-2 HISTORY
infection are associated with EMm and EMM and r Patients typically present with an acute onset of a for HSV may reveal an etiology but is not necessary
may lead to recurrent disease. for diagnosis, which is clinical.
centripetal rash in an acral distribution with r Skin biopsy by a dermatologist may differentiate
r An immunogenetic predisposition has been noted characteristic target lesions described above.
with increased incidence of certain HLA types r Rash is asymptomatic but may have associated pain other conditions such as vasculitis or systemic lupus
associated with recurrent EM (HLA-DQ3, B15, B35, erythematosus, that mimic the rash characteristic of
or burning and rarely pruritis.
A33, DR53, DQB1). r 50% of patients experience a nonspecific prodrome EM.
r Male gender of fever, malaise, headache, sore throat, upper Pathological Findings
r Previous history of EM respiratory symptoms, chest pain, arthralgias, EM is characterized by a T-lymphocytic infiltrate at the
myalgias, vomiting, or diarrhea. dermalepidermal junction with edema, keratinocyte
GENERAL PREVENTION r 2550% of children will develop oral lesions necrosis, and subepidermal bullae.
Since EM is typically associated with infectious causes,
prevention is difficult. Suppression of recurrent herpes concurrently with cutaneous lesions (2).
labialis with antiviral medication may be effective in
patients with recurrent disease.
PATHOPHYSIOLOGY
r The exact pathophysiology of EM is unclear, but it is
thought to represent an immune-mediated
(lymphocyte) hypersensitivity reaction to an
infectious or exogenous antigen.
320
ERYTHEMA MULTIFORME
DIFFERENTIAL DIAGNOSIS DISPOSITION 3. Sun Y, Chan RK, Tan SH, et al. Detection and
r Stevens-Johnson syndrome (SJS): genotyping of human herpes simplex viruses in
Admission Criteria
Systemic symptoms often present r EM is a self-limited disease and should not require cutaneous lesions of erythema multiforme by
Lesions are widely distributed but <10% BSA, hospital admission. nested PCR. J Med Virol. 2003;71:423428.
atypical, and flat (rather than typical raised acral r Rarely, patients with inability to tolerate oral intake 4. Riley M, Jenner R. Towards evidence based
targets in EM). despite analgesics may require hospitalization for emergency medicine: Best BETs from the
Multiple mucous membranes involved: Oral pain management and IV fluids. Manchester Royal Infirmary. Bet 2. Steroids in
(buccal, palatal, vermillion border, with children with erythema multiforme. Emerg Med J.
hemorrhagic erosions, pseudomembranes, ulcers, Discharge Criteria 2008;25:594595.
r The patient must have reliable caregivers and follow
crusts), ocular, and genital
Nikolsky sign positive up with a primary care physician.
r Toxic epidermal necrolysis (TEN): r The diagnosis of EM should be clear and must be ADDITIONAL READING
Systemic symptoms usually present distinguished from life-threatening rashes such as
r Assier H, Bastuji-Garin S, Revuz J, et al. Erythema
Lesions are widespread (>10% BSA), poorly SJS, TEN, and purpura fulminans.
multiforme with mucus membrane involvement and
defined erythematous macules and flat targets. Issues for Referral
r Doubt as to the diagnosis should prompt referral to Stevens-Johnson Syndrome are clinically different
Epidermal detachment in >10% of BSA
disorders with distinct causes. Arch Dermatol.
Multiple mucous membranes involved: Oral dermatology.
r Ocular involvement should prompt consultation with 1995;131:539543.
(similar to SJS), ocular, esophageal, genital, rarely r Leaute-Labreze C, Lamireau T, Chawki D, et al.
colonic ophthalmology.
r Urticaria
r Kawasaki disease
Diagnosis, classification, and management of
erythema multiforme and Stevens-Johnson
E
r Drug eruptions FOLLOW-UP syndrome. Arch Dis Child. 2000;83:347352.
r Contact dermatitis See Also (Topic, Algorithm, Electronic
r Behcet disease r Discharge instructions and medications: Media Element)
r DermNet NZ: http://dermnetnz.org/reactions/
r Rocky Mountain spotted fever Anticipatory guidance:
r Serum sicknesslike reaction Rash will typically resolve in 13 wk without erythema-multiforme.html
r DermAtlas: http://dermatlas.med.jhmi.edu/derm/
r Herpes gingivostomatitis scarring
r Purpura fulminans Temporary hypo- or hyperpigmentation may result.cfm?Diagnosis=34
occur.
Recurrence may be seen in up to 1/3 of children
TREATMENT with EM. CODES
Oral analgesics as needed
INITIAL STABILIZATION/THERAPY r Activity: ICD9
r EM does not cause severe systemic symptoms. If No restrictions r 695.10 Erythema multiforme, unspecified
stabilization is required, this suggests an alternate r 695.11 Erythema multiforme minor
diagnosis.
PROGNOSIS r 695.12 Erythema multiforme major
r The expected duration is 13 wk, with an average of
r Symptomatic treatment for pain associated with
7 days. The rash is usually self-limited, and there are
mucosal involvement is detailed below. no serious or long-term sequelae.
MEDICATION r Recurrences are possible if associated with HSV or PEARLS AND PITFALLS
First Line with accidental exposure to an offending antigen. r Consider SJS and TEN, which are life-threatening
r Oral analgesics as needed: r Reactive hyper- or hypopigmentation may be seen.
illnesses with high morbidity and mortality. These
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN r Scarring is unusual in EM. typically have more severe clinical features,
Ketorolac 0.5 mg/kg IV/IM q6h PRN especially when multiple mucous membranes are
Naproxen 5 mg/kg PO q8h PRN COMPLICATIONS
r Dehydration is a complication of severe oral involved.
Acetaminophen 15 mg/kg/dose PO/PR q4h PRN r EM is rare in children under 3 yr of age, and
Codeine or codeine/acetaminophen dosed as involvement.
r Recurrence is possible, particularly in alternate diagnoses should be considered.
r Topical analgesics for oral lesions as needed HSV-associated disease.
(eg, viscous lidocaine)
r Recurrent HSV-associated disease may benefit from
suppressive therapy: 1. Bastuji-Garin S, Rzany B, Stern RS, et al. Clinical
Acyclovir 4080 mg/kg/day divided t.i.d.; classification of cases of toxic epidermal necrolysis,
adolescent/adult, 400 mg PO b.i.d. or Stevens-Johnson syndrome, and erythema
200 mg t.i.d. multiforme. Arch Dermatol. 1993;129:9296.
Famciclovir (adolescent/adult) 250 mg PO b.i.d. 2. Auquier-Dunant A, Mockenhaupt M, Naldi L, et al.
Valacyclovir (adolescent/adult) 500 mg or 1 g PO Correlations between clinical patterns and causes
daily of erythema multiforme majus, Stevens-Johnson
r Systemic steroid therapy may be of limited value for syndrome, and toxic epidermal necrolysis: Results
symptomatic treatment but does not change of an international prospective study. Arch
morbidity or mortality and is not recommended (4). Dermatol. 2002;138(8):10191024.
321
ERYTHEMA NODOSUM
Solomon Behar
r Other causes: DIAGNOSTIC TESTS & INTERPRETATION

BASICS Epstein-Barr virus Diagnosis is primarily clinical. Testing may be helpful
Hodgkin lymphoma to determine the underlying cause.
DESCRIPTION Behcet disease: Seen in 50%
r Erythema nodosum (EN) is characterized by Lab
Systemic mycoses (eg, histoplasmosis, r CBC: Leukocytosis in infection, sarcoidosis
self-limited painful nodules that originate in the coccidiomycosis) r ESR: Elevation in rheumatologic disease, infection,
hypodermal fat layer below the skin, usually located Inflammatory bowel disease
in the anterior lower extremities. sarcoidosis
TB (BCG vaccine and PPD administration have r Rapid strep test, throat culture, antistreptolysin O
r Nodules last up to 2 wk, with new lesions been linked as well)
developing up to 6 wk after onset. Pregnancy (ASO) titers to confirm streptococcal infection
r EN is a symptom of an underlying condition and not Medication exposure (sulfonamides, oral Imaging
itself a disease. contraceptive pills) Consider obtaining a chest radiograph:
r Usually affects older children and teenagers r If TB risk factors/symptoms are present
r If sarcoidosis: Perihilar lymphadenopathy
EPIDEMIOLOGY DIAGNOSIS
r 15 in 100,000 (among adults) HISTORY r PPD skin test
r Prodromal illness 13 wk before onset: r Biopsy of the lesion is diagnostic.
r In older adolescents/adults, females are affected
Weight loss, malaise, low-grade fever, cough, and
37 times more frequently than males. Pathological Findings
arthralgia with or without arthritis
PATHOPHYSIOLOGY r This is followed by development of painful Acute septal panniculitis of hypodermal fat lobule
Delayed type IV hypersensitivity reaction to several subcutaneous nodules on lower extremities. without signs of true vasculitis
antigenic stimuli, generally developing 16 wk after DIFFERENTIAL DIAGNOSIS
the inciting event (eg, infection, medication exposure) PHYSICAL EXAM r Insect bites
r Symmetrical, poorly demarcated, tender
r Urticaria
ETIOLOGY nonulcerating nodules usually located on the
r Streptococcus and sarcoidosis are the most common r Folliculitis
anterior aspect of the lower extremities:
identifiable etiologies in adults: Can also be on the extensor surface of the r Erysipelas
Account for 98% of cases with an identifiable forearms and thighs r Nodular vasculitis
etiology from a Scandinavian study of 129 cases r Genitourinary ulcers occur with Behcet disease. r Thrombophlebitis
of EN (1) r Arthritis may occur with sarcoidosis.
r Variable based on geographic region r Lymphadenopathy or organomegaly is associated
r Upward of 50% of EN cases are idiopathic.
with malignancy.
322
ERYTHEMA NODOSUM
r Gonzales-Gay MA, Garcia-Porrua C, Salvarani C,

TREATMENT FOLLOW-UP et al. Erythema nodosum: A clinical approach. Clin
Exp Rheumatol. 2001;19:365368.
INITIAL STABILIZATION/THERAPY FOLLOW-UP RECOMMENDATIONS r Kakourou T, Drosatou P, Psychou F, et al. Erythema
Largely supportive treatment nodosum in children: A prospective study. J Acad
Bed rest Dermatol. 2001;44:1721.
MEDICATION Ibuprofen (10 mg/kg PO q6h PRN for pain) r Mert A, Ozaras R, Ozturk R, et al. Erythema
First Line r Activity:
r Treat underlying condition nodosum: An experience of 10 years. Scand J Infect
As tolerated Dis. 2004;36(6):424427.
r Ibuprofen 10 mg/kg/dose PO/IV q6h PRN r Schwartz, RA, Nervi SJ. Erythema nodosum: A sign
PROGNOSIS
Second Line Self-resolves in weeks, rarely months of a systemic disease. Am Fam Physician. 2007;
r Prednisone 1 mg/kg/day until lesions resolve: 75:695700.
Use if pain and lesions are persistent and COMPLICATIONS
debilitating None from EN
Rule out malignancy and infection before use CODES
r Colchicine if associated with Behcet syndrome REFERENCE
(pediatric dosing not established) ICD9
r Potassium iodide 150250 mg PO t.i.d.: 1. Cribier B, Caille A, Heid E, MD, et al. Erythema 695.2 Erythema nodosum
Use if NSAIDs have failed nodosum and associated diseases. A study of 129
cases. Int J Dermatol. 1998;37:667672. E
PEARLS AND PITFALLS
Consider biopsy if diagnosis is uncertain.
ADDITIONAL READING r Treatment is largely supportive.
DISPOSITION r Avoid ibuprofen use in cases of inflammatory bowel
EN is managed as an outpatient with appropriate pain r Fernandes NC, Maceira J, Muniz M. Erythema
medications. disease, as it may cause more GI bleeding.
nodosum: A prospective study of 32 cases. Rev Inst
Discharge Criteria Med Trop. 1994;36(6):507513.
Pain is under control r Garty BZ, Poznanski O. Erythema nodosum in Israeli
Issues for Referral children. Isr Med Assoc J. 2000;2(2):145146.
Refer to manage primary underlying conditions
323
ERYTHEMA TOXICUM
Solomon Behar
BASICS DIAGNOSIS r Neonatal herpes simplex infection:
Vesicular lesions
DESCRIPTION HISTORY Infant is ill appearing.
r Erythema toxicum is the most common pustular rash r Rash appearing on day 2 or 3 of life r Miliaria
of the newborn period, with an unclear etiology and r Most common in a full-term baby r Infantile acropustulosis: Pruritic on distal extremities
a benign course. r Baby is otherwise afebrile and healthy. r Bacterial folliculitis: Tender, red papules/macules
r Also known as erythema toxicum neonatorum r Lesions typically resolve spontaneously in days to r Transient neonatal pustular melanosis:
r Erythema toxicum is rare in preterm infants. weeks.
r Recurrence of lesions is possible but rare. Usually present at birth
r Only 10% of babies with erythema toxicum have it
More common in African Americans
at birth. PHYSICAL EXAM r Eosinophilic pustular folliculitis: Recurrent lesions
EPIDEMIOLOGY r 23-mm macules, papules, and pustules on face, tending to be on scalp
4070% of full-term babies trunk, and extremities, sparing palms and soles r Scabies: Rare
r Classically described as flea-bitten appearance
RISK FACTORS r Absence of signs of systemic illness
r Full-term babies
r Vaginal birth DIAGNOSTIC TESTS & INTERPRETATION
r Primiparous mothers Lab
Possible mechanism is mast cell degranulation as a None needed (peripheral eosinophilia may be noted if
reaction to commensal microbes (1,2) a CBC is sent)
ETIOLOGY
Skin scraping if diagnosis in doubt
Unknown
COMMONLY ASSOCIATED CONDITIONS Scraping of pustule reveals eosinophils with Gram,
Associated with a normal newborn Wright, or Giemsa stain.
324
ERYTHEMA TOXICUM
REFERENCES
TREATMENT CODES
1. Marchini G, Nelson A, Edner J, et al. Erythema
toxicum neonatorum is an innate immune response
Erythema toxicum is a benign neonatal rash that ICD9
to commensal microbes penetrated into the skin of
requires no treatment. Once distinguished from other 778.8 Other specified conditions involving the
the newborn infant. Pediatr Res. 2005;58(3):
rashes, no further intervention is necessary. integument of fetus and newborn
613616.
DISPOSITION 2. Nelson A, Ulfgren A-K, Marchini G, et al. Urticaria
Discharge Criteria neonatorum: Accumulation of tryptase-expressing PEARLS AND PITFALLS
All newborns with erythema toxicum may be safely mast cells in the skin lesions of newborns with
erythema toxicum. Pediatr Allergy Immunol. r If lesions are present on the palms and soles,
discharged home.
2007;18:652658. consider a different diagnosis.
3. Liu C, Feng J, Qu R, et al. Epidemiologic study of r The most dangerous rash in the differential diagnosis
FOLLOW-UP the predisposing factors in erythema toxicum is neonatal herpes, which causes lesions that may
neonatorum. Dermatology. 2005;210:269272. be initially erythematous macules that progress to
FOLLOW-UP RECOMMENDATIONS vesicular lesions rather than to ulcers. Certainty that
neonatal herpes is not causal is critical.
Routine care ADDITIONAL READING
r Activity:
Regular r Wagner A. Distinguishing vesicular and pustular
DIET
disorders in the neonate. Curr Opin Pediatr. E
1997;9:396405.
No special diet is necessary. Feeding with powdered
formula may be associated with the development of See Also (Topic, Algorithm, Electronic
erythema toxicum (3). Media Element)
r Herpes Simplex
PROGNOSIS r Rash, Maculopapular
Excellent; typically resolves without sequelae r Rash, Neonatal
COMPLICATIONS
Secondary bacterial infections
325
ESOPHAGEAL VARICES
Emily L. Willner

BASICS r Liver disease due to any cause:
Lab
Extrahepatic PV obstruction: Initial Lab Tests
DESCRIPTION Perinatal umbilical venous catheter with In order of priority:
r Esophageal varices are distended, tortuous, thrombosis r CBC for hemoglobin, platelets
submucosal veins that are superficial and may bleed Omphalitis
Bedside hemoglobin testing if available
spontaneously. Severe abdominal trauma r Type and cross-match for blood products
r In patients with portal HTN, which may result from a Intrahepatic PV obstruction: r Coagulation parameters (often abnormal, since
variety of causes, these veins form due to shunting of Cirrhosis due to any cause
blood from the portal to the systemic venous system. Cystic fibrosisrelated liver disease clotting factors are produced by the liver)
r Hemorrhage from esophageal varices can be r Basic metabolic panel (evaluate for electrolyte
Biliary atresia
massive: Congenital hepatic fibrosis disturbances, renal impairment)
Schistosomiasis r Ammonia (increased protein load from blood in GI
This topic will focus on variceal hemorrhage.
Posthepatic PV obstruction: tract can elevate ammonia)
EPIDEMIOLOGY Budd-Chiari syndrome r Liver enzymes and bilirubin (variable)
Incidence Veno-occlusive disease
r Incidence in children is unknown. Imaging
Cardiac disease r Useful in acute setting only if the diagnosis is in
r Esophageal variceal bleeding occurs in up to 10% of
doubt. Obtain while stabilizing hemodynamics and
children with portal HTN annually.
DIAGNOSIS controlling active bleeding:
Prevalence Upright abdomen x-ray (or cross-table lateral) to
r Variceal bleeding is a common cause of upper GI HISTORY check for perforation with free air
bleeding in the developing world. r Esophageal varices are normally asymptomatic. Hepatic US to check PV pressure if not known
r In developed countries, other causes (ulcers, r Esophageal variceal bleeding presents with hepatic disease or portal HTN
gastritis) predominate. hematemesis, with or without melena: r If hypoxemia or respiratory distress, CXR to check for
Obtain best estimate of blood loss. aspiration of blood
RISK FACTORS
r Identified varices on prior endoscopy Bleeding is typically painless. Diagnostic Procedures/Other
r Significant hemorrhage may lead to
r Portal venous pressure >5 mm Hg or portal vein Upper endoscopy is both diagnostic and therapeutic
light-headedness, syncope or near-syncope, and (3):
(PV) to hepatic vein (HV) gradient of >10 mm Hg:
pallor. r It should be performed in the setting of refractory or
PV to HV gradient >12 mm Hg is associated with r Patient/caregiver may report a history of liver
significantly increased risk of variceal bleeding (1). massive variceal bleeding OR
r Chronic liver disease of any etiology in order of disease or esophageal varices r Persistent slow bleeding despite medical
r If no history of liver disease, a detailed history of
highest risk (2): management
Extrahepatic PV obstruction recent symptoms is imperative to detect other
Congenital hepatic fibrosis causes of upper GI bleeding: DIFFERENTIAL DIAGNOSIS
Abdominal pain, jaundice, changes in stool, other For hematemesis:
Cirrhosis
bleeding or bruising, NSAID use r Gastric or duodenal ulcer
GENERAL PREVENTION r Gastritis, esophagitis
r Prophylaxis with nonselective beta-blockers may PHYSICAL EXAM
r If active variceal hemorrhage: r Mallory-Weiss tear
reduce bleeding rates in patients with known r Esophageal foreign body
varices, though pediatric data is limited. Tachycardia, hypotension, orthostatic vital sign
r Elective banding or injection sclerotherapy of large changes r Upper GI tract hemangioma/polyp
Pallor, delayed capillary refill r Dieulafoy lesion
varices decreases variceal bleeding (3).
Lethargy or agitation r Severe coagulopathy or thrombocytopenia
PATHOPHYSIOLOGY r Children with PV pressures high enough to cause r Swallowed blood from nasopharynx
r Increased pressure within the portal venous system esophageal varices frequently also have: r Ingested red food, drink, or medication
leads to shunting of portal venous blood to the Dilated periumbilical abdominal wall veins (caput r In infants: Swallowed maternal blood from birth or
lower-pressure systemic venous system. medusae)
r This causes dilation of normally very small vessels, Hemorrhoids
breast-feeding
forming engorged portosystemic collaterals in the: Splenomegaly
Distal esophagus r Abnormal liver exam:
TREATMENT
Upper stomach May be firm and small in end-stage cirrhosis or
Rectum enlarged in other conditions PRE HOSPITAL
Falciform ligament Typically not tender Assess and stabilize airway, breathing, and
Skin veins of the abdomen r Ascites and jaundice are variable, depending on circulation.
r Bleeding results when superficial submucosal underlying liver disease.
vessels in the esophagus and stomach become r Abdominal tenderness is variable, though usually INITIAL STABILIZATION/THERAPY
overdistended, fragile, and friable: not severe:
They may bleed spontaneously or with minor circulation.
Peritoneal signs suggest alternate diagnosis. r Prevent aspiration of vomited blood:
irritation.
Bleeding tendency is exacerbated by Consider intubation for airway protection if there
thrombocytopenia and deficiencies in clotting is obtundation, severe agitation, or respiratory
factors and fibrinogen related to end-stage liver distress.
disease.
326
ESOPHAGEAL VARICES
r Rapid assessment of circulation and perfusion: DISPOSITION REFERENCES

Obtain vascular access, preferably 2 large-bore Admission Criteria
peripheral IVs. r Hematemesis complicating varices usually requires 1. Garcia-Tsao G, Groszmann RJ, Fisher RL, et al.
Begin vascular volume resuscitation with isotonic admission for observation, monitoring, serial Portal pressure, presence of gastroesophageal
fluid. hemoglobin measurements, and consideration of varices and variceal bleeding. Hepatology.
In shock, push 20 mL/kg boluses of above fluid endoscopy. 1985;5(3):419424.
over 510 min, and repeat as necessary. r Critical care admission criteria: 2. Bernard O, Alvarez F, Brunelle F, et al. Portal
For massive ongoing bleeding with shock, Need for airway stabilization or IV vasoactive hypertension in children. Clin Gastroenterol.
transfuse unmatched type O, Rh negative blood as infusions, and those with: 1985;14(1):3355.
soon as available. Significantly altered mental status 3. Fox VL. Gastrointestinal bleeding in infancy and
r Place NG or orogastric tube and attach to low Shock refractory to volume resuscitation children. Gastroenterol Clin North Am. 2000;29:
intermittent suction: Significant ongoing blood loss 3766.
Do not use ice water lavage: This is ineffective and Persistent vital sign abnormalities (resting 4. Eroglu Y, Emerick KM, Whitingon PF, et al.
can cause hypothermia in children. tachycardia, orthostatic changes) or if need for Octreotide therapy for control of acute
r Urgent type and cross-match of blood products in frequent lab monitoring gastrointestinal bleeding in children. J Ped
patients with significant blood loss: Gastroenterol Nutr. 2004;38(1):4147.
Discharge Criteria
Transfuse the following as indicated if there is r Discharge is appropriate if it was determined that 5. Miga D, Sokol RJ, Mackenzie T, et al. Survival after
ongoing bleeding: first esophageal variceal hemorrhage in patients
Packed RBCs (10 mL/kg will raise hemoglobin there was no GI bleeding (eg, negative Gastroccult
with biliary atresia. J Pediatr. 2001;139(2):
2.53 g/dL) for symptomatic or rapidly
testing on red-colored emesis).
r Consider discharge in patients with a minimal 291296. E
worsening anemia
Platelets (1 unit per 10 kg body weight) if amount of blood in an emesis, normal vital signs for
thrombocytopenia (platelets <50,000/mm3 ) age, no ongoing blood loss, stable hemoglobin after ADDITIONAL READING
Fresh frozen plasma (10 mL/kg) if coagulopathy several hours of observation, reliable caregivers, and
close follow-up. r McDiarmid SV. End stage liver disease. In Kleinman
(INR >1.5)
Issues for Referral RE, Goulet O, Mieli-Vergani G, et al., eds. Walkers
MEDICATION r In the emergency department: Pediatric Gastrointestinal Disease. 5th ed. Ontario,
First Line Consult with a gastroenterologist for patients with Canada: BC Decker; 2008:11311147.
Octreotide and vasopressin decrease mesenteric blood known or suspected variceal bleeding. See Also (Topic, Algorithm, Electronic
flow. Note that vasopressin also causes significant Consult with a surgeon for patients with massive Media Element)
systemic vasoconstriction: or refractory variceal bleeding.
r Octreotide: 12 g/kg IV bolus, followed by Gastrointestinal Bleeding, Upper
Pediatric patients with refractory variceal bleeding
12 g/kg/hr IV infusion (pediatric dosing and should be transferred to a center with pediatric
safety not formally established) (4) gastroenterology and surgery. CODES
r Vasopressin: Start at 0.10.3 units/min, then titrate r Patients with newly diagnosed portal HTN or varices
dose as needed (0.0020.008 units/kg/min); max without bleeding should be referred to a pediatric
single dose 0.01 units/kg/min
ICD9
gastroenterologist. r 456.0 Esophageal varices with bleeding
Second Line r 456.1 Esophageal varices without mention of
r IV gastric acid reduction: More beneficial in ulcer
FOLLOW-UP bleeding
bleeding but recommended in significant upper GI r 456.20 Esophageal varices in diseases classified
bleeding until etiology is certain: FOLLOW-UP RECOMMENDATIONS elsewhere, with bleeding
Pantoprazole (Protonix) 1 mg/kg IV q1224h, max Patient Monitoring
single dose 40 mg r In patients with variceal bleeding: Continuous
r Antibiotics are recommended in adults with variceal
cardiovascular, respiratory, and pulse oximetry PEARLS AND PITFALLS
hemorrhage and cirrhosis to prevent infectious monitoring and frequent noninvasive BP checks
complications and to decrease rebleeding. Benefit in r Check CBC and coagulation tests every 26 hr r Early assessment of volume status and resuscitation
pediatric patients has not been established: depending on initial results, ongoing bleeding, and with fluids and blood are essential.
Ceftriaxone 50 mg/kg q24h, max single dose 1 g r Patients taking prophylactic beta-blockers may not
response to treatment.
COMPLEMENTARY & ALTERNATIVE be tachycardic despite significant blood loss.
DIET r Consider variceal hemorrhage in children with
THERAPIES NPO if upper GI bleeding
Esophageal balloon tamponade can be used to known liver disease presenting in shock of unknown
temporize refractory hemorrhage while awaiting PROGNOSIS etiology, even without history of hematemesis or
r Mortality in variceal bleeding in children with varices.
definitive treatment. However, the procedure is risky
and should only be attempted by a specialist with cirrhosis correlates with the severity of the
experience with the procedure. underlying liver disease (5).
r Patients with history of variceal bleeding have a high
SURGERY/OTHER PROCEDURES rate of rebleeding.
r Upper endoscopy with band ligation or injection
sclerotherapy of bleeding varices COMPLICATIONS
r Surgical portocaval shunting decreases portal r Hypovolemia and shock leading to end-organ
venous pressure and is considered when a hypoperfusion and subsequent dysfunction
r Aspiration of vomited blood
combination of medical and endoscopic
management fails:
Transjugular intrahepatic portosystemic shunt
(TIPS): Via venous access, a needle is passed from
the hepatic vein, via the liver parenchyma, into the
PV.
Surgical portocaval shunts are more invasive.
r Liver transplantation in patients with refractory
bleeding already on transplant list
327
ESOPHAGITIS
Michael E. Valente
Janet Semple-Hess
ETIOLOGY r Symptoms of infectious esophagitis include:

BASICS r GERD In older children: Mouth pain, mouth lesions,
r EE nausea, dysphagia, odynophagia, and retrosternal
DESCRIPTION r Caustic ingestions include: chest pain
r Esophagitis is defined as inflammation of the In younger children: Mouth lesions, nonspecific
Alkalis (lye, potassium hydroxide, and ammonium
esophageal mucosa and has numerous etiologies. hydroxide) found in drain cleaners, oven cleaners, symptoms including fussiness, refusal to drink,
r In the pediatric population, common causes of and dyspnea
and powdered laundry detergents
esophagitis are GERD, eosinophilic esophagitis (EE), Acids (hydrochloric, sulfuric, oxalic, and nitric In both age groups: Systemic symptoms may be
and caustic ingestions. acids) found in toilet bowl cleaners, drain cleaners, fever, chills, and nausea.
r Other etiologies include infection, radiation, and rust removers, and industrial bleaches History of immunodeficiency can lead to increased
trauma. r Infectious esophagitis (rare in children unless incidence and more diverse etiologies of infectious
immunocompromised): esophagitis.
EPIDEMIOLOGY
Candida and herpes simplex virus (HSV) are the PHYSICAL EXAM
Incidence r Assess vital signs for tachypnea and tachycardia.
most common pathogens.
>5,000 accidental caustic ingestions occur annually in
Bacteria, mycobacteria, fungi, and parasitic r Assess airway and respiratory system, especially
the U.S., which corresponds to 35% of reported
organisms such as Trypanosoma cruzi, following caustic ingestions.
accidental ingestions (1,2).
Cryptosporidium, and Pneumocystis are r Assess circulation and perfusion for signs of shock
Prevalence uncommon causes.
r Traumatic esophagitis may be caused by NG tube secondary to esophageal perforation and
The prevalence of esophagitis in the pediatric
hemorrhage.
population is unknown: placement and foreign bodies (zinc-containing r Evaluate for crepitus as a sign of esophageal
r A large cross-sectional survey found prevalence rates coins, toys, sharp objects, disc batteries).
r Radiation-induced esophagitis may occur in patients perforation and mediastinitis.
of 1.88.2% of symptoms associated with GERD (3). r Examine the oropharynx for erythematous plaques,
GENERAL PREVENTION after radiation therapy. ulcerations, thrush, or dental enamel erosions.
r Caregivers should be counseled to keep all caustic r Pill esophagitis results from prolonged contact with r Evidence of allergic shiners, eczema, and wheezing
agents out of childs reach and preferably in locked some medications (aspirin, potassium, NSAIDs) with in patients with suspected EE.
cabinets. the esophageal mucosa. r If GERD is a concern, observe feeding of the infant
r Coins and small toys should be kept out of reach of
to assess for symptoms of reflux.
young children and infants. DIAGNOSIS DIAGNOSTIC TESTS & INTERPRETATION
PATHOPHYSIOLOGY Lab
r GERD is the most common cause of esophagitis and HISTORY
r In older children, the most common symptoms are In the emergency department: If there is a concern for
is due to transient lower esophageal sphincter bleeding as a complication of esophagitis:
relaxation and reflux of gastric fluids: dysphagia, odynophagia, and substernal chest pain.
r In older children, symptoms of GERD and its r Stool occult blood
GERD esophagitis is characterized by changes in r Hematocrit
the esophageal mucosa, including basal cell resulting esophagitis often include chest pain after
hyperplasia, thickening of the papillae, and meals and at bedtime. Imaging
r In infants and young children, symptoms of GERD r In the emergency department: CXR can be used to
infiltration of inflammatory cells.
As severity increases, ulceration, scarring, and are varied: evaluate for aspiration pneumonia, to evaluate for
fibrosis with stenosis can be found. Symptoms of reflux: Frequent spitting up or evidence of perforation following a caustic
Barrett esophagus with a cellular metaplasia of vomiting ingestion, or if foreign body is suspected.
the columnar epithelium is rare in the pediatric Symptoms of esophageal pain: Crying, irritability, r As an outpatient, barium contrast radiography is
population. back arching (Sandifer syndrome), colic, and useful to evaluate for anatomic abnormalities of the
r EE may be based on allergic disorder and abnormal refusal to eat upper GI tract or to identify esophageal strictures
immunologic response or as a result of severe acid Respiratory symptoms (related to reflux and (avoid if concern for esophageal perforation).
reflux disease: aspiration): Apnea, cyanotic episodes, cough,
stridor, and excessive hiccups Diagnostic Procedures/Other
In contrast to GERD, EE can involve the mucosa,
r In all children with suspected caustic esophagitis, In the outpatient/referral setting:
submucosa, and muscularis. r Esophagogastroduodenoscopy (EGD) for diagnosis
r Ingestion of caustic agents can cause inflammation history is crucial to help predict severity of illness:
History of ingestion of alkali, acid, overheated and esophageal dilation of fixed esophageal
and necrosis at various levels of the esophageal
food/liquid, or disc battery strictures
mucosa and underlying muscularis: r Nuclear scintigraphy for pulmonary aspiration in
Severity of inflammation depends on type, Obtain original container or details of exact
amount, and concentration of the agent. product ingested, amount ingested, and patients with GERD
concentration of ingested agent r Esophageal pH probe studies for evaluating the
Full-thickness circumferential injury to the
esophagus carries a 20% mortality rate, so early Timing of ingestion efficacy of antisecretory therapy
surgical management is vital. Odynophagia or dysphagia following pill or
Temporal course of caustic esophagitis: medication ingestion
Acute phase (1st 2496 hr) with edema, Early symptoms: Coughing, crying, and vomiting
inflammation, and necrosis Late symptoms: Mouth or chest pain, drooling,
Ulceration and granulation phase (35 days hematemesis, respiratory distress, and stridor
r EE is usually diagnosed in patients with symptoms
after injury)
Chronic phase of scarring and stricture of relapsing or persistent GERD esophagitis that
formation (begins weeks after injury) does not respond to antireflux therapy. One should
have a higher index of suspicion in patients with:
Allergic conditions in the patient or family
Chronic respiratory complaints
328
ESOPHAGITIS

TREATMENT Admission Criteria r Dahms BB. Reflux esophagitis: Sequelae and
r Patents with caustic esophagitis should be
INITIAL STABILIZATION/THERAPY hospitalized in order to: differential diagnosis in infants and children
r Treatment of GERD esophagitis relies on improving Provide assistance if airway is compromised including eosinophilic esophagitis. Pediatr Dev
esophageal reflux in order to allow time for the Provide nutrition to allow esophageal healing: Pathol. 2004;7(1):516.
NPO with IV fluids r Furuta GT, Liacouras CA, Collins MH, et al.
esophagus to heal.
r Eosinophilic esophagitis: Total parenteral nutrition (TPN) AND/OR Eosinophilic esophagitis in children and adults: A
If known, removal of causative food antigens is Tube feedings systematic review and consensus recommendations
crucial. Obtain an EGD to evaluate for complications. for diagnosis and treatment. Gastroenterology.
A strict elimination diet with amino acidbased r For other types of esophagitis, hospitalization may 2007;133:13421363.
r Lovejoy FH Jr., Woolf AD. Caustic ingestions. Pediatr
formula is sometimes used in severe cases. be required if:
r Caustic esophagitis with alkalis or acids: Esophagitis is complicated by obstruction or Rev. 1995;16:473474.
perforation r Orenstein S, Peters J, Khan S, et al. The esophagus.
Evaluate and stabilize cardiorespiratory status
(intubation may be required if upper airway Patient is unable to tolerate PO intake or In Kliegman RM, Behrman RE, Jenson HB, et al.,
edema is present). gain/maintain normal weight for age eds. Nelson Textbook of Pediatrics. 18th ed.
Flush mouth and surrounding skin with water. Philadelphia PA: WB Saunders; 2007.
Issues for Referral r Pelclova D, Navratil T. Do corticosteroids prevent
Corticosteroid administration is controversial since r In the emergency department:
meta-analysis has failed to demonstrate a benefit. esophageal stricture after caustic ingestion? Toxicol
In 2nd- or 3rd-degree injuries and in all cases in
Notify a poison control center or consult a
toxicologist for potentially caustic ingestions. Rev. 2005;24(2):125129.
r Salzman M, OMalley R. Updates on the evaluation
E
which systemic corticosteroids are used, Surgical consult for suspected esophageal
prophylactic systemic antibiotics should be used perforation and management of caustic exposures. Emerg Med
(2,4). r Outpatient gastroenterologist referral: Clin North Am. 2007;25(2):459476.
r For infectious esophagitis, antiviral or antifungal
If endoscopy or biopsy is required for treatment or See Also (Topic, Algorithm, Electronic
therapy depending on suspected infectious agent, diagnosis Media Element)
severity of the esophagitis, and hosts age and In cases of GERD that are difficult to manage and r Gastroesophageal Reflux
immune status not responding well to first-line treatment r Pain, Chest
MEDICATION r Vomiting
r Treatment for GERD:
Histamine H2 antagonists: FOLLOW-UP
Ranitidine
Famotidine
FOLLOW-UP RECOMMENDATIONS CODES
r Follow-up after caustic ingestion is required to
Proton pump inhibitors (PPIs): monitor for development of strictures.
Omeprazole ICD9
r Follow-up for patients with GERD, EE, and infectious r 530.10 Esophagitis, unspecified
Lansoprazole
r Eosinophilic esophagitis treatment: esophagitis is required to follow effectiveness of r 530.11 Reflux esophagitis
initiated therapy and to monitor for complications. r 530.12 Acute esophagitis
Medical treatments investigated include systemic
corticosteroids, topical ingested steroids, and COMPLICATIONS
r Severe sequelae of reflux esophagitis include
leukotriene receptor antagonists.
Although PPIs do not treat EE directly, patients ulceration with chronic blood loss and Barrett PEARLS AND PITFALLS
with EE often have concurrent GERD that should esophagus. r All patients with suspected or confirmed esophageal
be treated with PPI therapy. r Significant complications of caustic esophagitis
caustic injury should be hospitalized.
Short courses of oral steroids may have a role in include esophageal perforation, mediastinitis, r If upper airway edema is present after a caustic
treating emergent EE patients: hemorrhage, and death.
Fluticasone propionate: Aerosolized fluticasone ingestion, early intubation to protect the airway is
indicated.
spray is swallowed instead of being inhaled. r Induction of emesis is contraindicated in all cases of
Prednisone 12 mg/kg/day, max single dose REFERENCES
60 mg/day caustic ingestion.
1. Rothstein FC. Caustic injuries to the esophagus in r Treatment of GERD does not immediately resolve
Leukotriene receptor antagonists: Evidence is children. Pediatr Clin North Am. 1986;33(3):
limited to adult EE studies. symptoms of GERD esophagitis, as time is required
665674. for the esophagus to heal.
SURGERY/OTHER PROCEDURES 2. Nelson SP, Chen EH, Syniar GM, et al. Prevalence
r Esophagitis with perforation requires surgical of symptoms of gastroesophageal reflux during
consultation in the emergency department. childhood: A pediatric practice-based survey. Arch
r Other surgical procedures may be referred for Pediatr Adolesc Med. 2000;154(2):150154.
outpatient follow-up: 3. De Jong AL, Macdonald R, Ein S, et al. Corrosive
Surgical correction of gastroesophageal reflux esophagitis in children: A 30-year review. Int J
(fundoplication) can be preformed if medical Pediatr Otorhinolaryngol. 2001;57(3):203211.
treatment has failed. 4. Wasserman RL, Ginsburg CM. Caustic substance
As EE does not improve with fundoplication, prior injuries. J Pediatr. 1985;107(2):169174.
to surgery for suspected GERD, EGD with biopsy
should be performed to rule out this disorder.
329
ETHANOL POISONING
David J. Story
Sari Soghoian
r Small amount metabolized via inducible cytochrome PHYSICAL EXAM

BASICS oxidases (MEOS pathway, mostly by CPY 2E1) r Vital signs may demonstrate tachycardia,
r 510% renally excreted unchanged bradycardia, hypotension, respiratory depression,
DESCRIPTION r Metabolism of ethanol interacts with key enzymes in and hypothermia.
r Ethanol, ethyl alcohol, traditional alcohol r Neurologic symptoms predominate:
the gluconeogenesis (NADH/NAD+) pathway and
r Component of beverages (beer, wine, liquor), Altered mental status: Drowsy to coma
may cause hypoglycemia and its sequelae (seizures,
mouthwash, cough and cold preparations, colognes, anoxic brain injury); young children with poor Slurred speech
hand sanitizers, and variety of other household items glycogen stores are at greatest risk. Ataxia
r CNS depressant causing motor incoordination, r Ethanol inhibits antidiuretic hormone (ADH) with Nystagmus
slurred speech, ataxia, and decreased level of diuretic effect. Dysconjugate gaze
consciousness r The average child can metabolize 20 mg/dL/hr of r Flushing and diaphoresis may be present.
r Ingestion may be intentional, typically among teens, r Nausea/vomiting
ethanol.
or inadvertent ingestion, common among toddlers r Disinhibition may occur with belligerent, loud,
ETIOLOGY
EPIDEMIOLOGY boisterous behavior.
Oral intake (intentional or unintentional ingestion)
Incidence DIAGNOSTIC TESTS & INTERPRETATION
r Unknown in young children COMMONLY ASSOCIATED CONDITIONS
r Intentional drug overdose Lab
r 80% of high school seniors report having used
r Trauma Initial Lab Tests
alcoho.l r Capillary blood glucose should be determined
r Hypoglycemia
r 9.5 million youth ages 1220 yr report having an immediately.
r Seizures
alcoholic drink in the past month, with 20% of r Serum ethanol level:
r Aspiration
those report being heavy drinkers (5 drinks at least
r Trauma Blood alcohol level >100 mg/dL typically
5 times in the last month). associated with significant sedation;
r Depression
RISK FACTORS >200 md/dL, often comatose; >300500 mg/dL
r Parents with alcoholism r Alcoholism associated with deep coma, respiratory
r Depression depression, seizures, hypotension
r Chemistry panel to check electrolytes and assess for
r Binge drinking with peers DIAGNOSIS an anion gap (if concerned for toxic alcohol
GENERAL PREVENTION HISTORY ingestion)
r Limit access to alcohol in the home r Child found near a source of ethanol or had easy r Serum osmolality
r Childproof cabinets/drawers used to store ethanol- access to ethanol r Pregnancy test in sexually mature females
and other alcohol-containing household products r Inappropriate behavior r Acetaminophen concentration if any concern for
r Increased drowsiness or lethargy depression, self-harm, or suicidality
PATHOPHYSIOLOGY
r Ethanol causes dose-dependent CNS depression. r Slurred speech
r Enhances GABA binding at the GABA receptor r Ataxia
A
(inhibitory CNS receptor) r Motor incoordination
r Inhibits NMDA receptor (excitatory CNS receptor) r Vomiting
r 8090% absorbed from stomach within 60 min
r 90% hepatic elimination by oxidation
r Metabolized by alcohol dehydrogenase to
acetaldehyde, then by aldehyde dehydrogenase to
acetate
330
ETHANOL POISONING
r Carbon monoxide poisoning
Admission Criteria r American Academy of Pediatrics. Alcohol use and
r Closed head injury r Loss of airway protective mechanisms
r Diabetic ketoacidosis r Profound serum concentration that will take several abuse: A pediatric concern. Pediatrics. 2001;
r Ethanol intoxication 108(1):185189.
hours to metabolize r Yip L. Ethanol. In Goldfrank LR, Flomenbaum NE,
r Hypoglycemia r Concern for patient safety at home
r Sedative/hypnotic ingestion r Labile glucose levels Lewin NA, et al., eds. Goldfranks Toxicologic
r Seizures r Concern for coingestion Emergencies. 8th ed. Stamford, CT: Appleton &
Lange; 2006.
r Starvation hetoacidosis r Seizure
r Toxic alcohol ingestion r Critical care admission criteria:
Unstable vital signs, particularly respiratory CODES
depression or hypotension unresponsive to IV fluid
TREATMENT therapy
ICD9
Associated trauma requiring intensive care
PRE HOSPITAL 980.0 Toxic effect of ethyl alcohol
r Assess and stabilize airway, breathing, and Discharge Criteria
circulation. Return to baseline mental status and ability to
r Assess for trauma, utilizing cervical collar and/or ambulate PEARLS AND PITFALLS
Issues for Referral r Smaller children lack significant liver mass and have
backboard as needed.
r Concern for child safety at home should prompt
fewer glycogen stores than adults and therefore are
E
INITIAL STABILIZATION/THERAPY child protective services or social work consultation.
r Assess and stabilize airway, breathing, and at increased risk for hypoglycemia in the setting of
r Intentional use warrants consideration for referral to ethanol intoxication.
circulation. r Children metabolize ethanol more rapidly than
r Intubation for unprotected airway psychiatrist, psychologist, or substance abuse
r Supportive care counselor. adults.
r Always check for ethanol content when assessing a
r IV fluids as needed
r Serial monitoring of capillary blood glucose FOLLOW-UP pediatric patient who has ingested household or
body care products.
MEDICATION FOLLOW-UP RECOMMENDATIONS r Proof of alcohol is numerically twice the
r Dextrose for hypoglycemia: Feed, if capable, or 1 Discharge instructions and medications: percentage of ethanol present. A 100-proof product
g/kg IV r Refrain from drinking alcohol. contains 50% alcohol.
r Antiemetics for nausea/vomiting: r Patients who reach emergency medical services in
PROGNOSIS
Metoclopramide 0.1mg/kg PO/IV q6h r Excellent for rapid, normal recovery for minor the setting of ethanol or other alcohol intoxication
Ondansetron 0.1 mg/kg PO/IV q8h may represent a subset of drinkers at higher risk of
r IV fluids: ingestions
r Prognosis worsens as blood alcohol level rises. trauma, comorbid psychiatric illness, and alcoholism.
Normal saline 20 mL/kg IV bolus 1 for
Blood alcohol level >500 mg/dL may result in
hypotension, repeat up to 2 times
severe morbidity and mortality.
COMPLEMENTARY & ALTERNATIVE r Unrecognized hypoglycemia causing seizure activity
THERAPIES places patient at increased risk for aspiration,
Use of caffeine-containing beverages, such as tea or traumatic bodily injury, and anoxic brain injury.
coffee, is commonly attempted by laypersons in an
COMPLICATIONS
attempt to make patient less sedated. r Hypoglycemia
r This is not demonstrated to be effective or safe and r Seizures
is not recommended for clinical use. r Permanent neurologic or neurocognitive injury
331
EYE, RED
Eric C. Hoppa
r Traumatic: PHYSICAL EXAM

BASICS Penetrating trauma: Ruptured globe r Fever: Infectious or inflammatory etiology
Blunt trauma: r Ophthalmologic:
DESCRIPTION Corneal/conjunctival abrasion Visual acuity: Decreased visual acuity in hyphema,
r Common causes of red eye(s) include infection, Subconjunctival hemorrhage: Resulting from iritis, chemical injury, orbital cellulitis, or glaucoma
trauma, caustic injury, and allergic or inflammatory direct trauma or increased intrathoracic pressure Proptosis may be seen in orbital cellulitis
conditions. from coughing or vomiting Eyelid edema and/or erythema: Trauma, allergy, or
r Ocular structures can be involved singularly or in Hyphema preseptal cellulitis
combination leading to the red eye. Traumatic iritis Eyelid: Presence of chalazion or hordeolum
Acute traumatic glaucoma: Associated with Eyelashes: Trichiasis or blepharitis
PATHOPHYSIOLOGY
r Bacterial or viral infection of the conjunctiva causes vision loss Attempt eversion of eyelids to assess for foreign
r Caustic Injury: body.
inflammation and injection of the conjunctival
vessels leading to a red eye. Alkaline injury may be more severe than acidic Extraocular movements (EOM): Painful or limited
r Infections in the orbital or preseptal areas can cause injury. EOM may been seen in orbital cellulitis, ruptured
Conjunctivitis from silver nitrate in neonates globe, or orbital fracture.
conjunctival injection. r Allergic conjunctivitis: Often associated with
r Corneal injury causes conjunctival injection leading Conjunctiva:
chemosis and prominent lymphatic tissue on the Diffuse injection: Infectious or allergic
to a red eye. conjunctivitis
r Blunt trauma may lead to hyphema or traumatic palpebral conjunctiva
r Systemic diseases: Prominent lymphoid tissue of palpebral
iritis. conjunctiva: Allergic conjunctivitis
r Burns from caustic chemicals cause conjunctival Kawasaki disease (KD)
Stevens-Johnson syndrome (SJS) Isolated bulbar conjunctival injection:
injection and corneal ulceration. Alkali substances Iritis/episcleritis: Juvenile idiopathic arthritis (JIA), Inflammatory disorders
cause liquifactive necrosis. sarcoidosis, TB, inflammatory bowel disease (IBD), Ciliary flush: Bulbar conjunctival injection
r Mast cell degranulation and histamine release from with limbic sparing can be seen in iritis or KD.
leukemia, collagen vascular diseases
allergen exposure causes conjunctival vessel r Disorders of the eyelids or lacrimal ducts: Subconjunctival hemorrhage
congestion and injection. Hordeolum (stye): Obstructed eyelid hair follicles Chemosis: Allergic conjunctivitis
r Systemic inflammatory conditions can lead to Pupillary exam:
or meibomian glands; often painful with purulent
inflammation of the conjunctiva, sclera, or the layers drainage Irregular shape: Ruptured globe
between. Chalazion: Painless granuloma of the meibomian Asymmetry: Iritis on the side with decreased
r Disruption of the tear film that lubricates the eye response
glands of the inner eyelid
surface can lead to irritation and red eye. Blepharitis: Inflammatory condition with crusting Cornea/anterior chamber:
of eyelashes Hyphema: Blood in anterior chamber seen with
ETIOLOGY tangential lighting either macroscopically or on
r Infectious: Trichiasis: Eyelashes folded onto the conjunctiva,
most often seen in Asian children slit lamp exam
Conjunctivitis: Corneal laceration: Iris may protrude through
Bacterial: Often unilateral with purulent Congenital nasolacrimal duct obstruction
Dry eye laceration
drainage. Causes include skin flora, r Skin:
Pseudomonas aeruginosa, and Moraxella Periorbital vesicles: HSV and VZV
catarrhalis. Neisseria gonorrhoeae and DIAGNOSIS Generalized rash: KD, SJS, or JIA
Chlamydia species may occur in sexually active r Lymphadenopathy:
adolescents. HISTORY
Corneal ulcers: P. aeruginosa in contact lens r Onset of symptoms Preauricular: Adenoviral conjunctivitis
r Systemic symptoms, such as fever Single large cervical node: KD
wearers
Neonatal: N. gonorrhoeae, Chlamydia r In neonates, maternal history of STIs DIAGNOSTIC TESTS & INTERPRETATION
trachomatis r History of trauma Lab
Viral: Usually bilateral and associated with upper r Exposure to alkali or acidic chemicals r Neonates with conjunctivitis: Gram stain, bacterial
respiratory infection (URI) symptoms. Causes r Associated ocular symptoms: Eye pain or drainage, culture, and Chlamydia DFA and culture
include adenovirus (20%), herpes simplex virus r Neonates with suspected N. gonorrhoeae
(HSV), echovirus, and coxsackievirus. eyelid swelling, visual changes, foreign body
sensation, or eye itching conjunctivitis or conjunctivitis associated with fever
Keratoconjunctivitis: HSV or varicella zoster should undergo a full sepsis evaluation.
r Associated systemic symptoms:
virus (VZV), associated with periocular vesicular r Older children with conjunctivitis: Gram stain and
lesions. Fever: Infectious or inflammatory etiologies
culture are not usually necessary.
Epidemic keratoconjunctivitis: Adenovirus URI symptoms: Viral conjunctivitis r In suspected orbital cellulitis, consider a blood
Orbital cellulitis: Extension of sinusitis caused by Rhinorrhea, sneezing, and itching: Allergic
conjunctivitis culture.
mixed flora r Send HSV culture/direct fluorescent antibody from
Preseptal/periorbital cellulitis: Extension of skin Rash and joint swelling: Inflammatory conditions
infection anterior to septal plate, caused by skin or r History of contact lens use vesicular lesions if suspecting HSV
upper respiratory flora r Associated medical conditions: JIA, IBD, leukemia, keratoconjunctivitis.
immunodeficiency
332
EYE, RED
Imaging r HSV keratoconjunctivitis:

r Suspected orbital fracture: CT orbit without contrast Acyclovir 30 mg/kg/day IV divided q8h or FOLLOW-UP
r Ruptured globe: CT orbit to rule out intraocular 80 mg/kg/day PO divided q8h
foreign body; strongly consider CT brain to rule out Trifluridine 1% ophthalmic solution to affected FOLLOW-UP RECOMMENDATIONS
intracranial injury. eye, 8 times a day
r Suspected orbital cellulitis: CT orbit with IV contrast In adults, treatment with topical trifluridine and Hand hygiene is critical to decrease spread of
topical or oral acyclovir for HSV infectious conjunctivitis to contact lenses.
Diagnostic Procedures/Other keratoconjunctivitis is associated with the best Children with a corneal abrasion should have
r Fluorescein exam:
clinical outcomes. The addition of topical follow-up for a repeat fluorescein exam within
Instill fluorescein into the eye and illuminate with interferon and topical steroid may also be of 24 hr.
a cobalt blue light. benefit given the extent of the keratitis (2). Narcotic pain medications may be necessary for
Uptake of fluorescein by corneal defects appear Treatment with oral acyclovir in children has been corneal abrasions
yellow/green shown to be beneficial (3). There are no studies Do not prescribe topic analgesic drops such as
Dendritic staining pattern with HSV infection comparing oral and topical antiviral therapies in proparacaine or tetracaine, as they interfere with
r Slit lamp examination: corneal healing.
children.
RBCs in anterior chamber: Microhyphema r Ruptured globe: r Activity:
WBCs in anterior chamber: Iritis Antibiotic prophylaxis: Cefazolin 100 mg/kg/day Rest for children with hyphema
DIFFERENTIAL DIAGNOSIS IV divided q8h
See Etiology section. Antiemetic: Ondansetron 0.15 mg/kg IV/PO q8h
Age-appropriate tetanus prophylaxis REFERENCES E
r Allergic conjunctivitis: Olopatadine HCl 0.2%:
1. Turner A, Rabiu M. Patching for a corneal abrasion.
TREATMENT 1 drop to each eye daily (children age >3 yr) Cochrane Database Syst Rev. 2006;(2):cd004764.
INITIAL STABILIZATION/THERAPY Second Line 2. Guess S, Stone DU, Chodosh J. Evidence-based
r Place an eye shield over the injured eye with Cycloplegic agent: Cyclopentolate 0.5%: 1 drop, can treatment of herpes simplex virus keratitis: A
suspected ruptured globe or intraocular foreign repeat in 5 min up to 3 times systematic review. Ocul Surf. 2007;5(3):240250.
body. SURGERY/OTHER PROCEDURES 3. Schwartz GS, Holland EJ. Oral acyclovir for the
r Apply topical anesthetic drops to relieve eye pain r Repair of ruptured globe treatment of herpes simplex virus keratitis in
prior to detailed exam. r Removal of intraocular foreign body children. Ophthalmology. 2000;107(2):278282.
r In chemical injury, perform eye irrigation immediately r Drainage of abscess with orbital cellulitis
with normal saline or Ringer lactate solution for ADDITIONAL READING
30 min and until ocular pH normalizes to 6.57.5. DISPOSITION
r Multiple studies show no clinical benefit of patching Admission Criteria r Greenberg MF, Pollard ZF. The red eye in childhood.
r Suspected gonococcal conjunctivitis
for corneal abrasions (1). Pediatr Clin North Am. 2003;50:105124.
r Performing hourly saline ocular lavage may prevent r Orbital cellulitis r Levin AV. Eyered. In: Fleisher GR, Henretig, eds. In
r Preseptal cellulitis with systemic symptoms or failing Fleisher GR, Ludwig S, eds. Textbook of Pediatric
corneal damage in N. gonorrhoeae conjunctivitis.
outpatient therapy Emergency Medicine. 6th ed. Philadelphia, PA:
MEDICATION r Ruptured globe Lippincott Williams & Wilkins; 2010.
First Line r Intraocular foreign body r Teoh DL, Reynolds S. Diagnosis and management of
r Anesthetic agents:
r Hyphema pediatric conjunctivitis. Pediatr Emerg Care.
Proparacaine hydrochloride 0.5%: 12 gtt 2003;19:4855.
Tetracaine hydrochloride 0.5%: 12 gtt Discharge Criteria
r Conjunctivitis: Most patients with red eye without systemic diseases
Erythromycin 0.5% ophthalmic ointment: 0.5-inch can be discharged with proper follow-up unless
meeting admission criteria above.
CODES
ribbon to each eye q.i.d. 7 days
Polymyxin B/trimethoprim sulfate ophthalmic Issues for Referral
solution: 12 drops q46h 510 days r Ophthalmologic consultation: ICD9
r 360.00 Purulent endophthalmitis, unspecified
Moxifloxacin HCl 0.5% ophthalmic solution: 1 Ruptured globe r 379.93 Redness or discharge of eye
drop t.i.d. 7 days Hyphema
r Neonatal conjunctivitis: r 921.3 Contusion of eyeball
Traumatic or inflammatory iritis
Gonococcal: Ceftriaxone 2550 mg/kg up to Suspicion of acute glaucoma
125 mg IV/IM 1 Significant chemical injury
Chlamydia: Erythromycin 50 mg/kg/day PO Neonate with gonococcal conjunctivitis PEARLS AND PITFALLS
divided q6h 14 days Suspicion of HSV/VZV keratoconjunctivitis r Pearls:
r Orbital cellulitis: Ampicillin/sulbactam (dosed as Orbital cellulitis
Conjunctivitis in contact lens wearers Anesthetic and cycloplegic agents should only be
ampicillin) 200 mg/kg/day IV divided q6h, max used for initial evaluation. They should not be
r Otorhinolaryngology consultation: Orbital cellulitis
single dose 2 g given to the patient at discharge.
r Preseptal cellulitis: Amoxicillin/clavulanic acid with sinusitis on CT
Early ophthalmologic consultation is imperative
(dosed as amoxicillin) 90 mg/kg/day PO divided with red eye and decreased visual acuity
q812h or ampicillin/sulbactam IV (as above) Most infectious conjunctivitis is viral, but topical
antibiotics are often prescribed to prevent
secondary infection.
Vertical corneal abrasion(s) may be indicative of a
foreign body trapped under the eyelid.
r Pitfalls:
Failure to differentiate orbital cellulitis from
preseptal cellulitis
Inadequate irrigation with chemical injury
333
EYE, STRABISMUS
r Restrictive strabismus: Corneal light reflex:

BASICS Orbital fracture: Normal light reflex should be symmetric in both
Orbital floor fracture may result in an eyes.
DESCRIPTION entrapment of the inferior rectus muscle. Temporal to the pupillary center is seen in an
r Several terms are used to describe the types of Medial wall fracture may result in an esotropic eye.
strabismus: entrapment of the medial rectus muscle. Nasal to the pupillary center is seen in an
Esotropia: Inward turning of the eyes (crossed Orbital hemorrhage, tumor, cellulitis, or abscess exotropic eye.
eye) Thyroid disease (Graves disease) Pupillary light reflex: CN III palsy may result in
Exotropia: Outward turning r Nonneurogenic nonrestrictive strabismus: dilated pupil.
Hypertropia: Upward turning Comitant childhood strabismus (benign or Extraocular movements (EOMs):
Hypotropia: Downward turning essential childhood strabismus) The strabismus is nonemergent if the patient has
Comitant or concomitant strabismus: The degree Sensory strabismus full and symmetric extraocular eye movements.
of misalignment remains nearly constant in all r See respective topics: Traumatic Brain Injury; Pain on attempted eye movement can be seen
gaze directions. The most common forms of Neoplasm, Brain; Otitis Media; Myasthenia Gravis; in orbital fractures.
childhood strabismus, including congenital Fracture, Orbital; and Hyperthyroidism. Decreased sensation along the cheek and upper
strabismus, fall into this category. lip is suspicious for an orbital floor fracture.
Incomitant strabismus: The degree of Palpation of the orbital rims for tenderness,
misalignment changes as the patient looks in DIAGNOSIS crepitus, and step-off to detect orbital fracture
different directions. This category includes Funduscopic exam may reveal papilledema in
neurologic palsy, extraocular muscle restriction, HISTORY patients with increased ICP.
r Onset of symptoms: Strabismus with acute or
CNS gaze disorders, and syndromic strabismus. Slit lamp exam can identify associated injuries
r This topic focuses on acute-onset strabismus. subacute onset is less likely to be congenital. such as corneal abrasion, hyphema, and
r The major causes of acute strabismus include Congenital strabismus may also worsen acutely. microhyphema in patients with trauma.
r Head trauma r Otoscopic exam: CN VI palsy may be caused by
neurologic palsy and extraocular muscle restriction.
r Orbital trauma
complicated otitis media.
PATHOPHYSIOLOGY r Double vision (diplopia): Presence of diplopia usually r Complete neurologic exam: Findings such as focal
r The 6 extraocular muscles are innervated by cranial
indicates acute or subacute onset of strabismus, neurologic deficits, CN palsies, and nystagmus
nerves (CNs) III, IV, and VI. whereas nonemergent childhood strabismus is
r CN III supplies the medial rectus, superior rectus, warrant investigation for intracranial mass and
usually not associated with diplopia. elevated ICP.
inferior rectus, and interior oblique muscles. The r Fluctuation of symptoms with the time of day and
parasympathetic innervation of the pupil and the fatigue with activity are suggestive of myasthenia DIAGNOSTIC TESTS & INTERPRETATION
levator palpebrae muscle are also supplied by CN III. gravis. Lab
r A complete CN III palsy results in exotropia, r Vomiting, headache, and ataxia may be seen in Routine lab testing is usually unnecessary.
decreased elevation, depression, and adduction as increased ICP. Imaging
well as ptosis and a dilated pupil. CN III palsy is r Recent illness: CN VI palsy may occur following a r CT of the orbit when orbital fracture is suspected:
often incomplete resulting in variations of Blowout fractures refer to fractures involving
viral illness.
presentation. r Underlying medical problems such as thyroid only the orbital bones.
r CN IV supplies the superior oblique muscle. A palsy
disease or myasthenia gravis Orbital floor fractures are more common in older
results in ipsilateral hypertropia. children.
r CN VI supplies the lateral rectus muscle. A palsy PHYSICAL EXAM
r General: Abnormal head tilt may compensate for the Orbital roof fractures with concomitant frontal
results in ipsilateral esotropia. bone fractures are more common in younger
r Conditions that restrict the movement of extraocular misalignment of the eyes. children.
muscles such as orbital fracture, orbital cellulitis, r Ophthalmologic: r CT of the head should be considered in patients
abscess, and tumors can result in misalignment Decreased visual acuity: with orbital fracture, especially roof fractures
when trying to look away from the restricting Abnormalities along the optical or neurologic extending from a skull fracture, to rule out
muscle. pathway can result in decreased visual acuity. associated intracranial injury.
Amblyopia, decreased visual acuity without r CT of the orbit may be needed to establish the
ETIOLOGY detectable organic cause in one eye, may be
r Neurologic palsies: diagnosis of thyroid eye disease if clinical
seen in patients with long-standing strabismus. presentation is atypical. CT shows thickened
CN III palsy: Less common: Ptosis:
Congenital CN III palsy
extraocular muscles without involvement of
Head trauma Myasthenia gravis
associated tendons.
Intracranial tumor r CT or MRI of the brain when a neurologic cause is
Retraction of upper lid:
Increased intracranial pressure (ICP) Thyroid disease suspected
CN IV palsy: Most commonly affected CN: Orbital hemorrhage
Congenital: May worsen acutely following viral
Enophthalmos or orbital dystopia (the affected eye
illness or head trauma is lower than the other) suggests orbital fracture.
Head trauma
Periocular ecchymosis and eyelid edema may be
Increased ICP
present in orbital fracture.
CN VI palsy: Proptosis:
Head trauma Thyroid disease
Increased ICP Orbital hemorrhage
Intracranial tumor
Postviral infection
Complicated otitis media
Abnormality of cavernous sinus
Traumatic extraocular muscle palsy
Myasthenia gravis
334
EYE, STRABISMUS
Diagnostic Procedures/Other r Timing of surgery to repair orbital fractures is ADDITIONAL READING

Diagnosis of myasthenia gravis: variable, from immediate, early, to delayed repair,
r Edrophonium: r Ehlers JP, Shah CP, Fenton GL, et al., eds. The Wills
depending on the type of fractures and the
IM, SC: Weight 34 kg, 2 mg; weight >34 kg, associated findings. Consult your surgeon for Eye Manual: Office and Emergency Room Diagnosis
5 mg institutional standard of care. and Treatment of Eye Disease. 5th ed. Philadelphia,
IV: 0.04 mg/kg given over 1 min followed by PA: Lippincott Williams & Wilkins; 2008.
DISPOSITION r Holmes JM, Mutyala S, Maus TL, et al. Pediatric
0.16 mg/kg given within 45 sec (if no response), Admission Criteria
max single dose 10 mg r Increased ICP third, fourth, and sixth nerve palsies: A population-
r Neostigmine IM: 0.0250.04 mg/kg as a single based study. Am J Ophthalmol. 1999;127:388392.
r Orbital fractures that require immediate surgery r Hoyt CS, Good WV. Acute onset concomitant
dose. Note: Atropine should be administered either r Critical care admission criteria:
IV (immediately prior) or IM (30 min before esotropia: When is it a sign of serious neurological
neostigmine). Increased ICP with concerns for cardiorespiratory disease? Br J Ophthalmol. 1995;79:498501.
instability or herniation r Levin AV. Eyestrabismus. In Fleisher GR, Ludwig S,
DIFFERENTIAL DIAGNOSIS Myasthenia gravis with concerns for respiratory eds. Textbook of Pediatric Emergency Medicine. 6th
See Etiology section. compromise ed. Philadelphia, PA: Lippincott Williams & Wilkins;
Discharge Criteria 2010.
r Orbital fractures that do not require immediate r Losee JE, Afifi A, Jiang S, et al. Pediatric orbital
TREATMENT
surgery fractures: Classification, management, and early
r Idiopathic childhood strabismus follow-up. Plast Reconstr Surg. 2008;122(3):
Eye shield should be applied if a ruptured globe is Issues for Referral
886897.
r Ticho BH. Strabismus. Pediatr Clin North Am.
E
suspected. r Consultation in the emergency department:
Ophthalmology consultation in patients with 2003;50:173188.
MEDICATION
First Line strabismus associated with:
r Orbital fracture: Prophylactic antibiotic is Diplopia
Eye pain CODES
recommended for orbital fractures involving a sinus.
CN palsies
Routine use of prophylactic antibiotic is
Visual impairment ICD9
controversial: r 378.00 Esotropia, unspecified
Hypertropia or hypotropia
Amoxicillin/clavulanate: 2040 mg/kg/day r 378.9 Unspecified disorder of eye movements
Orbital fractures
(amoxicillin component) PO in divided doses q8h r 378.10 Exotropia, unspecified
or 2545 mg/kg/day (amoxicillin component) Neurosurgery consultation in patients with
divided q12h for 1014 days OR strabismus associated with:
Head trauma
Azithromycin:
3-day regimen: 10 mg/kg (max single dose Increased ICP PEARLS AND PITFALLS
Intracranial tumor
500 mg/day) PO daily for 3 days
Otorhinolaryngologist or a plastic surgery r Pearls:
5-day regimen: 10 mg/kg PO on day 1 (max
consultation in orbital fractures Determine whether the strabismus is of acute
single dose 500 mg) followed by 5 mg/kg (max r Outpatient referral: onset.
single dose 250 mg/day) daily on days 25
Most patients with strabismus, who are not seen Strabismus with diplopia is usually associated with
Phenylephrine intranasal/spray. Note: Therapy
by ophthalmologist in the emergency department, emergent pathology.
should not exceed 3 continuous days:
26 yr: Instill 1 drop q24h of 0.125% solution should follow up with an ophthalmologist. Most patients with strabismus need evaluation by
Patients with small orbital fracture without ocular an ophthalmologist.
PRN r Pitfall:
612 yr: Instill 12 sprays or instill 12 drops muscle entrapment, enophthalmos, or orbital
q4h of 0.25% solution PRN dystopia may be referred to otorhinolaryngologist Failure to refer patients with orbital fracture for a
>12 yr: Instill 12 sprays or instill 12 drops or plastic surgeon. full eye exam by an ophthalmologist to rule out
q4h of 0.250.5% solution PRN All patients with orbital fractures should have associated ocular injury
r Treatment of myasthenia gravis: follow-up with an opthalmologist; orbital fractures
Pyridostigmine 7 mg/kg/day PO in 56 divided are frequently associated with ocular injury.
doses
Second Line FOLLOW-UP
Some experts recommend oral corticosteroids to
reduce the swelling in patients with orbital fractures FOLLOW-UP RECOMMENDATIONS
with limited EOM; consult with otorhinolaryngology at
your institution: Orbital fractures:
r Methylprednisolone: 12 mg/kg/day PO in divided Prophylactic antibiotics may be indicated (see
Medication section).
doses 12 times per day for 310 days, max single Nasal decongestant
dose 60 mg/day Consider oral corticosteroids in orbital fractures
SURGERY/OTHER PROCEDURES with EOM restriction
r May be warranted in patients with intracranial r Activity:
bleeding, brain tumor, and increased ICP Orbital fractures:
r Orbital fractures with the following conditions Advise patient not to blow the nose.
generally require surgery: Sleep with the head of the bed elevated.
Entrapment of orbital contents resulting in EOM Apply cold packs to the eye in the 1st 48 hr to
restriction or diplopia reduce swelling.
Enophthalmos
Vertical orbital dystopia
335
EYE, VISUAL DISTURBANCE

Kristen Breslin
Retinal detachment Pupillary exam:

BASICS Vitreous hemorrhage Irregular or peaked (tear drop) pupil occurs with
Traumatic optic neuropathy ruptured globe
DESCRIPTION CNS injury (cortical blindness) Afferent pupil defect (unilateral sluggish direct
r Visual disturbance includes sudden visual loss, r Binocular or monocular: response to light with normal indirect response):
change in acuity, diplopia, and abnormal images. Monocular diplopia: Corneal irregularity, cataract, Optic nerve or retinal disease
r Diagnoses more likely to present acutely are lens dislocation (ectopia lentis) Extraocular movements (EOMs): Limited
emphasized here. Binocular diplopia: movement due to CN palsies, orbital cellulitis, or
Cranial nerve (CN) III, IV, or VI palsy ophthalmoplegic migraine
PATHOPHYSIOLOGY
r Periorbital edema or lesions Thyroid eye disease Funduscopy:
r Obstruction or distortion of light as it travels Orbital cellulitis, tumor, or fracture Red reflex
CNS lesions: Mass, trauma, ventriculoperitoneal Leukocoria: Retinoblastoma, cataract, vitreous
through the cornea, anterior chamber, lens, or hemorrhage, retinal detachment, infection
shunt (VPS) malfunction, MS
posterior chamber Vertebrobasilar artery insufficiency Corneal clouding: Acute glaucoma
r Retinal pathology
Basilar or ophthalmic migraine Corneal opacities: Keratitis
r Disorders of the optic nerve or visual cortex Papilledema: Increased ICP
Venous sinus thrombosis
r Lack of coordination of eye movements Myasthenia gravis Retinal pallor: CRAO
Toxin: Alcohol, benzodiazepines, botulism Retinal hemorrhages, exudates, and dilated
ETIOLOGY r Abnormal visual images:
r Trauma retinal veins may be seen in CRVO.
r Infection: Uveitis, keratitis, endophthalmitis Floaters, flashes, or spots: Retinal detachment, Hyphema: Usually caused by trauma
r Autoimmune: Uveitis vitreous hemorrhage, migraine, occipital CNS Hypopyon: WBCs in anterior chamber, seen in
lesions, posterior uveitis, chorioretinitis keratitis, endophthalmitis, iritis
r Cardiovascular: Thromboembolic r Neurologic exam:
r Neurologic: Migraine, CNS lesion, increased Halos: Cataract, corneal edema, acute glaucoma,
vitreous opacities, ingestion (digitalis, chloroquine) Ataxia can be seen with vertebrobasilar
intracranial pressure (ICP) r Contact lens wearers: Increased risk of insufficiency or basilar migraine
r Toxic ingestion
pseudomonas and acanthamoeba keratitis DIAGNOSTIC TESTS & INTERPRETATION
r Photophobia: Uveitis, burns, migraines, corneal
Lab
DIAGNOSIS injury, CNS infection r Unexplained binocular vision loss: Consider
r Eye redness, watering, or discharge:
obtaining serum electrolytes, osmolarity, and
HISTORY Purulent discharge increases concern for bacterial methanol level for methanol toxicity.
r Eye pain: infection. r Hyphema: Sickle cell prep or hemoglobin
Pain with eye movement suggests optic neuritis or r Fever may be present with infectious causes,
electrophoresis in patients with unknown SCD
orbital cellulitis including periorbital and orbital cellulitis. status, as sickle cell trait increases the risk of
Pain with eye redness can indicate uveitis, r Vomiting may be present with increased ICP, increased intraocular pressure (IOP) (1).
keratitis, acute glaucoma, or endophthalmitis. migraine, acute glaucoma, and vertebrobasilar r PT, PTT, platelets in patients with spontaneous
r Visual loss or change in visual acuity:
insufficiency. bleeding
Sudden, painless vision loss: r Headache with visual loss can indicate:
Central retinal artery occlusion (CRAO) due to Imaging
Migraine r Head CT or MRI to evaluate for intracranial lesion in
emboli, thrombus, hypercoagulable state, Increased ICP including idiopathic intracranial
autoimmune disease, sickle cell disease (SCD), patients with abnormal neurologic findings or
HTN (pseudotumor cerebri)
trauma papilledema
CNS lesion: Mass, hemorrhage, VPS malfunction r CT head and orbits for orbital abscess in patients
Central retinal vein occlusion (CRVO) due to Venous sinus thrombosis
HTN, glaucoma, SCD, vasculitis, hypercoagulable Acute glaucoma with proptosis or limitation of EOM
state, oral contraceptives, external compression r Orbital CT for orbital fracture or FB:
Malignant HTN
Vitreous hemorrhage r Young children may manifest visual changes with MRI is contraindicated if metal is present.
Retinal detachment
abnormal eye contact, squinting, closing one eye, Diagnostic Procedures/Other
Toxic optic neuropathy: Methanol, ethylene r Mirror test for conversion disorder: Moving a mirror
difficulty walking, lack of interest in visual stimuli,
glycol, ethambutol, carbon monoxide, vitamin B and head tilt. placed close to the patients face and observing eye
deficiencies r Past medical history movements
Optic neuritis: Unilateral or bilateral r Medications or ingestions r Fluorescein exam for keratitis, corneal FB, abrasion,
Cortical blindness: Stroke, hemorrhage
r Duration and progression of symptoms or laceration
PHYSICAL EXAM r Tonometry: Normal IOP = 1021 mm Hg
r Constant or intermittent symptoms r Observation: Interactions, eye contact, response to
r Slit lamp exam of anterior chamber
r Trauma or precipitating triggers: visual stimuli
r BP: Malignant HTN r Lumbar puncture for opening pressure in idiopathic
Posttraumatic visual loss:
Periorbital swelling r Ophthalmologic exam: intracranial HTN
Corneal irregularity from chemical or thermal Inspection for periorbital lesions or edema, DIFFERENTIAL DIAGNOSIS
burn, corneal abrasion, or foreign body (FB) conjunctival injection, proptosis r Conversion disorder (hysterical blindness)
Hyphema Visual acuity r Malingering
Ruptured globe Visual field exam: Visual field loss can indicate r Hallucinations
Intraorbital FB glaucoma, retinal disease or detachment, CNS r Neck muscle pathology causing head tilt
Lens dislocation lesion, increased ICP, or optic neuritis. r Cerebellar disorder causing ataxia
Commotio retinae (retinal edema)
Retinal artery occlusion
336
EYE, VISUAL DISTURBANCE
TREATMENT r Topical steroids for hyphema:

REFERENCES
Prednisolone 1%: 12 gtt 48 times per day
INITIAL STABILIZATION/THERAPY r Cycloplegic agents to decrease ciliary spasm: 1. Lai JC, Fekrat S, Barron Y, et al. Traumatic hyphema
r Chemical burns, CRAO, and ruptured globe require Atropine 0.5% (children), 1% (adults): 1 gtt t.i.d.; in children: Risk factors for complications. Am J
immediate stabilization and emergent duration up to 1 wk Ophthalmol. 2001;119:6470.
ophthalmologic consultation. Cyclopentolate 0.5%: 1 gtt, cycloplegia and 2. Optic Neuritis Study Group. Visual function five
r Remove contact lenses, if present: mydriasis may last 24 hr years after optic neuritis: Experience of the Optic
Discontinue contact lens wear in the setting of r Hypotensive drops for emergent IOP reduction in Neuritis Treatment Trial. Arch Ophthalmol.
trauma, infection, or inflammation. consultation with ophthalmology: 1993;115:15451552.
r Chemical burns: Timolol 0.5%: 1 gtt q15min 2 3. Michael JG, Hug D, Dowd MD. Management of
Irrigate immediately with normal saline for corneal abrasion in children: A randomized clinical
SURGERY/OTHER PROCEDURES trial. Ann Emerg Med. 2002;40:6772.
30 min using a Morgan lens or IV tubing, and
Surgery may be indicated for ruptured globe,
continue until the ocular surface has a normal pH
intraorbital FB, retinal detachment, hyphema,
of 6.57.5. (See Burn, Chemical topic.)
Use of topical anesthetic facilitates this procedure
chemical burns, traumatic optic neuropathy, ADDITIONAL READING
full-thickness corneal laceration, lens dislocation,
by making it more comfortable.
glaucoma, orbital fracture, and some CNS lesions. r Dull K. Eyevisual disturbances. In Fleisher GR,
r Corneal abrasion:
Ludwig S, eds. Textbook of Pediatric Emergency
See Corneal Abrasion topic. DISPOSITION Medicine. 6th ed. Philadelphia, PA: Lippincott
r Ruptured globe: Admission Criteria Williams & Wilkins; 2010.
Apply eye shield; avoid manipulating the eye or r Ophthalmologic emergencies requiring emergent r Ehlers JP, Shah CP, Fenton GL, et al, eds. The Wills E
giving topical eye medications. ophthalmologic evaluation and possible Eye Manual: Office and Emergency Room Diagnosis
Consider orbital CT to look for intraocular FB admission: and Treatment of Eye Disease. 5th ed. Philadelphia,
Tetanus immunization for penetrating injuries Caustic burns PA: Lippincott Williams & Wilkins; 2008.
r Hyphema without a ruptured globe may also be Retinal artery occlusion
treated with topical steroids and cycloplegic agents Ruptured globe
in consultation with ophthalmology. (See Hyphema IOP >40 mm Hg with eye pain
Traumatic vitreous hemorrhage
CODES
topic.)
r To minimize increased IOP and decrease risk of Lens dislocation
Retinal detachment ICD9
rebleeding after hyphema, ruptured globe, or r 368.8 Other specified visual disturbances
vitreous hemorrhage: Acute vision loss of unknown etiology
r Infectious keratitis, endophthalmitis, and r 368.9 Unspecified visual disturbance
Antiemetics to prevent vomiting r 368.11 Sudden visual loss
Oral or IV pain control to decrease agitation symptomatic retinal detachment require
Bed rest with elevation of the head of bed ophthalmologic evaluation within 24 hr and often
r Orbital cellulitis should be treated with broad- require admission.
spectrum IV antibiotics. (See Orbital Cellulitis topic.)
r Admit patients with: PEARLS AND PITFALLS
r Central retinal artery occlusion: Orbital cellulitis r Pearls:
Start treatment immediately if the patient presents Orbital fractures requiring immediate surgery
Major causes of visual disturbance that require
within 24 hr of vision loss. Periorbital cellulitis that is severe or unresponsive
treatment in the emergency department include
Immediate digital ocular massage to dislodge to oral antibiotics
chemical burns and orbital trauma.
emboli: Pressure 5 sec, release 5 sec; repeat Hyphema if the patient has sickle cell trait,
Most patients with visual disturbance should be
for up to 15 min bleeding disorder, large hyphema, or strict bed
seen by an ophthalmologist for a full eye exam;
IOP reduction with acetazolamide IV/PO and/or rest or follow-up cannot be assured
this may be done in the emergency department or
topical ocular hypotensive drops such as timolol, a Optic neuritis for IV methylprednisolone
outpatient setting depending on acuity.
beta-blocker agent, in consultation with Idiopathic intracranial HTN with visual changes r Pitfalls:
ophthalmology CNS lesions
Venous sinus thrombosis Do not use an eye patch if infection is suspected.
Do not use acetazolamide in patients with SCD, as Do not use eye drops with steroids if the patient
it may cause metabolic acidosis, alter the pH of Malignant HTN
Significant injuries, CRAO, and acute glaucoma may have HSV keratitis.
the aqueous humor, and worsen sickling. Topical anesthetic drops inhibit epithelial healing
r Optic neuritis may be treated with IV steroids (2) in may require admission: Discuss with
ophthalmology. and should not be prescribed for outpatient use.
consultation with neurology. Do not use cycloplegic agents in acute glaucoma.
MEDICATION Do not apply pressure to a ruptured globe or an
r Consult ophthalmologist for the frequency and FOLLOW-UP eye with hyphema.
duration of treatment with antiviral agents,
mydriatic and cycloplegic agents, topical steroids, FOLLOW-UP RECOMMENDATIONS
r Ophthalmology follow-up for:
and hypotensive drops.
r Topical analgesic: Noninfectious uveitis, nontraumatic vitreous
hemorrhage, acute maculopathy, CRVO, and optic
Proparacaine: 12 gtt once in affected eye
neuritis within 48 hr
Tetracaine: 12 gtt once in affected eye
r Topical antibiotics for infection or prophylaxis Evaluation following uncomplicated corneal FB
removal in 2448 hr
following corneal injury: Leukocoria within days
Erythromycin eye ointment 0.5% daily to q.i.d. r Discharge instructions and medications:
Trimethoprim/polymyxin B/gramicidin 0.025%:
Eye patching does not improve healing for corneal
12 gtt q.i.d. to q1h
abrasions (3).
Moxifloxacin 0.5%: 1 gtt t.i.d. to q1h
Ofloxacin 0.3%: 12 gtt t.i.d. to q1h
r Topical antivirals for herpes simplex virus (HSV)
keratitis:
Trifluridine 1%: 1 gtt daily to 9 times per day
Vidarabine 3% ointment daily to 5 times per day
337
LWBK822-driver-F LWBK822-Hoffman ch168.xml April 15, 2011 14:11
FACIAL NERVE PALSY

Genevieve Santillanes
r Ramsey-Hunt syndrome: Peripheral nerve palsy due PHYSICAL EXAM

BASICS to varicella zoster reactivation. Patients usually have r Characteristic findings of the affected side for a
an associated vesicular rash of the ear, eardrum, peripheral 7th nerve palsy:
DESCRIPTION palate, or tongue. Flattening of the nasolabial crease
r Facial nerve (cranial nerve VII) palsy may be due to r External compression of facial nerve: Complicated Diminished ability to raise the corner of the mouth
central or peripheral etiologies. otitis media, cholesteatoma, parotid gland tumor, to smile
r Central causes are distinguished from peripheral tumor of the 7th nerve Diminished ability to completely close eyelid
nerve palsy by the presence of forehead sparing. r Lyme disease may be bilateral. (See Lyme Disease Inability to wrinkle the forehead: Special attention
r In peripheral nerve palsies, the upper and lower face topic.) should be paid to involvement of forehead
will be affected. r Sarcoidosis muscles:
r Differentiation between peripheral and central facial r Basilar or temporal bone fracture Paralysis of forehead muscles indicates a
nerve palsy is critical. r Brain tumor (gradual onset of symptoms, forehead peripheral cause.
r Nerve palsy may be complete, or partial nerve Forehead sparing raises concern for a central
sparing)
function may be retained. r Stroke (forehead sparing, generally has other cause.
r No predilection for right or left side of face r To rule out other causes, perform a complete
neurologic findings)
r Central neurologic disorders including stroke, MS, r MS neurologic exam with attention to all cranial nerves,
extremity strength, and reflexes.
and tumors can cause facial nerve palsy. r Guillain-Barre syndrome: Facial nerve palsy is r Perform a thorough exam of the oropharynx and
r This topic will focus on idiopathic peripheral facial
bilateral and usually presents with significant ears:
nerve palsy (Bell palsy). Other diagnoses will be weakness of extremities or palsy of other cranial Vesicles on the face, mouth, or ear are indicative
discussed in the Etiology section. nerves. of Ramsey-Hunt syndrome.
r Vaccines: Influenza vaccines not licensed in the U.S.
EPIDEMIOLOGY Otitis media, cholesteatoma, or parotid disease
r 30 per 100,000 annual incidence (1). have been associated with Bell palsy. can cause external compression of the facial nerve.
r 1 in 65 lifetime incidence
r Age: Peak between 10 and 40 yr; unusual before r Antecedent or even concurrent upper respiratory r Diagnosis is clinical. Testing should be performed
age 10 yr infection may be noted. only when the diagnosis is uncertain.
r Males and females are equally affected. r Many viral infections may have associated facial r In patients with forehead sparing, consider central
PATHOPHYSIOLOGY nerve palsy. If these infections are present, then the causes.
r Not definitively known resulting condition is not idiopathic Bell palsy:
Cytomegalovirus Lab
r Multiple causes of peripheral and central 7th nerve r Consider serologic testing for Lyme disease in
Epstein-Barr virus
palsy. endemic areas.
r Forehead involvement is spared in central etiologies Lyme disease r Consider testing for diabetes mellitus:
Mumps
because nerve fibers to the forehead originate from Rubella Testing for diabetes in children is not routinely
both cerebral hemispheres (1). r Diabetes mellitus (adult populations) recommended.
r Bell palsy is idiopathic, but it is widely believed to be
Imaging
secondary to viral infection: r CT/MRI indicated for:
Some evidence suggests that it is due to herpes DIAGNOSIS Gradual onset of symptoms
simplex virus (HSV)-1 reactivation (2,3). Sparing of the forehead OR
1 study showed an increased incidence of HSV-1 HISTORY
r History of tick bites or risk of exposure to ticks in Bilateral or recurrent cases
DNA in endoneurial fluid of patients with Bell r CT temporal bone if history of head trauma
palsy (3). Lyme-endemic areas
r Patients with Bell palsy have been noted to have r Recent vaccinations Diagnostic Procedures/Other
facial nerve swelling during decompression surgery r Rash or arthralgias suggest Lyme disease. Nerve conduction testing may be helpful as an
and on MRI: r Pain or vesicular rash suggest Ramsey-Hunt outpatient referral to determine the prognosis for
The facial nerve exits the pons at the syndrome. patients with complete paralysis. It is most clinically
cerebropontine angle and courses through the r Acute (<48 hr) or gradual onset. Gradual onset is useful when performed between 3 and 14 days of
internal auditory canal. Swelling of the facial nerve not typical of Bell palsy. onset of complete paralysis.
within the narrow canal can cause compression r Related symptoms: DIFFERENTIAL DIAGNOSIS
with resultant poor nerve conduction. Dry eyes See Etiology section.
Symptoms vary depending on the location of Dribbling or spilling liquid from corner of the
nerve damage. Proximal damage may diminish mouth
taste, tearing, and salivation. Damage at the Ipsilateral facial paresthesia
stylomastoid foramen results in facial paralysis r Associated neurologic symptoms. Other etiologies
without associated symptoms. should be investigated if there are any other
ETIOLOGY neurologic symptoms.
r The etiology of facial nerve paralysis in children is
diverse and includes (47):
Bell palsy (66%)
Infection (15%)
Trauma (13%)
Birth trauma (3%)
Leukemia (1%)
338
FACIAL NERVE PALSY
6. Shih WH, Tseng FY, Yeh TH, et al. Outcomes of

TREATMENT FOLLOW-UP facial palsy in children. Acta Otolaryngol. 2008;
15:16.
MEDICATION FOLLOW-UP RECOMMENDATIONS 7. Evans AK, Licameli G, Brietzke S, et al. Pediatric
r Patients should be followed weekly.
Need and utility of pharmacologic treatment is facial nerve paralysis: Management and outcome.
controversial. Spontaneous recovery is typical. r Discharge instructions and medications:
Int J Pediatr Otorhinolaryngol. 2005;69:
r Artificial tears: 2 gtt to affected eye q2h or PRN to Patients should use artificial tears during the day 15211528.
treat dry eye and eye lubricant at night if the eye cannot be 8. Quant EC, Jeste SS, Muni RH, et al. The benefits of
r Steroids: Not extensively studied in children: closed completely. steroids versus steroids plus antivirals for
Taping the eyelid shut may reduce risk of corneal treatment of Bells palsy: A meta-analysis. BMJ.
Prednisone 1 mg/kg daily for 7 days (various
abrasions and drying of the cornea. 2009;339:b3354.
lengths of treatment published in literature)
Best result when initiated early in course, Patient Monitoring 9. De Almeida JR, Al Khabori M, Guyatt GH, et al.
especially within 48 hr r Monitor for improvement on a weekly basis. Combined corticosteroid and antiviral treatment
Less likely to be of benefit when started >7 days r Consider closer monitoring if paralysis is complete. for Bell palsy: A systematic review and
after onset meta-analysis. JAMA. 2009;302(9):985993.
r Antivirals: Contradictory evidence on efficacy of PROGNOSIS
r 90% of children <15 yr of age have a full recovery, 10. He L, Zhou M, Zhou D, et al. Acupuncture for
antivirals for treatment of Bell palsy (8,9). Options Bells palsy. Cochrane Database Syst Rev.
often within 3 mo of onset (7).
include: r Older adolescents have an 84% chance of full 2006;(8):cd002914.
Acyclovir 80 mg/kg/day divided 5 times per day to 11. Teixeira LJ, Soares BG, Vieira VP, et al. Physical
recovery.
max 800 mg 5 times daily OR r Prognosis is best if some recovery occurs during the therapy for Bells palsy (idiopathic facial paralysis).
Valacyclovir 20 mg/kg/dose t.i.d. or to a max dose Cochrane Database Syst Rev. 2008;(3):cd006283.
of 1 g b.i.d. for adult dosing 1st week:
12. Grogan PM, Gronseth GS. Practice parameter:
Poor prognosis if no improvement within 3 wk (1)
Pregnancy Considerations r Bell palsy complicating pregnancy has a poorer Steroids, acyclovir and surgery for Bells palsy (an
r Acyclovir and valacyclovir are class B in pregnancy. evidence based review). Neurology. 2001;56:
r Prednisone is class C in pregnancy.
prognosis. 50% have persistent symptoms.
r Persistence of any aspect of symptoms, such as 830836. F
inability to close the mouth, facial paresthesia, pain,
THERAPIES
or inability to close eye, may result. ADDITIONAL READING
r Patch or taping eye closed, especially at night, is r Patients with retroauricular pain, diabetes, complete
r Gilden DH. Bells palsy. N Engl J Med. 2004;351(13):
often done to prevent corneal injury. paralysis, decreased salivary or tear production, or
dysgeusia have a worse prognosis. 13231331.
r Acupuncture has been used alone and in r Tiemstra JD, Khatkhate N. Bells palsy: Diagnosis
combination with medications for Bell palsy. COMPLICATIONS and management. Am Fam Physician. 2007;76:
Available evidence is inadequate to draw r Corneal abrasions or ulceration resulting from
9971002,1004.
conclusions about the efficacy of acupuncture, but inadequate tearing or eye closure
there is no evidence of harm (10). r Persistent facial weakness and asymmetry occurs in See Also (Topic, Algorithm, Electronic
r Physical therapy modalities such as exercise, up to 15% of patients Media Element)
electrostimulation, biofeedback, massage, and r 5% have permanent facial paralysis. Lyme Disease
others have been used to treat Bell palsy. Available r Motor synkinesis: Involuntary muscle movement
evidence is inadequate to draw conclusions about occurs with a voluntary muscle movement.
the efficacy, but there is no evidence of harm (11). r Autonomic synkinesis: Involuntary autonomic CODES
SURGERY/OTHER PROCEDURES response occurs with a voluntary muscle movement
Decompression surgery: (eg, tearing while eating). ICD9
r Loss of taste on affected side of tongue r 351.0 Bells palsy
r No conclusive evidence to support surgery (12)
r Rarely, muscle contracture r 351.9 Facial nerve disorder, unspecified
r May be considered in cases of complete paralysis if
no improvement after 1 wk
r If surgery is performed, it must occur within 2 wk of
REFERENCES PEARLS AND PITFALLS
onset of complete paralysis.
r Risk of permanent hearing loss after surgery 1. Peitersen E. Bells palsy: The spontaneous course r Bell palsy diagnosis is clinical. If acute-onset
of 2,500 peripheral facial nerve palsies of different unilateral peripheral 7th nerve palsy without other
DISPOSITION symptoms, no further investigation is needed.
etiologies. Acta Otolaryngol. 2002;549:430.
Admission Criteria 2. Khine H, Mayers MM, Avner JR, et al. Association r Consider other causes if symptoms have gradual
Admission may be warranted for workup if a central between herpes simplex virus-1 infection and onset, are bilateral or recurrent, or if other
cause is suspected. idiopathic facial paralysis in children and neurologic signs/symptoms are present.
Discharge Criteria adolescents. Pediatr Infect Dis J. 2008;27: r Ask about risk factors for Lyme disease.
Nearly all patients can be discharged. 468469. r Certain influenza vaccines not licensed in the U.S.
Issues for Referral 3. Murakami S, Mizobuchi M, Nakashiro Y, et al. Bell have been associated with facial nerve palsy.
r If bilateral nerve palsy, consider Lyme disease and palsy and herpes simplex virus: Identification of
refer for follow-up with primary care provider or viral DNA in endoneurial fluid and muscle. Ann
infectious disease specialist. Internal Med. 1996;124:2730.
r Refer recurrent 7th nerve palsy to neurologist or ENT 4. Cha CI, Hong CK, Park MS, et al. Comparison of
physician for nerve conduction testing. facial nerve paralysis in adults and children.
r Refer to a neurologist if no improvement in 23 wk. Yonsei Med J. 2008;49:725734.
Consider referral if complete paralysis persists at 5. Tsai HS, Chang LY, Lu CY, et al. Epidemiology and
1 wk: treatment of Bells palsy in children in northern
Consider referral for nerve conduction testing for Taiwan. J Microb Immunol Infect. 2009;42:
complete paralysis (on or after 3rd day). 351356.
339
FAILURE TO THRIVE
Michael E. Valente
Janet Semple-Hess
r Inadequate caloric absorption: r Birth history: To differentiate FTT from small for
BASICS Celiac disease gestational age
Cystic fibrosis r Chronic medical conditions
DESCRIPTION Protein-losing enteropathy r Stool pattern: Frequency and nature (diarrhea and
r Failure to thrive (FTT) is a term used to describe Food allergy constipation)
inadequate growth in early childhood. Inflammatory bowel disease r GI symptoms (evidence of milk protein allergy, GI
r Most definitions are based on failure to attain Vitamin or mineral deficiencies reflux)
growth parameters or growth velocity, with weight Hepatobiliary disease r Social history:
being the most commonly used indicator: Short gut syndrome
Changes at home at the time of onset
Weight for age <3rd or 5th percentile Parasitism
Availability of food
Weight as a percentage of median weight for age, Chronic constipation
Economic hardship
<80% or <90% Hirschsprung disease
Restrictive diet for social or religious reasons
Downward crossing (of weight for age) in 2 Malrotation
Home stressors
major percentile lines on a standard growth chart r Excessive caloric expenditure/Increased
Homelessness
EPIDEMIOLOGY metabolism:
Endocrine disorders (hyperthyroidism, diabetes PHYSICAL EXAM
Prevalence r Vital signs
r The prevalence of FTT in the general population is mellitus, diabetes insipidus, adrenal or pituitary
disease) r Plot weight, height/length, and head circumference
unknown. Malignancy on standard growth charts
r In 2007, the prevalence of underweight children r General assessment, including body fat and muscle
Chronic infection (HIV, immunodeficiency, TB)
(birth to age 5 yr) participating in U.S. nutrition and Renal disease (chronic renal insufficiency, renal mass
public health programs was 4.5% (1). tubular acidosis, recurrent urinary tract infections) r Assessment of respiratory status, including signs of
RISK FACTORS Hypoxemia (congenital heart defects, chronic lung hypoxemia
The following are associated with FTT: disease) r Pulmonary exam for evidence of chronic lung
r Underlying disease (diagnosed or undiagnosed) r Defective utilization:
disease or infection
r Lower socioeconomic status Inborn errors of metabolism r Cardiovascular assessment for congenital heart
r Crowded or unsanitary living environment Congenital infections disease and arrhythmia
r Poor emotional environment Genetic abnormalities r Abdominal exam evaluating for masses,
r Prematurity organomegaly, obstruction, constipation, and ascites
DIAGNOSIS r Assessment of hydration and evidence of renal
PATHOPHYSIOLOGY disease
Multiple disease (organic causes) and psychosocial r Plotting growth on standard growth charts is the r Neurologic exam including mental status,
factors (inorganic causes) can lead to FTT via: typical manner of diagnosis. developmental level, and tone
r Inadequate caloric intake r The goal of history, physical exam, and diagnostic r Signs of neglect or abuse
r Inadequate caloric absorption testing is to: r Dysmorphism suggestive of chronic disease or
r Excessive caloric expenditure Aid in the determination of the etiology genetic abnormalities
Guide therapy r Skin/mucosal changes
ETIOLOGY Determine appropriate follow-up
r Most children with FTT have mixed etiologies. These r Observe child/infant while eating/feeding:
etiologies can be organized by their HISTORY Caregiver and child interaction while eating
pathophysiology: r Complete dietary history: Positioning
r Inadequate caloric intake: Amount of food or formula in order to quantify Oral motor difficulties
Incorrect preparation of formula total caloric intake Distractibility
Recall of their last 24-hr intake is useful. r Quality of caregiver and child interaction
Inappropriate feeding (milk intake, juice intake)
Psychosocial factors (behavior problems, poverty, How formula is prepared
Intake of milk, juice, sodas, sugary drinks, and DIAGNOSTIC TESTS & INTERPRETATION
parentchild relationship problems, child
abuse/neglect, Munchausen syndrome by proxy) water Lab
r Feeding history: r Lab assessment has limited value in determining the
Mechanical feeding difficulties (cleft lip/palate,
Feeding routine: etiology of FTT, so diagnostic testing should be
choanal atresia, gastroesophageal reflux, pyloric
When? individualized based on the clinicians differential
stenosis)
Where? diagnosis after a thorough history and physical.
Neurologic (cerebral palsy, hypertonia or r Reasonable initial tests to be completed in the
hypotonia, generalized weakness) With/by whom?
Anorexia and nausea associated with chronic Food refusals emergency department:
illness Oversnacking Glucose
Appropriateness of feeding techniques for CBC with differential
developmental age Urinalysis
Problems with chewing, swallowing, emesis, or Urine culture
spit ups Electrolytes, including BUN and creatinine
Speed of feedings LFTs, including total protein and albumin
340
FAILURE TO THRIVE
r Further tests as indicated can be done in the MEDICATION r Bithoney WG, Dubowitz H, Egan H. Failure to
emergency department or an outpatient/inpatient Medication is dependent on the etiology. thrive/growth deficiency. Pediatr Rev. 1992;13;
setting depending on the case: 453459.
DISPOSITION r Gahagan S, Holmes R. A stepwise approach to
Lead level
PPD placement Admission Criteria evaluation of undernutrition and failure to thrive.
r Significant FTT, particularly in young infants or
HIV testing Pediatr Clin North Am. 1998;45:169187.
Sweat tests patients who lack follow-up to track catch-up r Krugman SD, Dubowitz H. Failure to thrive. Am Fam
IgA and antitransglutaminase (to evaluate for growth
r Patient without weight gain after appropriate close Physician. 2003;68(5):879884.
celiac disease) r Olsen EM. Failure to thrive: Still a problem of
Stool microscopy and culture outpatient treatment and follow-up
r Negligent or abusive caretakers definition. Clin Pediatr (Phila). 2006;45(1):16.
Stool fat
Urine organic and serum amino acids r Severe dehydration, malnutrition, or electrolyte See Also (Topic, Algorithm, Electronic
ESR abnormality with concern for refeeding syndrome Media Element)
Thyroid function tests r Medical causes of FTT identified in the emergency r Gastroesophageal Reflux
Iron studies department that require further inpatient workup r http://www.cdc.gov/growthcharts/
Serum insulinlike growth factor I (IGF-I) and/or treatment
Insulinlike growth factor binding protein (IGF-BP3)
Issues for Referral
Imaging r Social services for patients who have psychosocial CODES
r A CXR can be obtained in the emergency factors as a component to their FTT
department if there is clinical suspicion for TB, r Child protective services are required if neglect or ICD9
pneumonia, or cardiomegaly. r 779.34 Failure to thrive in newborn
abuse is suspected.
r Bone age, typically performed as an outpatient, may r Lactation consultant, nutritionist, and occupational r 783.41 Failure to thrive
be helpful to distinguish genetic short stature from therapist to guide appropriate feeding and maximize
constitutional delay of growth. caloric intake
r Medical specialist depending on etiology PEARLS AND PITFALLS F
It is important to differentiate FTT from normal r It is important to differentiate FTT from normal
variants in growth, including: variants in growth.
r Children who are following appropriate growth FOLLOW-UP r Most children with FTT have mixed etiologies.
curves for: FOLLOW-UP RECOMMENDATIONS r Admit all patients with FTT who lack follow-up to
Chromosomal abnormalities: Trisomy 13,18, and r Discharge only those patients in which follow-up is
track catch-up growth.
21, etc. OR ensured. r Child protective services notification is required if
Other syndromes affecting growth: Noonan r Children with FTT need a high-calorie diet for
neglect or abuse is suspected.
syndrome, Russell-Silver syndrome, fetal alcohol catch-up growth.
syndrome, and Prader-Willi syndrome, etc. r Diet modification may be needed in certain cases,
r Constitutional delay in growth
including high-protein diets and elemental formula
r Familial short stature in the case of milk protein allergy.
r Premature infants and infants with history of
intrauterine growth retardation who have normal
growth velocity: REFERENCE
When charting growth, corrections for gestational
1. Polhamus B, Dalenius K, Borland E, et al. Pediatric
age are necessary until at least 2 yr of age.
Nutrition Surveillance 2007 Report. Atlanta, GA:
CDC; 2009.
TREATMENT
r In the emergency department: ADDITIONAL READING
Evaluation and treatment of: r American Academy of Pediatrics, Committee on
Hypoglycemia Genetics. Health supervision for children with Down
Electrolyte abnormalities syndrome. Pediatrics. 2001;107(2):442449.
Dehydration r American Academy of Pediatrics, Committee on
Additional emergent treatment is guided by Genetics. Health supervision for children with Turner
etiology of FTT. syndrome. Pediatrics. 2003;111(3):692702.
r As an outpatient:
High-calorie diet and close follow-up to document
catch-up growth.
Vitamin and mineral supplementation
Additional workup and admission if failure to gain
weight in the outpatient setting
341
FASCIITIS
Emily L. Willner

BASICS Varicella vaccination reduces the risk of r Early physical findings in NF are similar to
varicella-related NF. cellulitis:
DESCRIPTION Fever and tachycardia are common.
r Fasciitis is defined as inflammation of the fascia. PATHOPHYSIOLOGY
Skin anesthesia and/or pain out of proportion to
r NF affects subcutaneous fat, muscle, and superficial
r Multiple etiologies of fasciitis (infectious, traumatic, exam are helpful if present.
and deep fascia, relatively sparing the skin.
autoimmune) with varied clinical presentations r Infection spreads rapidly along fascial planes, with Tissue crepitus occurs in a minority of cases
r Necrotizing fasciitis (NF) is severe inflammation of (1037%) but is highly suggestive (4).
progression over hours to days. Later findings are increased swelling,
the fascia and surrounding subcutaneous tissues r Bacterial virulence factors and microvascular
due to acute infection by virulent bacteria. It is purple/bluish skin discoloration, blisters, and
rapidly progressive, life and limb threatening, and occlusion with local ischemia cause necrosis. This hemorrhagic bullae in the affected area.
requires rapid diagnosis and treatment. damages sensory nerves in affected areas, causing May present in shock or multisystem organ
r Other types of fasciitis include the following: local anesthesia. dysfunction, especially with type II NF.
r NF may occur in any part of the body, though the r PF causes tenderness at the anteromedial calcaneus
Plantar fasciitis (PF): Overuse or repetitive minor
trauma of the foot, leading to inflammation of the trunk is most common in children (3). and along the plantar fascia. Pain may be elicited by
r Patients may present with shock, due to
plantar aponeurosis. Symptoms include plantar passive dorsiflexion of toes.
heel pain, especially morning pain and pain after streptococcal toxic shock syndrome (STSS) in
GAS-related cases. DIAGNOSTIC TESTS & INTERPRETATION
walking or exercising.
r GAS M proteins types 1 and 3, exotoxin A, and Lab
Nodular fasciitis: Benign growth of reactive
streptolysin O are virulence factors associated with Initial Lab Tests
fibroblasts in subcutaneous tissues, frequently
invasive disease including NF and STSS (4). In NF: Blood culture, CBC, electrolyte panel, calcium,
following minor trauma. It presents as a rapidly
BUN, creatinine, glucose, C-reactive protein (CRP):
growing, firm, and tender nodule. Common ETIOLOGY r The following are also helpful: PT/PTT, AST, ALT,
locations are the head and neck in infants and the r NF is classified into 2 types, differentiated by
forearms and back in others. It is rare in children. bilirubin, albumin, CPK, and lactate level.
microbiologic features: r Lab findings associated with NF include leukocytosis
Eosinophilic fasciitis: Autoimmune infiltration of Type I: Polymicrobial infection composed of
the fascia, especially in the extremities, though aerobic and anaerobic bacteria: with left shift; low sodium and calcium; and elevated
sparing the hands and feet. It is associated with More common in children <1 yr old, and those BUN, creatinine, CPK, CRP, lactate, and glucose.
peripheral eosinophilia and presents with edema with predisposing factors such as immune However, these are nonspecific and variable.
of affected areas, which progresses to indurated, compromise or diabetes mellitus Imaging
peau dorange skin. It is very rare in children. Common pathogens include Bacteroides, r NF is a clinical diagnosis. The following tests may be
r The focus of this article will be on NF, with some
Peptostreptococcus, Enterobacter, Klebsiella, helpful if NF is not clear:
attention to PF. and Proteus species; Escherichia coli, and Gas in soft tissue on x-ray of the affected area is
EPIDEMIOLOGY nonGAS or Clostridium species (1). uncommon but pathognomonic.
Called Fournier gangrene when perineal, and CT and MRI show subcutaneous/fascial
Incidence
r NF is rare in children: 0.080.3 cases per 100,000 Ludwig angina when cervical/intraoral. inflammation or tissue gas but are more useful in
Ludwig angina causes marked tongue and ruling out NF when clinical suspicion is low. If NF
children per year (1):
submandibular swelling and airway is strongly suspected, do not delay surgical
Increased incidence of group A beta-hemolytic
compromise; infection can track to the exploration.
streptococcus (GAS)-related NF during the 1990s
mediastinum. US shows a thickened, distorted fascial layer with
Estimated to cause 0.0180.03% of pediatric
Type II: Single pathogen, usually invasive GAS associated fluid accumulation. Limited data on
hospitalizations
r PF is common in older children and teens, especially (Streptococcus pyogenes): bedside US has shown some utility in diagnosis
Colloquially called flesh-eating bacteria (5).
athletes. It affects 10% of the general population. Associated with varicella infection r PF is a clinical diagnosis. Consider plain radiographs
RISK FACTORS More frequent than type I NF in healthy children if associated with acute trauma or if diagnosis is in
r NF: May follow minor skin trauma, surgical doubt.
Varicella infection, active or recent procedures, or be without a precipitant
Immune compromise (congenital or acquired) Staphylococcus aureus, including MRSA, is a less ALERT
Recent surgery common cause of type II NF. Do not delay surgical exploration for imaging if NF
Skin injury/trauma (may be minor) r PF is caused by repetitive microtears of the plantar is suspected. An exception is Ludwig angina, which
Chronic medical conditions aponeurosis, causing collagen degeneration in the requires CT imaging after airway stabilization and
Diabetes mellitus fascia. antibiotics to assess for mediastinal extension.
Malnutrition
IV drug abuse Diagnostic Procedures/Other
In neonates: Omphalitis, circumcision DIAGNOSIS r Expeditious surgical exploration and complete
NSAID use is reported as a risk factor in some debridement of necrotic tissue is diagnostic as well
HISTORY
studies, though not confirmed by others (2). r Diagnosis of NF can be very difficult, as early signs as therapeutic.
r PF: r Excisional biopsy may demonstrate necrosis or
and symptoms are nonspecific.
Rapid increase in weight-bearing physical activity, Initial symptoms mimic cellulitis: Fever, local bacteria, but a negative biopsy does not rule out NF
especially running swelling, pain, and erythema. where the index of suspicion is high.
Flat or high-arched feet, leg-length discrepancy, Pain is out of proportion to physical findings. Pathological Findings
tight gastrocnemius or soleus muscles Patients with concomitant STSS may report r Necrotic fascia and subcutaneous tissues
Hard running surfaces, worn shoes generalized pain, diffuse rash, malaise, myalgias, r Pathogen(s) frequently isolated from surgical
or diarrhea. specimen
r PF: Heel pain, classically worst in morning, or at
start of physical activity r NF: Cellulitis, gas gangrene, myositis, and
pyomyositis
r PF: Foot strain, overuse syndrome, stress fracture,
bony heel spur
342
FASCIITIS
SURGERY/OTHER PROCEDURES 3. Fustes-Morales A, Gutierrez-Castrellon P,

r Surgery is diagnostic and therapeutic, and surgical
TREATMENT Duran-Mckinster C, et al. Necrotising fasciitis:
re-exploration in 648 hr is required. Multiple Report of 39 pediatric cases. Arch Dermatol.
INITIAL STABILIZATION/THERAPY surgeries are common. 2002;138:893899.
r Assess and stabilize airway, breathing, and r Adjunctive hyperbaric oxygen therapy in NF is 4. Hasham S, Matteucci P, Stanley PRW, et al.
circulation. recommended by some experts, though data is Necrotising fasciitis. BMJ. 2005;330:830833.
r NF: conflicting on whether it improves outcome (7). 5. Yen ZS, Wang HP, Ma HM, et al. Ultrasonographic
Ensure adequate volume resuscitation, as NF DISPOSITION assessment of clinically-suspected necrotizing
causes capillary leak and results in intravascular fasciitis. Acad Emerg Med. 2002;12:14481451.
volume depletion.
Admission Criteria
r All patients with suspected NF should be admitted. 6. Anaya DA, Dellinger EP. Necrotizing soft-tissue
Early consultation with a surgeon r Those in whom the diagnosis is in question but not infection: Diagnosis and management. Clin Infect
r PF: NSAIDS, activity reduction, footwear change, Dis. 2007;44:705710.
highly likely should be admitted for antibiotics, serial
and stretching of the foot/calf 7. Jallali N, Withey S, Butler PE. Hyperbaric oxygen as
exams, and/or imaging.
MEDICATION r Critical care admission criteria: adjuvant therapy in management of necrotizing
fasciitis. Am J Surg. 2005;189:462466.
First Line The majority of patients diagnosed with NF
r Empiric antibiotics for broad-spectrum coverage of require ICU admission.
gram-negative anaerobes and streptococci. Any patient with airway compromise, ADDITIONAL READING
Consider MRSA coverage (vancomycin or linezolid) hemodynamic instability, or severe end-organ
until culture result (6): dysfunction requires ICU care. See Also (Topic, Algorithm, Electronic
Piperacillin/tazobactam: 240400 mg NF patients frequently develop significant Media Element)
piperacillin/kg/day IV divided q68h (max 18 g of coagulopathy and fluid shifts during surgery, so r Cellulitis
piperacillin/day) OR ICU admission postoperatively is recommended. r Toxic Shock Syndrome
Carbapenems such as meropenem (60 mg/kg/day Discharge Criteria
IV divided q8h (max 6 g/day), imipenem or
ertapenem, AND
Patients with PF may be discharged if otherwise
stable. CODES
F
Consider vancomycin 40 mg/kg/day IV divided
q6h (max 4 g/day)
Issues for Referral
r When GAS is identified as sole organism: Patients with NF should be transferred to a hospital ICD9
with surgery and an ICU. r 728.71 Plantar fascial fibromatosis
Penicillin G: 100,000400,000 units/kg/day IV r 728.86 Necrotizing fasciitis
divided q46h (max 24 million units/day) AND r 729.4 Fasciitis, unspecified
Clindamycin 2540 mg/kg/day IV divided q68h FOLLOW-UP
(max 4.8 g/day)
Clindamycin inhibits toxin production. Add when FOLLOW-UP RECOMMENDATIONS
GAS or Clostridium is strongly suspected or Patients with PF may follow up with their primary care PEARLS AND PITFALLS
identified. provider or a sports medicine or orthopedic specialist if r Consider NF in patients with apparent cellulitis and
r Use analgesics as needed. conservative treatment fails.
unexplained severe pain.
r NSAIDs r Patients with suspected NF should be given
PROGNOSIS
r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN r Mortality rate in NF is high, 1440% of all cases antibiotics and be transferred to a facility with
Second Line (adult and pediatric) (4): surgery and critical care support without delay.
r Alternative regimens in type I NF include: Early surgical intervention improves outcome.
r PF: 80% of cases resolve spontaneously or with
Cefotaxime 50 mg/kg/dose IV q68h
(max 2 g/dose) OR conservative treatments within 1 yr.
Ampicillin/sulbactam 100200 mg COMPLICATIONS
ampicillin/kg/day IV divided q6h (max 8 g/day) OR NF: Sepsis, acute respiratory distress syndrome,
Ciprofloxacin 2030 mg/kg/day IV divided q12h multisystem organ dysfunction, tissue loss leading to
(max 800 mg/day) AND cosmetic or functional difficulties, need for amputation
Clindamycin OR
Metronidazole 30 mg/kg/day IV divided q68h
(max 4 g/day)
r Consider addition of MRSA coverage and an
REFERENCES
aminoglycoside for extended gram-negative 1. Enelli I, Davies HD. Epidemiology and outcome of
coverage. necrotizing fasciitis in children: An active
r IV immunoglobulin administration in patients with surveillance study of the Canadian Paediatric
GAS STSS resulted in trends toward improved Surveillance Program. J Pediatr. 2007;151:7984.
outcome, but there is insufficient data to conclude 2. Lesko SM, OBrien KL, Schwartz B, et al. Invasive
benefit in invasive GAS disease (6). group A streptococcal infection and nonsteroidal
antiinflammatory drug use among children with
primary varicella. Pediatrics.
2001;107:11081115.
343
FEBRILE SEIZURE
Jennifer H. Chao
COMMONLY ASSOCIATED CONDITIONS Diagnostic Procedures/Other

BASICS r Fever EEG is indicated if necessary, such as if paralysis to
r Viral or bacterial illness effect endotracheal intubation is performed.
DESCRIPTION r Recent immunizations
r Febrile seizures are seizure activity associated with r Roseola (human herpesvirus 6)
r Febrile delirium
fever and no other identifiable cause (eg, no acute r Iron-deficiency anemia r Shivering
CNS or metabolic abnormalities).
r Febrile seizures can be divided into typical or r Breath-holding
r Apparent life-threatening event
simple/benign and atypical or complex. DIAGNOSIS r Idiopathic seizure
r Typical febrile seizures are seen in children between
ages 6 mo and 6 yr. They are generalized, occur once HISTORY r Seizure secondary to intracranial pathology
r Usually the child presents to the emergency
in 24 hr, stop spontaneously, and last <15 min. (trauma/mass/infection)
r Atypical febrile seizures include febrile seizures department having already returned to baseline r Epilepsy
outside of the usual age range, focal seizures, and neurologic function after having a generalized r Seizure from electrolyte, metabolic, or toxicologic
prolonged or multiple seizures in 24 hr. seizure while febrile that has self-resolved. These abnormality
seizures often stop in <5 min and are followed by a r Seizure due to shigella/shiga toxin:
EPIDEMIOLOGY brief postictal period.
r 25% of neurologically normal children have febrile r There is often no preceding history of illness, and the Rigors/chills with febrile illness
seizures. fever and seizure often are seen to have come out
r 90% occur between 6 mo and 3 yr of age.
of nowhere. TREATMENT
RISK FACTORS PHYSICAL EXAM
r Male gender r Vital sign evaluation including rectal temperature PRE HOSPITAL
r Multiple febrile episodes r Address airway, breathing, and respiration issues.
r A thorough neurologic exam should be conducted:
r History of prior febrile seizures r Cooling measures (undressing/antipyretics)
To detect both CNS abnormality r If actively seizing, apply oxygen via a nonrebreather
r Family history of febrile seizures To detect other findings of nuchal rigidity, Kernig,
r Precipitous change in temperature is possibly mask and consider benzodiazepine therapy.
or Brudzinski signs
contributory. r Physical findings are consistent with illness causing INITIAL STABILIZATION/THERAPY
fever r Oxygen
GENERAL PREVENTION r Cooling measures (undressing/antipyretics)
r Despite the common practice of aggressive DIAGNOSTIC TESTS & INTERPRETATION r If prolonged (>10 min), benzodiazepine therapy
antipyretic use, such as around-the-clock use of Lab
acetaminophen and/or ibuprofen, this has not been r Lab testing should only be utilized as is felt MEDICATION
demonstrated to prevent febrile seizure: necessary for evaluating the cause of the fever or First Line
In theory, any measure that prevents infections or etiology of seizure if diagnosis is uncertain. Antipyretics:
fever may reduce the occurrence of febrile seizure. r Assess anticonvulsant levels if patient is undergoing r Acetaminophen 15 mg/kg PO or up to 30 mg/kg PR
r Avoid treatment such as cool water bath or alcohol
therapy with a medication for which serum as initial dose repeated q4h PRN
bath during fever, as these may result in very rapid concentration assessment is available. r Ibuprofen 10 mg/kg PO/IV q6h PRN:
temperature drop. r Consider further workup including lumbar puncture
IV ibuprofen is newly approved by the FDA.
PATHOPHYSIOLOGY for an infectious etiology of the fever if the child is r IV acetaminophen is expected to receive FDA
See Etiology section. already on antibiotic therapy or does not return to approval in 2010:
baseline neurologic function in a timely manner. As parenteral antipyretics with 100%
ETIOLOGY r Further lab studies for electrolyte or metabolic
r Fever lowers the seizure threshold, resulting in bioavailability that can be safely and rapidly
abnormalities should be performed if there is administered during a seizure, these may play a
seizure activity.
r Rapid shift in temperature, rise or fall, is believed to suspicion for either based on history or physical. new role in febrile seizure management.
be a precipitant. Imaging
None unless intracranial pathology (trauma or mass) is
suspected from history or physical. If so, consider
cranial CT or MRI.
344
FEBRILE SEIZURE
Second Line Patient Monitoring See Also (Topic, Algorithm, Electronic

r Benzodiazepines: r Cardiorespiratory monitor for actively seizing Media Element)
Diazepam: IV (0.1 mg/kg), PR (0.5 mg/kg) max patients r Fever in Children Older than 3 Months
single dose 20 mg r Vital sign evaluation for postictal patients and r National Institute of Neurological Disorders and
Lorazepam: IV (0.050.1 mg/kg) max single dose patients who have returned to baseline Stroke. Febrile Seizures Fact Sheet. http://www.
4 mg r Monitor for further seizure activity. ninds.nih.gov/disorders/febrile seizures/detaiol
Midazolam: IV/IM (0.1 mg/kg), SL/IN (0.2 mg/kg) febrile seizures.htm
max single dose 10 mg PROGNOSIS r Seizure
r For refractory seizure activity: Recurrence is more likely if the child is younger at 1st r Status Epilepticus
Phenobarbital 20 mg/kg IV/IM seizure or has a lower temperature on presentation:
r 1/3 of patients will have recurrence.
Pentobarbital 5 mg/kg IV
Propofol 1 mg/kg IV r Incidence of epilepsy after 1 febrile seizure goes
Use of these medications may result in from 1%2%.
CODES
respiratory depression requiring respiratory r There are no known long-term neurologic
support including endotracheal intubation. consequences from simple febrile seizures. ICD9
r 780.31 Febrile convulsions (simple), unspecified
r Febrile seizures may be predictive for development
DISPOSITION r 780.32 Complex febrile convulsions
of epilepsy but are not considered causal.
Admission Criteria
r Patients requiring endotracheal intubation, with or COMPLICATIONS
without paralysis, and patients requiring prolonged If the child presents in status epilepticus, complications PEARLS AND PITFALLS
infusion of anticonvulsants to treat status are those associated with prolonged seizure activity:
r Injury associated with seizure activity in unsafe r Pearls:
epilepticus should be admitted to a critical care unit.
r Patients who have a febrile seizure in whom there is surroundings/falls Determination if the child has serious bacterial
any concern for other pathology as a cause should infection including meningitis is critical.
be admitted. Consider further lab/imaging evaluation with any
r Patients with status epilepticus should generally be ADDITIONAL READING child who presents with an atypical history or is F
admitted. <1 yr old.
r American Academy of Pediatrics. Practice parameter: Seizure without focal or other abnormal
Discharge Criteria The neurodiagnostic evaluation of the child with a neurologic findings is not consistent with or
r Return to baseline neurologic function
first simple febrile seizure. Provisional Committee on suggestive of meningitis.
r If the cause of the fever does not require admission Quality Improvement, Subcommittee on Febrile Caregiver education and reassurance is important
and may be treated as outpatient Seizures. Pediatrics. 1996;97(5):769772. to ensure proper care of the child and to assuage
r Green SM, Rothrock SG, Clem KJ, et al. Can seizures fears about the repercussions of febrile seizures.
Issues for Referral
be the sole manifestation of meningitis in febrile r Pitfalls:
If seizure is atypical>15 min, multiple in a 24-hr
period or focal, or if the patient is having frequent children? Pediatrics. 1993;92:527534. Failure to diagnose cause of fever that would
r Kimia AA, Capraro AJ, Hummel D, et al. Utility of warrant intervention, such as urinary tract
recurrences of simple febrile seizuresevaluation by
neurology should be considered. lumbar puncture for first simple febrile seizure infection or otitis media
among children 618 months of age. Pediatrics. Not recognizing febrile status epilepticus and
2009;123(1):612. treating for status epilepticus
FOLLOW-UP r Stengell T, Uhari M, Tarkka R, et al. Antipyretic Failure to allow 510 min of seizure activity
agents for preventing recurrences of febrile seizures. before giving a benzodiazepine:
FOLLOW-UP RECOMMENDATIONS Most febrile seizures cease spontaneously.
Arch Pediatr Adolesc Med. 2009;163(9):799804.
Discharge instructions and medications: r Teng D, Dayan P, Tyler S, et al. Risk of intracranial Benzodiazepines prolong sedation after postictal
r Patients should be discharged with instructions for
pathologic conditions requiring emergency period, making neurologic evaluation difficult.
fever control and any instructions and follow-up intervention after a first complex febrile seizure
pertinent to the illness causing the fever. episode among children. Pediatrics. 2006;
r Parents should be advised that if another seizure
117:304308.
occurs, they should not put anything in the childs
mouth and should lay the child on his or her side in
a safe place (to prevent injury). If the seizure lasts
>5 min or there is breathing difficulty, an
ambulance should be called. If the seizure
self-resolves rapidly, they should contact their doctor
or have their child evaluated in the emergency
department.
345
FELON
Yu-Tsun Cheng
Alan L. Nager

BASICS r Staphylococcus aureus is most common.
Lab
r Streptococcus organisms r Not necessary unless there is concern for more
DESCRIPTION r Growing incidence of MRSA. This may be difficult to serious infections, including septic arthritis
r A felon is a closed-space infection of the fingertip r Consider wound culture if the felon is incised and
determine clinically, but consider risk factors:
pulp or phalanx pad. Prior MRSA infection drained.
r One of several types of acute hand infections
Prolonged hospital stay
including paronychia, herpetic whitlow, flexor Imaging
Presence of invasive device or feeding tube r Consider imaging in chronic or severe cases where
tenosynovitis, and clenched-fist injuries Recent hospitalization or dialysis
there is concern for potential osteomyelitis
EPIDEMIOLOGY Residence in long-term care facility
r Gram-negative organisms: (including immunocompromised patients).
Prevalence r Plain film radiographs if there is concern for foreign
Among hand infections, felons account for 15%, Found in immunosuppressed patients
bodies
with the index finger and thumb being the most Consider in diabetic patients with frequent finger
sticks for serum glucose monitoring Diagnostic Procedures/Other
commonly affected digits. r Anaerobes or oral flora including Eikenella Consider use of US to identify abscess formation.
RISK FACTORS corrodens (13):
r Local trauma including abrasions, cuts, and puncture DIFFERENTIAL DIAGNOSIS
Consider in patients with a history of nail biting or r Paronychia:
wounds that may be complicated by the presence of thumb sucking Infection of the lateral soft tissue (paronychium)
wood splinters or bits of glass.
r Local spread from a paronychia COMMONLY ASSOCIATED CONDITIONS surrounding a fingernail
r Paronychia Most common infection of the hand
r Multiple finger-stick blood tests
r Immunosuppressed conditions, including diabetes May occur with or without felon
r Hangnails r Herpetic whitlow:
r Conditions predisposing to infection: and HIV
Less common viral infection of the hand
Patients on long-term steroid treatment Resulting from autoinoculation of herpes simplex
IV drug abusers DIAGNOSIS virus (HSV)-1 or HSV-2 into broken skin
Patients with a depressed immune system Typically presents with prodrome of 12 days of
HISTORY burning pain prior to development of skin
GENERAL PREVENTION r Pertinent history should be obtained, including
r Avoidance of predisposing factors for paronychia: erythema with characteristic grouped vesicular
whether or not there is minor penetrating trauma lesions
Nail biting such as wood splinters, cuts, nail biting, etc.
Thumb sucking r Often, there is no history of trauma. Unlike felons, pulp space of distal finger is not
usually tense and swollen.
Excessive dish washing with bare hands r Presence of paronychia(e)
Excessive manicuring Drainage is contraindicated, as this may lead to
r Fingertip swelling and/or redness complications including systemic spread.
r Early recognition and appropriate care of paronychia
r Throbbing sensation with tightness and pain, even r Osteomyelitis:
r Early recognition and appropriate, sterile care for
with mild pressure over the affected fingertip Consider in chronic cases of felon
minor trauma r Flexor tenosynovitis:
PHYSICAL EXAM
PATHOPHYSIOLOGY r Erythema and swelling of the affected fingertip Consider 4 cardinal signs, as originally described
r The fingertip pulp is compartmentalized by 1520
r There is often marked tenderness to palpation of the by Kanavel (4):
fibrous vertically oriented septa that originate from Symmetric swelling of the entire digit
fingertip (pulp):
the underlying periosteum of the distal phalanx and Digit semiflexed at rest
Swelling does not extend proximal to the distal
extend to the skin. Severe tenderness over the entire flexor tendon
r The small compartments contain multiple entities, interphalangeal joint of the affected digit.
r Inspection for fluctuance is important in determining Pain with passive extension of digit
including sweat glands and fat. Consider STI (disseminated Neisseria gonorrhoeae
r The skin surface provides a portal of entry for the need for drainage.
r At times, the pressure within the swollen fingertip infection), especially if atraumatic (5,6).
infection within these compartments. Requires parenteral antibiotics
r Routes of bacterial inoculation of the fingertip pulp leads to tension and spontaneous drainage via a
visible sinus tract.
include local trauma or spread from local infection. r Inspect for foreign bodies or associated paronychiae.
r Infection may begin with cellulitis and then progress
to abscess formation within these small, relatively
noncompliant compartments, resulting in swelling
within a closed space, pain, and ischemia of the
affected fingertip.
r Infection at an early stage may resolve
spontaneously or with conservative management.
346
FELON
SURGERY/OTHER PROCEDURES REFERENCES

TREATMENT If fluctuance is present on exam, incision and drainage
1. Connolly B, Johnstone F, Gerlinger T, et al.
is appropriate. Various methods exist for incision and
INITIAL STABILIZATION/THERAPY drainage. Care should be taken to avoid the digital Methicillin-resistant Staphylococcus aureus in a
Conservative treatment (without need for incision and neurovascular structures, flexor tendon sheath, and finger felon. J Hand Surg Am. 2000;25(1):
drainage) of early felons is appropriate: the nail matrix (see references 7 and 8 for more 173175.
r Warm water or saline soaks to promote circulation details): 2. Glickel SZ. Hand infections in patients with
and facilitate healing r The preferred method is a single volar longitudinal acquired immunodeficiency syndrome. J Hand Surg.
r Elevation to minimize edema and pain incision, which is least likely to injure nearby 1998;13(5):770775.
r Oral antibiotics neurovascular structures. 3. Newfield RS, Vargas I, Huma Z. Eikenella corrodens
r Tetanus prophylaxis when indicated r An alternative method is the high lateral incision infections. Case report in two adolescent females
r Identification of foreign bodies (dorsal midaxial hockey stick incision). with IDDM. Diabetes Care. 1996;19(9):
r Perform gentle decompression and irrigation to 10111013.
r Identification of abscess formation
allow drainage of all septal compartments. 4. Kanavel AB. Infections of the Hand. 4th ed.
r Careful determination for more severe infections
r Following either technique, the wound may be Philadelphia, PA: Lea & Febiger; 1921.
(osteomyelitis or flexor tenosynovitis) 5. Krieger LE, Schnall SB, Holtom PD, et al. Acute
packed with sterile gauze, which should be removed
MEDICATION in 12 days. gonococcal flexor tenosynovitis. Orthopedics.
First Line r Allow the wound to close by secondary intention. 1997;20:64950.
r A 710 day course of oral antibiotics is typically r Care should be taken to avoid the flexor tendon 6. Schaefer RA, Enzenauer RJ, Pruitt A, et al. Acute
sufficient. sheath, as trauma may lead to iatrogenic flexor gonococcal flexor tenosynovitis in an adolescent
r Empiric antibiotic coverage for S. aureus and tenosynovitis. male with pharyngitis. A case report and literature
streptococcal organisms is indicated: review. Clin Orthop. 1992;281:212215.
DISPOSITION 7. Barkin JA, Miki RA, Mahmood Z, et al. Prevalence
1st-generation cephalosporin (cephalexin):
Pediatric: 25100 mg/kg/day PO divided q6h Admission Criteria of methicillin resistant Staphylococcus aureus in
Adult: 500 mg PO q6h Concern for more serious infection, including flexor upper extremity soft tissue infections at Jackson F
Antistaphylococcal penicillin (dicloxicillin): tenosynovitis Memorial Hospital, Miami-Dade County, Florida.
Pediatric: 25 mg/kg/day PO divided q6h Discharge Criteria Iowa Orthop J. 2009;29:6773.
Adult: 500 mg PO q6h r Adequate drainage achieved if fluctuance is present 8. Pallin DJ, Egan DJ, Pelletier AJ, et al. Increased US
Macrolides if penicillin allergic (erythromycin): r Identification and removal of any foreign bodies emergency department visits for skin and soft
Pediatric: 3050 mg/kg/day PO divided q6h r Adequate follow-up available, particularly if incision tissue infections, and changes in antibiotic choices,
Adult: 500 mg PO q6h and drainage is performed
during the emergence of community-associated
methicillin-resistant Staphylococcus aureus. Ann
Second Line Emerg Med. 2008;51(3):291298.
r Consider coverage for MRSA (1,5):
Trimethoprim/sulfamethoxazole: FOLLOW-UP
Dose based on trimethoprim component ADDITIONAL READING
Pediatric: 810 mg/kg/day PO divided q12h r Discharge instructions and medications:
Adult: 160 mg PO q12h r Clark DC. Common acute hand infections. Am Fam
Elevate and splint affected finger.
Clindamycin: A 710 day course of oral antibiotics is typically Physician. 2003;68(11):21672176.
Pediatric: 1030 mg/kg/day PO divided q68h r Jebson PJ. Infections of the fingertip. Paronychias
sufficient.
Adult: 300 mg PO q68h and felons. Hand Clin. 1998;4:547555.
If incision and drainage is performed, the patient
r Consider additional coverage for anaerobes and oral r Ong YS, et al. Hand infections. Plast Reconstr Surg.
should follow up with the primary care provider in
flora if there is history of potential exposure: 12 days for unpacking of the wound and 2009;124(4)225e233e.
Amoxicillin/clavulanic acid: re-evaluation. r Watson PA, Jebson PJ. The natural history of the
Dose based on amoxicillin component r Activity: neglected felon. Iowa Orthop J. 1996;16:164166.
Pediatric: 2545 mg/kg/day PO divided q12h
Protect the affected finger until the wound heals
Adult: 500 mg PO q8h
and pain resolves.
Clindamycin does offer some anaerobic coverage CODES
but does not provide coverage for E. corrodens. PROGNOSIS
r Consider adding gram-negative coverage if the If treated appropriately and without delay, prognosis is
excellent. ICD9
patient is immunosuppressed: 681.01 Felon
If infection appears mild, oral COMPLICATIONS
trimethoprim/sulfamethoxazole, If left untreated, patients may develop:
amoxicillin/clavulanic acid, or a 3rd-generation r Osteomyelitis of distal phalanx PEARLS AND PITFALLS
cephalosporin (eg, cefdinir) provide moderate r Flexor tenosynovitis
gram-negative coverage: r Expand antibiotic coverage to include oral flora
r Skin necrosis
Cefdinir: Pediatric, 14 mg/kg/day PO divided (history of nail biting) and/or MRSA when indicated
r Septic arthritis
q12h; adult, 300 mg PO q12h (see Etiology section).
If concern for more serious infection, consider r Felons may mimic herpetic whitlow, in which case
hospital admission with parenteral beta-lactamase incision and drainage may cause spread to other
inhibitor: sites.
Piperacillin/tazobactam (dose based on r More severe infections (osteomyelitis, flexor
piperacillin component): Pediatric (>6 mo), tenosynovitis) may be prevented with appropriate
300400 mg/kg/day IV divided q68h; adult, and early management.
3 g IV q6h
347
FEVER IN CHILDREN OLDER THAN 3 MONTHS

Vincent J. Wang
r Specific bacterial causes include: PHYSICAL EXAM

BASICS Otitis media/Sinusitis: Commonly Streptococcus r The ability to determine serious bacterial illness (SBI)
pneumoniae, nontypeable Haemophilus by physical exam is difficult and unreliable in the
DESCRIPTION influenzae, Moraxella catarrhalis younger infant but improves over this age spectrum,
r Fever represents one of the most common chief Pneumonia: S. pneumoniae, nontypeable H. especially in patients >612 mo of age.
complaints in the emergency department. influenzae, Staphylococcus aureus, Mycoplasma r Specific findings:
r As compared to infants <3 mo old, older infants species, etc. Head: Localized swelling or tenderness
and children more reliably manifest signs and UTI: Escherichia coli and other gram-negative Ear: Red or bulging tympanic membrane, swelling
symptoms specific to the cause of fever: organisms of ear, tenderness of earlobe
The older the child, the more reliable the physical Unsuspected bacteremia: S. pneumoniae: Face: Swelling/induration, erythema, sinus
exam. Routine vaccination with the heptavalent tenderness
Infants 36 mo of age still demonstrate limited pneumococcal conjugate vaccine has decreased Eyes: Conjunctivitis, proptosis
ability to localize infection. the incidence of pneumococcal disease (3,5). Nose: Rhinitis, rhinorrhea
Children with developmental delay/mental Introduction of a decavalent pneumococcal Mouth/Pharynx: Lesions, redness, swelling, uvular
retardation also exhibit limited ability to localize conjugate vaccine in Europe in 2009 and deviation, trismus, gum swelling associated with
infection. utilization of newer vaccines in the U.S., such as dental caries
r Concern for acute fever without an obvious source Prevnar 13, should decrease the incidence Neck: Swelling, nodes, tenderness, decreased
depends on the height of fever and the age of the further. range of motion, meningismus
patient: Neisseria meningitidis, S. aureus, Haemophilus Chest: Rales, wheezing, decreased aeration,
Temperature >38 C or 100.4 F in infants <3 mo species, Salmonella species, and other egophony, splinting, tachypnea, grunting
of age organisms are less commonly reported. Abdomen: Location of tenderness, guarding,
Temperature >39 C or 102.2 F in infants Cellulitis/Abscess: rebound, referred pain
336 mo of age: Skin: Group A beta-hemolytic streptococcus Extremities: Swelling, tenderness, erythema,
Unsuspected (occult) bacteremia has been (GAS) and S. aureus predominate. decreased range of motion, decreased weight
defined as bacteremia in otherwise Dental: Anaerobes such as Bacteroides, bearing
well-appearing but febrile infants and toddlers Fusobacterium, and Peptostreptococcus species Dermatologic: Swelling, induration, fluctuance,
336 mo of age predominate. erythema
r In children >36 mo of age, most causes of fever can Osteomyelitis/Septic arthritis: Same as for
cellulitis: DIAGNOSTIC TESTS & INTERPRETATION
be identified clinically without the need for extensive r Any infant with fever and ill appearance should have
evaluation. Consider Neisseria gonorrhoeae in adolescents.
r An exhaustive list and description of all causes of Bacterial pharyngitis: GAS: a sepsis evaluation performed, empiric antibiotics
More common in school-age children initiated, and admission ordered for further
fever is beyond the scope of this topic; therefore, an management.
Unlikely <3 yr of age
overview will be presented. r Testing for UTI should be based on clinical
Other causes include but are not limited to other
EPIDEMIOLOGY bacterial infections, appendicitis, Kawasaki presentation and risk factors (1).
r Urinary tract infection (UTI)/pyelonephritis occurs in r Routine testing for bacteremia is not necessary,
disease, rheumatologic disease, oncological
310% of patients with fever (1,2) depending on problems, medication, etc. especially in the well-appearing, fully vaccinated
the age and risk factors. There is increased incidence patient >6 mo of age (4,5):
in: Consideration for blood testing for bacteremia can
Girls DIAGNOSIS be made in infants 26 mo of age but may not be
Boys <12 mo necessary (6).
Uncircumcised boys <24 mo HISTORY r Other testing should be based on clinical evaluation.
r Symptoms of disease may be nonspecific in infants
Children with underlying urologic conditions (eg, r Consider any of the following lab tests as indicated.
spina bifida, posterior urethral valves) and include history of fever, poor feeding, fussiness,
r Bacteremia occurs in <1% (35). sleepiness, seizure, rash, cough, rhinorrhea, and Lab
difficulty breathing. r Urinalysis and urine culture, especially in infants and
r Meningitis occurs in <<1%:
r In toddlers and older infants: children with risk factors
Decreased incidence of pneumococcal disease is r Serum CBC and blood culture
General: Malaise, irritability, decreased oral intake,
associated with decreased incidence of meningitis r Serum C-reactive protein and procalcitonin may play
decreased urine output
(3).
Pain: Ear, mouth, throat, joint, chest, head, a role in the assessment of febrile infants:
RISK FACTORS arm/leg, face, abdomen Their role has not yet been clearly defined.
r Innate immunologic deficiencies existing from birth HEENT: Eye redness/discharge, photophobia, facial Studies reveal mixed results in this age group.
that improve over time or periorbital swelling, gum swelling, muffled r CSF: WBC, RBC, glucose, protein, Gram stain, and
r Lack of or incomplete vaccinations voice, oral lesions CSF culture
r Day care attendance Neck: Neck pain, mass, or swelling r Viral testing (for respiratory syncytial virus, influenza,
Respiratory: Characteristics of cough, rhinorrhea, herpes simplex virus [HSV], etc.) based on
ETIOLOGY dyspnea
r Most causes of fever are due to viral infections symptoms, if diagnosis improves management
Abdomen: Vomiting, diarrhea, location of pain r Rapid streptococcal antigen testing and throat
(upper respiratory tract infections, acute Genitourinary: Dysuria, discharge, lesions
gastroenteritis, croup, viral syndromes, etc.). culture in age appropriate patients (>3 yr of age)
Extremities: Swelling, limp, pain, decreased range based on signs and symptoms
of motion
Dermatologic: Rash
348
FEVER IN CHILDREN OLDER THAN 3 MONTHS
Imaging r Occult bacteremia: Empiric treatment: 4. Lee GM, Fleisher GR, Harper MB. Management of
r Chest radiograph for suspicion of pneumonia: Ceftriaxone 50 mg/kg IM/IV (single dose) febrile children in the age of the conjugate
Wheezing and fever in the infant or toddler may r Meningitis: 3rd-generation cephalosporin: pneumococcal vaccine: A cost-effectiveness
be a sign of viral bronchiolitis, for which a chest Ceftriaxone 50100 mg/kg IV daily analysis. Pediatrics. 2001;108:835844.
radiograph is not routinely necessary. Cefotaxime 100200 mg/kg/day IV divided q6h 5. Rudinsky SL, Carstairs KL, Reardon JM, et al.
r CT scan or US of the specific site as indicated for r Septic arthritis: IV antibiotics for suspected Serious bacterial infections in febrile infants in the
suspicion of deep tissue infection, such as abscess, etiologies and operative intervention (see Arthritis, post-pneumococcal conjugate vaccine era. Acad
appendicitis, etc. Septic topic) Emerg Med. 2009;16:585590.
r Osteomyelitis: IV antibiotics for suspected etiologies 6. Hsiao AL, Chen L, Baker MD. Incidence and
r Transurethral catheterization or suprapubic bladder (see Osteomyelitis topic) predictors of serious bacterial infections among 57-
aspiration for urine testing r Bacterial gastroenteritis: Routine antibiotic to 180-day-old Infants. Pediatrics. 2006;117(5):
r Arthrocentesis for septic arthritis administration is not warranted until the stool 16951701.
r Suprapubic aspiration and arthrocentesis may be culture results are available. 7. Fleisher GR, Rosenberg N, Vinci R, et al.
guided by US. Intramuscular versus oral antibiotic therapy for the
SURGERY/OTHER PROCEDURES prevention of meningitis and other bacterial
r Operative irrigation for septic arthritis
DIFFERENTIAL DIAGNOSIS sequelae in young febrile children at risk for occult
r Incision and drainage for abscesses:
See Etiology section. bacteremia. J Pediatr. 1994;124:504512.
Abscess drainage may be guided by US
TREATMENT DISPOSITION
Admission Criteria
ADDITIONAL READING
r Ill appearance r Wang VJ. Fever and serious bacterial illness. In
r If ill appearing, address ABCs per Pediatric r Unreliable follow-up Tintinalli JE, Stapczynski J, Ma OJ, et al., eds.
Advanced Life Support algorithm. r Bacterial meningitis, septic arthritis, osteomyelitis, Tintinallis Emergency Medicine: Comprehensive
r Treat infection as diagnosed. pyelonephritis, rapidly spreading cellulitis Study Guide. 7th ed. New York, NY: McGraw-Hill;
r Most causes of fever are viral and require supportive r Pneumonia with hypoxemia or respiratory distress 2010. F
care alone. Discharge Criteria See Also (Topic, Algorithm, Electronic
r In well-appearing, febrile patients 336 mo of age r Well appearing Media Element)
without a focal source, if a CBC is obtained and the r Reliable follow-up r Arthritis, Septic
WBC >15,000/mm3 : r Ability to tolerate PO medications r Bacteremia
Consider treatment for occult bacteremia (7). r Fever in Infants 03 Months of Age
Treatment may also be limited to higher r Fever of Unknown Origin
thresholds of WBC count. FOLLOW-UP r Meningitis
MEDICATION r Osteomyelitis
First Line r 24-hr follow-up with the primary care provider (with r Otitis Media
r Acetaminophen or ibuprofen PRN r Pneumonia
access to culture results)
r The diagnosis guides antibiotic selection. r Discharge instructions and medications: r Urinary Tract Infection
r UTI: Acetaminophen or ibuprofen PRN
Cefixime 8 mg/kg/day PO daily or divided b.i.d. for Return for increased irritability, poor feeding,
10 days lethargy, decreased urine output CODES
Cephalexin 3060 mg/kg/day PO divided t.i.d. for
710 days PROGNOSIS
Depends on the results of the evaluation (eg, presence ICD9
Trimethoprim/sulfamethoxazole (dose on
of meningitis, bacteremia, pyelonephritis, etc.) 780.60 Fever, unspecified
trimethoprim component) 610 mg/kg/day PO
divided b.i.d. for 10 days COMPLICATIONS
r Pneumonia: r Complications depend on the site of infection.
r Death, urosepsis, seizures, hearing loss,
PEARLS AND PITFALLS
Amoxicillin (high dose) 8090 mg/kg/day PO
divided b.i.d. or t.i.d. for 10 days r Pearls:
developmental delay/mental retardation, abscess,
Amoxicillin/clavulanic acid (high dose amoxicillin limp, amputation, renal insufficiency/failure Recent vaccination improvements have
component) 8090 mg/kg PO divided b.i.d. or substantially decreased the incidence of SBI in this
t.i.d. for 10 days population. Check the vaccination status.
Azithromycin 10 mg/kg PO daily for 3 days REFERENCES Herd immunity does help, even for the
Cefuroxime 2030 mg/kg/day divided b.i.d. for unimmunized.
10 days 1. American Academy of Pediatrics. Practice r Pitfalls:
r Cellulitis or abscess: parameter: The diagnosis, treatment, and Not recognizing patients at risk for HSV infection
evaluation of the initial urinary tract infection in Performing an inadequate or incomplete
Cephalexin 60100 mg/kg/day PO divided q.i.d.
febrile infants and young children. Committee on evaluation
for 10 days
Quality Improvement, Subcommittee on Urinary Not applying vaccination status to your
Amoxicillin/clavulanic acid (see above)
r Cellulitis, abscess, MRSA: Tract Infection. Pediatrics. 1999;103(4):843852. decision-making process
2. Shaw KN, Gorelick M, McGowan KL, et al.
Clindamycin 30 mg/kg/day PO divided t.i.d. for
Prevalence of urinary tract infection in febrile young
10 days
children in the emergency department. Pediatrics.
Trimethoprim/sulfamethoxazole (see above) and
1998;102:e16.
cephalexin (see dose for cellulitis)
r Pharyngitis: 3. Invasive pneumococcal disease in children 5 years
after conjugate vaccine introductioneight states,
Penicillin VK 2550 mg/kg/day divided t.i.d. to
19982005. MMWR. 2008;57(6):144148.
q.i.d. max dose 3 g/day
Amoxicillin 4050 mg/kg/day divided b.i.d. or
t.i.d. for 10 days
349
FEVER IN INFANTS 03 MONTHS OF AGE

Vincent J. Wang
PHYSICAL EXAM r Other strategies:

BASICS r The ability to determine SBI by physical exam is Boston criteria (4):
difficult and unreliable for this age group. Temperature 38 C
DESCRIPTION r The physical exam may be normal. 2889 days of age
r Fever has traditionally been defined as a temperature r Signs may be nonspecific and may include: WBC 20,000/mm3
of >38 C or 100.4 F in an infant <23 mo of age. Fever Urinalysis negative
r Infants in this age group display limited ability to CSF WBC 10/mm3
Lethargy
demonstrate signs of infection (1). Irritability Applying Boston criteria to infants 12 mo of age
r Serious bacterial illness (SBI) is defined as Bulging fontanel Rochester criteria (5):
meningitis, sepsis, bacteremia, urinary tract infection Tachypnea, grunting, retractions Temperature 38 C
(UTI), pyelonephritis, pneumonia, osteomyelitis, Joint swelling 2 mo of age
acute gastroenteritis, cellulitis, abscess, and septic Abdominal distension No past medical history
arthritis. Rash WBC 5,000/mm3 or 15,000/mm3
r This topic focuses on occult fever (without obvious r Rectal temperatures are the gold standard and are Urinalysis negative
signs of bacterial infection, such as cellulitis, neck No CSF testing is included in these criteria.
strongly recommended over other methods. Axillary
abscess, etc). and tympanic membrane temperatures are not Imaging
r Viral infections, such as herpes simplex virus (HSV), reliable in this age group. r Obtain a chest radiograph for findings such as rales,
respiratory syncytial virus (RSV), or enterovirus, may tachypnea, grunting, or wheezing (6).
DIAGNOSTIC TESTS & INTERPRETATION r Wheezing and fever may be a sign of viral
also cause life-threatening illness. r Any infant with fever and ill appearance should have
EPIDEMIOLOGY a sepsis evaluation performed, empiric antibiotics bronchiolitis, for which a chest radiograph may not
initiated, and admission ordered for further be necessary.
Incidence r CT of the head is not routinely indicated in the
r UTI/Pyelonephritis occurs in 310%. management.
r Bacteremia occurs in 23%. r Consider the following lab tests. evaluation of neonatal meningitis.
r Meningitis occurs in 1%. Lab Diagnostic Procedures/Other
r Infants identified as high risk or ill appearing have a r Urinalysis and urine culture r Transurethral catheterization or suprapubic bladder
1321% incidence of SBI. r Serum CBC and blood culture aspiration for urine testing
r Rarely, arthrocentesis for septic arthritis.
r CSF WBC, RBC, glucose, protein, Gram stain, and
RISK FACTORS r Suprapubic aspiration and arthrocentesis may be
r Infants <3 mo have innate immunologic CSF culture
r Serum C-reactive protein (CRP) and procalcitonin guided by US.
deficiencies that improve over time.
r History of maternal fever during delivery may play a role in the assessment of these febrile DIFFERENTIAL DIAGNOSIS
r History of unexplained jaundice or admission for patients, although their role has not yet been clearly r Most causes of fever are due to viral infections, such
sepsis defined: as RSV, adenovirus, influenza, herpesvirus,
CRP is currently more readily available than coxsackievirus, or enteroviruses.
ETIOLOGY procalcitonin, but procalcitonin appears to be r Viral testing in combination with utilization of the
r Most causes of fever are due to viral infections. more promising (2). Boston, Rochester, or Philadelphia criteria may be
r SBI is most commonly due to Escherichia coli, group r Consider viral testing (for RSV, influenza, HSV, etc.) helpful to distinguish viral infections from bacterial
B streptococcus, and Listeria monocytogenes. based on season and symptoms, especially if a infections (7).
r Neisseria meningitidis, Streptococcus pneumoniae, positive test changes patient management or the
Staphylococcus aureus, Salmonella species, and amount of other testing done.
Haemophilus influenzae are less commonly reported. Lab: Established Protocols
TREATMENT
r Follow established protocols (if met, may discharge
DIAGNOSIS the patient) r If ill appearing, address ABCs per Pediatric
r Recommended: Philadelphia protocol (3):
Advanced Life Support algorithm.
HISTORY Temperature 38.2 C r If focal infection is identified, treat specifically (eg,
Symptoms of disease may be nonspecific and 2956 days of age meningitis, septic arthritis, UTI). See related topics
include: WBC 15,000/mm3 for these treatments.
r History of fever Urinalysis negative
r Poor feeding CSF WBC 8/mm3 MEDICATION
r Vomiting/diarrhea Serum band to neutrophil ratio 0.2 First Line
r Empiric treatment for term infants >3 kg
r Fussiness
r Age <1 mo: Combination therapy of:
r Sleepiness
r Seizure Ampicillin 200400 mg/kg/day IM/IV divided
q46h in combination WITH
r Rash
Cefotaxime 50 mg/kg IM/IV q68h OR
r Cough, rhinorrhea Gentamicin 2.5 mg/kg IV q8h
r Difficulty breathing Consider ceftriaxone (50100 mg/kg IM/IV
divided q1224h) instead of cefotaxime, but
AVOID use in infants with:
Potential or actual hyperbilirubinemia
Liver disease
Patients receiving calcium IV
350
FEVER IN INFANTS 03 MONTHS OF AGE
r Age >1 mo, admitted (failed established protocols): PROGNOSIS ADDITIONAL READING
Ceftriaxone or cefotaxime (consider adding Depends on the results of the evaluation (eg, presence
ampicillin) of meningitis, bacteremia, pyelonephritis, etc.) r American College of Emergency Physicians Clinical
r Age >1 mo, discharged: Policies Subcommittee on Pediatric Fever. Clinical
COMPLICATIONS policy for children younger than three years
No antibiotics (Philadelphia or Rochester criteria) r Complications depend on the site of infection
Ceftriaxone for low-risk patients (Boston protocol) r Death presenting to the emergency department with fever.
Ann Emerg Med. 2003;42(4):530545.
Second Line r Urosepsis r Bachur RG, Harper MB. Predictive model for serious
r Vancomycin (1015 mg/kg IV q68h) for suspected r Seizures
bacterial infections among infants younger than 3
S. aureus or S. pneumoniae meningitis r Hearing loss months of age. Pediatrics. 2001;108(2):311.
r Acyclovir (20 mg/kg/day IV q8h) for suspected HSV
r Developmental delay/mental retardation r Wang VJ. Fever and serious bacterial illness. In
infection r Abscess
r Dexamethasone (0.6 mg/kg/day IV divided q6h) for Tintinalli JE, Stapczynski J, Ma OJ, et al., eds.
r Limp Tintinallis Emergency Medicine: Comprehensive
presumed bacterial meningitis for infants >6 wk old r Amputation Study Guide. 7th ed. New York, NY: McGraw-Hill;
DISPOSITION r Renal insufficiency/failure 2010.
Admission Criteria See Also (Topic, Algorithm, Electronic
r Neonates <1 mo of age
Media Element)
r Ill appearance REFERENCES r Bacteremia
r Unreliable follow-up r Fever in Children Older than 3 Months
r Serum WBC >15,000/mm3 in Philadelphia protocol 1. Baker MD, Avner JR, Bell LM. Failure of infant
observation scales in detecting serious illness in r Meningitis
(may follow Rochester or Boston criteria instead) febrile 4- to 8-week-old infants. Pediatrics. r Urinary Tract Infection
(35) 1990;85(6):1040.
r CSF WBC >10/mm3
2. Maniaci V, Dauber A, Weiss S, et al. Procalcitonin
r CSF Gram stain showing bacteria
r Evidence of pyelonephritis
in young febrile infants for the detection of serious CODES F
bacterial infections. Pediatrics. 2008;122(4):701.
r Pneumonia 3. Baker MD, Bell LM, Avner JR. Outpatient ICD9
r Hypoxemia or respiratory distress management without antibiotics of fever in selected r 778.4 Other disturbances of temperature regulation
Discharge Criteria patients. N Engl J Med. 1993;329(20):1437. of newborn
r Well appearing 4. Baskin MN, ORourke EJ, Fleisher GR. Outpatient r 780.60 Fever, unspecified
r Reliable follow-up treatment of febrile infants 28 to 89 days of age
r Serum WBC 15,000/mm3 in Philadelphia protocol with intramuscular administration of ceftriaxone.
(may follow Rochester or Boston criteria instead)
J Pediatr. 1992;120:22. PEARLS AND PITFALLS
5. Jaskiewicz JA, McCarthy CA, Richardson AC, et al.
(35) r Pearls:
r Normal CSF indices Febrile infants at low risk for serious bacterial
infection an appraisal of the Rochester criteria Recent vaccination improvements (H. influenzae
r Urinalysis not suggestive of UTI type b and pneumococcal conjugate vaccines)
and implications for management. Pediatrics.
1994;94(3):390. have not substantially decreased the incidence of
6. Bramson RT, Meyer TL, Silbiger ML. The futility of SBI in this population.
FOLLOW-UP r Pitfalls:
the chest radiograph in the febrile infant without
FOLLOW-UP RECOMMENDATIONS respiratory symptoms. Pediatrics. 1993;92(4):534. Applying the fever criteria incorrectly
r 24-hr follow-up with the primary care provider (with 7. Byington CL, Enriquez FR, Hoff C, et al. Serious (Philadelphia, Boston, and Rochester criteria) by
access to culture results) bacterial infections in febrile infants 1 to 90 days selectively using and mixing the criteria
r If ceftriaxone was given, a repeat dose of old with and without viral infections. Pediatrics. Not recognizing patients at risk for HSV infection
ceftriaxone is optional. 2004;113(6):1662. Performing an inadequate or incomplete
r Discharge instructions and medications: evaluation
Not applying the birth and postpartum history
Acetaminophen 1015 mg/kg PO/PR q46h
Return for increased irritability, poor feeding,
lethargy, decreased urine output
351
FEVER OF UNKNOWN ORIGIN

Worapant Kriengsoontornkij
Vincent J. Wang
Relapsing fevers with periods during which PHYSICAL EXAM

BASICS patients are afebrile for 1 day between febrile r Absence of sweating in the presence of elevated or
episodes: Malaria, rat-bite fever, Borrelia changing body temperature:
DESCRIPTION infection, and lymphoma Consider dehydration, anhidrotic ectodermal
r The definition of fever of unknown origin (FUO) in Recurrent episodes of fever over periods of dysplasia, familial dysautonomia, or exposure to
children is commonly defined as: >6 mo duration: Metabolic defects, CNS atropine
Fever 38.3 C (101 F) dysregulation of temperature control, periodic r Purulent discharge in the nose or posterior pharynx,
Fever of at least 8 days in duration fever syndromes, immunodeficiency erythematous and boggy nasal mucosa, tenderness
No apparent diagnosis after the initial outpatient Temperatures 42 C (107.6 F) are most often on percussion over sinuses: Sinusitis
or hospital evaluation that has included: noninfectious in origin. r Ear pain, hearing loss, ear discharge, vertigo,
A thorough history and physical exam AND r Exposure to animals including household pets, bulging and redness of tympanic membrane (TM),
Initial lab assessment domestic animals in the community, and wild air-fluid levels behind the TM: Otitis media (OM)
r FUO is usually an atypical presentation of a common animals can cause zoonotic infections: r A cardiac murmur, often new onset: IE
childhood illness. Unpasteurized dairy products, contact with r Signs of respiratory distress (tachypnea, hypoxemia,
EPIDEMIOLOGY animals: Brucellosis retractions, nasal flaring, grunting) are more specific
Consumption of game meat, raw meat, or raw than fever or cough for pneumonia.
Incidence
r FUO accounts 1.5% of pediatric emergency shellfish: Brucellosis, toxoplasmosis, tularemia, r Skin:
hepatitis
department presentations (1). Petechiae in IE, bacteremia, viral and rickettsial
r In the general population, prevalence varies by Tick bites: Rocky Mountain spotted fever (RMSF),
infections
ehrlichiosis, tularemia, tickborne relapsing fever,
criteria for diagnosis of FUO, institution, and time of Rash begins on the ankles and wrists and spreads
or Lyme disease. North American mosquitoes and
studies. The prevalence is around 0.044% if the to the palms, soles, and centrally: RMSF
some ticks carry a variety of arboviruses.
duration of fever is >3 wk (2). A primary cutaneous papule or pustule develops
Tick bite, found in central Texas and eastern
approximately 310 days after an animal contact
RISK FACTORS Oklahoma, eastward throughout the southeastern
r Recent travel at a site of a scratch or bite: Cat scratch disease
U.S., and north along the Atlantic coastal plain
Eschar: Tularemia, scrub typhus
r Immunodeficiency (primary and secondary) into New England. Peak is MayAugust:
Macular salmon-pink rash: JRA
r Parenteral drug abuse Ehrlichiosis.
Malar erythema: Systemic lupus erythematosus
r Immigrant status Contact with urine of infected animals (eg, rats) in
(SLE)
water or soil: Leptospirosis
Palpable purpuric lesions: Vasculitis (eg,
PATHOPHYSIOLOGY Cat or dog bite: Pasteurella
polyarteritis nodosa)
r Resetting of the thermoregulatory center in the Contaminated food (undercooked meat, poultry or
Urticarial and/or serpiginous macular rash and
hypothalamus by the action of cytokines released in eggs): Salmonella
band of erythema at the lateral aspects of the
response to bacterial or viral pathogens, circulating Skinning, dressing, or eating infected animals
hands and feet: Serum sickness
immune complexes and pyrogens from tumor cells (squirrels, rabbits, hares, and muskrats): Tularemia
r Drug fever: By hypersensitivity reaction Erythema nodosum: Infection, malignancy, JRA,
Tick bite (rabbits, deer): Tularemia
r Travelers or immigrants from malaria-endemic areas SLE, inflammatory bowel disease (IBD)
r CNS: Direct damage to thermoregulatory centers (3)
A seborrheic rash can indicate histiocytosis.
r Inhaling aerosolized dust contaminated by
ETIOLOGY Sparse hair, particularly of the eyebrows and
r The 3 most common etiologic categories of FUO in parturient cats or by consuming unpasteurized eyelashes, and hypohidrosis may suggest
contaminated milk products: Q fever anhidrotic ectodermal dysplasia.
children are infectious diseases, connective tissue r Travel to or coming from endemic areas: r Eyes:
diseases, and neoplasms.
r The most common infections are Epstein-Barr virus North Carolina, Tennessee, Missouri, Oklahoma, Red weeping eyes: Connective tissue disease,
Arkansas, Virginia, Maryland, South Carolina, and especially polyarteritis nodosa
(EBV) infection, osteomyelitis, and urinary tract
Pennsylvania: RMSF Palpebral conjunctivitis: Coxsackievirus, measles,
infection (UTI).
Japan, Southeast Asia, west and southwest TB, EBV, cat scratch disease, lymphogranuloma
Pacific: Scrub typhus venereum
DIAGNOSIS r Pica (ingesting infected cat feces): Toxocara Bulbar conjunctivitis: Leptospirosis; if sparing the
infection, toxoplasmosis limbus, Kawasaki disease (KD)
HISTORY r Medication: Anticholinergic agents, dinitrophenol Petechial conjunctival hemorrhages: IE
r Fever:
and uncouplers of oxidative phosphorylation Uveitis: Sarcoidosis, JRA, SLE, KD, Behcet disease,
Intermittent fevers with a high spike and rapid r Genetic background: vasculitis
defervescence: Pyogenic infection, TB, lymphoma, Jewish descent: Familial dysautonomia Chorioretinitis: Cytomegalovirus (CMV),
and juvenile rheumatoid arthritis (JRA) Autosomal recessive transmission pattern in toxoplasmosis, syphilis
Remittent fevers with fluctuating peaks and a family: Hyperimmunoglobulin D syndrome, familial Proptosis: Orbital tumor, thyrotoxicosis, metastasis
baseline that does not return to normal: Mediterranean fever (neuroblastoma), orbital infection, Wegener
Intermittent fever with antipyretic agent r Continued, unexplained weight loss, excessive granulomatosis, pseudotumor cerebri
administration, viral infections, infective Lack of tears and absent corneal reflex: Familial
bruising or bleeding, limping: Neoplasm
endocarditis (IE), sarcoidosis, lymphoma, and r Past medical history: Lymphoma, rheumatic fever, dysautonomia
atrial myxoma Failure of pupillary constriction due to absence of
Sustained fevers persisting with little or no HIV infection
the sphincter constrictor muscle of the eye:
fluctuation: Typhoid fever, typhus, brucellosis, and Hypothalamic dysfunction
many other infections
352
FEVER OF UNKNOWN ORIGIN
r Skin and nails: Secondary Lab Tests Issues for Referral

Nail fold capillary abnormalities (dropout of r BUN, creatinine, and hepatic enzymes are obtained r Refer to infectious diseases doctor if cause of FUO is
capillary end loops, dilated, tortuous capillaries): to evaluate renal and/or hepatic involvement: undetermined.
Connective tissue diseases such as juvenile Elevated hepatic enzymes may be a clue to a viral r Connective tissue diseases, malignancy, and
dermatomyositis and systemic scleroderma infection without distinctive features (eg, EBV, miscellaneous diseases (eg, IBD, diabetes insipidus,
Petechiae, subcutaneous nodules, splinter CMV), or brucellosis. and periodic fever syndrome) should be referred to a
hemorrhages, clubbing: Vasculitis, IE r Serum electrolytes: Diabetes insipidus subspecialist.
r Oral cavity: r Lactate dehydrogenase (LDH): Cancer
Recurrent oral candidiasis: Various disorders of r HIV antibody
immune system r CSF testing should be performed in children with FOLLOW-UP
Smooth tongue with absence of fungiform suspected meningitis. FOLLOW-UP RECOMMENDATIONS
papillae: Familial dysautonomia r Serologic tests may aid in the diagnosis of EBV, No specific discharge instructions or activity limitations
Hyperemia of the pharynx: EBV, CMV, are warranted.
CMV, toxoplasmosis, salmonellosis, Lyme disease,
toxoplasmosis, salmonellosis, tularemia, KD,
tularemia, brucellosis, leptospirosis, cat scratch
leptospirosis PROGNOSIS
r Rectal and genitourinary exam: disease, rickettsial disease, JRA, and SLE. r Children with FUO have a better prognosis than do
r Immunoglobulin level: Congenital and acquired
Lymphadenopathy or tenderness can indicate adults.
immunodeficiency states (eg, HIV, Bruton r The outcome in a child is dependent on the primary
deep pelvic abscess, iliac adenitis, or pelvic
agammaglobulinemia)
osteomyelitis. disease process.
r Musculoskeletal: Imaging r In many cases, no diagnosis is established and fever
r CXR (recommended for all with FUO)
Point tenderness over a bone may suggest abates spontaneously.
r Consider sinus x-rays when upper respiratory r In up to 25% of FUO in which fever persists, the
osteomyelitis or neoplastic bone disease.
Tenderness over the trapezius muscle: infection symptoms are persistent >10 days, severe, cause is unclear after thorough evaluation.
Subdiaphragmatic abscess and worsening.
r Consider temporal bone CT scan for suspected COMPLICATIONS
Hyperactive deep tendon reflexes: Thyrotoxicosis
mastoiditis. This should be accompanied by an OM. Complications depend on the cause of FUO. F
DIAGNOSTIC TESTS & INTERPRETATION r Consider the following tests selectively:
Lab Echo: IE REFERENCES
Initial Lab Tests US: Intra-abdominal abscesses of the liver,
r CBC and blood smear (recommended for all children
subphrenic space, pelvis, or spleen 1. Ingarfield SL, Celenza A, Jacobs IG, et al. Outcomes
with FUO): CT or MRI: Detection of neoplasms or abscesses in patients with an emergency department
Anemia: Malaria, IE, IBD, SLE, TB, leukemia, Radionuclide scans: Tumors, abscesses, diagnosis of fever of unknown origin. Emerg Med
lymphoma osteomyelitis, localized pyogenic processes Australas. 2007;19(2):105112.
Thrombocytosis: KD MRI has the highest sensitivity and specificity for 2. Pasic S, Minic A, Djuric P, et al. Fever of unknown
Atypical lymphocytes: Viral infection detecting osteomyelitis in children. origin 185 pediatric patients: A single center
Bizarre or immature forms of lymphocytes: experience. Acta Paediatr. 2006;95(4):463466.
Leukemia Diagnostic Procedures/Other
r Tuberculin skin testing is recommended for all 3. Badjatia N. Hyperthermia and fever control in brain
Absolute neutrophil count >10,000/microL or injury. Crit Care Med. 2009;37(7 Suppl):
nonsegmented neutrophils >500/microL suggests patients with FUO without a recent skin test.
r Consider referral for laparoscopy, endoscopy, S250S257.
a higher likelihood of having a bacterial infection.
r ESR and C-reactive protein (CRP) (recommended for bronchoscopy, bone marrow exam, or biopsy (lymph
all children with FUO): General indicators of node, muscle or skin). ADDITIONAL READING
inflammation: DIFFERENTIAL DIAGNOSIS r Barkin RM, Zukin DD. Pediatric fever. In Marx J,
An elevated ESR or CRP excludes factitious fever. See Etiology, History, and Physical Exam sections.
A normal ESR or CRP: Noninflammatory conditions Adams J, Walls R, et al., eds. Rosens Emergency
(eg, dysautonomia, ectodermal dysplasia, thalamic Medicine: Concepts and Clinical Practice. 7th ed. St.
dysfunction, diabetes insipidus, drug fever) TREATMENT Louis, MO: Mosby; 2009.
The artificially lowered ESR: Consumption of
fibrinogen (such as disseminated intravascular INITIAL STABILIZATION/THERAPY
coagulopathy) r Support ABCs. CODES
An elevation occurs in noninflammatory disorders: r Initial treatment depends on the cause of FUO.
Hypergammaglobulinemia ICD9
ESR >30 mm/hr indicates inflammation: MEDICATION
See the respective topics for treatment of each of 780.60 Fever, unspecified
Infectious, autoimmune, or malignant diseases
ESR >100 mm/hr suggests TB, KD, malignancy, or these causes.
autoimmune disease. DISPOSITION PEARLS AND PITFALLS
r Urinalysis and urine culture to evaluate for UTI
Admission Criteria r The cause of FUO is more often a common disease
(recommended for all children with FUO) If the patient is ill appearing or outpatient
r Blood culture (recommended for all children with presenting in atypical fashion rather than a rare
investigation fails to reveal a cause of the fever, disease presenting in typical fashion.
FUO): Several sets should be obtained over 24 hr in inpatient admission may be necessary. r Careful and repeated history, physical exam, and
patients in whom IE, osteomyelitis, or deep-seated Discharge Criteria review and interpretation of lab data usually help to
abscesses are being considered. r Normal or baseline vital signs
determine the cause of FUO.
r Stable medical condition
r Follow-up ensured
353
FLAIL CHEST
Cathy E. Shin
ETIOLOGY Imaging
BASICS r Blunt chest wall trauma: r The AP CXR will identify most significant chest wall
Motor vehicle crashes (high speed) injuries but will not identify all rib fractures in the
DESCRIPTION Falls pediatric population. Lateral or anterior rib fractures
r A flail chest occurs when a segment (at least 2 r Nonaccidental trauma (5) will often be missed on the initial plain film.
fractures per rib) of the chest wall is separated from r Chest films may also identify:
the rest of the thoracic cavity: COMMONLY ASSOCIATED CONDITIONS
r Pulmonary contusion Subcutaneous emphysema
Respiratory distress is identified with paradoxical Broken ribs or other broken bones
r Rib fractures
movement of a segment of the chest wall (moving Hemothorax
inward on inspiration and moving outward on r Pneumothorax
Pneumothorax
expiration). r Hemothorax
Pulmonary contusion
r Compared to adults, flail chest is far less common in Diaphragmatic rupture
infants and children. r There is no role for chest CT scans to diagnose flail
r Due to the nature of the injury, the pediatric DIAGNOSIS
chest, but CT may be helpful to identify associated
population is at higher risk for associated pulmonary HISTORY injuries such as pulmonary contusion.
injuries (1). r High-speed motor vehicular crashes involving blunt
r Generally, the presence of a flail chest is associated DIFFERENTIAL DIAGNOSIS
chest or upper abdominal trauma
r Falls involving blunt chest or upper abdominal Other clinical diagnoses with similar presentations
with a mortality rate ranging from 1035%.
include:
EPIDEMIOLOGY trauma r Rib fractures: Clinically similar without paradoxical
r Conscious patients will complain of:
Prevalence chest wall movement
Flail chest complicates 513% of patients with Pain on palpation of the chest wall or on r Pulmonary contusion: Respiratory distress without
blunt chest trauma in the general population (2,3). inspiration
Shortness of breath flail chest or rib fractures
r Chest wall muscular strain: Chest wall splinting may
RISK FACTORS Difficulty with inspiration
r High-speed motor vehicle collisions Chest pain mimic flail chest
r Blunt trauma
PHYSICAL EXAM
PATHOPHYSIOLOGY r Respiratory distress: TREATMENT
r A transfer of significant kinetic energy in blunt Tachypnea
trauma to the rib cage or a crushing rollover injury is Intercostal and substernal retractions PRE HOSPITAL
the most frequent cause of flail chest. Air hunger
r The paradoxical movement of the rib cage will Nasal flaring circulation.
r All patients should initially be placed on 100%
adversely affect respiratory function via diminished Grunting
ventilation, pulmonary contusions, and atelectasis Chest wall splinting oxygen via a nonrebreathing face mask.
r Bruising, grazes, abrasions or seat belt signs are r IV analgesia as noted below
from hypoventilation.
r The negative intrathoracic pressure generated under visible on inspection. INITIAL STABILIZATION/THERAPY
the flail segment during inspiration results in the flail r Palpation may reveal the crepitus associated with r Management of chest wall injury is directed toward
segment being pulled inward. Similarly, the positive broken ribs. protecting the underlying lung and allowing
pressures with expiration cause the same segment r Decreased pulse oximetry readings adequate oxygenation, ventilation, and pulmonary
to push outward, thus creating a paradoxical r KEY EXAM: Paradoxical movement of a segment of toilet. This strategy is aimed at preventing the
appearance. the chest wallmoving inward on inspiration and development of pneumonia, which is the most
r Respiratory distress can be caused by the dynamics moving outward on expiration: common complication of chest wall injury.
of the chest wall or the underlying pulmonary injury. This is often better appreciated by palpation than r Pain management, judicious fluid resuscitation, and
r Derangement of chest wall mechanics results in by inspection. excellent pulmonary toilet are essential to stabilizing
reduced tidal volume, increased pulmonary the patient.
DIAGNOSTIC TESTS & INTERPRETATION r Isolated flail chest may be successfully managed
secretions, atelectasis, and cough, which in turn
increase the risk of pneumonia. Lab
with aggressive pulmonary toilet including face
r In pediatric patients, the ribs are more pliable and Initial Lab Tests
r No lab testing is necessary for the diagnosis of flail mask oxygen, CPAP, and chest physiotherapy.
less likely to fracture, although there may still be r Adequate analgesia is of paramount importance in
chest:
significant contusion of chest wall structures. patient recovery and may contribute to the return of
r In children, who have a more compliant chest wall, Consider obtaining a baseline arterial blood gas.
r The following may be helpful as part of the trauma normal respiratory mechanics.
flail chest is observed with lower frequency than r Early intubation and mechanical ventilation is
evaluation:
injury to the underlying structures, including the important in patients with refractory respiratory
CBC
lungs, heart, and mediastinal structures (4). failure or other serious traumatic injuries.
PT, PTT, INR
MEDICATION
First Line
r Analgesia is the mainstay of therapy for rib fractures.
r IV opioids:
then q2h PRN
Fentanyl 12 g/kg IV q2h PRN:
PRN
354
FLAIL CHEST
Second Line In several studies, the surgically repaired group 4. Smyth BT. Chest trauma in children. J Pediatr Surg.
r Once admitted, patient-controlled administration demonstrated: 1979;14(1):4147.
(PCA) is the best method for age-appropriate and Significantly fewer days on the ventilator and in 5. Gipson CL, Tobias JD. Flail chest in a neonate
cooperative patients. the ICU resulting from nonaccidental trauma. South Med J.
r An alternative is a continuous epidural infusion of a Lower incidence of pneumonia 2006;99(5):536538.
local anesthetic agent (with or without an opioid Better pulmonary function at 1 mo 6. Nirula R, Diaz JJJr., Trunkey DD, et al. Rib fracture
analgesic). Higher return to work percentage at 6 mo than repair: Indications, technical issues, and future
This provides complete analgesia allowing normal the nonoperative group (7,8) directions. World J Surg. 2009;33(1):1422.
inspiration and coughing without the risk of r In summary, most pediatric patients with flail chest
7. Voggenreiter G, Neudeck F, Aufmkolk M, et al.
respiratory depression. These can be placed in the may be treated successfully with intubation and pain Operative chest wall stabilization in flail
thoracic or high-lumbar positions. management alone, but a small group may benefit chestoutcomes of patients with or without
r Regional anesthesia by rib block may provide from operative correction of the flail segment. pulmonary contusion. J Am Coll Surg. 1998;
tremendous pain relief. DISPOSITION 187(2):130138.
COMPLEMENTARY & ALTERNATIVE Admission Criteria 8. Ahmed Z, Mohyuddin Z. Management of flail chest
THERAPIES Critical care admission criteria: injury: Internal fixation versus endotracheal
r Simple chest wall injury rarely requires intubation r Inpatient management is necessary for patients with intubation and ventilation. J Thorac Cardiovasc
and mechanical ventilation. Surg. 1995;110(6):16761680.
flail chest.
r Where ventilation is necessary, it is usually for r Poor respiratory effort requires early intubation and
hypoxemia due to underlying pulmonary contusions. mechanical ventilation. ADDITIONAL READING
Positive pressure ventilation may be required for
severe chest wall instability resulting in inadequate r Mayberry JC, Ham LB, Schipper PH, et al. Surveyed
spontaneous ventilation.
r Prolonged mechanical ventilation is associated with
FOLLOW-UP opinion of American trauma, orthopedic, and
thoracic surgeons on rib and sternal fracture repair.
the development of pneumonia and a poor
outcome. Tracheotomy and frequent flexible
r Discharge instructions and medications after
J Trauma. 2009;66(3):875879.
r Pettiford BL, Luketich JD, Landreneau RJ. The F
bronchoscopy should be considered to provide inpatient admission: management of flail chest. Thorac Surg Clin.
effective pulmonary toilet. Oral pain medications 2007;17(1):2533.
r Activity:
SURGERY/OTHER PROCEDURES Ad lib but no airplane travel if pneumothorax is See Also (Topic, Algorithm, Electronic
r Chest tube placement: Patients with rib fractures
present Media Element)
who are intubated are at an increased risk of http://www.trauma.org
developing a pneumothorax or tension Patient Monitoring
r Follow-up CXR 1 wk after the traumatic injury
pneumothorax due to laceration of the lung by the
sharp fracture end. In these cases, a prophylactic r Pulmonary function testing
CODES
chest tube is recommended. PROGNOSIS
r In most cases, positive pressure ventilation (CPAP or r Overall, patients with flail chest have 510% ICD9
intubation) allows for a nonoperative internal reported mortality if they reach the hospital alive. 807.4 Flail chest
stabilization of the chest wall, and fixation is not r Patients who do not need mechanical ventilation do
necessary. This is the conservative approach and is better statistically, and overall mortality seems to
applicable to most patients who have a flail chest.
r However, there is a small subgroup that may benefit increase with severity, age, and number of total rib PEARLS AND PITFALLS
fractures involved. r The diagnosis of flail chest is largely clinical.
from operative repair:
Internal fixation may: COMPLICATIONS Diagnosis: Observe paradoxical respirations while
Shorten duration of mechanical ventilation r Pneumonia the examiners hand is on the thorax (feel broken
Decrease the complication rate r Empyema ribs and crepitus).
Decrease the length of hospital stay r Bronchial pleural fistula r Consider associated injuries, particularly
Be cost-effective (68) r Chest wall deformity intrathoracic injuries.
Some indications for surgical repair include: r Chronic chest wall pain r Immediate treatment: Oxygen and pain
Failure to wean from the ventilator r Dyspnea on exertion management followed by possible intubation and
Paradoxical movement visualized during chest tube
weaning
Absence of pulmonary contusion REFERENCES
Absence of significant brain injury
Refractory pain despite narcotics or epidural 1. Garcia VF, Gotschall CS, Eichelberger MR, et al. Rib
pain catheter fractures in children: A marker of severe trauma.
J Trauma. 1990;30(6):695700.
2. Wanek S, Mayberry JC. Blunt thoracic trauma: Flail
chest, pulmonary contusion, and blast injury. Crit
Care Clin. 2004;20(1):7181
3. Ciraulo DL, Elliott D, Mitchell KA, et al. Flail chest
as a marker for significant injuries. J Am Coll Surg.
1994;178:466470.
355
FOOD POISONING
Nahar D. Alruwaili
Brent W. Morgan
r Ciguatera toxin: Produced by dinoflagellates that r Botulism presents with impaired cranial nerve
BASICS bioaccumulate, ultimately concentrating in reef fish. activity such as difficulty swallowing or handling oral
The mechanism of intoxication may involve secretions, constipation, hypotonia with progressive
DESCRIPTION increased sodium permeability in sodium channels symmetric paralysis, absent deep tendon reflexes,
r There are many lay definitions of food poisoning. and stimulation of central or ganglionic cholinergic and apnea.
This topic will focus on illness created by receptors. r Patients with scombroid poisoning may present with
microorganism-generated toxins contained in foods. skin flushing, urticaria, bronchospasm, tachycardia,
r The most common bacterial toxins causing ETIOLOGY
See Pathophysiology. and hypotension.
foodborne illness will be discussed, including: r Ciguatera toxin may present with myriad symptoms:
Staphylococcal enterotoxin B (SEB) COMMONLY ASSOCIATED CONDITIONS Diarrhea; abdominal cramps and/or vomiting; CNS
Bacillus cereus toxin r Vomiting
symptoms, including sensory changes such as
Scombroid toxin r Diarrhea blurred vision, change in temperature perception
Ciguatera toxin (temperature reversal, which is considered specific
Botulinum toxin is discussed briefly. Also see the for ciguatoxin); sensation of teeth being painful or
Botulism topic. DIAGNOSIS loose; paralysis; and respiratory arrest.
EPIDEMIOLOGY HISTORY PHYSICAL EXAM
r An estimated 76 million cases of foodborne disease r Food poisoning most often presents as r The most important element of the physical exam is
occur each year in the U.S. gastroenteritis with nausea, vomiting, diarrhea, and the assessment of the patients hydration status,
r 325,000 hospitalizations in the U.S. annually abdominal pain. signs of bacteremia, sepsis, or shock.
r Estimated 5,000 deaths in the U.S. annually r Constitutional symptoms (fever, malaise, myalgias) r Vital signs: Tachycardia, tachypnea, hypotension
r SEB, B. cereus, botulism, and scombroid occur may be suggestive of invasive bacteria or systemic with dehydration, or toxin related
throughout the U.S. disease. r The patients general appearance: Well or ill or in
r Ciguatera poisoning occurs most frequently in r Oliguria may be suggestive of dehydration or renal
shock
Florida and Hawaii. failure. r HEENT: Presence or absence of tears; dry or moist
r Ask about:
RISK FACTORS mucous membranes; whether the eyes appear
r Risk factors vary with specific etiology. Timing of illness in relation to ingestions sunken; depressed or flat fontanelles
r Improper storage of food
Associated abdominal and systemic symptoms r Chest: Decrease of the air entry or wheezing
History of similarly exposed persons with related (bronchospasm); dysrhythmia may occur with
GENERAL PREVENTION symptoms ciguatera.
Proper cooking and storage of foods Type of food consumed: r Skin: Skin turgor, capillary refill, skin flushing,
Prepared foods: Meats, pastries, salads (SEB)
PATHOPHYSIOLOGY Contaminated fried rice (emetic B. cereus toxin) urticaria
r Toxins released by microorganisms into food may r CNS: Evaluate for neurologic involvement such as
or meatballs (diarrheal B. cereus toxin)
cause a variety of diseases. Carnivorous reef fish such as mackerel, paresthesias, motor weakness, ataxia, visual
r SEB: Heat-stable enterotoxin acts by stimulating barracuda, amberjack, and grouper (ciguatera disturbances, cranial nerve palsies, and temperature
release of cytokines from T cells in the intestines, toxin) reversal.
leading to inflammatory reaction and cell Large fishpoorly refrigerated: Tuna, bonito, DIAGNOSTIC TESTS & INTERPRETATION
destruction: albacore, mackerel (scombrotoxin) Lab
Enterotoxins also may act on receptors in the gut Home-canned foods No lab testing is absolutely necessary, but consider the
that transmit impulses to the emesis center in the r SEB:
following:
brain. Characterized by the abrupt onset of vomiting r Bedside glucose: Hypoglycemia can occur in patients
In severe poisoning, SEB may cause systemic within minutes to hours; vomiting is the most
illness, shock, and multisystem organ failure. with inadequate oral intake.
prominent finding. Severe abdominal cramps and r Serum electrolytes, BUN, creatinine
r B. cereus toxin: 2 recognized types of illness are diarrhea may occur. In severe illness, r CBC and C-reactive protein to evaluate inflammation
caused by 2 distinct toxins: low-gradefever or mild hypothermia can occur.
r B. cereus toxin2 clinical syndromes: r Urinalysis
The vomiting (emetic) type of illness (short
incubation and duration) is believed to be caused r Blood gas to evaluate oxygenation and perfusion
Emetic syndrome: Like staphylococcal foodborne
by a heat-stable toxin. r Stool culture and WBC: For severe diarrhea, fever,
illness with severe vomiting, but presentation may
The diarrheal type of illness (long incubation and be delayed, occurring in several to 15 hr after persistently bloody stools, neurologic findings,
duration) is caused by heat-labile toxins that ingestion. severe abdominal pain, or if patient is
increase intestinal secretions by activation of Differentiation between the B. cereus emetic immunocompromised or very young
adenylate cyclase in the intestinal epithelium. syndrome and SEB is difficult and may be based r Blood culture: If the patient is notably febrile
r Scombroid: Results from improper refrigeration or on the type of food involved. r When epidemic poisoning is suspected, state public
preservation of large fish, which results in bacterial Diarrhea syndrome has a slightly longer health departments or the CDC may be able to
degradation of histidine to histamine: incubation period of 816 hr. analyze suspect food for toxins.
Scombrotoxin is a term sometimes used to Both syndromes are mild and usually are not r Botulinum: Stool sample for botulinum spores and
describe histamine in this scenario. associated with fever. toxin
The histamine poisoning resembles an allergic r The health department may assay food for SEB, B.
reaction, with any combination of flushing, cereus, botulinum, ciguatoxin, and scombroid.
urticaria or other acute pruritic rash, vomiting,
diarrhea, cough, wheezing, stridor, or diaphoresis.
356
FOOD POISONING
Imaging Second Line r SEB: Onset 16 hr after exposure; duration on

Abdominal radiographs (flat and upright): If Antidiarrheals: average 14 hr but as long as 2448 hr. Usually
obstructive symptoms or perforation are suggested r Generally not used in children <5 yr of age self-limited to vomiting:
Diagnostic Procedures/Other r Loperamide: 20% of patients visiting emergency departments
ECG: In patients with any ciguatera poisoning If <30 kg, 2 mg PO initially, then may repeat will require admission, and 4% of admitted
12 times daily. patients are severely ill and die from multisystem
DIFFERENTIAL DIAGNOSIS If >30 kg, 4 mg PO initially, then may repeat organ failure, typically the elderly and young
r SEB and B. cereus: children.
2 mg PO after each loose stool to maximum of
Infectious gastroenteritis is the main differential r B. cereus: Emetic syndrome onset is 16 hr,
12 mg/day.
diagnosis. r Bismuth subsalicylate (Kaopectate): diarrheal syndrome onset is 816 hr; resolves within
Inflammatory bowel disease 2448 hr.
Children 100 mg/kg/day divided in 5 equal doses
Colitis r Scombroid: Onset immediate, usually lasting several
for maximum 3 days
Irritable bowel syndrome hours and resolves within 2472 hr
Adolescent/adult: 2 tablets (262 mg each) or
Surgical abdominal causes: Intestinal obstruction,
30 mL of liquid q3060min until symptoms are r Ciguatera: Onset variable but <24 hr; long-lasting
appendicitis, intestinal malrotation or volvulus, effects of weeks to months, sometimes with only
controlled, maximum 8 doses/day for maximum of
intussusception partial resolution
r Scombroid: 3 days.
r Botulinum: Onset hours to days; duration depends
Allergic, anaphylactoid, and anaphylactic reactions COMPLEMENTARY & ALTERNATIVE
on treatment with IG. Resolution within days to
are the main differential diagnoses for scombroid THERAPIES weeks with IG. For patients not receiving IG
Ethanol ingestion in aldehyde Ciguatera: treatment, convalescence may last months:
dehydrogenasedeficient patients such as Asians r Mannitol is sometimes used as therapy; clinical trials
r Botulism: After the patient has survived the paralytic phase
have not demonstrated effectiveness. of botulism, the outlook for complete recovery is
Guillain-Barre syndrome r Amitriptyline, given as a sodium channel blocker to excellent.
Myasthenia gravis counteract the sodium channel opening of the
COMPLICATIONS
Cerebrovascular accident
Transverse myelitis
ciguatera toxin, may have some effectiveness,
though clinical trials evaluating this therapy are
r SEB: Shock, multisystem organ failure, death F
r Ciguatera: r Botulism: Paralysis, pneumonia, sepsis, death
lacking.
Organophosphate and carbamate toxicity r Ciguatera: Persistence of neurologic and cognitive
Scombroid DISPOSITION changes
Botulism Admission Criteria r Dehydration secondary to vomiting or diarrhea
r Patients with intractable vomiting, diarrhea, r Hypoglycemic secondary to vomiting
Meningitis
Tetrodotoxin poisoning dehydration, pain
r Severe illness, expected deterioration, or need for
inpatient therapy/evaluation (eg, botulism) ADDITIONAL READING
TREATMENT r Critical care admission criteria:
r American Academy of Pediatrics. Appendix IX.
Hypotension, dysrhythmia, unstable vital signs,
PRE HOSPITAL paralysis, shock Clinical syndromes associated with foodborne
Assess and stabilize airway, breathing, and diseases. In Pickering LK, Baker CJ, Kimberlin DW, et
circulation. Discharge Criteria al., eds. Red Book: 2009 Report of the Committee
r Symptoms are controlled to a degree compatible
on Infectious Diseases. 28th ed. Elk Grove Village,
INITIAL STABILIZATION/THERAPY with discharge.
r Assess and stabilize airway, breathing, and IL: Author; 2009:860863.
r Patient not dehydrated r CDC. FoodNet 2007 Surveillance Report. Atlanta,
circulation. r No signs of toxicity or systemic disease
r Correct dehydration and/or hypoglycemia. GA: U.S. Department of Health and Human Services;
Issues for Referral 2009.
MEDICATION r Poison control center for additional information and
First Line patient care recommendations
r Antiemetics: r For suspected outbreaks of infective pathogens, call CODES
May be necessary for SEB, B. cereus, scombroid, the local health department.
or ciguatera ICD9
Ondansetron 0.150.2 mg/kg IV q68h PRN r 005.0 Staphylococcal food poisoning
vomiting FOLLOW-UP r 005.89 Other bacterial food poisoning
Metoclopramide 0.1 mg/kg IV q6h PRN vomiting r 005.9 Food poisoning, unspecified
r Scombroid: FOLLOW-UP RECOMMENDATIONS
r Because most cases of food poisoning are
Diphenhydramine: 1 mg/kg/dose PO/IV q6h PRN,
self-limited, prolonged follow-up care is not
max 300 mg/day
required. PEARLS AND PITFALLS
Cimetidine: PO/IV 510 mg/kg q6h r Discharge instructions and medications: r The main differential diagnosis of most food
For severe histamine reaction/anaphylactoid
reaction, epinephrine and/or albuterol may be Antiemetics or antidiarrheals for 12 days poisoning is gastroenteritis. General supportive care
necessary. See Anaphylaxis topic. H1- and H2 blockers for 35 days is similar for both.
Corticosteroids are not indicated or useful in r Antibiotic therapy is not indicated in most
DIET
managing scombroid poisoning. r Eliminate contaminated food. foodborne illnesses.
r Botulinum: Treatment is mainly supportive: r Dietary restrictions are not standard care. r Notify the health department for foodborne illnesses.
Baby BIG: A human-derived antitoxin is used to
treat cases of infant botulism and is available from PROGNOSIS
r Most gastroenteritis secondary to food poisoning is
the California Department of Public Health.
Botulinum antitoxin: In cases of suspected mild and self-limited.
r Recovery is complete in 25 days in most individuals.
foodborne botulism, it is most effective if
r In the very young, the prognosis is more guarded
administered early in the disease course. (Contact
the local or state health department or the CDC.) because these patients can become dehydrated
See the Botulism topic for more detailed dosing quickly.
information.
357
FOREIGN BODY ASPIRATION

David D. Lowe
Joshua Nagler
r Ball valve obstruction: r Respiratory:

BASICS FB dislodges during expiration and reimpacts Cough very common
during inspiration. Varied respiratory distress depending on location
DESCRIPTION Results in atelectasis of obstruction
r Foreign body aspiration (FBA) is the inhalation of r Stop valve obstruction: Stridor with proximal airway obstruction
foreign matter that deposits within the airway, from Complete obstruction of air Abnormal auscultation in 75% of cases
the larynx to the distal bronchioles. Results in distal collapse or consolidation Asymmetric breath sounds, wheeze, or both are
r Presentation varies from asymptomatic to airway r More distal FBAs cause less acute symptoms. the most common ausculatory findings.
obstruction and respiratory failure. r Prolonged inability to clear secretions distal to the r Negative exam cannot rule out FBA (3).
r Most cases occur in infants and toddlers.
FB can lead to postobstructive pneumonia (often DIAGNOSTIC TESTS & INTERPRETATION
r Most patients present after an acute choking event recurrent), lung abscess, or bronchiectasis.
with symptoms including coughing and wheezing or r Aspiration of liquid or fine particulate substances, Lab
Initial Lab Tests
respiratory findings. such as hydrocarbons or talc, do not result in r No specific lab testing for FBA
r Delayed diagnosis can occur when the aspiration obstruction but may result in pneumonitis with r WBC count and inflammatory markers may be
event is not witnessed or reported: severe morbidity and potential mortality.
elevated with retained FBA but are nonspecific.
Initial presentation is often ascribed to an r Blood gas analysis may be indicated to evaluate
alternative diagnosis (eg, asthma). ETIOLOGY
r Organic materials are the most frequently aspirated ventilatory function.
Increased rates of postobstructive infection
r A careful history is the best diagnostic tool: objects:
Imaging
Nuts, popcorn, and seeds are most common (3). r Patients with highly suggestive history and
Physical exam and radiographic findings can r Inorganic objects are found more commonly in older
provide supporting evidence. respiratory compromise may be taken directly to
r Bronchoscopy is the gold standard for diagnosis and children. bronchoscopy without imaging.
management of solid object aspiration. r PA and lateral chest radiographs are the first-line
EPIDEMIOLOGY DIAGNOSIS imaging choice for stable patients.

r May reveal and localize radiopaque FB (1020% of
Incidence HISTORY cases) (6)
r Peak incidence occurs between 1 and 2 yr of age. r A suggestive history is the most sensitive and r Nonradiopaque foreign bodies will not be seen
r 80% of patients are <3 yr of age (1). specific means of diagnosis (1,4):
r Male to female ratio is 2:1. directly on conventional films, making the
Requires high level of suspicion and directed radiographic diagnosis more challenging.
r FBA is the most common cause of accidental death questioning r Films may demonstrate indirect findings consistent
in children <1 yr of age. Parents may otherwise forget a minor,
with FBA (5):
self-resolving choking event.
RISK FACTORS r The most common symptoms are coughing, Asymmetric hyperlucency and mediastinal shift
r Younger age suggests air trapping.
r Absence of molars choking, or gagging (5). Atelectasis or consolidation can occur distal to the
r Other presenting symptoms may include:
r Developmental delay FB.
Shortness of breath, chest pain, vomiting (often Sensitivity increases with:
GENERAL PREVENTION posttussive), fever, hemoptysis Inspiratory and expiratory films taken
r Regulation of nonfood choking hazards r The constellation of a choking episode with cough
sequentially OR
r Public education, including anticipatory guidance and unilateral wheeze or decreased breath sounds is Decubitus views in young or noncooperative
from primary care physicians not found in most cases (3). patients (5,7)
r Avoidance of high-risk foods in children with r Delayed diagnosis may present with: r Fluoroscopy is favored in some centers (2):
inadequate dentition or development Chronic cough, fever, hemoptysis Abnormal movement of hemidiaphragm or
PHYSICAL EXAM mediastinal swing suggests air trapping.
PATHOPHYSIOLOGY r Findings depend on location, degree of obstruction, r More proximal FBs (above the carina) are less likely
r Large objects in the proximal airway may cause
and time delay to presentation: to have abnormal radiographic findings.
complete airway obstruction and respiratory failure. r Lateral neck radiographs may be useful in patients
r Irritation of the larynx may cause laryngospasm. May be normal
r Check valve obstruction: r Vital signs: with stridor or drooling when looking for FB or
Tachypnea alternative diagnosis (prevertebral soft tissue
Diameter of bronchus increases during inspiration, swelling, abnormal epiglottis).
allowing air passage, but recoil during expiration Hypoxemia
prevents airflow around foreign body (FB) (2). Diagnostic Procedures/Other
r Rigid bronchoscopy in the operating room (OR) is
Results in localized hyperinflation
the definitive diagnostic and therapeutic procedure
for FBA.
r Flexible bronchoscopy may be used; however, FB
removal may be more difficult.
358
FOREIGN BODY ASPIRATION
DIFFERENTIAL DIAGNOSIS Issues for Referral 4. Fontoba JEB, Gutierrez C, Lluna J, et al. Bronchial
r Asthma Patients with low suspicion for FB with negative exam foreign body: Should bronchoscopy be performed in
r Bronchiolitis and radiographs may follow up with their primary care all patients with a choking crisis? Pediatr Surg Int.
r Croup providers, with referral to otolaryngology/surgery if 1997;12:118120.
r Epiglottitis symptoms recur or persist. 5. Black RE, Johnson DG, Matlak ME. Bronchoscopic
r Laryngotracheal malacia removal of aspirated foreign bodies in children.
r Pneumonia J Pediatr Surg. 1994;29:682684.
FOLLOW-UP
r Tracheitis 6. White DR, Zdanski CJ, Drake AF. Comparison of
r Vascular rings or slings FOLLOW-UP RECOMMENDATIONS pediatric airway foreign bodies over fifty years.
Patients discharged from the hospital are presumed South Med J. 2004;97:434436.
not to have FBA and should follow up with primary 7. Assefa D, Amin N, Stringel G, et al. Use of
TREATMENT care provider in 2448 hr to ensure symptoms have decubitus radiographs in the diagnosis of foreign
improved or resolved. body aspiration in young children. Pediatr Emerg
PRE HOSPITAL Care. 2007;23:154157.
r Administer supplemental oxygen. Patient Monitoring
r All patients with possible FBA should be on
r Basic life support for airway obstruction
continuous cardiopulmonary monitoring including ADDITIONAL READING
INITIAL STABILIZATION/THERAPY pulse oximetry until definitive care is provided.
r Complete airway obstruction per Basic Life Support r Capnography may be a useful adjunct for impending Schunk JE. Foreign body aspiration/ingestion. In
guidelines: respiratory failure. Fleisher GR, Ludwig S, eds. Textbook of Pediatric
Heimlich, chest thrusts may relieve complete Emergency Medicine. 6th ed. Philadelphia, PA:
DIET Lippincott Williams & Wilkins; 2010:307314.
obstruction. Keep patient NPO for possible anesthesia.
Needle cricothyrotomy may be necessary pending
surgical cricothyrotomy or tracheostomy. PROGNOSIS
r Patients generally have a favorable prognosis. CODES
High-flow oxygen and vascular access
Consult anesthesia or otolaryngology PRN. r Worse prognosis with: F
Rapid transfer to OR for bronchoscopy Complete airway obstruction ICD9
r Partial obstruction: Missed aspiration r 933.1 Foreign body in larynx
Keep patient comfortable, and avoid painful r 934.0 Foreign body in trachea
COMPLICATIONS
procedures. r Increased risk of complications with delayed r 934.9 Foreign body in respiratory tree, unspecified
High-flow oxygen diagnosis
Anesthesia and otolaryngology consultation r Due to FB:
r Stable patients with supportive history and/or
Early: PEARLS AND PITFALLS
exam: Asphyxiation
Radiographic evaluation to help localize FB r Pearls:
Postobstructive pulmonary edema
Rigid bronchoscopy is diagnostic and therapeutic. A careful history is the most useful diagnostic
r Stable patients with low suspicion: Late:
Pneumonia evaluation for FBA.
Screening CXR or fluoroscopy; if negative, consider Lung abscess Expiratory films may exaggerate localized
close observation and repeat films in 2448 hr. Bronchiectasis hyperinflation on chest films and are more helpful
Erosion with airway perforation or hemoptysis than inspiratory films.
MEDICATION In young children, evaluating for persistent
Fistula formation
First Line r Due to bronchoscopy: hyperinflation in the dependent hemithorax may
r No specific medications for FBA itself suggest air trapping.
r Nebulized racemic epinephrine 2.25% (0.5 mL in Anesthetic complications Radiographic changes evolve over time, so in the
2.5 mL normal saline): Oral trauma stable patient, follow-up films may provide an
May temporarily decrease swelling and Laryngeal edema alternative to immediate bronchoscopy.
obstruction in patients with stridor Bronchospasm r Pitfalls:
r Antibiotics for associated pneumonia: Atelectasis
A normal exam or negative radiographic studies
Retained fragments
Ampicillin/Sulbactam 50 mg/kg IV q6h cannot exclude FBA.
Ceftriaxone 50100 mg/kg IV q24h
Dexamethasone 0.15 mg/kg IV q6h for 24 hr:
r If significant inflammation noted on bronchoscopy 1. Ciftci AO, Bingol-Kologlu M, Senocak ME, et al.
Bronchoscopy for evaluation of foreign body
SURGERY/OTHER PROCEDURES aspiration in children. J Pediatr Surg. 2003;38:
r Rigid bronchoscopy is the gold standard and is 99% 11701176.
effective in removal of large solid FB. 2. Mu LC, Sun DQ, He P. Radiological diagnosis of
r Thoracotomy is required for failed bronchoscopy. aspirated foreign bodies in children: Review of 343
cases. J Laryngol Otol. 1990;104:778782.
DISPOSITION
3. Digoy GP. Diagnosis and management of upper
Admission Criteria aerodigestive tract foreign bodies. Otolaryngol Clin
r Patients being evaluated by bronchoscopy require
North Am. 2008;41:485496, viiviii.
admission.
r Persistent hypoxia, respiratory distress, or
pneumonia
Patients with significant respiratory distress or
airway inflammation after bronchoscopy
Endotracheal intubation
359
LWBK822-driver-F LWBK822-Hoffman ch178a.xml April 15, 2011 14:11
FOREIGN BODY INGESTION

Cynthia Lodding
Garth Meckler
r Characteristics of the FB are important to the risk of Diagnostic Procedures/Other

BASICS impaction or complications such as perforation: r Handheld metal detectors may be helpful in
Objects >2.5 cm have difficulty passing through localizing ingested coins and metallic FBs and may
DESCRIPTION the pylorus. obviate the need for x-rays when available (eg,
r Foreign body (FB) ingestion is defined as a Sharp objects have a higher rate of perforation, metallic objects located below the diaphragm can
suspected or confirmed FB that has been swallowed especially in areas of angulation including the C be safely observed as outpatients) (5).
and is located anywhere along the GI tract. loop of the duodenum, and the ileocecal valve. r Barium swallow may be useful for suspected FBs
r The focus of this topic will be FBs that are objects Ingestion of multiple magnets may lead to that are radiolucent.
rather than medications or toxic ingestions. Also, impaction through attraction across adjacent r Endoscopy (flexible or rigid) may be indicated for
caustic ingestions are not discussed in this topic. loops of bowel leading to pressure necrosis (7). symptomatic radiolucent FBs, impacted or sharp FBs,
Please see various topics on toxicologic ingestions Button batteries may cause local erosion and and retained button batteries or ingested multiple
and the Esophagitis and Burn, Chemical topics. perforation if retained (6). magnets.
EPIDEMIOLOGY ETIOLOGY Pathological Findings
r Nearly 100,000 FB ingestions are reported annually r Coins are the most commonly reported FB Mucosal edema, erosion, or perforation may be noted
in the U.S. ingestions in the U.S. and Europe, comprising up to during endoscopy or open surgical exploration of
r 80% of FB ingestions occur in children, with a peak 76% of ingested FB (5), while 530% of FB impacted FBs.
incidence between 6 mo and 3 yr of age. ingestions are sharp objects (9,10).
r Fish bone ingestion is more common in Asia. DIFFERENTIAL DIAGNOSIS
RISK FACTORS r The differential diagnosis of ingested FB presenting
r Young age r Sharp and multiple metallic objects (eg, nails) are
with respiratory symptoms includes:
r Advancing food inappropriate for developmental often associated with intentional ingestion in Aspirated FB
adolescents with psychiatric disease. Upper/Lower airway infections (eg, croup,
age
r Inappropriate toys for developmental age (small, COMMONLY ASSOCIATED CONDITIONS bronchiolitis, pneumonia)
Psychiatric disease in adolescents r The differential diagnosis of ingested FB presenting
separate pieces)
r Developmental delay may increase the risk for older with drooling, dysphagia, dysphonia, and
children compared to peers. odynophagia includes:
r Psychiatric disease may predispose adolescents to DIAGNOSIS Infections (eg, retropharyngeal or peritonsillar
FB ingestion. abscess, stomatitis)
HISTORY
r The majority (80%) of ingested FBs are witnessed. Oropharyngeal trauma
GENERAL PREVENTION r Younger patients (<2 yr of age) are more likely to Esophagitis (eg, viral, candidal)
r Close supervision during meals and while playing
Tear or other injury to esophageal or
with toys may help prevent accidental ingestion of have an unwitnessed ingestion and may present oropharyngeal mucosa may give the patient a
FBs. with symptoms such as coughing, drooling, or sensation of a FB at the site of injury.
r Careful inspection and storage of toys and batteries respiratory symptoms (8).
r 764% of FB ingestions are asymptomatic.
PATHOPHYSIOLOGY r Symptoms: Dysphagia/Odynophagia, FB sensation, TREATMENT
The pathophysiology of FB ingestion and the potential drooling, vomiting, refusal to eat, gagging, choking,
for impaction depend on characteristics of the patient or respiratory symptoms (stridor, wheezing) PRE HOSPITAL
and the FB: r Assess and stabilize airway, breathing, and
r Anatomic considerations include areas of PHYSICAL EXAM circulation.
physiologic narrowing: Findings depend on site of the FB as well as its r Ingested FB associated with loss or severe limitation
Cricopharyngeus muscle and thoracic inlet in the characteristics:
r Proximal pharyngeal or esophageal FBs may of airway patency should be treated with the
upper 1/3 of esophagus Heimlich maneuver or abdominal thrust in toddlers
Aortic arch in the middle 1/3 of esophagus produce drooling, gagging, or coughing. and older children and back blows and chest
Lower esophageal sphincter in the distal 1/3 of r Distal, blunt FBs are often associated with a normal
compressions in infants.
esophagus physical exam. r Support ABCs.
Pylorus r Rarely, resulting perforation may be associated with
FBs in the large intestine are likely to pass mediastinitis or peritonitis. INITIAL STABILIZATION/THERAPY
spontaneously without complication.
Rectal FBs may be the result of sexual activity and DIAGNOSTIC TESTS & INTERPRETATION circulation.
Lab r Oxygen and monitoring should be provided for
in prepubertal children may represent sexual
abuse (see Foreign Body, Rectal topic). Initial Lab Tests patients with respiratory symptoms.
r Underlying medical conditions such as congenital or r Routine lab testing for ingested FBs is not indicated. r Symptomatic patients should kept NPO in
r Leukocytosis associated with prolonged impaction anticipation of the potential need for anesthesia for
acquired strictures of the GI tract may predispose to
FB impaction. of foreign bodies is associated with an increased procedural removal of the FB.
incidence of complications (11). r Asymptomatic, blunt ingested FB below the
Imaging diaphragm can be safely managed expectantly as an
Plain radiographs of the chest and abdomen may outpatient for spontaneous passage in 12 wk.
demonstrate radiopaque foreign bodies: MEDICATION
r Lateral views may be helpful to distinguish
First Line
esophageal from tracheal foreign bodies and to help r Analgesia may be necessary.
define the anatomic location of FB if further along r Opioids:
the GI tract. Morphine 0.1 mg/kg IV/IM/SC q2h PRN:
then q2h PRN.
360
LWBK822-driver-F LWBK822-Hoffman ch178a.xml April 15, 2011 14:11
FOREIGN BODY INGESTION
Fentanyl 12 g/kg IV q2h PRN: Discharge Criteria 6. Sharma A, Chauhan N, Alexander A, et al. The risks
Initial dose of 1 g/kg IV may be repeated r Asymptomatic patients with a blunt FB below the and the identification of ingested button batteries
q1520min until pain is controlled, then q2h diaphragm (except multiple magnets) can be safely in the esophagus. Pediatr Emerg Care. 2009;25(3):
PRN. discharged with expectant outpatient management: 196199.
Codeine or codeine/acetaminophen dosed as Patients in whom esophageal bougienage has 7. Cauchi JA, Shawls RN. Multiple magnet ingestion
0.51 mg/kg of codeine component PO q4h PRN successfully pushed the FB into the stomach and gastrointestinal morbidity. Arch Dis Child.
Hydrocodone/Acetaminophen dosed as 0.1 mg/kg r Esophageal FB has been removed. 2002;87(6):539540.
of hydrocodone component PO q46h PRN
Issues for Referral
Second Line Asymptomatic ingested FBs that fail to pass
Glucagon has not been demonstrated to increase the spontaneously after 23 wk should be referred to a
ADDITIONAL READING
rate of spontaneous passage of esophageal coins in pediatric gastroenterologist or surgeon for possible r Loh KS, Tan LKS, Smith JD, et al. Complications of
children and is not recommended (4). endoscopic or surgical removal. foreign bodies in the esophagus. Otolaryngol Head
SURGERY/OTHER PROCEDURES Neck Surg. 2000;123(5):613616.
r Endoscopic removal may be necessary: r Louie JP, Alpern ER, Windreich RM. Witnessed and
FOLLOW-UP unwitnessed esophageal foreign bodies in children.
Sharp objects are a greater risk for complications,
though there is no consensus on guidelines for FOLLOW-UP RECOMMENDATIONS Pediatr Emerg Care. 2005;21(9):582585.
endoscopic or surgical removal. r Waltzman M. Management of esophageal coins.
Patient Monitoring
Button batteries are a risk for erosive r Parents may be instructed to examine the stool for Pediatr Emerg Care. 2006;22(5):367373.
complications that may occur within hours in the r Wyllie R. Foreign bodies in the intestinal tract. Curr
the ingested FB over the ensuing days to weeks.
esophagus (6). When past the pylorus, they r Discharged patients with ingested distal FBs should Opin Pediatr. 2006;18:563564.
usually pass uneventfully; when retained in the seek immediate medical care if there is fever,
esophagus or stomach >12 hr, they usually abdominal pain, vomiting, or bloody stools.
require removal. CODES
Magnets, when multiply ingested, are at risk for DIET
impaction and pressure necrosis across adjacent No dietary restrictions
ICD9
F
loops of bowel and should be endoscopically or PROGNOSIS r 935.1 Foreign body in esophagus
surgically removed (7). r >90% of ingested FBs pass spontaneously without r 935.2 Foreign body in stomach
r No single strategy for the management of
complication. r 938 Foreign body in digestive system, unspecified
esophageal FBs exists, and several options can r Prolonged impaction, ingested button batteries,
be considered (see Foreign Body, Esophagus sharp objects, and multiple magnets are associated
topic):
A brief period (816 hr) of observation with
with serious complications (3,9,10). PEARLS AND PITFALLS
maintenance of NPO status and repeat x-rays may COMPLICATIONS r Ingested button batteries in the esophagus can
r Esophageal perforation with abscess formation,
be appropriate, as 2530% of FBs will pass cause erosion or perforation within hours and
without complication (1). mediastinitis, sepsis
r Arterial-esophageal fistula with hemorrhage should be emergently removed.
Esophageal bougienage with or without sedation r Ingestion of multiple small magnets can lead to
may be effective to push the esophageal FB into r Stricture formation
pressure necrosis of adjacent loops of bowel and
the stomach (2). r GI perforation with peritonitis, sepsis
require removal regardless of location within the GI
Removal using McGill forceps (for proximal FB) or tract.
a balloon-tipped catheter (usually under r Though >50% of patients with ingested FB are
fluoroscopy, performed in the Trendelenberg REFERENCES asymptomatic, 7590% will have a history of
position) may be effective in a minority of cases
1. Waltzman ML, Baskin M, Wypij D, et al. A ingestion when specifically questioned.
(3). r The rate of spontaneous passage of esophageal
Endoscopy using a rigid or flexible endoscope is randomized clinical trial of the management of
the mainstay of removal of most impacted esophageal coins in children. Pediatrics. foreign bodies is highest for those located in the
esophageal FBs (4). 2005;116(3):614619. distal 1/3, followed by the middle 1/3, and finally
r Ingested FB with signs or symptoms of perforation 2. Arms JL, Mackenbergo-Mohn MD, Bowen MV, the proximal 1/3; a brief period of observation may
et al. Safety and efficacy of a protocol using be warranted.
or distal GI impaction may require surgical
exploration and removal. bougienage or endoscopy for the management of
coins acutely lodged in the esophagus: A large case
DISPOSITION series. Ann Emerg Med. 2008;51(4):367372.
Admission Criteria 3. Soprano JV, Mandl KD. Four strategies for the
r Symptomatic patients, patients with ingestion if
management of esophageal coins in children.
multiple magnets, signs and symptoms of Pediatrics. 2000;105(1):e5e10.
perforation 4. Mehta D, Attia M, Quintana E, et al. Glucagon use
r Patients with ingested button batteries that have
for esophageal coin dislodgment in children: A
not passed the esophagus within 12 hr and stomach prospective, double-blind, placebo-controlled trial.
within 24 hr are at risk for erosive complications and Acad Emerg Med. 2001;8(2):200203.
should be admitted. 5. Lee JB, Ahmad S, Gale CP. Detection of coins
r Asymptomatic patients with impacted esophageal
ingested by children using a handheld metal
FBs who fail 816-hr observation should be detector: A systematic review. Emerg Med J.
admitted for endoscopic removal. 2005;22(12):839844.
Signs and symptoms of GI perforation:
Mediastinitis or peritonitis with unstable vital
signs may require admission to an ICU.
361
FOREIGN BODY, CORNEA

Kimberly A. Giusto
Joshua A. Rocker
Organic and certain inorganic materials can cause r Pupil:

BASICS significant localized response: If significant irritation has occurred, signs of
Organic materials: traumatic iritis or uveitis may be present. This may
DESCRIPTION Soil, plant materials, insect parts, and animal cause the pupil to have an abnormal shape.
r Corneal foreign bodies (FBs) commonly occur from matter (fur) r Anterior chamber:
workplace and environmental exposures. Acids Use a slit lamp to look for flare or cells in anterior
r They can occur in any age group: Bases chamber.
More common in school-age children and Oxidizing materials:
adolescents Metals, such as iron and copper, can cause DIAGNOSTIC TESTS & INTERPRETATION
r Signs and symptoms range from mild irritation to rust rings. Imaging
r Plain radiographs may be useful, especially if a
severe inflammatory reaction (1):
High-speed, smaller projectiles may not produce metallic FB is suspected (3).
DIAGNOSIS r If an intraocular FB is suspected, CT or US can be
pain initially.
r If the FB penetrates the full layers of the cornea and used for evaluation.
HISTORY r MRI is not recommended because of the possibility
enters the anterior chamber, it is considered an r Obtain history of exposure:
intraocular FB and should not be considered a of metallic FB.
High-speed FBs have a greater risk of deeper
corneal FB. penetration. Diagnostic Procedures/Other
Important to note the FB material: r Slit lamp exam
EPIDEMIOLOGY r Fluorescein exam:
r One of the most common ophthalmologic reasons Rust rings can be created from retained iron
for emergency department visits: pieces (2). Seidel test:
FB may or may not still be present. Patient may just complain of FB sensation without A positive Seidel test is the appearance of
r Most common in young males known exposure. dilution of the fluoroscein at the site of the
r Patient may complain of photophobia or blurry corneal injury. This will give the look of a
RISK FACTORS vision. waterfall or fluid moving from the site of the
Certain jobs and outdoor activities may increase a r Patient may complain of excessive lacrimation. injury. This reveals the presence of an anterior
persons exposure to small projectile objects (1): r Note reported visual acuity and pain. chamber leak through the cornea and thus, by
r Metal- and woodworkers fall into this group. r Note history of contact lens usage. definition, is a globe rupture (2).
GENERAL PREVENTION PHYSICAL EXAM DIFFERENTIAL DIAGNOSIS
Wearing protective eyewear during high-risk activities r General: r Corneal abrasion
may reduce the likelihood of corneal FB. r Corneal laceration or perforation
Excessive tearing from affected eye
r Visual acuity: r Corneal ulcer
PATHOPHYSIOLOGY r Conjunctival FB
r Occurs when a FB projected toward the eye lodges Check visual acuity using Snellen chart (or
equivalent) prior to further exam, and note r Retained FB under the upper lid
in the cornea:
An underlying corneal abrasion or laceration may whether or not corrective lenses are used. r One also should consider more serious injuries such
be present. r Slit lamp exam: as globe rupture, hyphema, intraorbital FB, or
An inflammatory response may cause vascular Important for complete ophthalmologic exam keratitis secondary to prolonged inflammatory
dilation, which may result in edema to the cornea, r Lids: response.
conjunctiva, or lids: Lid edema may be present.
If the inflammatory response is not controlled or The upper and lower lids should be everted to
the FB is not removed, localized tissue necrosis look for retained FB: TREATMENT
may occur. Presence of a linear vertical corneal abrasion
r If the FB penetrates beyond the cornea, it then INITIAL STABILIZATION/THERAPY
may represent a retained FB in the upper eyelid. r Any toxic exposure to the cornea requires immediate
becomes an intraocular FB, which has a much higher r Conjunctiva:
morbidity associated with it. and copious irrigation:
May be a hyperemic, secondary to local irritation Make sure the eye is anesthetized prior to
ETIOLOGY causing chemosis. attempted removal of a corneal FB.
r Composition of the FB can affect the localized Corneal FB may be visualized during slit lamp It may be impossible to examine the eye
corneal inflammatory response (1): exam or with a direct ophthalmoscope. secondary to the patient squinting or refusing to
Inert objects can cause minimal responses: A rust ring, or a rusty stain at site of the FB, open the eye, so a topical anesthetic should be
Nonoxidizing metals, glass, and plastic should be noted. applied 1st:
However, larger-sized objects can cause a Fluorescein exam: If the patient has significant pain improvement
localized response. Use a fluorescein strip to perform a fluorescein
with a topical anesthetic, the injury can be
exam to look for any disruption of the cornea. localized to the superficial layers of the eye, the
cornea, or conjunctiva.
1st attempt removal using normal saline with
gentle jet stream irrigation.
A moist cotton swab can also be used:
Gently touch it to the corneal FB.
362
FOREIGN BODY, CORNEA
r If these methods are unsuccessful, a tuberculin ADDITIONAL READING

syringe with a 25- or 27-gauge needle attached can FOLLOW-UP r Augeri PA. Corneal foreign body removal and
be used while using the slit lamp for visual
assistance: FOLLOW-UP RECOMMENDATIONS treatment. Optom Clin. 1991;1(4):5970.
r Topical antibiotics should be continued until the r Babineau MR, Sanchez LD. Ophthalmologic
The FB is approached with the needle tangential
to the globe. corneal defect is completely healed. procedures in the emergency department. Emerg
The FB is then pushed off the cornea using the r Patients can follow up with their primary care Med Clin North Am. 2008;26:1734.
beveled tip of the sterile needle, paying close doctors in 12 days for re-examination. r Levin. Ophthalmic emergencies. In Fleisher GR,
attention not to penetrate the cornea. r Large defects should follow up with ophthalmology Ludwig S, eds. Textbook of Pediatric Emergency
Perform a Seidel test after attempting FB removal within 24 hr (2). Medicine. 6th ed. Philadelphia, PA: Lippincott
to look for any disruption in the cornea. Williams & Wilkins; 2010.
r If the FB is a metal, then a rust ring may remain PROGNOSIS
r Prognosis is generally good, with no long-term See Also (Topic, Algorithm, Electronic
after FB removal (3):
effects. Media Element)
Ophthalmologic consultation is recommended, r A prolonged delay in FB removaldays to r Conjunctivitis
but a rust ring does not need to be removed r Eye, Red
emergently. weeksincreases the risk of serious inflammatory
and infectious complication. r Eye, Visual Disturbance
Removal of a rust ring is performed using an r Development of severe inflammation and infection
ophthalmic burr under a slit lamp (3).
r After FB removal, copiously irrigate the eye with worsens the prognosis.
normal saline and apply topical antibiotics: COMPLICATIONS CODES
Topical antibiotics should be applied until the r Infection, scarring, corneal perforation, partial
corneal defect has completely healed (2). retained FB, traumatic iritis, hyphema, conjunctival ICD9
hemorrhage, and conjunctivitis may occur secondary 930.0 Corneal foreign body
MEDICATION
to corneal FB or its removal.
First Line r Complications can occur if there is delayed removal
r Topical ophthalmologic antibiotics:
of rust rings (2): PEARLS AND PITFALLS F
Choice of antibiotics include ophthalmic drops
Iron decay causing staining r Pearls:
such as:
Polymyxin B sulfate/trimethoprim: 1 drop OP Chronic inflammation Most corneal FBs can safely be removed by
Coats ring: emergency medicine physicians. Antibiotics can be
t.i.d. Circular scar in Bowman membrane of the
Ofloxacin: 1 drop OP t.i.d. used to help prevent infection, and follow-up
Tobramycin: 1 drop OP t.i.d. cornea should occur in 12 days depending on the size of
Corneal vascularization or necrosis the defect.
Consider ophthalmic ointment in younger children
such as: Consider ophthalmologic consult in cases of larger
Bacitracin: 0.5-inch ribbon in subconjunctival REFERENCES defects or suspected intraocular FB.
sac q.i.d. A fundoscopic exam should always be attempted.
r Oral NSAIDs can be given for pain control (4). 1. Bansal R, Ramasubramanian A, Jain AK, et al. At minimum, confirm the presence of bilateral red
r Topical anesthetics: Polyethylene foreign body on the cornea. Cornea. reflexes.
Proparacaine 0.5%: 12 drops OP once 2008;27(5):605608. Always evert the eyelids to look for retained FBs.
r Pitfalls:
Tetracaine 0.5%: 12 drops OP once 2. Sharma S. Ophthaproblem: Corneal rust ring. Can
Fam Med. 1997;43:13531360. Corneal abrasions can give the sensation of FB.
Second Line Eye pain and clinical evidence of FB sensation
r Cycloplegic agents have not proved effective in 3. Donnenfeld ED, Selkin BA, Perry HD, et al.
Controlled evaluation of a bandage contact lens should raise concern of corneal injury.
studies but can be considered in cases of extreme Reduction of visual acuity or visual fields should
pain or photophobia (5): and a topical non-steroidal anti-inflammatory drug
in treating corneal abrasions. Ophthalmology. prompt immediate referral to an ophthalmologist.
Homatropine 25%
r Check the tetanus status, and update if necessary. 1995;102:979984.
4. Calder L, Balasubramanian S, Stiell I. Lack of
COMPLEMENTARY & ALTERNATIVE consensus on corneal abrasion management:
THERAPIES Results of a national survey. CJEM. 2004;6(6):
Patching is not recommended but can be considered in 402407.
cases of large defects. 5. Sigurdsson H, Hanna I, Lockwood AJ, et al.
DISPOSITION Removal of rust rings, comparing electric drill and
hypodermic needle. Eye. 1987;1:430432.
Admission Criteria
Admission only needs to be considered if more serious
ophthalmologic injuries are present.
Discharge Criteria
Patients can be safely discharged home after removal.
363
FOREIGN BODY, DISC BATTERY

Michelle J. Alletag
Marc A. Auerbach
PATHOPHYSIOLOGY Imaging
BASICS r Alkaline or lithium batteries cause corrosion and r Plain abdominal and chest radiographs to locate the
coagulation necrosis of esophageal or GI mucosa, battery should be obtained on any patient with
DESCRIPTION skin, or nasal/ear mucosa. potential ingestion:
r Disc batteries are an exception to the benign nature r Less commonly, batteries may cause pressure In small children, it is often possible to include a
of most ingested foreign bodies: necrosis, mucosal burns (from small electrical significant portion of the abdomen with a chest
Found in watches, hearing aids, and other small activity), or toxic metal absorption if corrosion radiograph.
electronics, these small round candy-sized objects occurs: r If these radiographs are negative, consider a lateral
can be enticing to small children. Disc batteries may contain lithium (Li), manganese neck radiograph. This may locate a battery in the
r These batteries are often alkaline in composition (Mn), mercury (Hg), nickel (Ni), silver (Ag), or zinc hypopharynx or nasopharynx.
(consisting of metal oxidesusually silver, mercury, (Zn). r The structure of a disc battery gives it a double-ring
or manganese) and can result in corrosive injuries. r Ingested batteries with higher voltage or of larger appearance on plain radiographs. Coins appear as a
r Older toys or those from other countries may have size (sizes range from 823 mm) have a higher rate homogeneous circle without a 2nd ring.
higher risk due to inadequate seal/coating. of complications:
r The increasingly popular lithium batteries contain Diagnostic Procedures/Other
Additionally, larger batteries are less likely to pass Endoscopy can be used both for removal and to assess
several organic solvents and can also cause severe into the stomach. the extent of injury.
corrosive injuries.
r Ingestion is the most common cause of injury, but ETIOLOGY Pathological Findings
r Placement of a disc battery into an orifice for
disc batteries can be inserted into other orifices such Burns, coagulation necrosis, and mucosal sloughing
curiosity or entertainment by a child given the may be seen on endoscopy.
as the ear or nose. semblance to candy or age-appropriate oral behavior
r While generally benign once past the esophagus, r Primarily unintentional ingestions: DIFFERENTIAL DIAGNOSIS
disc or button batteries can result in rapid r Other foreign body ingestion
Only 446 of 10,213 cases reported in 2007 were
esophageal corrosion and/or hemorrhage and r Pill esophagitis
described as intentional.
should be removed emergently when identified to r Coin ingestion (coin is generally larger)
be in the esophagus. r Caustic ingestion
EPIDEMIOLOGY
DIAGNOSIS
Incidence HISTORY
r Disc batteries account for 2% of foreign body r Note time of exposure or insertion of battery into TREATMENT
ingestions (1). the orifice. PRE HOSPITAL
r The American Association of Poison Control Centers r Most often asymptomatic after observed or reported
Children with airway compromise should be managed
reports thousands of disc battery ingestions per year ingestion according to the Pediatric Advanced Life Support
(10,213 in 2007) (1). r Patients or their guardians may report history of
algorithm.
r The overall incidence of nasal button batteries is drooling, vomiting or gagging, throat or chest pain,
unknown (2). dysphagia, anorexia, abdominal pain or distension, INITIAL STABILIZATION/THERAPY
r 2 cases of severe corrosive burns to the skin have r Assess and stabilize airway, breathing, and
hematemesis, or diarrhea.
been reported when a button battery has been circulation.
PHYSICAL EXAM r Batteries should be removed emergently, regardless
lodged under a hard cast (3). r Usually asymptomatic, though fever, tachycardia,
r Button battery aspiration, with coagulation necrosis of time of last oral intake:
and/or hypotension are suggestive of GI tract Patients should be made NPO and prepared for
of the hypopharynx and respiratory mucosa, has perforation surgery.
also been reported: r Drooling may be a sign of pharyngeal or esophageal r Antibiotics should be given if there are concerns of
May lead to the formation of tracheoesophageal obstruction (more common with larger batteries) or
fistulas (4). GI tract perforation.
represent late effects such as necrosis or perforation. r Analgesic agents should be administered as needed
RISK FACTORS r Nasal bleeding or erythema
r Age (preschool years most common): for pain.
r Ear discharge or bleeding r Neutralizing agents have not been shown to
Over half of reported ingestions in 2007 occurred decrease complications.
in children <6 yr. DIAGNOSTIC TESTS & INTERPRETATION
r Agents that increase GI motility also have not been
r Developmental delay in older children Lab
r Ingestions often occur in a grandparent or elderly Initial Lab Tests shown to be effective (5).
r Unnecessary for uncomplicated cases
relatives home. MEDICATION
r For cases in which obstruction or perforation is
First Line
GENERAL PREVENTION suspected, CBC, serum electrolytes, BUN, and r Opioids:
r Prevent toddlers from having access to button
creatinine should be obtained. Morphine 0.1 mg/kg IV/IM/SC q2h PRN:
batteries. Avoid toys with button batteries. r If the removed battery containing mercury or Initial morphine dose of 0.1 mg/kg IV/SC may
r Make sure that a toys battery compartment is
cadmium is not intact, mercury or cadmium levels be repeated q1520min until pain is controlled,
properly secured. may need to be assayed. However, cases of systemic then q2h PRN.
toxicity have not been reported. Codeine/Acetaminophen dosed as 0.51 mg/kg of
codeine component PO q4h PRN
PO q46h PRN
364
FOREIGN BODY, DISC BATTERY
r NSAIDs: Issues for Referral 4. Slamon NB, Hertzog JH, Penfil SH, et al. An unusual
Relatively contraindicated in oral ingestions r Any significant esophageal injury necessitates close case of button battery-induced traumatic
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN follow-up with the surgeon for stricture formation tracheoesophageal fistula. Pediatr Emerg Care.
Ketorolac 0.5 mg/kg IV/IM q6h PRN and new or recurrent fistulas. 2008;24(5):313316.
Naproxen 5 mg/kg PO q8h PRN r ENT or pediatric surgery specialists should be 5. Litovitz T, Butterfield AB, Holloway RR, et al.
r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN contacted for operative removal of nasal or ear Button battery ingestion: Assessment of
Second Line foreign bodies in the operating room under direct therapeutic modalities and battery discharge state.
Broad-spectrum antibiotics with anaerobic coverage visualization and for follow-up if necrosis. J Pediatr. 1984;105(6):868873.
for perforation:
r Cefoxitin: FOLLOW-UP ADDITIONAL READING
Adult dose: 12 g IV q68h FOLLOW-UP RECOMMENDATIONS r Fergusson JA. Lead foreign body ingestion in
r Clindamycin: r Discharge instructions and medications: children. J Ped Child Health. 1997;33(6):542544.
30 mg/kg/day IV divided q8h, max single dose Return for respiratory distress, poor feeding, fever, r Kost KM, Shapiro RS. Button battery ingestion: A
900 mg IV q8h or chest pain. case report and review of the literature.
r Piperacillin/Tazobactam (Zosyn): r Activity: J Otolaryngol. 1987;16(4):252257.
<6 mo old: 150300 mg/kg/24 hr IV div q68h Regular activity as tolerated
>6 mo old and children: 240400 mg/kg/24 hr IV Patient Monitoring Media Element)
div q68h Children will need to be monitored as outpatients by r Burn, Chemical
Adult dose: 3 g IV q6h the primary care provider, surgeon, or r Burn, Thermal
SURGERY/OTHER PROCEDURES gastroenterologist for further complications. r Foreign Body Aspiration
r Removal techniques vary by institution: r Foreign Body, Ear
DIET
Disc batteries in the esophagus should typically be In patients with esophageal injury, NG tube feeds or r Foreign Body, Esophagus
removed promptly without delay:
Improvements in the sealing of such batteries,
pureed foods may be necessary until wounds are fully r Foreign Body Ingestion F
healed. r Foreign Body, Nose
making them less prone to leak their caustic
contents, has led some clinicians to allow a brief PROGNOSIS
period of hours to see if battery will pass to the Patients with prompt removal (prior to any esophageal
stomach. burns) of the foreign body have excellent prognosis. CODES
We do not recommend this strategy. COMPLICATIONS
Techniques include endoscopy under anesthesia, r Esophageal perforation and tracheoesophageal ICD9
magnet extraction (orogastric tube with attached r 931 Foreign body in ear
fistula formation if the battery remains in the
magnet) using fluoroscopy, and surgical removal. r 932 Foreign body in nose
esophagus or stomach more than 34 hr
r Nasal and ear foreign bodies require surgical r Gastric hemorrhage and aortoesophageal fistulas r 935.1 Foreign body in esophagus
removal if not easily extracted with an ear curette or with hemorrhage have also been described.
other small hook in the emergency department: r Children with esophageal injuries are at risk for
Alligator forceps may rarely break or damage the developing esophageal strictures, feeding PEARLS AND PITFALLS
cell, causing increased tissue damage and should difficulties, or tracheoesophageal fistulas with r Pearls:
not be routinely used. (See Foreign Body, Nose resultant pulmonary complications.
and Foreign Body, Ear topics for more details.) r Nasal septal perforation and saddle-nose deformity Esophageal disc batteries are highly concerning
for their ability to cause caustic or electrical injury.
DISPOSITION are common complications when disc batteries are Prompt removal is recommended.
Admission Criteria nasal foreign bodies. Prompt recognition and treatment can prevent
r Patients with minor esophageal burns should be significant morbidity and mortality.
monitored in the hospital. The frequent lack of initial symptoms and rapid
r NG tube feedings are recommended until wounds REFERENCES onset of mucosal injury place children at high risk
heal. 1. Bronstein AC, Spyker DA, Cantilena LR, et al. 2007 for potentially life-threatening esophageal injuries.
r Critical care admission criteria: Annual Report of the American Association of r Pitfalls:
Known esophageal rupture or hemorrhage Poison Control Centers National Poison Data Failure to appreciate the significant morbidity that
Patients with respiratory difficulty or unstable vital System (NPDS): 25th annual report. Clin Toxicol. may result from button battery ingestion, even in
signs 2008;46(10):9271057. initially asymptomatic children, may be disastrous.
Discharge Criteria 2. Glynn F, Amin M, Kisella J. Nasal foreign bodies in
r If a battery located in the ear, nose, nasopharynx, or children. Pediatr Emerg Care. 2008;24(4):
esophagus has been removed without complication, 217218.
the patient may be discharged after appropriate 3. Moulton SL, Thaller LH, Hartford CE. A wound
postsedation recovery. caused by a small alkaline cell battery under a
r Hospitalized patients should demonstrate ability to plaster cast. J Burn Care Res. 2009;30(2):355357.
tolerate feeds (either by mouth or by NG tube if
wounds necessitate).
r Consider follow-up endoscopy prior to discharge to
assess for any damage not seen on the initial
evaluation.
365
FOREIGN BODY, EAR

James A. ODonnell
r Delayed discovery of objects can result in DIFFERENTIAL DIAGNOSIS

BASICS inflammation as well as infection: r Cerumen impaction, otitis externa (OE)/otitis media
Necrotizing otitis externa (NOE): (OM)
DESCRIPTION Symptoms include severe tenderness around the r Abrasions to ear canal
r Ear foreign bodies (FBs) can be found anywhere in auricle, headache, ear drainage, and granulation r Bleeding secondary to traumatic damage to ear
the external auditory canal. tissue at the junction of the osseous and canal without FB
r Common types of FBs include (1,2): cartilaginous portions of the external ear. r TM perforation
Food: Beans, seeds, corn kernels Facial nerve palsy, mastoiditis, sepsis, r Cholesteatoma or tumor
Toys: Crayons, beads, play dough, toy parts osteomyelitis, and sigmoid sinus thrombosis can
Miscellaneous: Sponge foam, Styrofoam, pebbles, be features (5).
buttons, pencil erasers, button batteries, cotton, Children have a higher incidence of facial nerve TREATMENT
insects, earrings palsy earlier in the disease course than do
adults (6). PRE HOSPITAL
EPIDEMIOLOGY Possible causes also include retained FB and r Comfort measures
Incidence button battery erosion (1). r Keep patient NPO.
0.050.45% emergency department visits (1,3)
ETIOLOGY INITIAL STABILIZATION/THERAPY
Prevalence r Most are self-inserted due to a childs curiosity r Provide comfort measures and reassurance:
Most cases are seen below the age of 8 yr. Can be (1): Consider NSAID medication in anticipation of
seen in children as young as 12 yr. 43% of cases Can be inserted accidentally or during play prolonged pain and inflammation.
occur between the ages of 4 and 8 yr (4): r Insects can fly or crawl into the ear canal.
r No difference in occurrence in gender or right or left Keep NPO in case procedural sedation is needed
r Munchausen by proxy syndrome for removal or CT scan.
ear predilection r Need to have a cooperative patient who will lie still
r Bilateral incidence is 0.8%.
to permit adequate visualization of the ear canal
r An incidental finding in 5% DIAGNOSIS with magnification:
r Most commonly seen in the summer months If patient is uncooperative, may need to consider
HISTORY the use of procedural sedation.
RISK FACTORS r Local pain (47%)
r 45% of cases have a previous history of FB insertion. r Application of topical anesthesia to the ear canal is
r Verbal admission by child (33%)
r History of pica or developmental delay (1) r Insertion witnessed by caregiver (7%) not effective due to the impermeable keratinized
epithelial surface of the canal.
r Bleeding (4%) r The need for removal is more urgent if there is an
GENERAL PREVENTION
r Keep small objects out of reach of children. r Discharge (0.9%)
infection, if a button battery is noted in the ear
r Proper supervision of children r Foul odor coming from ear canal, or if vegetable matter has become wet.
r Parental and child education r Rare: Cough, nausea, vomiting, excessive eye r If an insect is the suspected FB, administer fluid to
tearing, headache, hearing loss (2,4) rapidly immobilize and kill the insect:
PATHOPHYSIOLOGY
r The ear canal narrows at the junction of the PHYSICAL EXAM Microscope immersion oil agent has the most
cartilaginous and osseous portions. FBs deeper in r Assess both ear canals for FB: rapid onset of action against insects (2,7):
This is typically available only if microscopy is
the canal are more difficult to remove, as are those Pulling the pinna superiorly and laterally will
straighten the external auditory canal for performed within the emergency department.
closer to the tympanic membrane (TM).
r Type of insult depends on nature of material placed adequate visualization. Mineral oil is also effective.
r Note any drainage or discharge, bleeding, evidence Benzocaine/Antipyrine has physical and
in the ear canal: pharmacologic properties that kill the insect and
Alkaline batteries (eg, button batteries) can cause of infection, or the presence of fever.
provide anesthesia to the ear canal and TM:
alkaline burns and liquefaction necrosis. DIAGNOSTIC TESTS & INTERPRETATION Of the viscous agents used, this is most likely to
Insects cause injury from movement or stinging. be readily available.
This can induce a local inflammatory or systemic Lab
r Usually no lab testing is required. Lidocaine, tetracaine, proparacaine, or alcohol
anaphylactic response: r Wound culture if infection is suspected may also be used
Have an increased incidence of damage to the
Mineral oil or microscope immersion oil are more
ear canal or infection Imaging effective than alcohol or 1% lidocaine (1,7):
Food items such as vegetable matter or breads Consider temporal bone CT scan if unable to visualize Lidocaine can make an insect exit an ear canal,
can swell with moisture exposure and induce an FB or liquefaction necrosis is suspected due to a but the movement can alarm your patient.
inflammatory response. button battery. These agents may cause middle ear inflammation
Diagnostic Procedures/Other or nystagmus if the TM is not intact.
Visualization using otoscope with an instrumentation
MEDICATION
or operating head
First Line
Antibiotics:
r Topical antibiotics:
A wide variety of these are available. A Cochrane
review indicates that these agents are currently
judged to be equally effective (8):
Polymyxin B/Neomycin solution: 4 drops b.i.d.
Ofloxacin 0.3%: 2 drops or 0.25 mL b.i.d. for
7 days if age >1 yr
366
FOREIGN BODY, EAR
r Oral antibiotics: DISPOSITION REFERENCES

Consider oral antibiotics for FBs that have been in Admission Criteria
place for >48 hr. Admit patients with malignant OE, NOE, or necrotic 1. Ansley JF, Cunningham MJ. Treatment of aural
Oral antibiotics should be given if there is cellulitis tissue damage for IV antibiotics. foreign bodies in children. Pediatrics.
of the face or neck, severe ear canal edema, or 1998;101(4):638641.
perforation of the TM or if an obstruction would Discharge Criteria 2. Brown L, Dannenberg B. A literature based
r Discharge if FB is removed and there are no further
prevent penetration of a topical antibiotic approach to the identification and management of
agent: FBs and TM is intact. pediatric foreign bodies. Pediatr Emerg Med Rep.
r If TM is perforated, recommend follow-up with ENT.
Amoxicillin 80 mg/kg/day divided b.i.d.t.i.d. 2002;7(2):93104.
Amoxicillin/Clavulanic acid 80 mg/kg/day Issues for Referral 3. McLaughlin R, Ullah R, Heylings D. Comparative
divided b.i.d.t.i.d. r ENT consultation or follow-up may be needed (48% prospective study of foreign body removal from
Clindamycin 30 mg/kg/day divided t.i.d. of cases) (2,3) external auditory canals of cadavers with right
r Consider IV antibiotics for patients with: r ENT follow-up may be needed if: angle hook or cyanoacrylate glue. Emerg Med J.
Liquefaction necrosis, malignant OE, or NOE: FB cannot be removed: 2002;19:4345.
Cefepime 100 mg/kg/day divided q12h Patient will require sedation that cannot be 4. Ngo A, Ng KC, Sim TP. Otorhinolaryngeal foreign
Piperacillin 150300 mg/kg/day divided q68h accomplished in the emergency department bodies in children presenting to the emergency
Clindamycin 2540 mg/kg/day divided q68h Round solid subjects department. Sing Med J. 2005;46(4):172178.
Second Line Object wedged in canal or up against TM 5. Rubinstein E, Ostfeld E, Ben-Zaray S, et al.
Analgesic otic solution: Glass or other sharp objects Necrotizing external otitis. Pediatrics.
Bleeding is an indication that the object may
r Benzocaine/Antipyrine (Auralgan) otic drops 1980;66:618620.
be sharp (1,2). 6. Rubin J, Yu VL, Stool SE. Maligant external otitis
SURGERY/OTHER PROCEDURES Damage to the TM has occurred. media in children. J Pediatrics. 1988;113(6):
r Surgical debridement and repair of necrotic tissues if r ENT consultation in the emergency department may 965970.
NOE is present. be needed if: 7. Kaushik V, Malik T, Saeed SR. Interventions for
r Styrofoam beads can be dissolved by spraying them
with ethyl chloride or acetone:
There is an inordinate amount of bleeding.
FB is a button battery.
acute otitis externa. Cochane Database Syst Rev.
2010;(1):CD004740.
F
Avoid the use of either if the TM is not intact or Liquefaction necrosis is suspected. 8. Lettler S, Cheney P, Tandberg D. Chemical
the lining of the ear canal is abraded. This may immobilization and killing of intra-aural roaches:
increase the risk of systemic absorption of either An in vitro comparative study. Ann Emerg Med.
agent. FOLLOW-UP 1993;22(12):17951798.
r Cooperativity and/or restraint of the patient is
FOLLOW-UP RECOMMENDATIONS See Also (Topic, Algorithm, Electronic
paramount for safe removal of FBs. r Discharge instructions and medications:
r Irrigation of the ear canal: Media Element)
Patient needs to be rechecked by the primary care Foreign Body, Disc Battery
Instill lukewarm water by means of flexible Silastic provider within 23 days post-discharge,
tubing attached to a syringe. especially if there are retained remnants of an
Irrigation is contraindicated if the TM is perforated insect or other organic matter, which can cause an
or if the FB is suspected to be a button battery, inflammatory reaction or serve as a nidus for
CODES
bean, or other vegetable material. infection in the ear canal.
r Suction: ICD9
Always consider discharging on antibiotic drops.
Limited usefulness Use oral antibiotics for OM or more serious cases 931 Foreign body in ear
Noise may frighten patient. of OE.
May push FB deeper into the canal Consider analgesic agents for home use at
The Schuknecht FB suction catheter works best. discharge.
PEARLS AND PITFALLS
r Katz Extractor: A mini Foley catheter-like device r Activity: r Pearls:
inserted past the FB then inflated and withdrawn Avoid swimming and getting water into ear canal Examine the TM and ear canal before and after
r Right angle, nerve hook, or angled curette: until the damage resulting from the aural FB has any attempted removal to look for additional FBs,
Insert past FB, rotate 90 degrees, and withdraw. healed. remnants, or damage to the canal or TM.
Can cause pain or damage to canal or TM if Examine the opposite ear and nose, as children
Patient Monitoring
inserted improperly can place multiple FBs.
r Alligator or Hartman forceps: Advise family to observe the patient for increased
r Pitfalls:
pain, foul-smelling discharge from the ear canal,
Most successful with small objects in the lateral swelling around the ear, persistent fevers, or altered Avoid cold water irrigation of the ear canal, as this
3rd of the canal mental status. can induce vertigo and nystagmus.
Can push FB deeper into the canal Almost 50% of aural FBs cannot be primarily
Not best choice for removing a large or smooth PROGNOSIS removed. Repeated attempts lead to increased
FBs Children do well if a timely diagnosis is made. complications.
r Cyanoacrylate (Super Glue) (3): Unless the treating physician has a reasonable
COMPLICATIONS
Place 1 drop of cyanoacrylate on the tip of a r Trauma to the canal expectation that the FB can successfully be
cotton swab or hollow plastic stick. Press this r Facial nerve palsy removed, it is preferable to have ENT attempt
against the FB for 2560 sec. Once adherent to r Ear canal laceration or hematoma removal.
the swab, remove the FB and stick from canal. r OE
Best for smooth and dry FBs (eg, beads) r Perforation of the tympanic membrane
This technique is unsuitable for uncooperative
r Auditory ossicle dislocation
patients or those with a tortuous canal, large
tragus, or poorly visualized FBs.
Can result in glue stick being cemented to the ear
canal or pushing the FB in deeper
367
FOREIGN BODY, ESOPHAGUS

Marc A. Auerbach
Lilia Reyes
r Once a swallowed foreign body reaches the stomach r Physical findings may be due to complications of
BASICS within a normal GI tract, it is likely to pass through foreign body migration or esophageal perforation. In
within 46 days and less likely to lead to this situation, the following will be found:
DESCRIPTION complications: Drooling, pooling of secretions
r Foreign bodies discussed here are coins, sharp Possible problem sites more distal include the Rales, swelling or crepitus in neck, or peritonitis
foreign bodies, long or large objects, magnets and pylorus, the fixed curves of the C loop of the Respiratory distress that can manifest as:
lead, and impacted food. duodenum (ie, secondary to its retroperitoneal Stridor
r Coins are the most common ingested foreign body location), and the ileocecal valve. Wheezing
in the U.S. and Europe. Increased work of breathing
r In Asia and other countries where fish is a large ETIOLOGY
r Food boluses DIAGNOSTIC TESTS & INTERPRETATION
component of the diet, fish bone ingestion and r Esophageal abnormalities
impactions are common.
Imaging
r Oral behavior of younger children r Chest/Abdominal radiography is most useful given
r Meat/Food impaction is common in adolescents and
that most foreign bodies ingested by children are
adults. COMMONLY ASSOCIATED CONDITIONS radiopaque.
Esophageal abnormalities r Coins in the esophagus appear in an en face
EPIDEMIOLOGY
Data from the American Association of Poison Control position on an AP view and the edge of the coin will
Centers suggest that in 2007 there were more than DIAGNOSIS be seen on the lateral view, while the opposite if the
125,000 cases of foreign body ingestion by children coin is in the trachea.
<19 yr old: HISTORY r If the swallowed object is below the diaphragm,
r Incidence is highest in children ages 6 mo to 4 yr of r Children present after a caregiver witnesses the
further radiography is generally unnecessary since
age. ingestion of a foreign body or after a child reports the object should pass through the GI tract in the
r 98% of foreign body ingestions in children are ingestion to a caregiver. setting of normal anatomy.
r Often presents asymptomatically r Radiolucent objects in the esophagus may be better
accidental (1).
r May have vague symptoms that do not promptly visualized if the study is done after having the
RISK FACTORS suggest foreign body ingestion patient drink a small amount of dilute contrast (ie,
r Foreign body entrapment and subsequent
r The child may present with signs or symptoms of a should not be done if endoscopy is planned).
perforation are more likely at the site of a congenital r CT scan or MRI is rarely indicated.
complication of ingestion.
malformation or at the site of prior surgery. r Esophageal foreign body symptoms:
r 95% of meat impaction has underlying esophageal Diagnostic Procedures/Other
Dysphagia Handheld metal detectors have been shown to have
pathology that contributes to impaction:
Food refusal 100% sensitivity and 92.4% specificity in experienced
Pathology includes peptic ulcers, caustic injury, or
Drooling hands in identifying the location of ingested metallic
postoperative strictures.
Emesis/Hematemesis objects (2).
A more recently recognized pathology is
Foreign body sensation
eosinophilic esophagitis. DIFFERENTIAL DIAGNOSIS
r Food impaction may also be associated with Chest pain
r Esophagitis
Sore throat
underlying motility disorders. Stridor r Viral or streptococcal pharyngitis
r Mental retardation and psychiatric illness are r Croup or retropharyngeal abscess
Cough
associated with foreign body ingestion. Unexplained fever r Upper respiratory tract infection
r Stomach/Lower GI tract foreign body symptoms: r Psychological sensation or hysteria
GENERAL PREVENTION
r Parents should be advised to keep coins, sharp Abdominal distention/pain
foreign bodies, long or large objects, magnets, and Vomiting
lead-based toys out of reach of small children. Hematochezia TREATMENT
r Education on cutting food into manageable Unexplained fever
proportions and complete mastication of food prior PRE HOSPITAL
PHYSICAL EXAM Assess and stabilize airway, breathing, and
to swallowing r Physical exam is usually normal.
r Signs mentioned in the History section may be circulation.
PATHOPHYSIOLOGY r Using abdominal thrusts to dislodge a foreign body
r 3 main locations: Esophagus, stomach, and lower GI present.
r Abrasions, blood streaks, or edema in the in a spontaneously breathing patient without
tract respiratory distress is not advised.
r Esophagus has 3 typical locations of impaction: hypopharynx may be evidence of proximal
6070% impact at thoracic inlet, 1020% lodge swallowing-related trauma. INITIAL STABILIZATION/THERAPY
r Inspection of the oropharynx may reveal an r Patients with drooling, marked emesis, or altered
in the mid-esophagus at the level of the aortic
notch, and 20% lie just above the lower impacted foreign body. mental status may need supportive measures to
esophageal sphincter: r Drooling or pooling of secretions suggests an protect the airway.
The thoracic inlet is the area between the r Coin ingestion:
esophageal foreign body but may be due to an
clavicles on CXR. esophageal abrasion. Emergent endoscopic removal of esophageal coins
In the esophagus, there is an anatomic change should be performed in symptomatic patients
from skeletal muscle to the smooth muscle. unable to swallow their secretions or who are
The cricopharyngeus sling at C6 may provide an experiencing acute respiratory symptoms.
area of further entrapment of foreign body.
368
FOREIGN BODY, ESOPHAGUS
r If asymptomatic, can delay to allow for appropriate SURGERY/OTHER PROCEDURES

r Endoscopy by subspecialist
REFERENCES
fasting prior to endoscopy:
If the coin passes beyond the esophagus, routine r Foley catheter method for removal of blunt 1. Bronstein AC, Spyker DA, Cantilena LR Jr., et al.
removal is not indicated. esophageal foreign body: 2007 Annual Report of the American Association
r Repeat radiograph to see if object has moved. Only experienced personnel should perform this of Poison Control Centers National Poison Data
r Glucagon, benzodiazepines, and nifedipine have not procedure. System (NPDS): 25th annual report. Clin Toxicol.
been shown to be effective in the passage of This procedure should be reserved for healthy 2008;46(10):9271057.
esophageal foreign bodies in children. children and those with a history of witnessed 2. Seikel K, Primm PA, Elizondo BJ, et al. Handheld
r The majority of coins that pass asymptomatically to ingestion of blunt foreign body <24 hr prior. metal detector localization of ingested metallic
the stomach or distally can be managed r Bougienage method for removal of blunt foreign bodies: Accurate in any hands? Arch
conservatively to see if they spontaneously pass esophageal foreign body: Pediatr Adolesc Med. 1999;153(8):853857.
through the GI tract. Only experienced personnel should perform this 3. Traub SJ, Nelson LS, et al. Pediatric body packing.
r When multiple coins are ingested, they may adhere procedure. Arch Pediatr Adolesc Med. 2003;157:174177.
to each other, impairing transpyloric passage. 4. Blaho KE, Merigian KS, Winbery SL. Guideline for
DISPOSITION
r Sharp foreign bodies: Safety pin ingestion is a fairly the management of ingested foreign bodies.
Admission Criteria Gastrointest Endosc. 2002;55:802806.
common sharp ingestion for children. Nonstraight- r Children who require endoscopic foreign body
pin sharps may require endoscopic or, in some cases, 5. Kay M, Wyllie R. Pediatric foreign bodies and their
removal usually require admission. management. Curr Gastroenterol Rep. 2005;7(3):
surgical removal. r Critical care admission:
r Long or large objects: 212218.
Esophageal perforation and/or respiratory
Primary sites of impaction are the esophagus, the compromise
pylorus (ie, may not allow passage of objects
>15 mm in diameter), and the duodenal C loop Discharge Criteria ADDITIONAL READING
r Patient may be discharged soon after successful
(ie, may not allow for passage of objects >10 cm Schunk J. Foreign body-ingestion/aspiration. In
in length). endoscopic removal foreign body without
Fleisher GR, Ludwig S, eds. Textbook of Pediatric
r Endoscopy may be performed on a patient who is complications.
r Asymptomatic patients in whom the foreign body Emergency Medicine. 6th ed. Philadelphia, PA: F
asymptomatic after appropriate preanesthesia Lippincott Williams & Wilkins; 2010.
fasting. has been removed or has passed to the stomach
r Urgent endoscopy is required in symptomatic See Also (Topic, Algorithm, Electronic
Issues for Referral
r Surgery or GI specialists should be consulted for Media Element)
patients despite the risk of aspiration or impaired r Foreign Body Aspiration
visualization of the object. endoscopic removal of foreign bodies. r Foreign Body Ingestion
r Magnets and lead: r A healthy child with repeated foreign body
Ingestion of >1 magnet may be hazardous impaction should be evaluated for an underlying
because magnets are able to attract each other, esophageal disorder.
resulting in fistulization, obstruction, and/or CODES
perforation.
Early endoscopic removal is recommended if FOLLOW-UP ICD9
>1 magnet is visualized on radiography. 935.1 Foreign body in esophagus
Given that lead-based foreign bodies ingested can
cause lead toxicity, early endoscopic removal is r Return for any respiratory distress, chest pain,
recommended. PEARLS AND PITFALLS
r Food impaction: drooling, neck swelling, abdominal distension or r Children without symptoms may still have an
Symptomatic patients unable to handle their pain, or inability to swallow.
esophageal foreign body that requires removal.
secretions require urgent endoscopic PROGNOSIS When in doubt, obtain a radiograph.
disimpaction. Those who can handle their Excellent r Consider foreign body ingestion in young children
secretions require endoscopy within 12 hr. who present with their 1st episode of wheezing,
Papain or meat tenderizer should not be used, COMPLICATIONS
r Intestinal perforation is a risk for battery or magnet stridor, or drooling.
as this may lead to hypernatremia and severe
esophageal injury. ingestion.
r Swallowed drug packages: r Esophageal rupture or perforation from attempted
Children and adults swallow drug-filled balloons, removal or displacement using Foley catheter
condoms, finger cots, and plastic kitchen wrap in a method or bougienage
variety of sizes:
The asymptomatic patient can be observed for
passage with administration of activated
charcoal to prevent further drug absorption
followed by nonoil-based oral cathartic (ie,
polyethylene glycol) (3).
Symptomatic patients with drug toxicity or
obstruction require stabilization and surgical
therapy for ruptured cocaine packets (4,5).
r Disc batteries should be removed emergently,
regardless of time of last oral intake.
These pose risk of esophageal injury, including
perforation from both conducted electrical current
and caustic material that may leak.
369
FOREIGN BODY, NOSE

Ee Tein Tay
BASICS DIAGNOSIS r Nasal tumor or mass
r Nasal polyp
DESCRIPTION HISTORY r Septal hematoma
r Nasal foreign bodies are most commonly found on r Most nasal foreign bodies are often asymptomatic
r Foreign body that has already been removed or
floor of nasal passage, below the inferior turbinate. and incidentally noted by the caregiver or patient.
r Common types of foreign bodies inserted: r Can often elicit a history of child placing a foreign dislodged by the time of the emergency department
visit
Food: Corn kernels, seeds, beans body in the nose
Toys: Crayons, beads, play dough, plastic toy parts r Foul chronic nasal discharge, usually unilateral
Miscellaneous: Paper, Styrofoam, magnets, rocks, r Epistaxis TREATMENT
buttons, erasers r Pain or discomfort
r Sneezing PRE HOSPITAL
EPIDEMIOLOGY Assess and stabilize airway, breathing, and
r Snoring
Incidence circulation.
r Mouth breathing
0.1% of pediatric emergency department visits
Prevalence PHYSICAL EXAM r Assess and stabilize airway, breathing, and
r Most common in children between 2 and 4 yr of age r Foreign body visualized in nasal cavity
circulation.
r Gender ratio depends on type of foreign body: r Fever r Prevent child agitation to decrease the risk of airway
Beads: Male to female ratio is 1:1.9. r Nasal discharge
aspiration.
Plastic toys: Male to female ratio is 1:1. r Epistaxis r Patient may need to be appropriately restrained with
r May have septal laceration or perforation a papoose or sedated to achieve optimal conditions
GENERAL PREVENTION
r Keep small objects out of the reach of children. r Enlarged nasal turbinate or mucosal edema to remove the object.
r Parental and child education r Bony destruction
r Granulation tissue from chronic foreign body MEDICATION
r Proper child supervision r 1% lidocaine without epinephrine drops to nasal
r Requires a light source for visualization such as an
PATHOPHYSIOLOGY cavity for local anesthesia, up to 5 mg/kg:
otoscope, a nasal speculum, or an illuminated Consider using 2% viscous lidocaine as lubricant
Pathophysiology depends on the composition of the
magnifying glass to fully examine the patient when using a Foley catheter for removal.
foreign body:
r 0.5% phenylephrine spray to decrease mucosal
r Battery corrosion may release alkaline material DIAGNOSTIC TESTS & INTERPRETATION
Lab swelling, 12 sprays in affected nostril
when in contact with moist mucosa, producing r Antibiotics:
thermal burn. CBC, ESR, C-reactive protein, and/or blood culture if
r Nasal foreign bodies may exert a mass and pressure infection is suspected Consider Cephazolin if suspected facial cellulitis:
25100 mg/kg/24 hr q68h IV.
effect. Imaging
r Certain items such as food can cause a local and Consider ampicillin/sulbactam if suspected sinus
Consider radiographic imaging of nasal bones if involvement: 100200 mg/kg/24 hr q6h IV or IM.
systemic inflammatory response that results in unable to visualize a radiopaque foreign body in the
increased swelling. nasal cavity.
ETIOLOGY Diagnostic Procedures/Other
Insertion of a foreign body for curiosity or r Visualization using an otoscope, an illuminated
entertainment by a child magnifying glass, or a nasal speculum
r Use of a fiberoptic scope either by an emergency
Foreign body in the opposite nasal passage or another department physician or an otolaryngologist
body orifice
370
FOREIGN BODY, NOSE
r Use a light source and nasal speculum during
Discharge Criteria
r Well appearing with normal vital signs
ADDITIONAL READING
foreign body removal. r No airway compromise or concerns r Davies PH, Benger JR. Foreign bodies in the nose
r Techniques for removal: and ear: A review of techniques for removal in the
Issues for Referral emergency department. J Accid Emerg Med.
Parents kiss: Otolaryngology referral if removal is anticipated to be
Caretaker applies positive pressure through the 2000;17(2):9194.
difficult, attempt at removal is unsuccessful, or r Hein SW, Maughan KL. Foreign bodies in the ear,
childs mouth and simultaneously occludes the perforation or mass is suspected
contralateral nostril nose and throat. Am Fam Physician. 2007;76(8):
Oral insufflations with a bag valve mask: 11851189.
Positive pressure applied similar to parents FOLLOW-UP r Kadish HA, Corneli HM. Removal of nasal foreign
kiss bodies in the pediatric population. Am J Emerg Med.
Hooked probe or alligator forceps for foreign body FOLLOW-UP RECOMMENDATIONS 1997;15(1):5456.
r Discharge instructions and medications: r Kiger JR, Brenkert TE, Losek JD. Nasal foreign body
close to anterior nares
Balloon catheter: Follow up with a primary care physician or return removal in children. Pediatr Emerg Care. 2008;
Insert a 58 French Foley or 46 Fogarty to the emergency department if there is prolonged 24(11):785789.
catheter past foreign body, inflate balloon epistaxis, respiratory difficulty, or signs and
23 mL, then withdrawal catheter with foreign symptoms of infection.
body. Routine antibiotics are not recommended for CODES
Suction catheter for round, smooth object close to patients without septal perforation or signs of
the anterior nares bacterial infection.
r Activity: ICD9
Saline washout: 932 Foreign body in nose
Use a high-pressure bulb syringe filled with May resume normal routine without activity
isotonic sodium chloride to the contralateral restrictions
nostril.
PROGNOSIS PEARLS AND PITFALLS
Saline can also cause objects to swell or change
in consistency.
Usually full recovery after retrieval of foreign body r Pearls: F
Organic matter/food COMPLICATIONS Sedation may reduce the cough or gag reflex if a
Forceful injection of saline can be a powerful r Nasal foreign body gets into trachea foreign body is pushed into the pharynx, resulting
choking stimulus. r Epistaxis in airway compromise.
Cyanoacrylate glue: r Nasal septal ulceration or perforation Reinspect the nose and other orifices for a 2nd
Apply a small amount on a cotton swab, press r Nasal meatal stenosis foreign body prior to discharge.
onto object for 60 sec, then attempt removal. r Thermal burn with button batteries Consider using viscous lidocaine as a lubricant
Magnet for use for retrieval of metallic objects r Pressure necrosis with magnets when using a Foley catheter for removal.
r Pitfalls:
DISPOSITION r Pain and discomfort from removal
r Laceration Risk of aspiration or pushing object further into
Admission Criteria the nasal cavity, particularly if removal is
r Aspiration of foreign body resulting in airway r Barotrauma from positive pressure
attempted in an uncooperative child
compromise r Accidental adhesion of glue to mucosa
r Removal requiring surgical intervention r Infection risks:
r Infection requiring parenteral antibiotics
Acute otitis media
Sinusitis
Facial cellulitis
Periorbital cellulitis
371
FOREIGN BODY, RECTUM

Mandisa A. McIver
Robert F. Gochman
BASICS DIAGNOSIS r DRE
r Anoscopy
DESCRIPTION HISTORY r Rigid sigmoidoscopy
r The frequency of rectal foreign bodies encountered r There may be a history of anal manipulation, foreign
in the emergency department is increasing. body insertion, or sexual abuse: Pathological Findings
r Patients are reluctant to disclose their presence, Ask how long the foreign body has been in the r Intra-abdominal free air
rectum. r Peritoneal signs on abdominal exam
which only delays their removal.
r The most serious complication is perforation of the Inquire as to how many attempts have been made r Rectal bleeding
rectum or colon. to remove the object.
If self-introduced or concealing an object, the DIFFERENTIAL DIAGNOSIS
r There is a high success rate for outpatient r Constipation
history is often vague or inconsistent. r Rectal tear
management. r The patient may complain of anal or abdominal
r Hemorrhoids
EPIDEMIOLOGY pain, constipation, rectal bleeding, difficulty voiding,
r Intestinal polyp
Incidence or fever.
r Increasing incidence due to increasing popularity of r Perirectal abscess
PHYSICAL EXAM
anal eroticism r On external exam, look for signs of trauma.
r 33% of patients with self-introduced rectal foreign r Attempt to palpate the foreign body on digital rectal TREATMENT
bodies do not initially admit to the act (1). exam (DRE) or anoscopy for better visualization,
Prevalence only if a sharp object is not suspected: PRE HOSPITAL
Unknown r Pain management
Low-lying objects are normally palpable by DRE
and are often easily removed in the emergency r NPO for possible sedation/general anesthesia
RISK FACTORS r Do not attempt to remove a rectal foreign body.
r Young children department.
r Psychiatric patients High-lying objects above the rectosigmoid
junction are difficult to visualize and remove. INITIAL STABILIZATION/THERAPY
r Victims of assault r Sphincter relaxation is mandatory for removal of
High-lying objects are 2.25 times more likely to
require operative intervention (2). large foreign bodies.
GENERAL PREVENTION r In consultation with surgery, consider the
Careful insertion of rectal thermometers and enema r Abdominal exam may reveal tenderness to palpation
or peritoneal signs if perforation or obstruction is following methods of analgesia and foreign body
tips
present. removal (4):
PATHOPHYSIOLOGY r There may be bloody discharge from the rectum or Local infiltrative anesthesia or IV sedation is
r Delay in presentation and multiple attempts at useful.
loose sphincter tone.
self-removal may lead to mucosal edema and injury For digital extraction, lubricate the area with
as well as muscular spasm. DIAGNOSTIC TESTS & INTERPRETATION lidocaine jelly and use the other hand to apply
r Perforation of the rectal wall can lead to extension Lab abdominal pressure.
of injury into the peritoneum or perineum: Initial Lab Tests Grasp the edge of the object with forceps and
2/3 of the rectum is extraperitoneal. r No labs are required for emergency department apply traction while the patient bears down to
management. perform a Valsalva maneuver.
ETIOLOGY r CBC may reveal leukocytosis, which is suggestive of For anal block, inject local anesthetic with a
r Most objects found in children are self-introduced or
perforation. 30-gauge needle. Raise an intradermal wheal at 6
placed iatrogenically (ie, tip of thermometer).
r They are also found in psychiatric patients, victims of r Preoperative labs may be indicated if the patient is and 12 oclock positions. Then, with a larger
needle, inject circumferentially along the internal
assault, cases of concealment (ie, weapons or drug requiring surgical removal of the object.
sphincter muscles along the anal canal.
packets), patients with constipation, and from sex Imaging If the object has created a vacuumlike effect, pass
practices. r Plain abdominal radiographs can detect
a well-lubricated Foley catheter beyond the object
r It is possible to have an ingested foreign body intra-abdominal free air: and inflate a balloon to break the seal and aid in
lodged in the rectum (ie, toothpick, chicken bone). An upright image can assist in looking for free air removal.
r Sexual assault and child abuse must be considered. under the diaphragm. For removal, you may need to use a vaginal
r Radiographs are also used to determine the number speculum, obstetric forceps, or an obstetric
r Psychiatric disorder of foreign bodies as well as the shape, surface vacuum extractor.
outline, location, and direction (3). r Limit time for attempts at removal to 30 min (4).
r Constipation
r May need serial images to follow progress of object r In patients where multiple exams or attempts to
through rectum remove the foreign body occur, admit the patient for
r Radiographic study with contrast: a higher level of anesthesia and more invasive exam
Use water-soluble contrast if perforation is techniques.
suspected.
372
FOREIGN BODY, RECTUM
r If there is concern for ischemic anorectal mucosa, DISPOSITION REFERENCES

more invasive exams should be performed in the Admission Criteria
operating room under general anesthesia. r Failed extraction attempts in the emergency 1. Ooi BS, Ho YH. Management of anorectal foreign
r Consider broad-spectrum antibiotics (3rd-generation department that require surgical removal in the bodies: A cause of obscure anal pain. Aust N Z J
cephalosporins) for risk of perforation or if excessive operating room. Surg. 1998;68(12):852855.
manipulation has been performed. r May admit for observation for possible descension 2. Lake JP, Essani R, Petrone P, et al. Management of
r For suspected perforation/peritonitis, consider of high-lying object into rectum retained colorectal foreign bodies: Predictors of
antibiotic combinations that cover gram-positive, r Critical care admission criteria: operative intervention. Dis Colon Rectum.
gram-negative, and anaerobic organisms. Signs of perforation 2004;47(10):16941698.
Rectal laceration 3. Kingsley AN, Abcaman H. Colorectal foreign
MEDICATION bodies: Management Update. Dis Colon Rectum.
Peritonitis/Sepsis
First Line 1985;28(12):941944.
Obstruction
Benzodiazepine to relax patient and anal sphincters: 4. Wigle R. Emergency department management of
r Diazepam 0.10.2 mg/kg/dose mg IM/IV/PO q12h Discharge Criteria retained foreign bodies. Am J Emerg Med.
r Stable after observation for 12 hr
as needed, max single dose 10 mg 1998;6(4):385389.
r No signs of perforation, peritonitis, or sepsis
Second Line r Normal postextraction sigmoidoscopy 5. Clarke DL, Buccimazza I, Anderson FA, et al.
r Antibiotics: Colorectal foreign bodies. Colorectal Dis. 2005;
For suspected perforation/peritonitis, consider the Issues for Referral 7(1):98103.
following antibiotic combinations for r Psychiatric counseling 6. Azman B, Erkus B, Guvenc H. Balloon extraction of
gram-positive, gram-negative, and anaerobic r Social work if sexual abuse is suspected: a retained rectal foreign body under fluoroscopy,
coverage. In this case, all children in the family should be case report and review. Pediatr Emerg Care.
r Single drug therapy might be accomplished by evaluated. 2009;25(5):345347.
piperacillin/tazobactam (Zosyn) alone:
Piperacillin/Tazobactam (Zosyn): FOLLOW-UP
>6 mo and children 240400 mg/kg/day IV ADDITIONAL READING F
divided q68h; Adult: 3 g IV q6h FOLLOW-UP RECOMMENDATIONS r Busch DB, Starling JR. Rectal foreign bodies: Case
r Cefotaxime and metronidazole (Flagyl): r Discharge instructions and medications:
reports and a comprehensive review of the worlds
Cefotaxime: Follow up with primary care physician in 24 hr. literature. Surgery. 1986;100(3):512519.
Infants >30 days and children: 150 mg/kg/day Follow up with surgeon within 3 mo for loss of r Koornstra JJ, Weersma RK. Management of rectal
IV divided q8h anal sphincter tone or fecal incontinence. foreign bodies: Description of a new technique and
Adult dose: 2 g IV q8h Return for abdominal pain or distension, fever, clinical practice guidelines. World J Gastroenterol.
Metronidazole: vomiting, or severe rectal bleeding. 2008;14(27):44034406.
Metronidazole 1550 mg/kg/day IV divided Stool softeners r Memon JM, Memon NA, Khatri MK, et al. Rectal
q8h; Adult dose: 500750 mg IV q8h Pain medication
r Ciprofloxacin and clindamycin: r Activity: foreign body: Not a rarity. Gomal J Med Sci. 2007;
5(2):7274.
Ciprofloxacin: As tolerated r Roberts JR, Hedges JR, eds. Anorectal procedures. In
Max single dose 1.2 g/day
Patient Monitoring Clinical Procedures in Emergency Medicine. 5th ed.
After removal, watch the patient for any intestinal Philadelphia, PA: Saunders; 2009.
Clindamycin: strictures, abdominal distension, obstruction, or r Shah BR, Lucchesi M, eds. Gastrointestinal
inability to pass stools. disorders. In Atlas of Pediatric Emergency Medicine.
Max single dose 900 mg IV q8h
DIET Columbus, OH: McGraw-Hill; 2006.
SURGERY/OTHER PROCEDURES No restrictions
Surgical consult should be obtained for (2,4,5): See Also (Topic, Algorithm, Electronic
r Large foreign body PROGNOSIS Media Element)
r High-lying foreign body (above rectosigmoid r Most patients do well post extraction. Trauma, Perineal
r Serious complications are rare.
junction)
r Foreign bodies in place >2 days with surrounding r Operative repair may include colostomy.
CODES
rectal edema COMPLICATIONS
r Smooth objects without a natural lever r Failure to remove the foreign body
r Fragile objects ICD9
r Perforation (most serious)
937 Foreign body in anus and rectum
r Sharp objects r Deep mucosal tear
r Unsuccessful attempts in emergency department r Perianal infection (bacteremia/sepsis)
r Peritonitis PEARLS AND PITFALLS
r Intestinal perforation r If the history suggests a foreign body with a sharp
r Postremoval sigmoidoscopy is recommended (2).
edge, the physician should forego the DRE.
r It is recommended to remove all mercury deposits
from a broken mercury thermometer to prevent local
mercury absorption (6).
r Use of enemas or cathartics may increase the risk of
perforation (especially with sharp foreign bodies).
r Concomitant drug intoxication or moving
battery-operated objects may require delay of
surgery until conditions are safe.
373
FOREIGN BODY, SOFT TISSUE

Jeranil Nunez
RISK FACTORS r Complaint of FB sensation

BASICS r History of an object that has shattered (glass), r Pain with passive movement of the area
splintered (wood, metal), or broken (teeth) on r In the preverbal child, a nonresolving infection
DESCRIPTION contact with open skin or has contaminated a refractory to antibiotic therapy (cellulitis,
r Patients presenting with open wounds or where skin wound (debris, gravel, chemicals) culture-negative abscess, persistent purulent
has been penetrated (eg, abrasions, lacerations, r Deep wounds (>5 mm) drainage) or bony changes on radiographic studies
puncture wounds) have risk of retained foreign body r Wounds whose depth is not visible may be the only clue to retained FB.
(FB). r Puncture wounds through clothing or shoes
r FBs in soft tissue can cause: r Prior attempt at removal (possible retention of PHYSICAL EXAM
r FBs may be visible to the naked eye either as a mass
Toxic or allergic reactions fragments)
Damage to vital structures such as nerves, or discoloration in the epidermis.
GENERAL PREVENTION r Suspicion for a retained FB when there is:
tendons, vessels, or joints
Infection resistant to antibiotic therapy Appropriate protective gear Pain with deep palpation over a puncture wound
Acute or chronic, recurrent inflammation or a palpable, tender mass
PATHOPHYSIOLOGY Puncture wounds +/ signs of infection:
Destruction of surrounding soft tissue or bony r The bodys normal transient inflammatory reaction
abnormalities Surrounding erythema
r Some soft tissue FBs should or need to be removed in response to soft tissue injury is often prolonged in Induration
the presence of a retained FB, resulting in delayed Tenderness
immediately. The size, composition, location, and wound healing. If excessive, there may be
accessibility of the FB, potential tissue damage from Drainage
destruction of surrounding soft tissue. Abscess
wound exploration, difficulty of FB extraction, and r Increased granulocyte and macrophage proliferation r Patency of circulation and neurologic function
risks of future complications should all be weighed with release of collagenases and proteases attempt
against the benefits of removal. (sensory, motor) should be carefully assessed in all
r Indications for removing FBs (1): to dissolve and extrude the foreign material. patients with open wounds and FBs.
r If unable to destroy the FB, macrophages that have
Reactive material likely to cause: ingested the foreign material coalesce into DIAGNOSTIC TESTS & INTERPRETATION
Intense inflammation or infection (thorns,
multinucleated giant cells that then become encased Lab
spines, vegetative material) in a dense fibrous capsule (granuloma). Once Wound culture/fungal culture if there is purulent
Allergic reaction
encapsulated, the inflammatory response subsides drainage or an abscess
Toxicity (heavy metals, spines with venom)
but can recur with minor trauma to the area. Imaging
Impingement on or damage to tendons, vessels, or r Vegetative, organic foreign materials such as wood, r Radiopaque FBs:
nerves
thorns, and plant spines may trigger an intense Plain radiographs (min 2 views):
Heavy bacterial contamination
Impairment of mechanical function
inflammatory reaction and can lead to infection Surface markers (paper clips, needles, grids)
(usually fungal). placed over the puncture wound can aid in
Intra-articular or intravascular location r In some instances, the inflammatory response can
Proximity to fractured bone localization.
Potential for migration toward important anatomic represent an allergic reaction (blackthorns, rose Likely visible: Metal, glass >2 mm, gravel/stone,
structures (glass, metal, plastic) thorn, cactus spine) or a toxin-mediated reaction bone, aluminum, teeth, pencil graphite
Persistent pain (sea urchin spines with venom, heavy metals). In Fluoroscopy: Most useful intraoperatively
very rare cases, systemic toxicity can result from r Radiolucent FBs:
Established inflammation or infection
Cosmetic deformity or psychological distress exposure (lead, mercury) (3). US:
r FBs embedded in the thoracic cavity, abdominal ETIOLOGY Best method to visualize wood, vegetative
cavity, or neck should be left in place and surgical r FB embedded in soft tissue as sustained from direct material, and rubber
consultation sought for wound exploration and FB trauma or a fall onto a dirty surface CT or MRI are recommended in cases of:
removal under general anesthesia. r Penetration of skin by FBs with retention of material Failed exploration or persistent infection with
r High-pressure injection accidents (eg, paint guns) (thorns, splinters, cacti, branches, nails, needles, negative radiographic findings
Foreign material embedded in area
require urgent surgical consultation. Injected paint, glass, fish hooks, etc.)
Need for 3-dimensional analysis for better
grease, and hydrocarbons can lead to intense local
inflammation, tissue destruction, and necrosis with
COMMONLY ASSOCIATED CONDITIONS surgical approach and exploration
r Lacerations
possible need for amputation. r Puncture wounds Diagnostic Procedures/Other
All open wounds should be thoroughly irrigated and
EPIDEMIOLOGY
carefully inspected before and after attempted FB
Incidence
In 1 prospective study, the most common complication
DIAGNOSIS removal. If there are multiple FBs present, repeat
imaging studies after removal are recommended.
of pediatric lacerations was retained FB (2%) (2): HISTORY
r Glass, wood, and metal accounted for the majority r Detecting FB in soft tissue can be difficult. DIFFERENTIAL DIAGNOSIS
r Cellulitis
of the retained FBs. r Detailed history of mechanism of injury is
r Abscess
essential: r Soft tissue mass
All elements listed in the Risk Factors section
r Vascular thrombosis
Composition, size, and location of possible FB
Multiple wounds r Septic or traumatic arthritis
Time elapsed from injury (Wounds >24 hr old are r Bone cyst, tumor
more difficult to examine and have increased risk
of infection.)
374
FOREIGN BODY, SOFT TISSUE
r Cactus spines can be pulled out with careful traction PROGNOSIS

r Most inflammatory responses resolve completely
TREATMENT along the axis of insertion:
If many cacti are present, depilatory wax or after FB extraction.
PRE HOSPITAL woodworking glue can be used for simultaneous r Retained FBs that cause recurrent inflammation,
r Hemostasis: Sterile dressings should be placed over extraction. infection, and tissue damage or migrate toward vital
exposed surface areas to minimize contamination of r FBs in the hand may be removed in the emergency structures can cause significant morbidity.
open wounds and control active bleeding. department if:
r In cases of hypotension, IV fluid boluses COMPLICATIONS
Visible through the existing wound r Delayed wound healing with recurrent inflammation
r Pain management as needed No additional skin incisions are needed
and scarring
Minimal bacterial contamination r Infection: Cellulitis, culture-negative abscess,
INITIAL STABILIZATION/THERAPY No tendon or neurovascular injuries
r Hemostasis lymphangitis, bursitis, synovitis, arthritis,
Otherwise, consultation with a surgical hand
r Superficial wound irrigation and exploration osteomyelitis
specialist is recommended. r Bony abnormalities: Periosteal thickening, bone
r Skin debridement of devitalized tissue
MEDICATION pseudotumors, osteolytic lesions
r Small, inert material (glass, metal, plastic)
First Line r Migration of FB
r Pain management: embedded in benign locations not readily accessible r Vascular thrombosis
Local anesthetics: for removal can be left in place and removed
r Loss or limitation of function
Injected lidocaine with or without epinephrine electively if necessary.
r Wound closure as needed:
SC
Lidocaine/Epinephrine/Tetracaine (LET) topically Delayed primary closure and prophylactic
antibiotics are recommended for wounds >24 hr
REFERENCES
if minimal risk of infection
Not to be used in patients with high-pressure old or with heavy bacterial contamination. 1. Lammers RL, Magill T. Detection and management
injection injuries r Surgery/Plastic surgery/Orthopedic surgery of foreign bodies in soft tissue. Emerg Med Clin
Opioids: consultation as indicated based on location of FB North Am. 1992;10:767781.
DISPOSITION 2. Baker MD, Lanuti M. The management and F
Admission Criteria outcome of lacerations in urban children. Ann
be repeated q1520min until pain is r Inpatient ward admission criteria: Emerg Med. 1990;19:10011005.
controlled, then q2h PRN. 3. Lammers RL. Soft tissue foreign bodies. Ann Emerg
Fentanyl 12 g/kg IV q2h PRN: Need for parenteral antibiotics
FBs embedded in critical areas requiring surgical Med. 1998;17:13361345.
exploration and intervention (tendons, nerves, or 4. Kaiser WC, Slowick T, Spurling KP, et al. Retained
q1520min until pain is controlled, then q2h foreign bodies. J Trauma. 1997;43:107111.
PRN. vessels or those causing ischemia or hemorrhage)
Anaphylactic shock associated with a retained FB
0.51 mg/kg of codeine component PO q4h
that cannot be removed immediately
ADDITIONAL READING
PRN
Hydrocodone/Acetaminophen dosed as Toxin-mediated reaction or systemic toxicity with Brennan J, Friedland H. Subcutaneous foreign bodies.
0.1 mg/kg of hydrocodone component PO significant end organ dysfunction (heavy metals, In King C, Henretig FM, King BR, et al., eds. Textbook
q46h PRN venomous spines) or tissue necrosis of Pediatric Emergency Procedures. 2nd ed.
r Tetanus prophylaxis and immune globulin as Discharge Criteria Philadelphia, PA: Lippincott Williams & Wilkins;
indicated (See Tetanus Prophylaxis topic.) r Established hemostasis with appropriate wound 2008:10551064.
Second Line irrigation and careful exploration
r Wound management and follow-up as needed
Prophylactic antibiotics are not usually necessary but CODES
are recommended in wounds: Issues for Referral
r With history of animal or human bites Outpatient surgical referral (general surgery,
r With heavy bacterial contamination (soil) ICD9
orthopedics, plastics) is recommended for any patient
729.6 Residual foreign body in soft tissue
r Over sterile sites (tendons, joints, or bones) who is discharged from the emergency department
r In immune-compromised patients with a retained FB (within 4872 hr).
r With retained FBs PEARLS AND PITFALLS
SURGERY/OTHER PROCEDURES FOLLOW-UP r Chronic or recurrent infections resistant to
r A time limit of 15 min should be set for wound antimicrobial therapy or wounds with persistent
exploration in the emergency department. Adequate Discharge instructions and medications: pain or limitation of function should raise suspicion
anesthesia, hemostasis, and lighting are essential r Antibiotic treatment as needed for a retained FB.
for successful exploration. r Superficial objects that are easily visible and located
r Some wound margins may need to be extended in r Wound care instructions
in benign locations can be safely removed in the
order to fully explore the area or to safely grasp and Patient Monitoring emergency department or office.
remove a foreign object: Close follow-up is recommended for patients with a r Retained, missed FBs are a common cause for
In some cases, block excision of the tissue retained FB or for patients who had extensive wound malpractice claims against treating physicians (4).
containing the FB may be necessary: exploration (within 4872 hr). r Careful, meticulous exam and documentation are
Superficial location but difficult to grasp crucial in all circumstances.
Contamination of tissue
Toxic reaction
375
FRACTURE, CERVICAL SPINE

Marc A. Auerbach
Lawrence Siew

BASICS r Majority of cervical spine fractures result from r Close monitoring of vital signs:
trauma to top of the head or back of the neck. Can Apnea or hypotension may result from injuries at
DESCRIPTION occur from: the level of diaphragmatic control.
r Cervical spine fractures are rare in children. Motor vehicle and bike accidents Hypotension, bradycardia, or temperature
r Injury can occur through flexion, extension, vertical Pedestrian accidents instability may result from spinal shock.
compression, rotation, or a combination of these Falls r Neck exam:
mechanisms. Diving injuries Maintain in-line stabilization
r Age-related anatomic considerations account for Sports-related injuries Tenderness, muscle spasm, or deformity over
differences in the types of injuries: r Mechanism of injury can predict type of injury (24): spinous process
Younger children are more susceptible to fractures Hyperflexion (most common): r Respiratory signs:
of the growth plate and ligamentous injuries Wedge fractures: Diaphragmatic breathing
involving the upper cervical spine. Pure flexion injury with compression of the r Abdominal/Genitourinary signs:
Older children are more susceptible to vertebral anterior vertebral body and without disruption Ileus
and arch fractures involving the lower cervical of posterior elements Fecal incontinence
spine. Teardrop: No rectal tone with rectal exam
r Most spinal cord injuries result from direct Flexion with vertical compression causing
Urinary retention
compression or disruption of the cord by fracture anterior displacement of triangular bony r Neurologic signs:
fragments or subluxed vertebrae: fragment Muscle tone:
Spinal cord injury without radiologic abnormality Clay-Shoveler: Flaccid tone may indicate lower motor neuron
(SCIWORA) may occur, especially in children <8 yr Abrupt flexion with lower neck muscular
lesion or spinal shock.
of age. contraction resulting in oblique fracture at Muscle strength:
base of spine process, most commonly at Focal weakness
EPIDEMIOLOGY C7-T1 Paralysis:
Incidence Hyperextension: Partial cord syndromes (central cord, anterior
14% of children admitted to major trauma centers, Compression of posterior elements and cord, Brown-Sequard, and dorsal cord
6080% of all pediatric vertebral injuries: disruption of anterior longitudinal ligament
r Male > female (teenagers) syndromes)
Hangman fracture: Complete cord syndrome (paraplegia,
r As high as 80% are bony spine injuries (1). Affects the arch of C1 or the bilateral pedicles
quadriplegia)
of C2 Sensation:
RISK FACTORS Axial loading:
r Down syndrome: Isolated sensory deficit is the most common
Compressive downward forces that cause burst finding with cervical spine injury.
15% have atlantoaxial instability or comminuted fractures of the arches of C1 or
r Klippel-Feil syndrome Deep tendon reflexes
vertebral bodies of lower cervical spine Rectal exam
r Morquio syndrome: Jefferson burst fracture:
Mucopolysaccharidosis IV with associated Fractures of the arches of C1 and lateral DIAGNOSTIC TESTS & INTERPRETATION
hypoplasia of the odontoid displacement of C1 with respect to C2 Imaging
r Larsen syndrome: Rotational injuries: r Children with suspected cervical spine injury must
Associated with cervical vertebrae hypoplasia Fracture or dislocation of vertebral facets undergo radiologic evaluation.
r Previous cervical spine surgery r Radiologic imaging may be deferred if the suspicion
GENERAL PREVENTION r Facial fractures of cervical spine injury is low. This may be guided by
r Proper adult supervision r Head injuries age of child (>8 yr), low risk mechanism of injury,
r Avoidance of high-risk activities such as r Spinal cord injuries no distracting pain or injuries, awake and able to
cooperate with exam, no mental status changes, no
trampolines, contact sports neck pain or limitation of movement, and no
r Age-appropriate restraints in motor vehicles
DIAGNOSIS neurologic deficits (5):
PATHOPHYSIOLOGY Preferred initial radiographs are cross-table
Children <8 yr of age are more susceptible to HISTORY lateral, anteroposterior, and odontoid. The series
fractures of the growth plate and injuries of the upper r Nature of trauma (fall, motor vehicle injury, sports must include all 7 cervical vertebrae as well as
cervical spine (C1-3): injury, etc.): odontoid and lateral masses.
r Growth centers are susceptible to sheer forces Mechanism of injury Flexion-extension views may be required in the
r Local pain, muscle spasm, or decreased range of alert, cooperative patient who still complains of
during rapid deceleration or hyperflexion-extension.
r Fulcrum of the cervical spine progresses caudally motion neck pain and there are concerns of ligamentous
r Transient or persistent paresthesias injury (6).
(C2-3 at birth to C5-6 at 8 yr of age). r Neck CT should be obtained for:
r There is greater mobility of the cervical spine r Weakness
because of weaker cervical musculature and r Ask about signs of other types of neck trauma: Inadequate 3-view plain radiographs
Changes in voice, hoarseness, dysphagia, Suspicious plain radiographs
increased laxity of ligaments.
r Incomplete ossification of the odontoid process and odynophagia, tenderness, or hematemesis Fracture-displacement seen on plain radiographs
High index of suspicion for injury despite normal
relative larger head compared to body also plain radiographs
contribute.
r Immature vertebral joints and facets allow more
sliding (2).
376
FRACTURE, CERVICAL SPINE
r MRI is superior to CT for soft tissue and ligamentous SURGERY/OTHER PROCEDURES REFERENCES
injuries. It has limited utility in the emergent setting Surgical management is reserved for neurologic injury
because of availability and accessibility. and/or unstable fractures: 1. Kokoska ER, Keller MS, Rallo MC, et al.
r SCIWORA: r Conservative treatment includes skeletal traction Characteristics of pediatric cervical spine injuries.
See objective signs of myelopathy as a result of and closed reduction (halo vest). J Pediatr Surg. 2001;36(1):100105.
trauma in the absence of findings on plain r Surgical treatment includes cervical spine 2. Fesmire F, Luten R. The pediatric cervical spine:
radiographs and CT. decompression and fusion. Developmental anatomy and clinical aspects.
535% of patients with myelopathy may have J Emerg Med. 1989;7:133142.
SCIWORA (7) DISPOSITION 3. Viccellio P, Simon H, Hoffman JR, et al. A
MRI should be performed or CT myelography if Admission Criteria prospective multicenter study of cervical spine
MRI is unavailable. r Radiographic evidence of cervical spine fracture or injuries in children. Pediatrics. 2001;108:e20.
dislocation 4. Patel J, Tepas JJ. Pediatric cervical spine injuries:
Diagnostic Procedures/Other r Symptoms of spinal cord injury with negative
Somatosenosry evoked potentials: Defining the disease. J Pediatr Surg. 2001;36(2):
r Electrical impulse in response to stimuli radiographic imaging (SCIWORA) 373376.
r Critical care admission criteria: 5. Khanna G, El-Khoury GY. Imaging of cervical spine
DIFFERENTIAL DIAGNOSIS All patients with proven or suspected spinal cord injuries in childhood. Skeletal Radiol. 2007;36:
r Ligamentous injury injuries and progressing neurologic exam or 477494.
r Muscles strain abnormal vital signs 6. Ralston ME, Chung K, Barnes PD, et al. Role of
r Cauda equina syndrome Unstable fractures or dislocations at high risk for flexion-extension radiographs in blunt pediatric
r Spinal cord infections, neoplasms causing spinal cord injury cervical spine injury. Acad Emerg Med.
r Vertebral artery dissection Discharge Criteria 2001;8:237245.
r Resolution or improvement/stabilization of 7. Pang D, Polack I. Spinal cord injury without
neurologic symptoms: radiographic abnormality in childrenthe
TREATMENT Disposition to physical rehabilitation facility as SCIWORA syndrome. J Trauma. 1989;29:654664.
PRE HOSPITAL
required
r Adequate pain control
8. Short DJ, Masry WS, Jones PW. High dose F
r Assess and stabilize airway, breathing, and methylprednisolone in the management of acute
spinal cord injurya sytematic review. Spinal
circulation. Issues for Referral
Cord. 2000;38(5):273286.
r Immobilization of spine with cervical collar and long Suspected spinal cord injury should have neurosurgery
spine board is necessary: and/or orthopedic consultations.
If properly fitting cervical collars are unavailable, ADDITIONAL READING
splinting the head and body with towels or foam FOLLOW-UP
blocks and tape is a reasonable option. Kilmo P, Ware ML, Gupta N, et al. Cervical spine
Maintain the patient in a neutral position, and FOLLOW-UP RECOMMENDATIONS trauma in the pediatric patient. Neurosurg Clin North
avoid head and neck movement while full spinal r Discharge instructions and medications: Am. 2007;18(4):599620.
immobilization is being applied. Maintain cervical spine immobilization. See Also (Topic, Algorithm, Electronic
INITIAL STABILIZATION/THERAPY Adequate pain control Media Element)
r Assess and stabilize airway, breathing, and r Activity: r Fracture, Coccyx
circulation per Advanced Trauma Life Support (ATLS) Restricted with no contact activities until cleared r Spinal Cord Compression
and Pediatric Advanced Life Support guidelines: by physician r Strangulation
If suspicion for cervical spine fracture, immobilize Patient Monitoring r Trauma, Neck
the patient with a rigid cervical collar and a long r Monitor for any new neurologic deficits or r Trauma, Spinal Cord
spine board if not done earlier. progression of pre-existing deficits.
Evaluate for associated injuries. r Monitor for parathesias or inability to void or
Perform serial neurologic exams. incontinence. CODES
r Control of pain, preventing further injury, and
stabilize associated injuries PROGNOSIS
r Related to associated spinal cord injury ICD9
r Early, timely consultations with neurosurgery and/or r 805.00 Closed fracture of cervical vertebra,
r Mortality from spinal cord injury decreased 24%
orthopedic surgery: unspecified level
over past 30 yr; 80% of patients hospitalized for
If subspecialty care is not available, arrange r 805.01 Closed fracture of first cervical vertebra
transfer to trauma center. spinal cord injury survive (1).
r 805.02 Closed fracture of second cervical vertebra
MEDICATION COMPLICATIONS
r Spinal or neurogenic shock
First Line r Paralysis
r Morphine 0.1 mg/kg IV/IM/SC q2h PRN: PEARLS AND PITFALLS
r Cord syndromes (complete, incomplete, anterior
Initial morphine dose of 0.1 mg/kg IV/SC may be r Pearls:
repeated q1520min until pain is controlled, then cord, Brown-Sequard)
r Horner syndrome Younger children are more susceptible to upper
q2h PRN.
r Fentanyl 12 g/kg IV q2h PRN: cervical injuries, unlike older children who are
more likely to have lower cervical spine
involvement.
q1520min until pain is controlled, then q2h PRN. r Pitfalls:
Second Line Improper immobilization
Consider methylprednisolone: 30 mg/kg IV over Do not remove a cervical collar on a patient with
15 min, then 5.4 mg/kg/hr over the next 23 hr. abnormal mental status.
(Caution: Dosage based on adult guidelines; lack of
high-level pediatric evidence):
r Previously, steroids were recommended by the ATLS
guidelines, but based on recent data this
recommendation has been withdrawn.
r Routine use is institution dependent (8).
377
FRACTURE, CLAVICLE
Louis A. Spina

BASICS r Mechanism of injury causing a fractured clavicle is
Imaging
typically a direct fall onto the affected shoulder r Routine radiographs of the affected clavicle are often
DESCRIPTION during sports or play. obtained to confirm the diagnosis of a fracture:
r The clavicle connects the shoulder to the trunk and r Lateral compression during a crush injury, as can Fractures are often not visible on every
is one of the most commonly injured structures in occur in some motor vehicle accidents, may also radiographic view.
the shoulder girdle. result in a fracture of the clavicle (2). Midshaft fractures are usually transverse or
r The clavicle is the most commonly fractured bone in r Less commonly, clavicular fracture can be caused by oblique, and displacements with comminution are
the pediatric population. a fall onto outstretched hand (FOOSH), with common.
r Clavicular fractures can be divided into fractures of transmitted forces causing the fracture. Medial fractures are at risk for displacement of the
the midshaft, the medial end (or medial 3rd), and section lateral to the fracture:
the lateral end (or lateral 3rd). Displacement can be either posterior or anterior.
r Most of the fractures (90%) in the pediatric DIAGNOSIS Occasionally require further radiographs or CT
population occur in the midshaft of the clavicle. scans to determine the direction of displacement
HISTORY if not readily apparent on physical exam.
(1,2): r Common presentation is pain in the affected area.
Greenstick fractures of the clavicle are common. r Some providers may defer radiographs on younger
Verbal children will spontaneously complain of pain,
patients with midclavicular tenderness and make a
EPIDEMIOLOGY and younger children may cry, avoid use of affected
r Clavicular fractures are most common in children arm, or cradle the affected arm with the opposite clinical diagnosis.
r CT:
between 2 and 10 yr of age: extremity.
>50% of all clavicular fractures occur in children r Often, there is an associated trauma reported by the If there is concern about posterior displacement,
<10 yr of age. patient or the caregiver: chest CT scan with IV contrast can be helpful to
r Clavicular fractures are also seen in the newborn However, there are times, especially in younger determine if there is compression of the
children, when there is no known mechanism of underlying vessels or the trachea.
period. r Angiography:
r Fractures of the medial aspect of the clavicle are rare injury.
in young children and raise the question of abuse. r In older children, a history of a sports-related injury If there is a concern about vascular injury resulting
(direct blow or FOOSH) may be present. from a displaced fracture, angiography may be
RISK FACTORS necessary.
r Participation in contact sports increases the risk of PHYSICAL EXAM
clavicular fracture. r Exam of the clavicle will often reveal swelling due to DIFFERENTIAL DIAGNOSIS
r Humeral fractures
r A difficult vaginal delivery can increase the risk of a hematoma over the area of fracture with r Shoulder dislocation and contusion
clavicular fracture in the neonatal population. tenderness in this area:
r Acromioclavicular separation
Crepitus can sometimes be palpated at the site of
PATHOPHYSIOLOGY fracture. r Sternoclavicular separation
r Midshaft fractures of the clavicle are often r Sternal fractures
Medial clavicular fractures can have either anterior
greenstick fractures without significant angulation or posterior displacement, which is often palpable r Rotator cuff injury
or displacement: on exam. r Muscular injuries to the shoulder and chest
Associated neurovascular injury is rare but may be Lateral fractures are infrequently displaced in
seen secondary to severe forces causing children (1).
significant displacement. r Children often have limited active range of motion TREATMENT
r Lateral clavicular fractures usually occur through the
of the shoulder on the affected side. Limited
physis, where the coracoclavicular and abduction of the shoulder is usually present. PRE HOSPITAL
acromioclavicular ligaments anchor the clavicle and r Determine if the fracture is open or closed: r A sling should be utilized in the prehospital setting
prevent dislocation. to help stabilize the affected extremity.
r Medial clavicular fractures often occur through the Open wounds should be apparent, but tenting of
r Ice packs to the affected region
the skin overlying the fracture site should alert the
medial physis with either posterior or anterior examining physician for potential puncture of the r Pain management
displacement of the distal fragment: skin at a later time.
Posterior displacement can cause compression of r Examine the surrounding joints and bones for INITIAL STABILIZATION/THERAPY
the mediastinal vessels or the trachea. Most clavicle shaft fractures can be adequately
fractures, dislocations, and subluxations: stabilized using a figure-of-eight dressing or using a
Sternal fractures or dislocation sling and swathe.
Humeral fractures
Shoulder dislocations
r Evaluate the patient for associated life-threatening
injuries:
Rib fractures
Cervical or thoracic spine fractures
Intrathoracic injuries
Pneumothorax
378
FRACTURE, CLAVICLE
MEDICATION DISPOSITION REFERENCES

First Line Admission Criteria
r Once immobilized, most fractures will require r Most clavicular fractures do not require admission 1. Postacchini F, Gumina S, De Santis P, et al.
over-the-counter medications to control associated unless surgical stabilization is necessary. Epidemiology of clavicle fractures. J Shoulder Elbow
pain: r Concerns about possible child abuse may necessitate Surg. 2002;11(5):452456.
NSAIDs: admission to ensure the safety of the child. 2. Bishop JY, Flatow EL. Pediatric shoulder trauma.
Consider NSAID medication in anticipation of Clin Orthop Relat Res. 2005;432:4148.
Discharge Criteria 3. Kubiak R, Slongo T. Operative treatment of clavicle
prolonged pain and inflammation.
Some clinicians prefer to avoid NSAIDs due to Stable patients with clavicular fracture that have been fractures in children: A review of 21 years. J Pediatr
adequately immobilized may be safely discharged Orthop. 2002;22:736739.
theoretical concern over influence on
home.
coagulation and callus formation.
Animal studies have raised concerns that Issues for Referral
NSAIDs may negatively influence bone healing; r Most clavicular fractures do not require immediate ADDITIONAL READING
however, there is no clinical evidence in humans. orthopedic evaluation or follow-up. Most of these
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN injuries can be managed by the primary care See Also (Topic, Algorithm, Electronic
Ketorolac 0.5 mg/kg IV/IM q6h PRN provider. Media Element)
r Open fractures, unstable distal fractures, grossly r Fracture, Humerus
r Trauma, Chest
Acetaminophen 15 mg/kg/dose PO/PR q4h PRN displaced midshaft fractures, and posteriorly and
r Open fractures require prompt administration of r Trauma, Shoulder
severely anteriorly displaced medial fractures and
antibiotics: any fracture with neurovascular compromise will
Initial treatment with cefazolin IV at a dose of require orthopedic consultation in the emergency
50100 mg/kg/day divided into 3 doses per day department. CODES
(q8h) is preferred.
Second Line ICD9
FOLLOW-UP r 810.00 Closed fracture of clavicle, unspecified part
r Opioids:
r 810.01 Closed fracture of sternal end of clavicle F
Morphine 0.1 mg/kg IV/IM/SC q2h PRN: FOLLOW-UP RECOMMENDATIONS
Initial morphine dose of 0.1 mg/kg IV/SC may r Discharge instructions and medications: r 810.02 Closed fracture of shaft of clavicle
be repeated q1520min until pain is controlled, Sling should be worn for the initial 3 wk and then
then q2h PRN. for comfort.
Fentanyl 12 g/kg IV q2h PRN: Parents should be warned that a lump in the area PEARLS AND PITFALLS
Initial dose of 1 g/kg IV may be repeated of the fracture might form during healing, which r Pearls:
q1520min until pain is controlled, then q2h can take several months to resolve.
Ibuprofen is typically adequate for pain control. Clavicular facture is the most common fracture of
PRN.
r Activity: childhood.
The majority of clavicular fractures may be treated
0.51 mg/kg of codeine component PO q4h PRN Usually kept in sling for 6 wk.
conservatively with immobilization and do not
Hydrocodone or hydrocodone/acetaminophen After 6 wk, the sling may be removed if patients
need immediate orthopedic referral.
dosed as 0.1 mg/kg of hydrocodone component pain allows. r Pitfalls:
PO q46h PRN Athletes should not return to sports until they
r For those requiring antibiotics and allergic to have normal painfree range of motion and no Posterior displacement of a medial clavicular
tenderness to palpation over injured region. fracture may result in compression of the
cephalosporins, clindamycin administered IV at
mediastinal vessels or the trachea.
dosing of 30 mg/kg/day divided q8h is an
PROGNOSIS In younger children (<2 yr of age) presenting with
acceptable alternative. r Most clavicular fractures heal well due to the clavicular fractures and inconsistent histories, the
SURGERY/OTHER PROCEDURES excellent remodeling capabilities of children. possibility of an inflicted injury should be
r Most clavicular fractures in childhood do not require r Very few clavicular fractures in children require considered.
surgery due to excellent remodeling potential: surgical repair.
Only 15 patients during a 21-yr period required
surgery in 1 review (3). COMPLICATIONS
r Pneumothorax / hemothorax
r Indications for surgery:
r Brachial plexus injury
Open fractures r Injuries to the subclavian artery or vein
Neurovascular compromise
Irreducible fractures that carry the risk of
becoming open fractures:
Often has tenting of the skin overlying the
fracture site
Nonunion of fracture site (usually after 3 mo)
379
FRACTURE, COCCYX
Nazreen Jamal
Bruce L. Klein
r MRI or CT scan should be reserved for select cases

BASICS DIAGNOSIS (2):
Each of these scans is more sensitive for
DESCRIPTION HISTORY diagnosing a coccyx fracture than the lateral
r The coccyx, commonly called the tailbone, consists History of recent trauma to the coccygeal region, most radiograph.
of up to 5 separate or fused vertebrae. commonly a direct fall onto the buttocks: Adjacent nonbony injury may be identified as well,
r Pain in and around the region of the coccyx is r Immediate pain in the coccygeal region following but these associated injuries are rarely serious.
referred to as coccydynia (or coccygodynia). the event While an MRI or CT scan can be ordered when the
r Worse pain while sitting or rising from the sitting lateral radiograph is normal or indeterminate,
PATHOPHYSIOLOGY
r Trauma to the coccygeal region can cause a fracture position identifying a coccyx fracture usually does not
r May also complain of pain on defecation change the initial management.
of the coccyx and coccydynia.
r Coccydynia with or without a fracture can be a PHYSICAL EXAM DIFFERENTIAL DIAGNOSIS
r Pain on external palpation of the coccyx r Contusion
consequence of parturition.
r Coccydynia without a fracture can also result from r Rectal exam r Sacrococcygeal dislocation
nontraumatic etiologies: Pain on internal palpation of the coccyx r Sacral fracture
Nearby septic arthritis r Abnormal mobility of the coccyx may be r Pilonidal cyst
Malignant metastases appreciated: r Perirectal abscess
Idiopathic in origin However, in normal adults, the tip of the coccyx r Constipation
ETIOLOGY can be moved up to 30 degrees anteriorly and 1 r Tumor
r Direct trauma to the coccygeal region: cm laterally (1).
r Perform a complete neurologic exam:
A fall in the half-seated position, with the impact
of the fall directed to the coccyx, is a common Isolated coccyx fractures should not have TREATMENT
cause (1). neurologic deficits.
r If the history and physical exam suggest coccyx
A kick to the buttocks can also result in a fracture DIAGNOSTIC TESTS & INTERPRETATION fracture, treat as such even if radiographs appear
of the coccyx. Imaging
r Coccyx fractures can be caused by obstetric or normal.
r Lateral radiograph of the coccyx (with the hips r Virtually all coccyx fractures are initially managed
gynecologic maneuvers. flexed maximally): conservatively and in the same manner.
Displaced fractures of the coccyx may be r Supportive care is recommended:
identified, but nondisplaced ones may be missed. Analgesics
Interpretation can be difficult given the natural Sitz baths
variations in coccygeal angulation. Stool softeners
If no fracture is visible radiographically, but the Inflated doughnut cushion to sit upon to relieve
history and physical exam seem consistent with pressure off the coccyx
one, the injury should be treated as a fracture. Activity restrictions
r Symptoms typically abate within 26 wk, although
some patients, usually adults, will be refractory to
conservative management.
r Manual reduction of an angulated or displaced
fracture is rarely ever necessary, especially upon
initial presentation.
380
FRACTURE, COCCYX
First Line See Also (Topic, Algorithm, Electronic

r Opioids: FOLLOW-UP Media Element)
Morphine 0.1 mg/kg IV/IM/SC q2h PRN: r Pain, Back
Initial morphine dose of 0.1 mg/kg IV/SC may FOLLOW-UP RECOMMENDATIONS r Pilonidal Cyst
be repeated q1520min until pain is controlled, Follow up with the patients primary care provider or r Spinal Cord Compression
then q2h PRN. an orthopedic surgeon if the pain persists after r Trauma, Perineal
Fentanyl 12 g/kg IV q2h PRN: 46 wk of conservative therapy. r Trauma, Spinal Cord
Initial fentanyl dose of 1 g/kg IV may be
PROGNOSIS
repeated q1520min until pain is controlled, Complete healing usually occurs in 612 wk.
then q2h PRN.
Codeine or codeine/acetaminophen dosed as COMPLICATIONS CODES
r Isolated coccyx fractures should have no neurologic
PRN deficits. ICD9
Hydrocodone or hydrocodone/acetaminophen r Rarely, chronic pain may result. 805.6 Closed fracture of sacrum and coccyx without
dosed as 0.1 mg/kg of hydrocodone component mention of spinal cord injury
PO q46h PRN
r NSAIDs: REFERENCES
Consider NSAID medication in anticipation of PEARLS AND PITFALLS
1. Traycoff RB, Crayton H, Dodson R. Sacrococcygeal
prolonged pain and inflammation: pain syndromes: Diagnosis and treatment. r Treat all patients with a history and physical exam
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN consistent with coccyx fractures conservatively with
Orthopedics. 1989;12(10):13731377.
Ketorolac 0.5 mg/kg IV/IM q6h PRN supportive care regardless of the imaging results.
Naproxen 5 mg/kg PO q8h PRN 2. Williamson JB, Raissaki MT. Fracture dislocation of
the sacro-coccygeal joint: MRI evaluation. Pediatr r If pain persists after 46 wk, the patient should be
Radiol. 1999;29:642643. referred to an orthopedic surgeon.
SURGERY/OTHER PROCEDURES 3. Wray CC, Easom S, Hoskinson J. Coccydynia:
Some adults with refractory coccydynia (from diverse Aetiology and treatment. J Bone Joint Surg. F
etiologies, not just from fractures) have benefited from 1991;73-B(2):335338.
local anesthetic and steroid injections, manipulation of 4. Cebesoy O, Guclu B, Kose KC, et al. Coccygectomy
the coccyx under general anesthesia, or coccygectomy: for coccygodynia: Do we really have to wait? Injury.
r These procedures are rarely, if ever, performed or 2007;38:11831188.
necessary in pediatric patients with coccyx fractures
(3,4).
ADDITIONAL READING
DISPOSITION
Admission is usually not required. r Bucholz RW, Heckman JD, Court-Brown C, et al.,
eds. Rockwood and Greens Fractures in Adults. 6th
Discharge Criteria
r Most patients can be discharged home with ed. Philadelphia, PA: Lippincott Williams & Wilkins;
2006.
prescriptions for an analgesic and a stool softener as r Widmann RF. Fractures of the pelvis. In Beaty JH,
well as instructions regarding supportive care.
r Activity: Kasser JR, eds. Rockwood and Wilkins Fractures in
Children. 6th ed. Philadelphia, PA: Lippincott
Avoid contact sports such as wrestling or football.
Williams & Wilkins; 2006.
Issues for Referral
If the pain does not resolve in 46 wk, the patient
should be referred to an orthopedic surgeon.
381
FRACTURE, FEMUR
Tara Webb
Marc Gorelick

BASICS r In premobile children, nonaccidental trauma is the
Lab
most likely cause of a femur fracture. r No lab tests are absolutely indicated for isolated
DESCRIPTION r Ambulatory, small children can sustain femur femur fractures:
Femur fractures are classified by level, pattern, open fractures from relatively minor trauma, such as Consider CBC to assess for significant
vs. closed, degree of displacement and angulation, tripping or twisting a leg. hemorrhage.
and degree of comminution: r School-age children are likely to sustain femur Although uncommon, hemodynamically significant
r Femoral shaft fractures are the most common, fractures when struck by motor vehicles. bleeding may occur in these fractures (3).
accounting for 70% of femur fractures. r Adolescents can sustain femur fractures from r Lab testing should focus on evaluation for other
r Subtrochanteric (12 cm below the lesser high-velocity automobile collisions. suspected injuries based on mechanism of injury.
trochanter) and supracondylar fractures (just above r Pathologic fracture secondary to tumors,
Imaging
the origin of the gastrocnemius) are less common osteogenesis imperfecta, bone cysts, or osteoporosis r AP and lateral radiographs of the affected limb
and require unique management. should include both the hip and the knee to check
r Pattern types commonly include transverse, oblique, COMMONLY ASSOCIATED CONDITIONS
r In a pedestrian vs. auto collision, the Waddell triad for other associated fractures or dislocations.
and spiral. r Skeletal survey may be indicated if nonaccidental
r Degree of comminution described by Winquist and refers to the constellation of femur fracture, thoracic
or abdominal injury, and head injury. trauma is suspected.
Hansen: r When a fracture of the femur is present, the joint r Other imaging as indicated by clinical suspicion of
Grade I: Fracture with small fragment <25% associated injuries
width of femoral shaft, stable in axial plane and above and below must be examined to rule out
rotational direction associated hip and tibial injuries. DIFFERENTIAL DIAGNOSIS
Grade II: Fracture with 2550% width of femoral r Hip fracture, dislocation, or contusion
shaft, stable in axial plane; possible rotational r Thigh hematoma or contusion
DIAGNOSIS r Knee fracture, dislocation, or contusion
instability
Grade III: Fracture with >50% width of femoral HISTORY r Overuse pain
shaft, unstable in axial plane and rotationally r Thigh pain, swelling, and inability to ambulate are
Grade IV: Circumferential loss of cortex as well as expected.
instability in axial plane and rotationally r Mechanism of the fracture TREATMENT
r Associated injuries during the event such as head,
EPIDEMIOLOGY PRE HOSPITAL
Incidence thoracic, or abdominal injuries that may be more r Assess and stabilize airway, breathing, and
Incidence of femoral shaft fractures in children is immediately life threatening
r Screen for nonaccidental trauma risk factors or signs circulation.
19.15 per 100,000 (1): r Consider cervical collar and spine board if necessary.
r Peak incidence is during early childhood (<5 yr of of systemic disease if mechanism of injury seems r Early immobilization using traction devices should
inconsistent with clinical findings.
age) and in adolescence. be performed prior to hospital care:
PHYSICAL EXAM Always ensure presence of distal lower extremity
RISK FACTORS r Complete physical exam to evaluate hemodynamic
r Patients who are male gender or black race have a pulses.
stability and rule out other life-threatening Traction may be contraindicated with fractures
higher incidence of femur fractures.
r Rickets or diet poor in vitamin D or calcium injuries: close to the knee, hip, or pelvis.
r Osteogenesis imperfecta Patient could be tachycardic or hypotensive from
hemorrhage into the affected thigh. INITIAL STABILIZATION/THERAPY
r Presence of pre-existing bone cysts r In the affected limb: r Assess and stabilize airway, breathing, and
r Physical abuse circulation.
Check skin overlying injury to classify fracture as r Determination if any acute, life-threatening injuries
r Motor vehicle accident open vs. closed.
Look for obvious deformity. are present.
GENERAL PREVENTION r Adequate analgesia
Prevention may be accomplished by general injury Assess neurovascular status distal to the injury to
assess for vascular integrity and compartment r Placement of the affected limb into traction splint
prevention and child abuse prevention techniques.
syndrome.
PATHOPHYSIOLOGY r Determine if other injuries are present in the same MEDICATION
r Direct force tends to produce a transverse fracture. First Line
limb (rarely, ipsilateral femoral neck fractures can r Opioids:
r Torsional force results in spiral fractures: occur) (2).
Spiral fractures are seen with falls from height. Morphine 0.1 mg/kg IV/IM/SC q2h PRN:
Spiral fractures also strongly suggest
nonaccidental trauma in younger children. be repeated q1520min until pain is controlled,
r Children rarely have open fractures due to increased then q2h PRN.
bone elasticity. Initial fentanyl dose of 1 g/kg IV may be
repeated q1520min until pain is controlled,
then q2h PRN.
PO q46h PRN
382
FRACTURE, FEMUR
r NSAIDs: r Children ages 610 yr are typically treated with

REFERENCES
Consider NSAID medication in anticipation of closed reduction and flexible intramedullary rod
prolonged pain and inflammation: fixation. 1. Hinton RY, Lincoln A, Crockett MM, et al. Fractures
Ibuprofen 10 mg/kg IV/PO q6h PRN r Children >11 yr of age are treated with either of the femoral shaft in children. J Bone Joint Surg.
Ketorolac 0.5 mg/kg IV/IM q6h PRN intramedullary fixation with rigid rods or casting 1999;81A(4):500509.
Naproxen 5 mg/kg PO q8h PRN with external fixation, depending on characteristics 2. Agrawal A, Agrawal R, Meena DS. Ipsilateral
Some clinicians prefer to avoid due to theoretical of the fracture. femoral neck and shaft fractures in children.
concern over influence on coagulation and callus r Distal femur fractures are close to the growth plate J Trauma. 2008;64(4):E47E53.
formation. and therefore are managed using wire or screw 3. Lynch JM, Gardner MJ, Gains B. Hemodynamic
Second Line fixation with careful avoidance of the growth plate significance of pediatric femur fractures. J Pediatr
Local anesthetic: (4). Surg. 1996;31(10):13581361.
r Femoral nerve blockade with long-acting local DISPOSITION
4. Kanlic E, Cruz M. Current concepts in pediatric
anesthetic has been demonstrated to effect femur fracture treatment. Orthopedics.
Admission Criteria 2007;30(12):10151019.
significant analgesia and reduce opioid requirement r Most patients are initially admitted to the
in adults. hospital:
May be considered in any patient, particularly if Parents of patients who are placed in spica casts
there is concern for hypotension due to opioid or must receive training in how to care for the child
CODES
preference to reduce opioid use. in the cast.
Lidocaine max single dose 5 mg/kg Most patients are placed into traction until proper ICD9
r Antibiotics as indicated for open fractures: r 820.00 Fracture of unspecified intracapsular section
bone end apposition occurs to permit proper
Cefazolin 25100 mg/kg/day IV/IM divided q68h surgical repair. of neck of femur, closed
r Patients who receive operative care must be r 820.10 Fracture of unspecified intracapsular section
Gentamicin 2.5 mg/kg/dose IV/IM q8h
r Tetanus prophylaxis as necessary: admitted for monitoring and recovery. of neck of femur, open
r Critical care admission criteria: r 821.00 Fracture of unspecified part of femur, closed
Tetanus toxoid 0.5 mL IM for booster:
If unimmunized, combined antigen vaccine is Patients with significant hemorrhage,
F
recommended. compartment syndrome or other complications, or
Tetanus Ig 250 IU IM all ages multiple traumatic injuries may require ICU PEARLS AND PITFALLS
SURGERY/OTHER PROCEDURES monitoring. r Pearls:
All children with femur fractures should receive an When a femoral shaft fracture is present, always
orthopedic consult for definitive management: FOLLOW-UP obtain radiographs of the joint above and below
r Femoral neck fractures have a high risk for the injury.
FOLLOW-UP RECOMMENDATIONS r Nonaccidental trauma must be strongly considered
hematoma formation, which can impair blood flow
to the femoral head. Presence of a hematoma Patient Monitoring in the differential diagnosis of femur fractures in
requires surgical drainage. Patient and caregivers should monitor for evidence of nonambulatory children.
r Femoral neck fractures are repaired using either compartment syndrome or other complications of r Pitfalls:
open reduction with fixation or closed reduction, casting. Failure to recognize and treat coexisting
followed by immobilization. Spica cast may be used life-threatening injuries
PROGNOSIS Clinical presentation is usually very obvious; there
in children <2 yr of age. r Children have an increased femoral blood supply
r Femoral shaft fractures in small children are is risk that the clinician may fail to recognize other
compared to adults, resulting in excellent prognosis
managed conservatively, as they are usually injuries that may be more subtle.
for fracture healing and union.
relatively stable fractures. Pavlik harnesses are used r Most patients are able to bear weight by 6 wk and Failure to recognize concomitant fractures in the
in children 04 mo of age; spica casts are used in pelvis or femoral neck when a femoral shaft
return to normal activity in 3 mo. fracture is present
small children above this age with stable fractures.
COMPLICATIONS
r Overgrowth of the affected limb and leg length
discrepancy
r Thigh compartment syndrome
r Fat embolism
r Acute respiratory distress syndrome
r Avascular necrosis of the femoral head after femoral
neck fractures
r Nonunion is very uncommon.
383
FRACTURE, FOOT
Bhawana Arora
Usha Sethuraman

BASICS r Ligament injuries, as with Lisfranc injuries
Imaging
r Compartment syndrome seen with crush injuries r Plain film radiographyAP, lateral, and oblique:
DESCRIPTION r Ankle fractures Ottawa foot rules predict need for radiography for
r Fractures of the foot bones are common. r Lower spine fractures (5% of calcaneal fractures) midfoot fractures. Need to obtain radiograph if
r Occur in all of the 26 bones of the foot: r Other injuries in multisystem/high-energy trauma there is pain in the midfoot zone and any of the
2 bones in the hindfoot (calcaneus, talus), 5 bones following 3 findings (4):
in the midfoot (navicular, cuboid, 3 cuneiforms), Point tenderness over the base of 5th metatarsal
and 19 bones in the forefoot (5 metatarsals, DIAGNOSIS Point tenderness over the navicular bone
14 phalanges) Inability to take 4 steps, both immediately after
HISTORY injury and in the emergency department
EPIDEMIOLOGY r Description of pain characteristics:
r Account for 58% of all pediatric fractures and for Although the Ottawa rules were designed for
Onset, location, character, duration those >18 yr of age, studies have shown they
7% of all physeal fractures (1) Change with activity or rest
r The incidence increases with age. may be used in adolescents 10 yr (5).
Aggravating factors Jones fracture:
r Metatarsal physeal fractures are the most common r Trauma (new or repetitive): Involves the proximal diaphysis of the 5th
fractures, accounting for 60% of pediatric foot Time between injury and the onset of pain metatarsal and has a high incidence of
fractures, with fractures of the base of the 5th r Mechanical symptoms (locking, clicking) nonunion/delayed union
metatarsal accounting for 22% (2,3). r Neurologic symptoms (eg, altered sensation, Pseudo Jones fracture:
r Phalangeal fractures account for as much as 18% of
numbness, discoloration of foot) Avulsion of 5th metatarsal base, usually a pull
pediatric foot fractures (2). r Gait and current function by peroneus brevis
r Talar and calcaneal fractures represent 2% each of
r Effect of previous treatment. Nondisplaced fractures of the phalanx are
all pediatric foot fractures (1). r Usual mechanisms of fractures are: common:
RISK FACTORS Usually Salter-Harris I or II types
Talar fractures: Forceful dorsiflexion of ankle r Special plain film imaging views may be needed for
r Congenital foot deformities
Calcaneal fractures:
r Nutritional deficiencies Occur with high velocity, axial loading, with the the diagnosis of specific fractures:
r Stress fractures due to change in activity talus being driven into the calcaneus Lisfranc fractures require a high index of suspicion
r High-impact or repetitive motion sports (eg, Tarsometatarsal complex injuries: because spontaneous reduction may occur
Athletes with these injuries tend to have subtle masking the true extent of injury:
gymnastics, basketball, tennis, running) Need stress views with weight bearing
r Improper foot wear or inadequate conditioning clinical and radiographic findings.
Can be from low- or high-force injuries due to Calcaneal fracture requirements:
GENERAL PREVENTION flexion or abduction. Lateral view is important because it allows
r Injury prevention and sports conditioning Include Lisfranc fractures: measurement of the Bohlers angle, which is
r Wearing well-fitting, supportive athletic shoes Forceful plantarflexion of the foot with axial measured at the intersection of 2 lines on
loading, or a direct crush injury superior surface of calcaneus:
PATHOPHYSIOLOGY Bohlers angle normally measures 2040
r Fractures can be localized to the forefoot, midfoot, Commonly missed diagnosis
Metatarsal fractures (indirect or direct injuries): degrees but is reduced in fractures

and hindfoot. These regions are demarcated by 3
Indirect injuries result from axial loading, Need to also consider lumbosacral spine films
jointsLisfranc, Chopart, and subtalar: Talar fractures require 45-degree internal oblique
The Lisfranc (tarsometatarsal) joint separates the inversion, or rotation
Direct injuries often result from the impact of films.
midfoot from the forefoot, which includes the 5 r Other imaging modalities such as bone scanning, CT
metatarsophalangeal joints: falling objects.
Phalangeal fractures result from objects falling scanning, MRI, and US may help diagnose occult
The tarsometatarsal joints have intrinsic stability
onto the foot or stubbing of toe: foot fractures:
as a result of both the osseous architecture and CT scan:
the associated ligaments. Proximal phalangeal fractures are more
common than distal phalangeal fractures. Many bones are not ossified, so this is useful.
The Chopart joint separates the midfoot from the Bony tarsal coalitions not seen on radiographs
hindfoot and includes the joint between the Hallux injuries are more common than those of
the lesser toes. may be seen on CT.
calcaneus and the cuboid bone and the talus and Useful for assessing for tarsometatarsal complex
navicular bone: Stress fractures occur in adolescents who are
injury
Supination and pronation occur at this joint. involved in repetitive intense training.
MRI:
The subtalar joint separates the talus and PHYSICAL EXAM Permits increased soft tissue contrast
calcaneus. The 3 articulating facets of calcaneus r Inspect the injured foot for swelling, bruises, Better visualization of muscles, ligaments,
form a complex subtalar joint with the deformity, and open wounds. cartilage, periosteum, and subchondral bone
corresponding talar facets: r Palpation along the foot will show point tenderness
The talus is unusual in that: DIFFERENTIAL DIAGNOSIS
A large portion of its surface is articular
at the fracture site. r Osteochondroses: Kohler, Freiberg disease
r With displaced fractures and dislocations, a
cartilage. r Calcaneal apophysitis: Sever disease
Blood supply is limited, making it prone to
deformity of the foot is usually apparent. r Tarsal coalition, infections
Rotational deformity is present if the nail bed does r Pathologic fractures through a neoplasm
osteonecrosis after a talar neck fracture:
not lie in the same plane as that of the
The calcaneus has numerous muscle and tendon r Accessory bones or sesamoids may mimic
corresponding toe on the opposite foot.
attachments. r Test range of motion and joint function.
ETIOLOGY r Conduct a careful neurologic exam of the foot,
r Simple falls/accidents
including both motor and sensory functions.
r Fall from heights, especially calcaneal fractures r Palpate for pulses and assess capillary refill.
r Twisting injuries and stress fractures r Look for compartment syndrome with crush injuries
r Objects falling onto the foot or stubbing of toe
of the midfoot:
r Crush injuries (eg, lawn mower injuries) Hallmark of compartment syndrome is excessive
pain on passive flexion of toes.
384
FRACTURE, FOOT
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN COMPLICATIONS

r Osteonecrosis, especially with talar fractures
TREATMENT Ketorolac 0.5 mg/kg IV/IM q6h PRN
r Compartment syndrome
PRE HOSPITAL r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN r Arthritis with intra-articular toe fractures
Ice application, splint immobilization, elevation r Antibiotics for open fractures: r Infection in open fractures
Cefazolin 25100 mg/kg/day IV divided q68h, r Nonunion/Delayed union as with Jones fractures
r Immobilization: Posterior/Stirrup splint max 12 g/day r Growth arrest from great toe fractures
r Pain control r If open fracture, give tetanus toxoid if not current. r Residual pain after tarsometatarsal complex injuries
r Nondisplaced talar fractures: Immobilization in a SURGERY/OTHER PROCEDURES (eg, Lisfranc fractures)
nonweight-bearing long leg cast for 68 wk r Nail bed injuries involving the germinal matrix
r Calcaneal fractures: Extra-articular fractures can be should be repaired, and significant subungual
treated with immobilization for 56 wk. hematomas (>40% of nail bed) should be drained. REFERENCES
r Lisfranc injuries: r Operative management is suggested for:
1. Mizuta T, Benson WM, Foster BK, et al. Statistical
Nondisplaced fractures at the level of the Unstable displaced talar fractures analysis of the incidence of physeal injuries.
tarsometatarsal joint complex may actually be Displaced intra-articular calcaneal fractures J Pediatr Orthop. 1987;7:518523.
injuries that were initially displaced but then Tarsometatarsal complex injuries 2. Peterson CA, Peterson HA. Analysis of the
spontaneously reduced. Markedly angulated fractures or displaced incidence of injuries to the epiphyseal growth plate.
Patients with such injuries may be treated with a intra-articular fractures of the proximal phalanx of J Trauma. 1972;12:275281.
posterior plaster splint for up to 1 wk, followed by the great toe
3. Peterson HA, Madhok R, Benson JT, et al. Physeal
a nonweight-bearing short leg cast for a month Open fractures require irrigation and debridement
fractures: Part 1. Epidemiology in Olmsted County,
and then a short walking cast for an additional and IV antibiotic therapy.
Minnesota, 19791988. J Pediatr Orthop.
2 wk. DISPOSITION 1994;14(4):423430.
r Tarsal fractures: Avulsion or stress fractures can be
Admission Criteria 4. Stiell IG, Greenberg GH, McKnight RD, et al.
treated in a short walking cast for 23 wk.
r Metatarsal fractures: If fracture is not proximal, they
r Children who sustain Lisfranc injuries due to Decision rules for the use of radiography in acute F
high-energy trauma have significant soft tissue injury ankle injuries. Refinement and prospective
can be treated with weight bearing as tolerated in a and should be observed for compartment syndrome. validation. JAMA. 1993;269:1127.
short walking cast or a cast shoe for 3 wk: r Need for open reduction and internal fixation 5. Dowling S, Spooner CH, Liang Y, et al. Accuracy of
In proximal, 1st through 4th metatarsal fractures, r Other significant nonorthopedic injuries Ottawa ankle rules to exclude fracture of the ankle
consider possibility of a Lisfranc injury. and midfoot in children: A meta-analysis. Acad
If Lisfranc injury is ruled out, treat with a Discharge Criteria Emerg Med. 2009;16:277.
nonweight-bearing short leg cast for 4 wk. r Stabilization of fracture
r Pseudo Jones fracture: 6 wk walking cast r Adequate pain control 6. Kavanaugh JH, Brower TD, Mann RV. The Jones
r Good follow-up fracture revisited. J Bone Joint Surg. 1978;60A:
r Jones fractures are more recalcitrant to treatment.
776782.
These fractures should be treated with at least 6 wk Issues for Referral
in a nonweight-bearing cast (6). r Complex open fractures
r Toe fractures: Immobilization by taping the injured r Unstable fractures CODES
toe to the adjacent toe (buddy taping): r Displaced intra-articular fractures
A piece of cotton or felt should be placed between r Lisfranc injuries ICD9
the toes to avoid maceration. r Compartment syndrome r 825.0 Fracture of calcaneus, closed
A rigid-soled shoe or surgical cast shoe aids in
r Need for open reduction and internal fixation r 825.1 Fracture of calcaneus, open
immobilization and comfort. r 825.20 Fracture of unspecified bone(s) of foot
Immobilize injured toe until point tenderness has
(except toes), closed
resolved, which usually requires 34 wk.
FOLLOW-UP
MEDICATION
First Line FOLLOW-UP RECOMMENDATIONS PEARLS AND PITFALLS
r Opioids: r Rest, ice, and elevation
r Adequate analgesia r Foot fractures in children usually have a good
Initial morphine dose of 0.1 mg/kg IV/SC may r Proper instruction in crutch walking prognosis and usually are treated nonoperatively.
r Resume normal activity when pain free after r A high index of suspicion is needed to diagnose
then q2h PRN. assessment by a physician. tarsometatarsal complex injuries.
r Follow up with orthopedics/primary care physician r Watch for compartment syndrome in children with
Initial dose of 1 g/kg IV may be repeated depending on nature of fracture. crush injuries and high-energy foot injuries.
q1520min until pain is controlled, then q2h r Follow up initially after 1 wk and then regularly until
PRN. patient has a well-healed fracture and is pain free.
Codeine/Acetaminophen dosed as 0.51 mg/kg of
Patient Monitoring
Watch for signs of compartment syndrome.
dosed as 0.1 mg/kg of hydrocodone component PROGNOSIS
PO q46h PRN Prognosis is generally excellent with appropriate and
r NSAIDs: timely treatment.
prolonged pain and inflammation:
Some clinicians prefer to avoid NSAIDs due to
theoretical concern over influence on
coagulation and callus formation.
Animal studies have raised concerns that
NSAIDs may negatively influence bone healing;
however, there is no clinical evidence in humans.
385
FRACTURE, FOREARM/WRIST
Dante Pappano
Darshan Patel
ETIOLOGY r For all fractures, note the following:

BASICS r Acute accidental trauma related to play and sports Involved portion of bone(s): Diaphysis,
activity, especially FOOSH metaphysis, or epiphysis
DESCRIPTION r Acute trauma of other types: Major multitrauma, Type of fracture: Buckle, plastic deformity,
r The bones of the forearm and wrist are at risk for greenstick, oblique, spiral, or complete
penetrating missile, electrical injury (5)
traumatic injury as part of reflexive attempts at r Nonaccidental trauma Physeal involvement and grading according to
deceleration of the body when falling (sometimes r Repetitive stress Salter-Harris/Ogden classification system
called FOOSH, or fall on outstretched hand) (1). r Pathologic fractures Angulation: Degree and direction
r In adolescents, fatigue-type stress fractures Displacement: Percentage and direction
(especially those related to sports activities) while COMMONLY ASSOCIATED CONDITIONS Measurement of overlap or shortening
less common than in the lower extremity, may also r Fracture/Dislocations: Presence of fragments
occur (2). Monteggia r Gustilo and Anderson (GA) grading system for open
Galleazzi fractures (7):
EPIDEMIOLOGY r Sprains/Soft tissue injury
r Upper extremity fractures are the most common Type I: Laceration <1 cm, minimal soft tissue
r Lacerations damage or contamination
fractures in children. After clavicle fractures, forearm r Head/Neck injury
fractures are the most common, comprising Type II: Laceration >1 cm, minimal soft tissue
1045% of all pediatric fractures (3). damage or contamination
r Wrist injuries make up 2.5% of all emergency Type III: Extensive soft tissue damage
department visits:
DIAGNOSIS DIFFERENTIAL DIAGNOSIS
6070% of these are scaphoid fractures (1), while r Normal variant radiographic findings
HISTORY
all other carpal fractures are rare. r Context and mechanism r Sprains and soft tissue injury
r The National Electronic Injury Surveillance System r Screen for associated trauma.
estimates that >250,000 pediatric forearm and r If reported mechanism and actual injury do not
wrist fractures occurred in 2008 (4): seem to agree, consider nonaccidental trauma.
TREATMENT
Most occur during biking, football, snowboarding,
skateboarding, roller skating, other sports, and PHYSICAL EXAM PRE HOSPITAL
r Primary trauma survey and management of ABCs r Temporary splint in position of comfort with easily
playground/slides/swings/trampolines (4)
when appropriate removable splinting material:
RISK FACTORS r Bone: Note deformity, overlying soft tissue swelling, Check pulses pre- and post splinting.
r Underlying bone weakness due to osteogenesis r Pain medication
tenderness, erythema:
imperfecta, osteoporosis, unicameral bone cysts, or For scaphoid fractures, note snuffbox tenderness r Ice and elevation
neoplasms or pain on compression of the thumb along the
r Stress fractures of the forearm and wrist related to INITIAL STABILIZATION/THERAPY
longitudinal axis. r Elevate and rest the affected extremity.
specific sports (2): r Joint: Note effusion, range of motion, swelling,
Olecranon: Javelin, baseball, weight lifting r Apply ice and administer analgesics.
tenderness r Immobilization:
Ulnar shaft: Softball, tennis, volleyball, bowling r Skin integrity
Distal radius: Gymnastics r Vascular integrity, Doppler exam if needed Most forearm fractures: Apply sugar tong splint.
Wrist: Gymnastics, shot put, tennis r Neurologic (sensory and motor) exam Scaphoid fracture (or clinically suspected fracture):
Apply thumb spica splint.
GENERAL PREVENTION
r Adult supervision of high-risk play activities DIAGNOSTIC TESTS & INTERPRETATION Buckle fracture: Removable splint and even
r Safety equipment, wrist protectors Imaging prefabricated splint may be options.
r Graduated training schedules and interruption of r Plain radiography: Ulnar styloid: None
r Open fracture: IV antibiotics, cover with sterile or
activity at the earliest signs of injury Study of choice for forearm fractures
Can perform contralateral comparison views anti-infective (eg, betadine) impregnated gauze (7):
PATHOPHYSIOLOGY r MRI or bone scan: GA type I:
r Childrens process of skeletal maturation (3): In consultation with an orthopedic surgeon,
Studies of choice for stress fractures and
Increased porosity suspected wrist fractures, however, after splinting option of irrigation in the emergency
Thicker periosteum may be performed nonemergently. department, admission, and observation on IV
Presence of growth plates r CT scan: antibiotics (7)
r The above pediatric physiology allows for (2): GA types II and III:
When necessary, can show improved anatomic Administer IV antibiotics.
Plastic deformity: definition over plain films, especially for suspected
Less prone to comminution Will need operative management
wrist fractures
Buckle/Torus fracture MEDICATION
Greenstick injuries Diagnostic Procedures/Other
US performed by the emergency department physician First Line
Growth plate injuries r Opioids:
Standard complete or adult-type fractures (6)
Greater remodeling potential: Pathological Findings Initial dose of 0.1 mg/kg IV/SC may be repeated
Nonunion is more rare than in adults. r Forearm fractures have overt cortical disruption or
plastic deformity on plain films. PRN.
r Monteggia fracture: Fracture of the proximal ulna
with radial head dislocation Initial dose of 1 g/kg IV may be repeated
r Galeazzi fracture: Fracture of the radius with
disruption of the radioulnar joint and ulnar luxation PRN.
PO q46h PRN
386
FRACTURE, FOREARM/WRIST
r NSAIDs: Issues for Referral

r Acute traumatic fractures need orthopedic follow-up.
REFERENCES
prolonged pain and inflammation: r Stress fractures need sports medicine or orthopedic 1. Perron AD, Brady WJ. Evaluation and management
Some clinicians prefer to avoid NSAIDs due to follow-up. of the high-risk orthopedic emergency. Emerg Med
theoretical concern over influence on r Report suspected nonaccidental trauma. Clin North Am. 2003;21(1):159204.
coagulation and callus formation. 2. Anderson MW. Imaging of upper extremity stress
Animal studies have raised concerns that fractures in the athlete. Clin Sports Med.
NSAIDs may negatively influence bone healing; FOLLOW-UP 2006;25(3):489504.
however, there is no clinical evidence in humans. 3. Carson S, Woolridge DP, Colletti J, et al. Pediatric
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN FOLLOW-UP RECOMMENDATIONS upper extremity injuries. Pediatr Clin North Am.
Ketorolac 0.5 mg/kg IV/IM q6h PRN 2006;53(1):4167.
Naproxen 5 mg/kg PO q8h PRN Orthopedic surgery follow-up within 1 wk
4. National Electronic Injury Surveillance System.
r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN Always wear splint (except for torus fracture).
Available at http://www.cpsc.gov/LIBRARY/
Wear sling only while up and awake.
Second Line neiss.html. Accessed May 8, 2010.
Apply ice, and elevate affected extremity.
Open fracture infection prophylaxis (7): Pain medications 5. Pappano D. Radius fracture from an electrical injury
r Tetanus immunoprophylaxis as indicated r Activity: involving an electric guitar. South Med J. 2010;
r GA type I: Cefazolin 25100 mg/kg/day IV divide 103(3):242244.
Rest the affected extremity.
q68h Avoid activities that could result in reinjury. 6. Patel DD, Blumberg SM, Crain EF. The utility of
r GA types II and III: Cefazolin dosing as above and bedside ultrasonography in identifying fractures
Patient Monitoring and guiding fracture reduction in children. Pediatr
gentamicin 2.5 mg/kg/dose IV q8h Advise patients to return for inadequate pain control, Emerg Care. 2009;25(4):221225.
SURGERY/OTHER PROCEDURES additional trauma to the injured area, numbness, or 7. Lobst CA, Tidwell MA, King WF. Nonoperative
r Regional anesthesia may significantly or completely discoloration of fingers/thumb. management of pediatric type I open fractures.
eliminate need for other analgesics: PROGNOSIS J Pediatr Orthop. 2005;25(4):513517.
Ulnar nerve block, radian nerve block, hematoma
block
r Forearm fracture: Excellent healing and functional F
outcome is expected.
r Closed reduction in the emergency department or r Scaphoid fractures carry moderate risk of nonunion ADDITIONAL READING
close outpatient orthopedic follow-up for diaphyseal and avascular necrosis.
and metaphyseal forearm fractures with: See Also (Topic, Algorithm, Electronic
>15-degree angulation COMPLICATIONS Media Element)
r Complications of general forearm fracture care are r Fracture, Hand
Overlapping ends or significant displacement r Fracture, Scaphoid
r Urgent orthopedic consultation for: rare but include the following (3):
Compartment syndrome r Fracture, Torus
Monteggia and Galeazzi fracture/dislocations
Neurovascular compromise from immobilization r Trauma, Elbow
Neurovascular compromise
Open fracture (casting or splinting)
Physeal or displaced intra-articular injury Refracture
r Operative management (namely, closed reduction in Nonunion CODES
Synostosis
the operating room, open reduction, or internal or
Physeal injury with growth arrest
external fixation) anticipated for (3,7): ICD9
Angulation with unacceptable functional outcome r 813.00 Closed fracture of upper end of forearm,
Difficult to reduce fractures r Scaphoid fractures are at higher risk of
Unstable fractures unspecified
Displaced scaphoid fracture complications: r 813.10 Open fracture of upper end of forearm,
GA types II and III open fractures Moderate risk of nonunion (1)
unspecified
Discretionary operative management if severe Avascular necrosis complicates 510%, with risk r 813.80 Closed fracture of unspecified part of
angulation/displacement and skeletally mature of subsequent collapse or SLAC wrist (1).
r Complications of fracture reduction: forearm
DISPOSITION Completion of greenstick fracture or iatrogenic
Admission Criteria fracture of nonfractured bone
r Open fracture Secondary displacement
PEARLS AND PITFALLS
r Anticipated surgery (relative indication) Iatrogenic neurovascular injury r Pearls:
r Increased risk of compartment syndrome Risk of infection with open fracture When only a single forearm bone is fractured, look
r Suspected nonaccidental trauma for dislocation of the nonfractured bone.
Discharge Criteria Salter-Harris type I fracture of the distal radial
r Skin intact (no open fractures) physis is the most common growth plate injury
r Displacement/Angulation is effectively reduced or and may have a normal radiograph.
r Pitfalls:
close orthopedic follow-up is assured
r Documentation of satisfactory neurovascular exam Failure to screen for compartment syndrome and
document the neurovascular exam
post immobilization
r Recovery from sedation (if provided)
387
FRACTURES, GREENSTICK/BOWING
Rasha Dorothy Sawaya
Cindy Ganis Roskind

BASICS Usually secondary to a fall on outstretched hand r Nonpathologic bowing
(FOOSH) with or without a rotator movement r Pediatric growth plates have nutrient vessels that
DESCRIPTION may be mistaken for fracture lines.
r Bowing and greenstick fractures are incomplete COMMONLY ASSOCIATED CONDITIONS r Rickets
r Bowing or greenstick fractures of one bone are
fractures involving the diaphyses or metaphyses of r Osteogenesis imperfecta
the long bones, most commonly of the forearm: frequently associated with injury to an adjacent
bone or joint: r Other metabolic bone disease
Usually caused by trauma r Pathologic fractures
r Both are often associated with a complete fracture Supracondylar fractures: Frequently associated
with diaphyseal greenstick fractures of the
of another adjacent bone.
r Both can angulate further without adequate therapy. radius/ulna
r Bowing fractures: Monteggia fracture-dislocation: Dislocation of the TREATMENT
proximal radius with greenstick or bowing fracture
Plastic deformation without any cortical defect of the proximal ulna PRE HOSPITAL
Most commonly involve the radius, ulna, and r Immobilization of the injured limb with a splint:
Galeazzi fracture: Fracture of distal radius with
occasionally the fibula. distal radioulnar joint injury Ensure intact distal pulses pre- and
r Greenstick fractures: r Nerve injury: post-immobilization.
An extension of a bowing fracture, with a cortical r Ice, elevate, and administer analgesic.
Case reports of median or ulnar nerve injury with
and periosteal defect on the convex side of the greenstick fractures (5,6) INITIAL STABILIZATION/THERAPY
bone r Pain management as needed (see below)
Most commonly involve the radius and ulna r Procedural sedation for fracture reduction as needed
EPIDEMIOLOGY
DIAGNOSIS r Bowing fracture:
Incidence HISTORY No consensus on management of bowing
r Greenstick fractures are common: r FOOSH fractures. Early pediatric orthopedic involvement
Highest incidence between 7 and 12 yr of age (1) r History of axial or transverse trauma to the site of during the emergency department course is highly
r Bowing fractures are relatively rare: injury recommended for all bowing fractures (2).
Occur in children 28 mo to 16 yr r Symptoms: Decision to immobilize with sugar tong splint or a
Highest incidence between 4 and 10 yr (2) Pain, decreased movement, or use of affected limb long arm cast or to perform a closed reduction
Tenderness of affected limb depends on several factors. Older age is a
RISK FACTORS significant factor for reduction:
r Rickets Visible deformity
r Past medical history of metabolic bone disease Age of the child:
r Diet deficient in vitamin D or calcium
Children <4 yr old remodel well and
r Osteogenesis imperfecta PHYSICAL EXAM reduction may not be required.
r Affected limb: Children 410 yr old: No consensus
GENERAL PREVENTION
r Fall prevention Deformity Children >10 yr old: Closed reduction is
r Playing on playgrounds with safe surfaces Greenstick fractures: Usually rotational and generally advised (4).
r Proper adult supervision visually dramatic with skin-line changes at the Degree of bowing:
level of the fracture >1020-degree bowing and >6 yr old:
PATHOPHYSIOLOGY Swelling Closed reduction is recommended (1,2).
r Long bones have an elastic limit and a plastic Tenderness Associated fractures or dislocations:
limit. Pain Lack of reduction of a bowing fracture
r Bowing fracture: Limitation of motion, especially pronation and associated with a fracture or dislocation of a
An axial compression force applied to a long bone supination second bone impedes appropriate healing of
r Neurovascular exam: the latter (2,4).
in an amount exceeding its elasticity results in a
bowing deformity maintained after the force is Sensation and movement distal to the site of injury Amount of functional limitation upon initial
removed. Pulse and capillary refill distal to the site of injury exam:
Multiple microfractures seen on histopathology r Evaluate the other bones and joints of the injured Significant loss of supination or pronation or
without evidence of hematoma or callus formation limb. clinical deformity requires reduction (4,7).
(3) r Greenstick fracture:
r Greenstick fracture: DIAGNOSTIC TESTS & INTERPRETATION
Angular deformity remodels well, however
Imaging rotational deformity (most common) often
An axial compression force with a twisting force r Plain radiographs of affected limb:
applied to a long bone in an amount exceeding its requires closed reduction.
At least 2 views: AP and lateral 2 types of reduction techniques: Rotational
plasticity results in a classic fracture with cortical
Always include the joints above and below the method of reduction and fracture method of
and periosteal disruption of the convex surface.
suspected fracture. reduction:
The cortex and periosteum of the inner curvature r A certain degree of bowing may be normal for a
remains intact though deformed. Rotational method: Rotating the bone in the
Hematoma and callus formation child: direction opposite to the deforming force (1):
r Case reports of transverse forces causing bowing Comparison films of the unaffected limb may be Easier and less painful
helpful to assess the degree of abnormal (excess) Most commonly used
(2,4)
bowing. Fracturing method: Completing the fracture:
Has lower refracture rate
Risk of reangulation if not adequately rotated
More painful and traumatic (8)
Associated complete fracture may require
completing the greenstick fracture for better
outcome of closed reduction and alignment of
now both completely fractured bones.
388
FRACTURES, GREENSTICK/BOWING
MEDICATION Issues for Referral 5. Huang K, Pun WK, Coleman D. Entrapment and
r Transfer to a center with a pediatric orthopedic transection of the median nerve associated with
First Line
r Oral opioids: specialist if: greenstick fractures of the forearm: Case report
Codeine or codeine/acetaminophen dosed as Nerve impingement and review of the literature. J Trauma. 1998;
0.51 mg/kg of codeine component PO q4h PRN Vascular supply injury 44(6):11011102.
Hydrocodone or hydrocodone/acetaminophen Compartment syndrome 6. Prosser AJ, Hooper G. Entrapment of the ulnar
dosed as 0.1 mg/kg of hydrocodone component r Associated supracondylar fractures or joint nerve in a greenstick fracture of the ulna. J Hand
PO q46h PRN dislocation Surg Br. 1986;11(2):211212.
r Oral NSAIDs: r Refer all bowing and greenstick fractures to a 7. Komara J, Kottamasu L, Kottamasu S. Acute
Consider NSAID medication in anticipation of pediatric orthopedic specialist for follow-up. plastic bowing fractures in children. Ann Emerg
prolonged pain and inflammation: Med. 1986;15(5):585588.
Some clinicians prefer to avoid NSAIDs due to 8. Noonan K, Price C. Forearm and distal radius
theoretical concern over influence on FOLLOW-UP fractures in children. J Am Acad Orthop Surg.
coagulation and callus formation. FOLLOW-UP RECOMMENDATIONS 1998;6:146156.
Animal studies have raised concerns that r Timely orthopedic follow-up within 510 days, 9. Clarke D, Lecky F. Best evidence topic report. Do
NSAIDs may negatively influence bone healing; depending on initial management non-steroidal anti-inflammatory drugs cause delay
however, there is no clinical evidence in humans r Oral pain management: Ibuprofen as first-line in fracture healing? Emerg Med J. 2005;22(9):
(9). 652653.
therapy in the 1st 72 hr (10)
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN r Rest, ice, and elevation of cast or splint for at least 10. Drendel AL, Gorelick MH, Weisman SJ, et al. A
Naproxen 5 mg/kg PO q8h PRN randomized clinical trial of ibuprofen versus
r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN 48 hr post cast/splint to avoid compartment
syndrome acetaminophen with codeine for acute pediatric
Second Line arm fracture pain. Ann Emerg Med. 2009;
IV pain management: ACTIVITY 54(4):553560.
r Morphine 0.1 mg/kg IV/IM/SC q2h PRN: No physical activity until further recommendation by a
Initial morphine dose of 0.1 mg/kg IV/SC may be
pediatric orthopedic surgeon.
ADDITIONAL READING
F
repeated q1520min until pain is controlled, then PROGNOSIS
q2h PRN. r Generally favorable
r Fentanyl 12 g/kg IV q2h PRN: r Children have good remodeling potential of the
Media Element)
Initial dose of 1 g/kg IV may be repeated forearm. r Fracture, Forearm/Wrist
q1520min until pain is controlled, then q2h PRN. r Depends on age, degree of angulation, and r Fracture, Supracondylar
r Ketorolac 0.5 mg/kg IV/IM q6h PRN supination/pronation of the affected area r Fracture, Torus
r When possible, pediatric orthopedic consultation in r Bowing fractures if untreated or incompletely
the emergency department is suggested prior to treated: CODES
splinting/casting or reduction. Limitation of motion:
r Closed reduction depending on significance of Loss of complete supination, pronation, and ICD9
bowing (see above) and other associated fractures especially rotator motion r 813.04 Other and unspecified closed fractures of
r Rarely, open reduction may be required. May prevent proper healing of concurrent proximal end of ulna (alone)
fractures (7) r 813.07 Other and unspecified closed fractures of
DISPOSITION r Greenstick fractures if incomplete reduction/rotation proximal end of radius (alone)
Admission Criteria or immobilization: r 813.14 Other and unspecified open fractures of
r Open fractures
1020% redisplacement rate with volar proximal end of ulna (alone)
r Fractures with compartment syndrome or angulation (1)
neurovascular compromise Refracture
r Suspected nonaccidental trauma r Medullary cyst formation PEARLS AND PITFALLS
r Posttraumatic cortical cysts
Discharge Criteria r Pearls:
r Stable vital signs and no other associated injuries
A 2nd adjacent bone is often involved.
that may require hospitalization
r Intact neurovascular exam REFERENCES Greenstick fractures have been described in
patients with vitamin D deficiency.
r Pain adequately controlled with oral medications 1. Davis D, Green D. Forearm fractures in children: r Pitfalls:
r Adequate reduction and immobilization of affected Pitfalls and complications. Clin Orthop Relat Res. Bowing fractures may be subtle on radiographs.
bone with a double sugar tong splint or long arm 1976;(120):172183. Injuries to the proximal or distal joint must be
cast 2. Vorlat P, De Boeck H. Bowing fractures of the ruled out when the radius or ulna are fractured or
r Ability to follow-up with pediatric orthopedic forearm in children: A long-term followup. Clin bowed.
surgeon: Orthop Rel Res. 2003;413:233237. Consider child abuse if the history does not fit the
Document intact neurovascular function after 3. Chamay A. Mechanical and morphological aspects injury.
emergency department therapy and casting. of experimental overload and fatigue in bone. Inadequate rotation during reduction of greenstick
J Biomech. 1970;3:263270. fractures
4. Vorlat P, De Boeck H. Traumatic bowing of
childrens forearm bones: An unreported
association with fracture of the distal metaphysis.
J Trauma. 2001;51(5):10001003.
389
FRACTURE, HUMERUS
Donna M. Simmons
PATHOPHYSIOLOGY Radial nerve injury:

BASICS r Fractures of the proximal humeral physis are most Numbness over the dorsum of the hand
common in adolescents during the period of rapid between the 1st/2nd metacarpals
DESCRIPTION growth when the physis is weakest. Decreased thumb and wrist extension
r The humerus is the largest bone in the upper r The axillary and radial nerves are at risk for injury Decreased forearm supination/wrist drop
extremity and is an important component of the with displaced proximal humeral head and midshaft Assess motor function by having the patient make
shoulder. humeral fractures, respectively: a thumbs up (radial nerve), tight fist over the
r The proximal humerus has 2 ossification centers: Fortunately, these injuries are rare. thumb (median nerve), and an OK sign (anterior
The medial ossification center may be present at Usually just see temporary loss of function interosseous nerve).
birth but generally appears by 2 mo of age. (neurapraxia) without a physical nerve disruption Presence of radial, ulnar, and brachial pulses and
The lateral ossification center generally appears by r The thick periosteum of the humerus limits capillary refill in all digits
9 mo of age in girls and by 14 mo in boys. displacement, and the growth potential of the DIAGNOSTIC TESTS & INTERPRETATION
The ossification centers fuse by 57 yr of age. proximal epiphysis allows for significant remodeling
r Closure of the proximal humeral epiphysis does not Imaging
of proximal and shaft fractures with minimal r AP and lateral radiographic views of humerus:
occur until 1619 yr of age. deformity.
r The proximal humeral epiphysis accounts for 80% of Must include shoulder and elbow joints
ETIOLOGY r Obtain dedicated shoulder and elbow radiographs
the longitudinal growth of the humerus. r Direct blow to shoulder on the lateral aspect of the
r Proximal physeal fractures most commonly occur in for concerns of injury of those joints.
arm. r Assess fracture location, fracture pattern, and the
children 1117 yr of age and are usually r Fall on outstretched hand (FOOSH) presence of displacement or angulation:
Salter-Harris type II. r High-energy trauma, motor vehicle accidents,
r In the younger child, proximal humerus fractures are Suspect Salter-Harris type I fracture if there is
contact sports, falls tenderness over the proximal humeral physis
typically Salter-Harris type I. r Birth trauma despite normal radiographs.
r Humeral shaft fractures occur in all ages but are
r Consider child abuse when shaft fractures occur in Comparison views may show widening of the
more common in children ages <3 yr and >12 yr physis.
children <3 yr of age.
(1). r Electrical shock, seizures r US or MRI may be helpful in diagnosing fractures in
r Supracondylar humeral fractures are discussed in a
neonates.
separate topic. COMMONLY ASSOCIATED CONDITIONS
Shaft fractures are commonly pathologic in children DIFFERENTIAL DIAGNOSIS
EPIDEMIOLOGY r Clavicle fracture
312 yr of age and are associated with bone cyst or
Incidence r Shoulder dislocation/rotator cuff injury
tumor.
The incidence of proximal humeral fractures is r Brachial plexus palsy
13 cases/1,000 population per year. r Shoulder joint infection
Prevalence DIAGNOSIS r Osteomyelitis of humerus
r Shaft fractures are not common, representing r Tumor
HISTORY
<10% of all fractures in children (2). r Typically, there is a FOOSH or other significant r Little league shoulder or osteochondrosis of
r Humerus fractures are the 2nd most common
trauma. proximal humeral epiphysis
fractures in neonates. r Shoulder or arm pain with and without movement r Tendinitis
RISK FACTORS r Irritability in a neonate when upper extremity is r Bursitis
r Unicameral bone cyst or tumor of humerus moved or decreased movement of upper extremity
r Obesity (pseudoparalysis)
r Malignancy, metastasis to bone TREATMENT
PHYSICAL EXAM
r Prior radiation treatment r Swelling of the proximal, midshaft, or distal humerus PRE HOSPITAL
r Osteoporosis r Shortening of the upper extremity suggests r Immobilize the fracture
r Contact sports displacement. r Manage the patient with multiple trauma according
r Pain on palpation to Advanced Trauma Life Support (ATLS) principles.
GENERAL PREVENTION r Ask young children to point with 1 finger to locate
r Proper parental supervision INITIAL STABILIZATION/THERAPY
r Proper education of sports safety the injury. r Assess and stabilize airway, breathing, and
r Athletic protective equipment r Decreased range of movement of shoulder or elbow
circulation per ATLS guidelines, and identify all
r Correction of osteoporosis r Perform a detailed neurovascular exam:
injuries.
Brachial plexus injury can cause decreased r Immobilization:
sensation or pain in the affected arm. Sling or shoulder immobilizer
Axillary nerve injury: Check neurovascular status before and after
Numbness over the deltoid placement.
Shoulder weakness r Administration of adequate analgesia facilitates
Inability to raise or abduct shoulder
exam and eases pain during imaging.
r Application of ice
390
FRACTURE, HUMERUS
r Nonoperative treatment for most despite angulation SURGERY/OTHER PROCEDURES COMPLICATIONS

and displacement: r Open fractures and fractures with associated r Radial nerve palsy with shaft fractures
Sling and swathe for infants and young children neurovascular injury may require surgical repair. r Deltoid nerve injury with proximal fractures
with proximal and humeral shaft fractures with Most neurapraxias will resolve spontaneously. r Growth retardation without functional limitation
arm wrapped close to trunk for 34 wk r Displaced or angulated fractures for which and usually not clinically significant
Adolescents may also use sling/swathe or can use alignment cannot be maintained with closed r Nonunion is rare.
shoulder immobilizer for proximal and shaft reduction may undergo percutaneous pinning or r Avascular necrosis is rare.
fractures if there is no significant displacement. open reduction with internal fixation.
r Acceptable angulation and displacement is as
DISPOSITION
follows (without need for reduction):
Admission Criteria
REFERENCES
For proximal fractures: r Patients requiring surgery
<5 yr of age: 70-degree angulation, minimal 1. Caviglia H, Garrido CP, Palazzi FF, et al. Pediatric
r Trauma victims with multisystem injuries fractures of the humerus. Clin Orthop Relat Res.
apposition
512 yr: <45-degree angulation, <50% r Children who are victims of abuse 2005;432:4956.
apposition r Neurovascular compromise 2. Shrader MW. Proximal humerus and humeral shaft
Adolescents: 25-degree angulation, <30% fracture in children. Hand Clin. 2007;23:431435.
Discharge Criteria
apposition r Patients with fractures amenable to nonoperative 3. Beaty JH. Fractures of the proximal humerus and
For shaft fractures: management shaft in children. Instr Course Lect. 1992;41:369.
<5 yr of age: Up 70-degree angulation, 100% r May discharge if there is no suspicion of 4. Hwang RW, Bae DS, Waters PM. Brachial plexus
displacement palsy following proximal humeral fractures in
512 yr: 4070-degree angulation nonaccidental injury
patients who are skeletally immature. J Orthop
>12 yr: Up to 40-degree angulation, 50% Issues for Referral Trauma. 2008;22(4):286290.
displacement (3) r Refer to an orthopedic surgeon immediately for:
Bayonet apposition of 11.5 cm is acceptable: Open fractures
Traction may be required if bone segments are Neurovascular injury ADDITIONAL READING F
overriding too much. Significantly displaced/angulated fractures
Rotational deformity may require correction. Intra-articular fractures See Also (Topic, Algorithm, Electronic
r For complete or moderately displaced fractures, Compartment syndrome Media Element)
Multisystem trauma r Fracture, Clavicle
coaptation splint, modified Velpeau bandage, and
r Child protective services for nonaccidental injury. r Fracture, Forearm/Wrist
functional bracing are options.
r Long arm cast for distal 3rd fractures Transverse and spiral fractures may be associated r Fracture, Scapula
r Hanging arm casting for humeral shaft fractures with abuse. r Fracture, Supracondylar
require upright position during sleep and may not be r Trauma, Shoulder
effective.
r Open humeral fractures require sterile dressings,
FOLLOW-UP
tetanus prophylaxis, parenteral antibiotics, and FOLLOW-UP RECOMMENDATIONS CODES
surgical repair.
Refer to an orthopedic surgeon in 710 days. ICD9
MEDICATION See Medication section. r 812.00 Fracture of unspecified part of upper end of
r Opioids: r Activity:
Morphine 0.1 mg/kg IV/IM/SC q2h PRN: humerus, closed
For fractures treated nonoperatively, patients can r 812.10 Fracture of unspecified part of upper end of
usually resume light activities and active range of humerus, open
be repeated q1520min until pain is controlled, motion after 46 wk. They should have followed r 812.20 Fracture of unspecified part of humerus,
then q2h PRN. up with their orthopedic surgeon before this and
Fentanyl 12 g/kg IV q2h PRN: closed
received their advice to progress.
Resume vigorous activities gradually.
q1520min until pain is controlled, then q2h No contact sports until 6 mo following the
PRN. humeral shaft fracture
PEARLS AND PITFALLS
Codeine/Acetaminophen dosed as 0.51 mg/kg of r Pearls:
codeine component PO q4h PRN Patient Monitoring
r Neurapraxia usually resolves by 3 mo. If not, refer to Always consider nonaccidental trauma with spiral
dosed as 0.1 mg/kg of hydrocodone component an orthopedic surgeon for possible surgical fractures of the humerus, especially for children
PO q46h PRN exploration (2). <3 yr of age.
r NSAIDs: r Patients requiring pinning for unstable fractures are r Pitfalls:
Consider NSAID medication in anticipation of followed weekly with radiographs to determine Failing to evaluate for neurovascular injury
prolonged pain and inflammation: when pins can be removed. Failing to consider nonaccidental injury if the
Some clinicians prefer to avoid NSAIDs due to mechanism of injury is inconsistent with level of
PROGNOSIS development in a healthy child <3 yr of age.
theoretical concern over influence on r Usually full recovery without loss of function
coagulation and callus formation. r Nearly all cases of radial nerve palsy fully resolve.
Animal studies have raised concerns that r Complete recovery of brachial plexus injury in
NSAIDs may negatively influence bone healing;
neonates in 9 mo (4)
however, there is no clinical evidence in humans.
391
FRACTURE, MANDIBULAR
Hnin Khine
r Condylar fractures are common in younger children r Assess the difficulty of mouth opening, range of
BASICS and decrease with increasing age. motion, and stability of the temporomandibular joint
r Multiple fracture sites along the mandible can be (TMJ):
DESCRIPTION found in 4060% of the cases. This is especially Place a finger into the external auditory canal and
r The mandible makes up the lower jaw of the face locate the TMJ. Then, ask the patient to move his
more common in older children.
and houses the lower teeth. or her jaw to assess its stability.
r It is the largest and strongest bone of the face. ETIOLOGY Place a wooden tongue blade laterally between
r In younger children, most mandibular fractures are
r The mandible is composed of 2 hemimandibles the teeth on either side and assess for the
the result of motor vehicle accidents (MVAs) or falls. patients ability to hold the blade in place without
fused at midline by a vertical symphysis. r With increasing age, altercations (35%), MVAs
r Facial fractures are rare in children for the following pain while the examiner attempts to pull the blade
(28%), bicycle accidents (12%), and falls (7%) with twisting motions.
reasons:
cause the majority of mandibular fractures (2). Assess the bite status (normal or abnormal).
Underdeveloped facial skeleton and paranasal
COMMONLY ASSOCIATED CONDITIONS r Paresthesia of the lower lip or gums suggests
sinuses
Unerupted teeth provide additional strength. r Among hospitalized trauma patients, facial fractures damage to the inferior alveolar nerve, which also
Lower center of gravity during falls with less are associated with: provides sensation to the teeth.
resultant force on impact (1) Higher injury severity score DIAGNOSTIC TESTS & INTERPRETATION
r Many patients with mandibular fractures (3060%) Longer ICU stays
Longer hospital stays (1)
Imaging
have serious associated injuries: r Dental panoramic views (Panorex)
Strong forces are required to break the mandible r Can see concomitant thoracoabdominal,
8692% sensitive
(2): intracranial, spine, extremity, and other facial Require the patients cooperation
This is especially true for the mandibular injuries.
r Chin lacerations or contusions should raise suspicion Useful in isolated mandibular injury
symphysis, which is rarely fractured due to its r A series of plain radiographs may be more useful in
thickness. for mandibular fractures (3).
r Among the hospitalized trauma patients, r Mandibular dislocations patients who are unable to cooperate to take
panoramic views:
mandibular fractures are the most common type of Lateral oblique view: To view the condyle,
facial fracture (1).
DIAGNOSIS coronoid process, body, ramus, and angle of
EPIDEMIOLOGY mandible
r Very rare in children <5 yr of age HISTORY PA view: To view the ramus, angle, and body of
r Incidence increases with increasing age r Obtain the mechanism of injury, including the mandible
r Mandibular fractures were found in 1.5% of all time of injury and circumstances surrounding the Towne view: To view the condyles
hospitalized trauma patients (1). injury: Mandibular occlusal views: To view a symphyseal
r Male to female ratio of 3:1 Mechanism of injury will help determine the fracture
possible site of fracture. Dental radiograph: To view alveolar or dental root
RISK FACTORS r Symptoms of mandibular fracture include: fractures
r Lack of proper restraints in motor vehicles r Computerized tomogram (CT):
Facial swelling with localized pain
r Participating in sports without proper protective gear Pain and difficulty with mouth opening and closing 100% sensitive
r Interpersonal violence Dental pain or abnormal bite May be useful when other facial fractures are
r Use of substances that impair mental abilities Numbness of the lip and chin suspected as well.
CXR to look for unaccounted teeth
GENERAL PREVENTION ALERT
r Use of appropriate protective equipment during r Important to correlate the history with physical DIFFERENTIAL DIAGNOSIS
r Mandibular dislocations or contusions
sports findings
r Use of proper restraints in motor vehicles r Suspect child abuse if there are inconsistencies in r Traumatic hemarthrosis of TMJ
r Appropriate use of child safety precautions at each r Dental trauma resulting in referred pain
the history or physical exam. r Related skull fractures
developmental stage
r Proper adult supervision of children during play
PHYSICAL EXAM
r General exam using Advanced Trauma Life Support
PATHOPHYSIOLOGY TREATMENT
r Fractures can occur along any part of mandible: (ATLS) protocols to exclude life-threatening injuries
Greenstick fractures are common in the younger r Maintain cervical spine immobilization until PRE HOSPITAL
age group due to the high elasticity of bone with significant spine injuries are excluded. r Assess ABCs per ATLS and Pediatric Advanced Life
thick medullary spaces and thin bony cortices. r Assess for associated injuries focusing on the CNS, Support (PALS) guidelines:
r Pediatric fractures are less likely to be comminuted. spine, airway, and other facial injuries. Cervical spine immobilization if necessary
r The site of fracture is dependent on the mechanism r Inspection: r Collect and preserve any avulsed teeth:
of injury: Deformity or swelling See Trauma, Dental topic for proper technique for
Forces directed to the chin can cause fractures of Ecchymosis: External or inner mucosa of mouth preservation of teeth.
the condyles or symphysis. Lacerations: External or intraoral INITIAL STABILIZATION/THERAPY
Direct assaults usually result in a fracture of the Any tooth trauma, including dental avulsion; r Address ABCs per ATLS and PALS guidelines:
body or angle of the mandible at the point of dental luxation, subluxation, concussion, Look for other life-threatening injuries.
impact. intrusion, and extrusion; or enamel, crown, root, Recognize that mandible fractures may make
and alveolar bone fractures orotracheal intubation difficult.
r Palpation: r Ensure a patent airway by removing any material
Palpate along the entire mandible to look for that could obstruct the airway, such as blood,
step-off, bony disruption, or point tenderness. vomitus, bone fragments, and foreign bodies.
Palpate each tooth for pain and stability. r Control bleeding locally with pressure. Consider
nasal packing if there is persistent epistaxis.
392
FRACTURE, MANDIBULAR
r Consider use of an antiemetic (eg, ondansetron) to Discharge Criteria 3. Zachariades N, Mezitis M, Mourouzis C, et al.
prevent vomiting. r Stable vital signs Fractures of the mandibular condyle: A review of
r Judicious pain therapy r Adequate pain control achieved 446 cases. Literature review, reflection on
r Use of routine antibiotic prophylaxis is controversial. r No respiratory difficulties and associated CNS treatment and proposal. J Craniomaxillofac Surg.
r Consider prophylactic antibiotics in: issues 2006;34:421432.
Heavily contaminated wounds r Reliable family for follow-up 4. Norholt SE, Krishnan V, Sindet-Pedersen S. Pediatric
Severely comminuted fractures condylar fractures: A long term follow-up study of
Issues for Referral 55 patients. J Oral Maxillofac Surg. 1993;51(12):
Severely macerated soft tissues Follow up with the surgical service that initiated initial
Delayed fracture treatment 13021310.
therapy.
Prolonged operative time 5. Leake D, Doykos J, Habal MB. Long-term follow-up
Uncomplicated fractures in patients with valvular of fractures of mandibular condyle in children. Plast
heart disease FOLLOW-UP Reconstr Surg. 1971;47(2):127131.
MEDICATION FOLLOW-UP RECOMMENDATIONS
First Line r Discharge instructions and medications: ADDITIONAL READING
r Pain therapy is guided by severity:
Soft or liquid diet
Mild pain: Pain control as needed See Also (Topic, Algorithm, Electronic
Acetaminophen 15 mg/kg PO q4h PRN Antibiotics to be taken as prescribed Media Element)
r Dislocation, Temporomandibular Joint
Moderate to severe pain: Consider antiemetic agent as needed
Codeine/Acetaminophen dosed as 0.51 mg/kg r Activity: r Trauma, Dental
of codeine component PO q4h PRN r Trauma, Facial
Avoid rigorous activity.
Hydrocodone or hydrocodone/acetaminophen No contact sports until the treating surgeon clears
dosed as 0.1 mg/kg of hydrocodone component the patient
PO q46h PRN
Patient Monitoring
CODES
Initial morphine dose of 0.1 mg/kg IV/SC may Return sooner for re-evaluation if:
ICD9
F
r Worsening pain
be repeated q1520min until pain is r 802.20 Closed fracture of unspecified site of
controlled, then q2h PRN. r Difficulty breathing or swallowing
r Ondansetron: mandible
r Severe headache, drowsiness, or weakness r 802.30 Open fracture of unspecified site of mandible
0.15 mg/kg IV/PO q48h, max single dose 8 mg r Fever or other serious complaints
Second Line DIET
r Consider tetanus prophylaxis: PEARLS AND PITFALLS
Soft or liquid diet
Td 0.5 mL IM or DTaP 0.5 mL IM r Pearls:
r If antibiotics are considered, use: PROGNOSIS
r Dysfunction resulting from condylar fractures Remember to assess for associated injuries since
Penicillin G sodium aqueous:
100,000400,000 units/kg/day IV divided increases with increasing age at the time of trauma patients admitted with facial fractures have a
q46h, max single dose 24 million units/day, OR (4). higher injury severity score than those without
r If occlusion is normal after swelling has resolved, facial fractures.
Amoxicillin:
2550 mg/kg/day PO divided b.i.d. or t.i.d. early mobilization is associated with excellent results Remember to assess for mandibular injuries in
orally for 35 days (5). patients with chin lacerations.
r Pitfalls:
For penicillin-allergic patients, clindamycin: COMPLICATIONS
1030 mg/kg/24 hr PO or IV divided q68h for r Immediate: Beware that bilateral mandibular fractures may be
35 days, max single dose 2.7 g/day PO/IV present.
Wound infection or sepsis
r Delayed:
r Definitive repair of a mandibular fracture is not a Growth disturbance with facial asymmetry
surgical emergency. Malocclusion or trismus
r Wide range of management available: Nonunion or malunion
Analgesia alone Tooth loss or ankylosis
r Paresthesias
Physiotherapy
Mandibulomaxillary fixation r TMJ dysfunction
Open reduction with internal fixation
r Most pediatric mandibular fractures can be
managed with closed reduction. REFERENCES
r Every attempt should be made to manage
1. Imahara SD, Hopper RA, Wang J, et al. Patterns
prepubertal children with mandibular fractures and outcomes of pediatric facial fractures in the
conservatively to minimize trauma to permanent United States: A survey of the National Trauma
dentition. Data Bank. J Am Coll Surg. 2008;207:710716.
DISPOSITION 2. Smartt JM Jr., Low DW, Bartlett SP. The pediatric
Admission Criteria mandible: II. Management of traumatic injury of
r Patients with significant dental or mandibular fracture. Plast Reconstr Surg. 2005;116:28e.
trauma who cannot tolerate PO intake
r Other associated system trauma requiring admission
As determined by the injury severity score
Unstable fracture with potential airway
compromise
393
FRACTURE, NASAL
Hnin Khine
r Naso-orbito-ethmoid fractures: r Exam of nares:

BASICS Occur as a result of a direct blow to the mid face Elevate the tip of the nose to maximize the view.
Seen as complete separation of nasal bones and Use an otoscope with an ear or nasal speculum to
DESCRIPTION medial orbital bones from frontal bone and the aid the exam:
r The nose is made up of bone and cartilage. infraorbital rim Remove any blood clots.
r The upper 1/3 is made up of paired nasal bones that r Swelling of the septum with a blue to purple
ETIOLOGY
articulate: intranasal mass is suggestive of septal
A majority results from direct trauma:
Superiorly with nasal process of frontal bone r In younger children, falls or motor vehicle accidents hematoma:
Laterally with frontal process of maxillary bones r Useful aids to help differentiate septal hematoma
Medially with each other (thicker above than (MVAs)
r In older children and adolescents, MVAs, falls, from edema
below) and spine of frontal and the perpendicular Application of topical vasoconstrictor:
plate of the ethmoid to form the bony septum sport-related trauma, and assault Application of phenylephrine hydrochloride or
Inferiorly with the cartilaginous framework COMMONLY ASSOCIATED CONDITIONS oxymetazoline
r The lower 2/3 consists of a cartilaginous framework. r Among hospitalized trauma patients, facial fractures No change in size seen with septal hematoma
r The middle 1/3 is made up of septal and lateral are associated with: Palpate the septum with a cotton-tipped
cartilaginous structures in the shape of a triangle. Higher injury severity score (ISS) applicator: Doughy consistency suggests septal
r The lower lateral cartilage is paired and joined in the Longer ICU stay hematoma or abscess.
middle to form the tip of the nose. Longer hospital stay (1) r The presence of clear fluid may indicate a CSF leak
r The nose has an abundant blood supply from both r It is important to look for other concomitant from an associated skull fracture.
the internal and external carotid arteries. intracranial, spinal, and facial injuries. r Mid-face instability or dental malocclusion is
r Facial fractures are rare in children for the following indicative of a midfacial Le Fort fracture.
reasons: DIAGNOSTIC TESTS & INTERPRETATION
Underdeveloped facial skeleton and paranasal DIAGNOSIS
sinuses
Lab
HISTORY Initial Lab Tests
Additional strength of the maxilla and mandible r Assess for associated injuries, mainly CNS, spine,
Consider coagulation studies for hemorrhage.
from unerupted teeth ocular, and other facial injuries.
Lower center of gravity during falls with resultant r Mechanism of injury can suggest the likelihood of Imaging
less force on impact (1) r Plain radiographs are rarely needed emergently.
associated injuries or symptoms: r Consider a CT scan if suspecting skull,
EPIDEMIOLOGY Symptoms include pain, bleeding, nasal
r Nasal fractures are the most common pediatric obstruction, anosmia, and deformity. naso-orbito-ethmoid, or other facial fractures.
facial fractures. Symptoms associated with septal hematoma DIFFERENTIAL DIAGNOSIS
r Nasal fractures are more common in young toddlers include severe localized nasal pain, tenderness on Other facial fractures such as orbital, maxillary sinus,
than adolescents. palpation of nasal tip, and significant nasal ethmoid sinus, and cribiform plate fractures
obstruction:
RISK FACTORS Symptoms of septal hematoma can be delayed.
r Sport, especially without protective gear
r Improper use of restraints in motor vehicles
Septal hematoma may occur even after minor TREATMENT
trauma (3).
Patients with septal abscess usually can have fever PRE HOSPITAL
GENERAL PREVENTION r Assess and stabilize airway, breathing, and
r Use of appropriate protective gear during sport in addition to the symptoms of a septal
hematoma. circulation per Advanced Trauma Life Support (ATLS)
activities
r Proper use of restraints in motor vehicles and Pediatric Advanced Life Support (PALS)
PHYSICAL EXAM guidelines:
r Child safety precautions r General exam to rule out severe life-threatening
Administer supplemental oxygen, preferably by
injuries nonrebreather mask, if necessary.
PATHOPHYSIOLOGY r Inspection of nose and face:
r Fracture can occur in both bony and cartilaginous Consider a cervical collar, if necessary.
structures. Deformity and swelling r Control epistaxis:
r The Kiesselbach plexus at the anterior septum is a Ecchymosis Application of pressure usually is effective:
Epistaxis Pinch nares together.
common site of nosebleed.
r Septal hematoma occurs when blood collects Shape of nose: Pugnacious nose with loss of
anterior projection on lateral view with increased INITIAL STABILIZATION/THERAPY
between septal cartilage and mucoperichondrium: r Assess and stabilize airway, breathing, and
intercanthal distance suggest naso-orbital-
May grow acutely or subacutely ethmoid fracture circulation per ATLS and PALS guidelines:
Can be bilateral with nasal fractures r Palpation: Administer supplemental oxygen, preferably by
Complications associated with septal hematoma nonrebreather mask, if necessary.
Tenderness:
include: At nasal tip: Suggests septal hematoma Assess nasal passage patency:
Septal abscess may extend to CNS (meningitis, Nasal intubation is contraindicated if the nasal
Over the frontal sinus: May indicate a frontal
intracranial abscess, orbital cellulitis, or passage is compromised or if a septal
sinus fracture
cavernous sinus thrombosis). hematoma is present.
Avascular necrosis of nasal septal cartilage with Deformity
Crepitus Consider a cervical collar, if necessary.
subsequent saddle nose deformity Displaced nasal fractures do not require reduction
Functional nasal obstruction due to scar tissue in the emergency department unless they
and cartilage overgrowth (2) compromise the airway.
394
FRACTURE, NASAL
r Control epistaxis: r Septal hematomas must be drained in the PROGNOSIS

Use pressure or a vasoconstricting agent. emergency department: Full recovery is typical unless complications from
Pack nares with gauze if necessary: After drainage, pack with petroleum jelly gauze to associated injury or infection occur.
Antibiotics may be prescribed if the patient is prevent reaccumulation.
r Consult otolaryngologist if: COMPLICATIONS
discharged home with packing. r Acute:
MEDICATION Uncontrolled epistaxis Septal hematoma or abscess
Significant deviation of external nares with nasal r Chronic:
First Line obstruction
r Pain therapy: Guided by the severity of injuries Cosmetic deformity: Saddle nose or bump
r Opioids: Suspicion for septal hematoma/abscess
Structural deformity: Septal deviation, deviation of
Naso-orbital-ethmoid fracture
Morphine 0.1 mg/kg IV/IM/SC q2h PRN: osseous and cartilaginous pyramid
Initial morphine dose of 0.1 mg/kg IV/SC may DISPOSITION r Functional:
be repeated q1520min until pain is controlled, Admission Criteria Nasal obstruction
then q2h PRN. r Most nasal fractures do not require admission. Obstructive sleep apnea
Codeine or codeine/acetaminophen dosed as r Admit patients with significant craniofacial injuries
0.51 mg/kg of codeine component PO q4h PRN (eg, nasoethmoid fractures).
Hydrocodone or hydrocodone/acetaminophen r Critical care admission criteria: REFERENCES
dosed as 0.1 mg/kg of hydrocodone component Unstable vital signs due to injury severity, altered 1. Imahara SD, Hopper RA, Wang J, et al. Patterns
PO q46h PRN mental status, or respiratory compromise
r NSAIDs: and outcomes of pediatric facial fractures in the
Airway obstruction United States: A survey of the National Trauma
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN Nasal obstruction in neonates requires immediate Data Bank. J Am Coll Surg. 2008;207:710716.
Naproxen 5 mg/kg PO q8h PRN intervention since they are obligate nose
r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN 2. Toback S. Nasal septal hematoma in an
breathers. 11-month-old infant: A case report and review of
r Vasoconstricting agents:
Discharge Criteria literature. Ped Emerg Care. 2003;19(4):265267.
r Stable vital signs and epistaxis controlled
Phenylephrine hydrochloride nasal spray:
Children 25 yr: Use 12 sprays or drops of r Adequate patent airway assured
3. Alvarez H, Osorio J, De Diego JI, et al. Sequelae
after nasal septum injuries in children. Auris Nasus
F
0.25% solution in each nostril q4h. r No evidence of significant head, face, neck, or other Larynx. 2000;27:339342.
Adults and children >6 yr of age: Use 2 sprays
injuries 4. Biswas D, Mal RK. Are systemic prophylactic
or drops of 0.5% solution in each nostril q4h. r Adequate pain control antibiotics indicated with anterior nasal packing for
Oxymetazoline nasal spray: r Reliable caregiver
Children 25 yr: Use 12 sprays or drops of spontaneous epistaxis? Acta Oto-Laryngologica.
2009;129:179181.
0.025% solution in each nostril q12h. Issues for Referral
Adults and children >6 yr of age: Use 2 sprays r Otolaryngologist referral for patients with any
or drops of 0.05% solution in each nostril q12h. significant amount of nasal swelling ADDITIONAL READING
Prolonged use of vasoconstricting agents will r Follow-up should be within 4872 hr:
cause rebound congestion with chronic swelling Patients with septal hematoma should follow up See Also (Topic, Algorithm, Electronic
of nasal mucosa. within 24 hr after emergency department septal Media Element)
Cocaine 4% solution, max single dose 1 mg/kg hematoma drainage. r Fracture, Orbital
topically to septum, max single dose 8 mL in r Bring a few recent photos of the patient to compare r Trauma, Head
adult: the shape of the nose before and after the trauma. r Trauma, Facial
Preferred for closed reduction, as it provides
vasoconstriction and anesthesia
Second Line FOLLOW-UP CODES
r Consider tetanus prophylaxis.
r Use of antibiotics with nasal packing is controversial FOLLOW-UP RECOMMENDATIONS
r Discharge instructions and medications: ICD9
(4): r 802.0 Closed fracture of nasal bones
Apply ice (1st 24 hr) and then heat/warm
If considered, use amoxicillin/clavulanate: compress (after 24 hr) to the affected area to r 802.1 Open fracture of nasal bones
2550 mg/kg/day dosed as amoxicillin divided minimize swelling.
b.i.d. or t.i.d. for 35 days Avoid nose blowing.
For penicillin-allergic patients, clindamycin: Pain medications as needed PEARLS AND PITFALLS
1030 mg/kg/24 hr PO divided q68h for r Activity:
35 days r Remember to assess for associated injuries since
Minimize activities until follow-up with
patients admitted with facial fractures have higher
SURGERY/OTHER PROCEDURES otolaryngologist.
r Most nasal fractures require closed reduction at a ISS score than those without facial fractures.
No contact sports until approved by treating r Have a high vigilance for septal hematomas. Consult
later date when the swelling has subsided. otolaryngologist or plastic surgeon
r If swelling has not yet occurred, immediate closed otolaryngologist early for septal hematomas.
Patient Monitoring r Septal hematoma can occur even with minor trauma.
reduction is preferred: Return sooner for re-evaluation if: r Consider prophylactic antibiotics, particularly those
Averts need for delay and potential use of general r Difficulty breathing
anesthesia with fracture reduction in ED.
r Pain increases
Useful if ability to follow up with subspecialist is r Worsening nasal obstruction
uncertain r Fever develops
Procedure is painful but brief, and the goal is to
r Recurrence of uncontrolled epistaxis
produce a symmetrical appearance.
r Nasal packing is needed if epistaxis is not controlled r Signs of increased intracranial pressure develop
by pressure.
395
FRACTURE, ORBITAL
Victoria Shulman
r Orbital floor fractures, also known as blowout

BASICS fractures, occur when an object strikes the eye. The DIAGNOSIS
force of the object displaces the globe posteriorly
DESCRIPTION and increases intraorbital pressure. This causes the HISTORY
r The orbit is made up of several facial bones: r When and how did injury occur?
weakest portion of the orbit (floor) to rupture.
The frontal bone makes up the superior and upper Several consequences can occur: Suspect underlying fracture when the mechanism
medial orbital ridge. Entrapment of the inferior rectus muscle and of injury indicates that a great force was applied
The zygoma makes up the lateral orbital rim. orbital fat leading to pain with or restriction of to the face even in the absence of significant
The maxilla comprises the inferior and lower movement of the eye and diplopia physical findings.
medial rims and floor of the orbit. r Blurry vision or decreased vision?
Injury to the infraorbital nerve with the associated
The ethmoid bone forms the medial and part of its decreased sensation of the cheek or upper teeth Hyphema, vitreous hemorrhage
posterior walls. Globe malpositioning such as enophthalmos or Retinal detachment
The sphenoid, lacrimal, and palatine bones form orbital dystopia r Double vision?
the remainder of the posterior orbit. r Trapdoor blowout fractures are most common in Entrapment
r The weakest parts of the orbit are the thin bones the pediatric population: Lens dislocation (causes monocular diplopia)
overlying the maxillary and ethmoid sinuses along Similar to a greenstick fracture, because of the r Pain with eye movement?
the orbital floor and medial wall: elastic nature of pediatric bones, the orbital floor, r Difficulty with eye movement in a specific direction?
However, these bones tend to be thicker in the instead of rupturing, may trap orbital fat and r Diplopia with eye movement in a specific direction
pediatric population than in adults until the muscle as the bones snap back into place (especially lateral or upward gaze)?
sinuses are fully aerated. potentially resulting in severe, restrictive r Sensitivity to light?
r Orbital roof fractures occur in younger children. This ophthalmoplegias. Suggests traumatic iritis or iridocyclitis
relates to the proportionally larger head and lack of There may be few periocular signs of trauma, r Numbness of a region of the face?
pneumatization of the frontal sinuses (1). and this is known as the white-eyed blowout Forehead: Suspect superior orbital rim or roof
r Orbital floor fractures occur primarily in older fracture: fracture
children (1). In addition to the relative lack of external signs
Cheek or upper teeth: Suspect orbital floor fracture
of trauma, there is also a decreased sensitivity r Nausea or vomiting?
EPIDEMIOLOGY of CT in identifying entrapment of the soft
r Trauma to the eye represents between 0.3% and 3% May indicate intraocular injury
tissues; therefore, a comprehensive evaluation
of all emergency department visits in the U.S. (2,3). Can also indicate muscle entrapment via the
r Facial fractures are rare in young children: of the patients ocular motion and visual acuity
oculocardiac reflex
must be performed.
The face of a child is small relative to the head, so Also may indicate intracranial injury
The recovery period in children who undergo
the majority of injuries involve the upper face and surgery within the 1st 5 days after trauma is PHYSICAL EXAM
skull. significantly shorter (5). r Since orbital fractures are the result of trauma,
Nasal, mandibular, and orbital fractures are the primary survey and attention to ABCs take priority
most common types seen. ETIOLOGY
r In younger children, motor vehicle accidents, falls, per Advanced Trauma Life Support (ATLS)
r The age distribution of orbital fractures has 2 peaks: guidelines:
1040 yr of age and >70 yr. and nonaccidental trauma are common causes of
Maintain cervical spine immobilization if indicated.
r Male to female ratio of 9:1 (4) orbital fractures. r After life-threatening injuries have been stabilized, a
r In older children and adolescents, sports-related
RISK FACTORS more specific exam of the face and orbits should
injuries and assaults become more common.
r Unrestrained car accident victims r Domestic violence should be considered as a cause occur:
r Certain sports, especially baseball or softball r Inspect:
in adolescent and older females.
r Male gender (4) Face for asymmetry while looking down from the
COMMONLY ASSOCIATED CONDITIONS head of the bed, as this allows for easier
GENERAL PREVENTION Since orbital fractures occur from significant trauma to evaluation of enophthalmos or exophthalmos
r Protective eyewear during sports activities the face and eye, other associated injuries may be Eyelids for lacerations:
r Proper use of motor vehicle restraints seen: May represent globe penetration
r Hyphema, vitreous hemorrhage Pupils for roundness and reactivity
PATHOPHYSIOLOGY r Ruptured globe, orbital hematoma Cornea for abrasions or lacerations
r Significant force is required to produce orbital
r Retinal detachment Anterior chamber for hyphema
fractures. Intercanthal distance:
r Orbital roof fractures, which are more common in r Traumatic optic neuropathy
Widening may indicate disruption of the medial
younger children, have a higher association with r Corneal abrasion or laceration
canthal ligament.
intracranial injury: r Intracranial injury
Nares for septal hematoma
Dural tears are associated with CSF leakage. r Related facial or cervical spine fractures r Palpate:
Ptosis and vertical ocular motility problems can be Supraorbital ridge and frontal bone for step-off
seen due to injury to the levatorsuperior rectus fractures
muscle complex. Zygoma along its arch and at its frontal, temporal,
r Orbital rim fractures are usually the result of a direct
and maxillary articulations
blow to the superior or lateral orbit. Mandible for swelling, tenderness, or step-off
Teeth for stability and/or malocclusion
r Check:
Ocular movements:
Make sure that eyes are symmetric and do not
cause pain with movement, especially with
upward and lateral gaze.
Visual acuity and presence of diplopia
Sensation to face
Orbital emphysema (soft tissue crepitance)
396
FRACTURE, ORBITAL
DIAGNOSTIC TESTS & INTERPRETATION Second Line

r Administer tetanus toxoid if appropriate.
REFERENCES
Imaging
r Since orbital fractures are often associated with r Oral antibiotics: 1. Koltai PJ, Amjad I, Meyer D, et al. Orbital fractures
other traumatic injuries, routine radiographs for Controversial, limited data (7) in children. Arch Otolaryngol Head Neck Surg.
trauma surveys should be considered. Consider if orbital fracture extends into a sinus 1995;121(12):13751379.
r Plain radiographs have poor sensitivity in diagnosing Amoxicillin 80 mg/kg/day PO divided b.i.d.t.i.d. 2. McGwin G Jr., Owsley C. Incidence of emergency
orbital fractures. However, they may be indicated Amoxicillin/Clavulanic acid 80 mg/kg/day PO department treated eye injury in the United States.
when: divided b.i.d.t.i.d. Arch Ophthalmol. 2005;123(5):662666.
CT is unavailable or there is low suspicion of Clindamycin 30 mg/kg/day PO divided t.i.d. 3. Bord SP, Linden J. Trauma to the globe and orbit.
orbital fractures r Corticosteroids: Emerg Med Clin North Am. 2008;26(1):97123.
Consider the Waters view when ordering plain May play a role in treatment of patients with 4. Antoun JS, Lee KH. Sports related maxillofacial
radiographs: limitation of ocular motility by differentiating fractures over an 11 year period. J Oral Maxillofac
This view best shows the inferior orbital rims, between edema-induced restriction of ocular Surg. 2008;66(3):504508.
nasoethmoid bones, and maxillary sinuses. movement (should resolve within a week) and 5. Kwon JH, Moon, JH, Kwon MS, et al. The
An air-fluid level in the maxillary sinus when the entrapment (will not resolve) (8) differences of blowout fracture of the inferior
patient is upright may indicate an orbital floor May decrease time of resolution of diplopia and orbital wall between children and adults. Arch
fracture. improve surgical outcome (8) Otolaryngol. 2005;131(8):723727.
The teardrop sign is an opacification in the Dosing recommended by consulting 6. Hatton MP, Watkins LM, Rubin PA. Orbital fractures
upper maxillary sinus representing orbital fat or ophthalmologist in children. Ophthal Plast Reconstr Surg. 2001;
an entrapped muscle. This may indicate an SURGERY/OTHER PROCEDURES 17(3):174179.
orbital floor fracture. r The goal of surgical intervention is to prevent visual 7. Martin B, Ghosh A. Antibiotics in orbital floor
The Caldwell view best displays the lateral orbital fractures. Emerg Med J. 2003;20(1):66.
loss and minimize late problems such as persistent
rim and ethmoid bone. 8. Millman AL, Della Rocca RC, Spector S, et al.
r CT scan of the orbits is usually considered the test diplopia and globe malpositioning (6).
r Isolated orbital floor fractures generally require Steroids and orbital blowout fracturesa new
of choice to diagnose orbital or other facial
fractures:
surgical repair if there is alteration of extraocular systematic concept in medical management and F
motility or orbital volume surgical decision making. Adv Ophthalmic Plast
Has increased sensitivity r The timing of surgery is still debated. Many surgeons Reconstr Surg. 1987;6:291300.
Useful in diagnosing associated injuries
Helpful in diagnosing orbital nerve involvement in will allow a few days for the orbital and periorbital
edema to resolve.
the fracture or intracranial injury r A trapdoor fracture has the potential for ischemia ADDITIONAL READING
Obtain a CT scan for severe pain, decreased visual
acuity, limitation of ocular movements, or to occur in the entrapped tissues, so these fractures See Also (Topic, Algorithm, Electronic
suspicion for orbital fracture. are generally repaired within 24 hr of the injury. Media Element)
Consider including CT of the brain for suspected DISPOSITION Globe Rupture
intracranial injury. Admission Criteria
r Severe herniation of orbital contents or similar injury
r Coincidental facial infections that threatens vision CODES
r Other facial fractures, including Le Fort fractures r Associated injuries that require admission
r Contusions to the face r Critical care admission criteria: ICD9
r 802.6 Closed fracture of orbital floor (blow-out)
r Dental trauma, including fractures Associated injuries, especially intracranial
r 802.7 Open fracture of orbital floor (blow-out)
Discharge Criteria r 802.8 Closed fracture of other facial bones
r Normal vital signs and adequate pain control
TREATMENT r Reliable caregiver and follow-up assured
PRE HOSPITAL PEARLS AND PITFALLS

FOLLOW-UP r Pearls:
circulation.
r Placement of metal shield if suspected globe injury FOLLOW-UP RECOMMENDATIONS Always check visual acuity in an age-appropriate
r Follow up as per surgical specialty service. manner since decreased visual acuity may be a
INITIAL STABILIZATION/THERAPY r All patients should have follow-up with an sign of optic nerve injury, retrobulbar hemorrhage,
r Assess and stabilize airway, breathing, and or other eye injury.
appropriate subspecialist within 1 wk. r Pitfalls:
circulation. r Discharge instructions and medications:
r Any suspicion of globe injuries should prompt Failure to identify nonaccidental injury
Cold packs to the eye to reduce swelling
immediate evaluation by an ophthalmologist. Failure to diagnose associated intracranial,
Elevate head of bed, and avoid nose blowing.
Medications to reduce coughing, sneezing, and cervical, or intraocular injuries
ALERT Failure to consult an ophthalmologist in the
Orbital fractures in children are associated with a vomiting may be helpful.
Pain medications as needed emergency department if the patient has a
high prevalence of ocular injury necessitating full significant loss in visual acuity, signs of
ophthalmologic evaluation (6). Patient Monitoring entrapment, or ocular hematomas
Patient should return promptly for:
MEDICATION r Any change in visual acuity, worsening pain
First Line r Fever, headache, facial tenderness
r Ibuprofen 10 mg/kg/dose PO q6h PRN
r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN COMPLICATIONS
r Visual loss from associated ocular injuries
r Codeine/Acetaminophen dosed as 0.51 mg/kg of
r Cosmetic defects such as enophthalmos or orbital
r IV fluids and antiemetics may be indicated if severe dystopia may occur.
r Persistent diplopia, especially in extreme excursions
nausea or vomiting occurs.
of gaze
397
FRACTURE, PATELLA
Sara Ahmed
Michele M. Nypaver

BASICS r Patellar dislocation
Imaging
r Patellar tendinitis r Plain x-rays are the initial imaging choice with AP,
DESCRIPTION r Patellar tendon rupture lateral, and sunrise views:
r The patella is the largest sesamoid bone in the body.
Traumatic fractures:
r It is enveloped within the quadriceps tendon and Occur at the middle 1/3
receives an excellent blood supply from the DIAGNOSIS Often comminuted with a high-riding patella
geniculate branches (inferior, middle, and superior) Stress fractures:
of the popliteal artery. HISTORY Occur at the junction of the middle and distal
r There are 3 types of patellar fracture: r Hearing a crack or feeling a popping sensation when
1/3 of the patella
Traumatic fracture injured Have sclerotic edges
r Pain, swelling, and tenderness at the knee:
Stress fracture (insufficiency/fatigue fracture) (1,2) If initial radiographs are negative, diagnosis may
Avulsion fracture (sleeve fracture): Superior, Inability to bear weight require serial radiographs over time or a bone
inferior, medial, and lateral Pain decreasing with rest but resuming with scan (6).
movement Avulsion:
EPIDEMIOLOGY Pain in the anterior knee Small bone fragment
Patellar fractures are rare (<5% of all fractures). Pain with weight bearing and extension of the High-riding patella in contrast to the
RISK FACTORS knee contralateral side
r Traumatic fractures: r MRI:
PHYSICAL EXAM
Occur in younger athletes (3,4) r Localized tenderness and a joint effusion are May be indicated to identify osteochondral
r Stress fractures (3,5): typically present: fractures from the patella
Young athletes due to overuse Inability to bear weight Diagnostic Procedures/Other
Children with osteoporosis or osteomalacia r Joint effusion
r Avulsion fractures: With significant mechanism or diminished distal
r High-riding patella: pulses, may need to consider an arteriogram to assess
Those who perform high-impact jumping activities Refers to situation when the patella does not rest the integrity of the vessels.
PATHOPHYSIOLOGY well within the trochlear sulcus with the knee
extended DIFFERENTIAL DIAGNOSIS
Fractures typically caused by: r Knee sprain
r Direct blow AND/OR r With a displaced fracture, a gap between the 2
r Ligament injury
r Sudden contraction of quadriceps fracture fragments may be palpated. r Patellar displacement
r The integrity of the extensor mechanism needs to be
r Meniscus injury
ETIOLOGY evaluated:
r Motor vehicle accident r Femur, tibia, and/or fibula fracture
For this, joint aspiration and lidocaine injection
r Direct blow/fall may be needed to differentiate limitation of r Quadriceps tendon rupture
r Sports related: extension based on pain or extensor injury: r Traumatic bursitis
Weight lifting Continued limitation of extension despite r Bipartite patella
Jumping and landing sports reduction of joint effusion and injection of r Vascular injury
lidocaine suggests extensor injury.
398
FRACTURE, PATELLA
Admission may be required if the patient requires 1. Jerosch JG, Castro WH, Jantea C. Stress fracture of
PRE HOSPITAL surgery. the patella. Am J Sports Med. 1989;17:579580.
r Immobilization 2. Zionts LE. Fractures around the knee in children.
r Nonweight bearing Discharge Criteria J Am Acad Orthop Surg. 2002;10:345355.
r Intact lower extremity neurovascular status
r Analgesia r Adequate pain control with oral medications 3. Pietu G, Hauet P. Stress fracture of the patella. Acta
r Ice Orthop Scand. 1995;66:481482.
Issues for Referral 4. Frank JB, Jarit GJ, Bravman JT, et al. Lower
INITIAL STABILIZATION/THERAPY Children with patellar fractures should be referred to extremity injuries in the skeletally immature athlete.
r Immobilization: Casting from groin to ankle or knee an orthopedic specialist. J Am Acad Orthop Surg. 2007;15:356366.
bracing with the knee in extension 5. Teitz CC, Harrington RM. Patellar stress fracture.
r Analgesia
Am J Sports Med. 1992;20:761765.
FOLLOW-UP
MEDICATION 6. Norfray JF, Schlachter L, Kernahan WT Jr., et al.
r Opioids: FOLLOW-UP RECOMMENDATIONS Early confirmation of stress fractures in joggers.
Morphine 0.1 mg/kg IV/IM/SC q2h PRN: r Discharge instructions and medications: JAMA. 1980;243:16471649.
Initial morphine dose of 0.1 mg/kg IV/SC may Rest, ice, elevation 7. Ogden JA, Tross RB, Murphy MJ. Fractures of the
be repeated q1520min until pain is controlled, Follow-up with orthopedics tibial tuberosity in adolescents. J Bone Joint Surg
then q2h PRN. Follow-up with physical therapy Am. 1980;62:205215.
Fentanyl 12 g/kg IV q2h PRN: Complete immobilization for 46 wk
Initial dose of 1 g/kg IV may be repeated Crutch walking to keep affected extremity
q1520min until pain is controlled, then q2h nonweight bearing ADDITIONAL READING
PRN. Pain control
r Activity: Harris RM. Fractures of the patella. In Bucholz RW,
Codeine/acetaminophen dosed as 0.51 mg/kg of
codeine component PO q4h PRN Complete immobilization for 46 wk followed by:
Heckman JD, eds. Rockwood and Greens Fractures in
Adults. 5th ed. Philadelphia, PA: Lippincott Williams &
F
Hydrocodone or hydrocodone/acetaminophen Physical therapy involving passive range of
Wilkins; 2002:1775.
dosed as 0.1 mg/kg of hydrocodone component motion and quadriceps strengthening
PO q46h PRN
r NSAIDs: Patient Monitoring
Check for distal extremity perfusion and presence of CODES
adequate pulses.
Some clinicians prefer to avoid NSAIDs due to PROGNOSIS ICD9
r 822.0 Closed fracture of patella
theoretical concern over influence on Good prognosis for full recovery
r 822.1 Open fracture of patella
coagulation and callus formation. COMPLICATIONS
Animal studies have raised concerns that r Infection
NSAIDs may negatively influence bone healing; r Loss of reduction
however, there is no clinical evidence in humans. r Failure of fixation
PEARLS AND PITFALLS
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN r Avascular necrosis r Pearls:
r Delayed union or nonunion/malunion Bipartite patella can mimic patellar fracture on
Acetaminophen 15 mg/kg/dose PO/PR q4h PRN r Chondromalacia radiographs.
r Traumatic arthritis Physical therapy will improve outcome.
COMPLEMENTARY & ALTERNATIVE r Pitfalls:
r Quadriceps weakness
THERAPIES r Extensor lag Assuming that weight bearing on the affected leg
Physical therapy once healing is complete excludes a patellar fracture
SURGERY/OTHER PROCEDURES Prolonged immobilization will result in muscle
Consultation with orthopedic surgery indicated for: atrophy.
r Open fractures requiring debridement:
Disruption of extensor mechanism
>2-mm displacement
>3-mm fragment separation
Dislocation with fracture
Associated patellar tendon rupture
399
FRACTURE, PELVIC AVULSION

Deirdre D. Ryan
Robert M. Kay

BASICS Sudden eccentric or concentric muscle force avulses Imaging
bone through the cartilaginous apophysis. r AP/Frog-leg pelvis x-rays will demonstrate most
DESCRIPTION fractures. This is helpful because it provides a view
r Avulsion fractures are typically caused by a powerful ETIOLOGY
r ASIS: Overpull of the sartorius muscle with the hip in of the contralateral side for comparison (1).
contraction of the attached muscle on a developing r Oblique/Axial pelvis x-rays can be performed if there
apophysis, or less commonly due to repetitive extension and the knee flexed
r AIIS: Avulsion by the direct head of the rectus is any difficulty seeing the fracture on the routine
traction of a muscle on a developing apophysis (1). pelvis x-rays (1).
r Muscle/Apophysis associations: femoris muscle most often occurs when the hip is
Sartorius muscle/anterior superior iliac spine (ASIS) hyperextended and the knee is flexed in kicking DIFFERENTIAL DIAGNOSIS
sports (eg, soccer, rugby, football). r Muscle strain
Direct head rectus femoris muscle/anterior inferior r Ischial tuberosity: Due to maximal exertion of the r Exuberant callus formation can mimic an
iliac spine (AIIS)
Hamstring muscles/ischial tuberosity hamstring muscles (eg, gymnastics, football, track) osteosarcoma if the x-ray is obtained more than
r Lesser trochanter: Due to overpull of the iliopsoas 710 days post-injury.
Adductor muscles/ischial tuberosity
Iliopsoas muscle/lesser trochanter muscle during hip flexion
Transversus abdominis muscle/iliac crest
Rectus abdominis muscle/pubic ramus TREATMENT
DIAGNOSIS
EPIDEMIOLOGY PRE HOSPITAL
Prevalence HISTORY r Rest
r Occurs in 16.4% overall in patients who report r Patient will complain of pain at the site of the r Positioning the hip and knee in a position of comfort
pelvic pain after sporting activity (2) avulsion fracture.
r Pelvic avulsion fractures breakdown (2): r Acute fractures: Sudden pain and a popping sound INITIAL STABILIZATION/THERAPY
r Chronic fractures: Slowly developing pain with Crutch use until pain resolves
54% ischial
22% AIIS repetitive activity that increases over time MEDICATION
r Pain may be mild or marked. Oral or parenteral pain medication:
19% ASIS
3% superior corner pubic ramus r Motion is limited. r Ibuprofen 10 mg/kg PO q6h PRN
1% iliac crest r Loss of muscular function r Naproxen 5 mg/kg PO q12h PRN
r Patients will complain of pain when sitting or r Acetaminophen 15 mg/kg PO q4h PRN
RISK FACTORS
r Active adolescent and young adult athletes moving on the involved tuberosity. r Morphine 0.1 mg/kg IV/IM/SC q2h PRN:
r Sports such as soccer, gymnastics, sprinting/hurdles, PHYSICAL EXAM Initial morphine dose of 0.1 mg/kg IV/SC may be
basketball, and tennis r Palpate for area of tenderness. repeated q1520min until pain is controlled, then
r Range of motion of the hip and knee will elicit pain q2h PRN.
GENERAL PREVENTION
r Thorough warm-up and stretching of affected in the localized area. COMPLEMENTARY & ALTERNATIVE
r Contraction or stretching of involved muscle will THERAPIES
muscles prior to participation in sports
r Sitting out of play if experiencing pain elicit pain. Physical therapy after pain resolves
r Ischial tuberosity fractures: Flexing the hip and
extending the knee elicit pain. Abducting the hip at
this point will increase the pain.
400
FRACTURE, PELVIC AVULSION

r Operative fixation is rarely indicated but is r Overall very good CODES
recommended by some for fragments displaced r Some patients may develop chronic pain due to
>2 cm (3). abundant callus formation that may need to be ICD9
r Occasionally, patients will require removal of addressed. r 808.2 Closed fracture of pubis
excessive callus formation at the ischial tuberosity if r 808.3 Open fracture of pubis
COMPLICATIONS
it leads to chronic pain and disability. r Pain due to abundant callus formation r 808.41 Closed fracture of ilium
DISPOSITION r Nonunion and persistent pain at the fracture site
Admission Criteria requiring operative intervention
Admit if pain is not controlled by oral pain medications PEARLS AND PITFALLS
(rarely necessary). r Oblique/Axial pelvis x-ray will show avulsions
Issues for Referral REFERENCES
difficult to see on AP pelvis x-ray.
Refer to orthopaedist as an outpatient. 1. Sundar M, Carty H. Avulsion fractures of the pelvis r Most fractures are successfully treated
in children: A report of 32 fractures and their conservatively.
outcome. Skeletal Radiol. 1994;23:8590. r Abundant callus formation can be mistaken for
FOLLOW-UP
2. Rossi F, Dragoni S. Acute avulsion fractures of the osteosarcoma; therefore, the history should be
FOLLOW-UP RECOMMENDATIONS pelvis in adolescent competitive athletes: carefully reviewed.
Discharge instructions and medications: Prevalence, location, and sports distribution.
r Weight bearing as tolerated with crutches Skeletal Radiol. 2001;30:127131.
r Oral pain medications PRN 3. Lynch SA, Renstrom PA. Groin injuries in sport:
r No sports participation until released for it by an Treatment strategies. Sports Med. 1999;28:
orthopaedist 137144.
Patient Monitoring
Orthopaedist will order follow-up x-rays at 46 wk. ADDITIONAL READING
F
Media Element)
r Dislocation, Hip
r Pain, Abdomen
r Trauma, Abdominal
401
FRACTURE, RIB
Kristin McAdams Kim
Michele M. Nypaver
BASICS DIAGNOSIS r Pathologic fracture
r Chest wall contusion
DESCRIPTION HISTORY r Pneumothorax
r Rib fractures can occur as a result of both major and r Multisystem trauma
r Sternal fracture or dislocation
minor trauma with and without concurrent r Severe blow to chest with blunt object
r Nontraumatic causes of chest pain:
intrathoracic injury: r Nonaccidental trauma, especially with posterior rib
Cardiac injury or compromise
Involves the fracture of 1 rib fractures
r 2 causes: r Difficulty breathing Pulmonary embolus
r Abdominal pain with trauma Pneumonia
Acute trauma Musculoskeletal chest wall strain
Stress fractures GI:
r Stable fractures are minimally displaced and do not PHYSICAL EXAM
r Expose the body to assess the nature of injury and GERD
involve >2 consecutive segments. Esophagitis
other associated injuries as outlined in the Advanced
RISK FACTORS Trauma Life Support (ATLS) recommendations. Dermatologic:
r Thoracic trauma r Pain with palpation of chest wall Herpes zoster
r Vigorous force such as rowing, weight lifting r Flail chest wall/unstable chest wall
r Osteopenia r Chest wall hematoma (due to intercostal vessel
r Osteogenesis imperfecta TREATMENT
laceration)
r May have shallow or rapid respirations PRE HOSPITAL
PATHOPHYSIOLOGY r Evaluate for any crepitus, bony deformity, or
r Fractures are due to significant force: Assess and stabilize airway, breathing, and
Elastic chest wall makes rib fractures rare in decreased breath sounds. circulation:
r Muffled heart sounds may indicate associated r Administer supplemental oxygen, preferably by
younger children.
r Mortality and morbidity are usually due to pericardial effusion. nonrebreather mask.
r Distended neck veins may suggest cardiac r Provide pain control.
associated internal injuries (1).
tamponade or tension pneumothorax. r Consider possible tension pneumothorax if clinically
ETIOLOGY
r Multiple trauma DIAGNOSTIC TESTS & INTERPRETATION evident.
r Blunt trauma to chest Imaging INITIAL STABILIZATION/THERAPY
r Stress fracture in athlete (2) r CXR (PA and lateral): Assess and stabilize airway, breathing, and circulation
r Nonaccidental trauma, especially in those <3 yr of To assess for pneumothorax or hemothorax as per ATLS and Pediatric Advanced Life Support
age (3): To assess heart size and width of mediastinum (PALS) guidelines:
Need to correlate injury with reported mechanism Very difficult to detect fracture on plain r Administer supplemental oxygen, preferably by
and make sure that there are not any radiograph: nonrebreather mask.
inconsistencies Rib plain film series with oblique views r Pain control
r Consider bone scan for high suspicion and negative r Treat pneumothorax/hemothorax.
COMMONLY ASSOCIATED CONDITIONS plain films. r Evaluate for flail chest.
r Pneumothorax r Consider CT or MRI for suspected costochondral
r Hemothorax r Look for paradoxical chest wall movement.
injury or internal thoracic injuries. r Look for other associated injuries during secondary
r Pulmonary contusion r If concerned about abdominal injury, consider FAST
r Injury to trachea, large neck vessels, brachial plexus, survey.
(Focused Assessment with Sonography for Trauma)
or spine is seen with fractures of 1st, 2nd, or 3rd ribs. and/or abdominal CT.
r Splenic and liver injuries are seen with injuries to r Consider skeletal survey for child abuse.
lower ribs.
r Flail chest:
Flail chest occurs when 3 consecutive ribs are
fractured in 2 places.
402
FRACTURE, RIB

First Line FOLLOW-UP r Adam A, Dixon AK, Grainger MB, et al., eds. Trauma
r Opioids:
Morphine 0.1 mg/kg IV/IM/SC q2h PRN: FOLLOW-UP RECOMMENDATIONS and intensive care radiology. In Grainger and
r Discharge instructions and medications: Allisons Diagnostic Radiology. 5th ed. Philadelphia,
be repeated q1520min until pain is controlled, Outpatient pain control with NSAIDs or oral PA: Churchill Livingstone; 2008.
narcotics as needed r DeLee JC, Drez D, Miller MD, eds. Shoulder. In
then q2h PRN.
Fentanyl 12 g/kg IV q2h PRN: Return to medical care if any respiratory DeLee and Drezs Orthopaedic Sports Medicine:
Initial fentanyl dose of 1 g/kg IV may be difficulty/distress, worsening chest or abdominal Principles and Practice. 3rd ed. Philadelphia, PA:
repeated q1520min until pain is controlled, pain, pain with swallowing, inadequate pain Saunders; 2009.
control, or activity intolerance. r Shilt J, Green N, Cramer KE. Nonaccidental trauma.
then q2h PRN.
r Activity: In Green NE, Swiontkowski MF, eds. Skeletal
0.51 mg/kg of codeine component PO q4h PRN Incentive spirometry may be helpful to prevent Trauma in Children. 4th ed. Philadelphia, PA:
Hydrocodone or hydrocodone/acetaminophen pneumonia. Saunders; 2009.
dosed as 0.1 mg/kg of hydrocodone component Several weeks of light activity
Limit risk for reinjury. See Also (Topic, Algorithm, Electronic
PO q46h PRN Media Element)
r NSAIDs: No contact sports until well healed and pain free r Child abuse
Consider NSAID medication in anticipation of Patient Monitoring r Hemothorax
prolonged pain and inflammation: r Follow up with primary care provider in 23 days.
r Pneumothorax/Pneumomediastinum
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN r May need serial chest radiographs to find healing
r Trauma, Chest
Ketorolac 0.5 mg/kg IV/IM q6h PRN fractures
r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN PROGNOSIS
r Simple rib fractures heal well. CODES
Second Line r Pain may continue for several weeks.
Local anesthetics: r Primarily determined by associated injuries ICD9
F
r Intercostal nerve block may be highly effective for r 807.00 Closed fracture of rib(s), unspecified
treatment of rib fracture pain. COMPLICATIONS r 807.01 Closed fracture of one rib
r Lidocaine, max single dose 5 mg/kg r Pneumothorax
r Hemothorax r 807.02 Closed fracture of two ribs
r Exercise care to avoid deep needle insertion that
r Pulmonary contusion:
violates the pleura.
Flail chest has high mortality due to pulmonary
SURGERY/OTHER PROCEDURES contusion. PEARLS AND PITFALLS
r Will depend on other injuries
r Pneumonia r Perform a thorough exam to look for other
r May need thoracostomy tube
r Nonunion or improper union of rib fracture associated injuries.
DISPOSITION r Chronic pain r Rib fractures in infants are very rare. Perform a
Admission Criteria r Splenic laceration thorough investigation for nonaccidental trauma in
r Parenteral analgesia requirement these situations.
r Respiratory compromise r Consider nonaccidental injury with posterior rib
r Concern for child abuse REFERENCES fractures in infants and toddlers.
r Fracture of 3 ribs r Flail chest can result in significant mortality from the
1. Bliss D, Silen M. Pediatric thoracic trauma. Crit Care
r Nature of other associated injuries Med. 2002;30:S409415. underlying pulmonary contusions.
r Patients with underlying lung or cardiac disease or r Fracture of the 1st, 2nd, or 3rd rib is associated with
2. Gregory PL, Biswas AC, Batt ME. Musculoskeletal
other concerning comorbidities problems of the chest wall in athletes. Sports Med. high morbidity and mortality due to the protected
r Critical care admission criteria: 2002;32:235250. location of these bones and degree of force required
Pulmonary contusion, cardiac contusion, to fracture them.
3. Williams RL, Connolly PT. In children undergoing r Conduct a thorough evaluation with 1st rib fractures,
respiratory distress, respiratory compromise, or chest radiography what is the specificity of rib
associated injuries may necessitate critical care fractures for non-accidental injury? Arch Dis Child. and strongly consider a trauma team evaluation.
admission. 2004;89:490492.
Discharge Criteria
r No underlying lung injury or compromise to
pulmonary function
r No concern for child abuse
r Simple rib fractures and no concerning concurrent
intrathoracic or intra-abdominal injuries
r Pain well controlled with oral medications
Issues for Referral
May need orthopedic follow-up
403
FRACTURE, SCAPHOID
Mark X. Cicero
BASICS DIAGNOSIS r Scapholunate dissociation:
An increased gap between these bones is evident
DESCRIPTION HISTORY on radiograph.
r Scaphoid, the name of the most commonly injured r FOOSH, as noted previously, is almost always r Fractures of other metacarpals
carpal bone, comes from the Greek skaphos, present and followed by deep dull pain in the wrist. r Fracture of the distal radius, including the radial
meaning boat. r Alternately, there may be a history of activity or
styloid
r The scaphoid is alternately referred to as the sports with repeated hyperextension and flexion, r Radioulnar joint injuries
navicular in some texts. such as tennis, gymnastics, or wood chopping. r De Quervain tenosynovitis:
r Its articulations include the distal radius, trapezium, r The pain worsens with gripping or squeezing.
Lateral wrist pain and tenderness over radial
and capitate bones. PHYSICAL EXAM styloid:
r Blood supply is from a branch of the radial artery r Snuffbox tenderness (100% sensitive, 80% specific) The tendons of the abductor pollicis longus and
and enters the bone distally: (2) extensor pollicis brevis are affected.
Blood vessels enter at the distal tubercle and the r Pain with supination against resistance, gripping, or Perform the Finklestein test where the examining
waist of the scaphoid. squeezing is sensitive but not specific. physician grasps the thumb while the hand is
The proximal portion of the bone has tenuous r Scaphoid tubercle tenderness while the wrist is in ulnarly deviated:
arterial blood flow and is prone to ischemia, extension has greater positive predictive value than If there is a sharp pain along the distal radius,
nonunion, and avascular necrosis with fracture. snuffbox tenderness (2). then De Quervain tenosynovitis is likely.
EPIDEMIOLOGY r Pain with axial compression of the thumb is
Incidence suggestive of scaphoid fracture.
r 350,000 new scaphoid fractures occur annually in r Contusion, swelling, or snuffbox fullness are seen TREATMENT
the U.S. (1). infrequently: PRE HOSPITAL
r The scaphoid is the most commonly fractured carpal A recent series suggested that 3 findings are r Immobilization with a simple splint
bone across all age groups. highly suggestive of scaphoid fracture (3): r Compression, such as an elastic bandage
r Among pediatric patients, males in late adolescence Volar scaphoid tenderness r Pain management
most frequently sustain scaphoid fractures. Pain with radial deviation of the hand r Ice
Pain with active wrist range of motion
RISK FACTORS r Elevation
Gymnastics, skateboarding, and other activities DIAGNOSTIC TESTS & INTERPRETATION
Imaging INITIAL STABILIZATION/THERAPY
increase the risk for a forceful fall onto outstretched r When a radiographically proven nondisplaced
hand (FOOSH); as a result, a scaphoid fracture occurs. r Obtain AP, lateral, and oblique radiographs of the
fracture is present, a short arm thumb spica cast is
wrist.
GENERAL PREVENTION r Additionally, a dedicated scaphoid view, in which applied with the wrist in neutral position. There is no
Wrist guards prevent hyperextension during skating added benefit to long arm casting.
the wrist is ulnarly deviated, is useful. r Clinically suspected fractures with no radiographic
and cycling-related falls. r Initial radiography has 7090% sensitivity for
PATHOPHYSIOLOGY evidence or nondisplaced fractures are managed
fracture.
r Momentum of the fall determines the likelihood of r If radiographs are negative and occult fracture is with the thumb spica splint or casting.
r Scaphoid fractures with displacement are splinted
wrist fracture. suspected, there are 3 options (listed below). The
r Wrist hyperextension determines whether the wrist should be immobilized if occult fracture is
until operative management occurs.
r Pain control will be necessary.
scaphoid is at risk for fracture. suspected (see Initial Stabilization/Therapy):
r Wrist flexion or extension <90 degrees is protective. Bone scintigraphy (bone scan) is a cost-effective MEDICATION
The force of the fall is transmitted proximally along option, either during the emergency department r Opioids:
the upper extremity in these situations. evaluation or soon after. Morphine 0.1 mg/kg IV/IM/SC q2h PRN:
MRI is an excellent choice for detecting occult Initial morphine dose of 0.1 mg/kg IV/SC may
ETIOLOGY
r FOOSH is the etiology. The forearm is prone during fractures of the scaphoid and adjacent bones as be repeated q1520min until pain is controlled,
well as ligamentous injuries. then q2h PRN.
the fall.
r There are rare reports of scaphoid stress fractures in Follow-up radiographs performed 2 wk after the Fentanyl 12 g/kg IV q2h PRN:
injury. Fractures should then be evident due to Initial dose of 1 g/kg IV may be repeated
athletes who compete in diving and racquet sports. remodeling and periosteal elevation. q1520min until pain is controlled, then q2h
COMMONLY ASSOCIATED CONDITIONS r The role of ultrasound is unclear. PRN.
Infrequently (512% of the time), there are concurrent Codeine/Acetaminophen dosed as 0.51 mg/kg of
fractures of another carpal bone or the distal radius. codeine component PO q4h PRN
PO q46h PRN
404
FRACTURE, SCAPHOID
r Oral NSAIDs:
REFERENCES
Consider NSAID medication in anticipation of FOLLOW-UP
prolonged pain and inflammation: 1. Christodoulou AG, Colton CL. Scaphoid fractures in
Some clinicians prefer to avoid NSAIDs due to FOLLOW-UP RECOMMENDATIONS children. J Pediatr Orthop. 1986;6(1):3739.
theoretical concern over influence on 2. Freeland P. Scaphoid tubercle tenderness: A better
coagulation and callus formation. Patients with a clinical suspicion for a displaced or indicator of scaphoid fractures? Arch Emerg Med.
Animal studies have raised concerns that nondisplaced fracture should be re-evaluated in 1989;6(1):4650.
NSAIDs may negatively influence bone healing; 12 wk by an orthopedic surgeon. 3. Evenski AJ, Adamczyk MJ, Steiner RP, et al.
however, there is no clinical evidence in humans. Displaced fractures are prone to mal- or nonunion Clinically suspected scaphoid fractures in children.
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN and are managed with operative fixation. Patients J Pediatr Orthop. 2009;29(4):352355.
Naproxen 5 mg/kg PO q8h PRN need to be seen promptly by orthopedic surgery.
r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN Patients and their families are given instructions
using the PRICE mnemonic: ADDITIONAL READING
SURGERY/OTHER PROCEDURES Pain control
r Displaced fractures require stabilization to prevent Rest r Anz AW, Bushnell BD, Bynum DK, et al. Pediatric
mal- or nonunion (see Complications). Orthopedic Ice, especially in the 1st 24 hr after the injury scaphoid fractures. J Am Acad Orthop Surg.
surgery needs to be consulted for these cases. Compression, achieved with the splint or cast 2009;17(2):7787.
r Orthopedic interventions include: Elevation: A sling can assist this goal. r Elhassan BT, Shin AY. Scaphoid fracture in children.
Percutaneous pin fixation r Activity: Hand Clin. 2006;22(1):3141.
Internal fixation with Kirschner wires or a screw Activities that risk reinjury during the healing r Perron AD, Brady WJ, Keats TE, et al. Orthopedic
Nonunions may require excision of the avascular process are to be avoided. pitfalls in the ED: Scaphoid fracture. Am J Emerg
proximal portion of the scaphoid, bone grafting, r Immobilization precludes wrist range of motion: Med. 2001;19(4):310316.
or radial stylectomy. Later management of scaphoid injuries includes See Also (Topic, Algorithm, Electronic
DISPOSITION rehabilitation with an occupational therapist or Media Element)
Admission Criteria
r Even displaced fractures are not routine grounds for
physical therapist.
Patient Monitoring
Fracture, Hand F
admission. Internal fixation is done as an outpatient r Caregivers are instructed to monitor the patient for:
operative procedure. Worsening pain in the wrist CODES
r Open fractures or the presence of other serious Numbness or paresthesias in the ipsilateral fingers
injuries will require admission. Cold, discolored, or swollen digits ICD9
r Patients with chronic fractures or malunion may be r These findings should prompt a speedy return to the r 814.01 Closed fracture of navicular (scaphoid) bone
admitted after surgical repair, especially if bone emergency department or a call to the primary care of wrist
grafting is involved. doctor or managing orthopedist. r 814.11 Open fracture of navicular (scaphoid) bone
Discharge Criteria PROGNOSIS of wrist
r Appropriate immobilization r Nondisplaced scaphoid fractures have an excellent
r Adequate pain control rate of union (95%), but the limb may be casted for
r Caretaker understands discharge instructions up to 10 wk when the fracture is through the PEARLS AND PITFALLS
r Follow-up with a pediatric or general orthopedist is scaphoid waist or more proximal. r Missed and misdiagnosed scaphoid fractures may
arranged. r Displaced fractures are more prone to mal- or
result in a lawsuit for malpractice.
Issues for Referral nonunion and have a more guarded prognosis. r Displaced fractures are prone to mal- or nonunion
r Refer all patients with scaphoid fractures to r Even with good union of the bony fragments,
and are managed with operative fixation. The
orthopedic surgery. In some centers, scaphoid patients may suffer chronic pain and limitation of emergency physician should arrange prompt
fractures are managed by hand-specific services: range of motion. consultation.
Displaced fractures are grounds for urgent referral. COMPLICATIONS r All clinically suspected scaphoid fractures should
r Advise patients about the concerns of scaphoid r Fractures through the middle (waist) of the scaphoid prompt thumb spica immobilization and referral to
malunion and avascular necrosis. and the proximal 3rd of the bone are prone to an orthopedic surgeon.
avascular necrosis and chronic wrist dysfunction.
r As noted previously, malunion of the scaphoid is of
particular risk when there is displacement.
Nonunion may occur even with nondisplacement:
Degenerative joint disease and osteoarthritis may
result.
405
FRACTURE, SCAPULA
Asha S. Payne
Bruce L. Klein
ETIOLOGY r Movement of the scapula and shoulder:

BASICS r Scapular body, spine, and/or neck fractures, Shoulder movement, especially abduction, causes
sometimes with extension into the intra-articular pain.
DESCRIPTION glenoid: Deep inspiration can be painful (due to scapular
r The scapula is a triangular-shaped bone that is Usually caused by high-energy trauma movement).
responsible for providing a stable anchor for the Most commonly, direct blunt trauma to the With some combinations of fractures and
movement of the arm: posterosuperior or lateral aspect of the ligamentous injuries, the shoulder can become
The scapula is flat, is relatively translucent at its forequarter or shoulder: unstable.
center, and has thickened borders and ridges that From a significant fall, motor vehicle crash, r Must perform careful neurologic and vascular exams
serve as sites for multiple muscle attachments. motorcycle accident, or contact sport injury of the adjacent thorax and upper extremity to
Attaches to the clavicle via the acromioclavicular (such as football or hockey) assess:
and coracoclavicular ligaments There are reports of scapula fractures following a Brachial plexus
Articulates with the humerus seizure or electric shock, without direct blunt Axillary, brachial, and subclavian artery function
Protected by the supraspinatus, infraspinatus, and trauma.
subscapularis muscles r Glenoid fractures: DIAGNOSTIC TESTS & INTERPRETATION
r Scapula fractures can involve the: Can be caused by lower-energy forces: Lab
Scapular body From a fall on an outstretched hand with Initial Lab Tests
Scapular spine transmitted force Lab tests would only be needed for associated
Scapular (glenoid) neck Anterior glenoid rim fracture: injuries:
Glenoid body/rim (intra-articular) Can result from a glenohumeral shoulder r CBC in situations with considerable hemorrhage
Acromion process and/or dislocation Imaging
Coracoid process r Acromion or coracoid avulsion fracture: r Scapular fractures can be subtle and may be missed
EPIDEMIOLOGY Can be caused by traction to the upper extremity on the initial trauma AP CXR.
r Scapular fractures are uncommon, as the scapula is r Standard radiographic series for the evaluation of a
a mobile bone and is mostly protected by thick r When the mechanism is a high-energy trauma, there scapula fracture includes:
muscles: very frequently are other, sometimes AP view of the scapula/glenohumeral joint
1% of all fractures (13) life-threatening, injuries (16): Axillary view:
35% of shoulder girdle fractures Thoracic (eg, clavicle and rib fractures, Velpeau axillary lateral view may be more
r Occurs predominantly in young and middle-aged hemo-/pneumothorax, pulmonary contusion) comfortable for the patient.
men: Upper extremity (including brachial plexus and Scapular Y view
Rare in children vascular [eg, axillary, brachial, and subclavian r CT scan of the scapula with 3-dimensional
arteries] injuries and fractures) reconstruction can help to more accurately define
RISK FACTORS
r High-speed activities, such as motorcycle riding Skull/Intracranial (eg, skull fracture, closed head the extent of the fracture and assist with surgical
r Contact sports injury) planning:
r Mountain climbing (due to falls) Spinal (eg, vertebral fracture, spinal cord injury) Particularly useful when a fracture of the glenoid
Intra-abdominal neck or intra-articular body/rim is suspected on
r Child abuse
Pelvic (eg, fractures), among others conventional x-rays as well as for angulated or
r Traction to the upper extremity can result in brachial comminuted fractures
GENERAL PREVENTION r Often additional imaging studies (eg, CXR or CT
Standard protective equipment specific to the various plexus and vascular injuries.
sports may help prevent fractures. scan, angiogram/CT angiogram) are needed to rule
out associated injuries.
PATHOPHYSIOLOGY DIAGNOSIS
Usually caused by high-energy trauma: DIFFERENTIAL DIAGNOSIS
r A normal growth center in a child may be confused
r Strong forces overwhelm the protection of the soft HISTORY
r History of a direct blow to the scapula as a fracture:
tissues and the normal mobility of the scapula and r Pain in the scapula or shoulder area following Fractures of the coracoid and acromion can be
shoulder, resulting in fracture.
trauma to the ipsilateral forequarter or upper distinguished from their normal physes based on
extremity the patients age and the usual locations of these
physes.
PHYSICAL EXAM r Os acromiale, a failure of the acromion ossification
r Visualization of the scapula and shoulder:
centers to ever close, occurs in a small percentage of
Abrasions, contusions, and/or edema may be patients and is frequently bilateral:
present. X-ray of the contralateral scapula may help
The shoulder sometimes appears deformed or distinguish an os acromiale from a true fracture.
flattened. r Adjacent soft tissue (eg, ligamentous) injury
The arm is typically held in adduction. r Clavicle, rib, or proximal humerus fracture
r Palpation over the fracture site elicits tenderness.
406
FRACTURE, SCAPULA
r For surgical repair or irrigation/debridement 1. Cole PA. Scapula fractures. Orthop Clin North Am.
PRE HOSPITAL r When there is inadequate pain control with 2002;33:118.
r Immobilize the spine, including the cervical spine, 2. Newton EJ, Love J. Emergency department
immobilization (sling and swathe) and oral analgesia
when injury is due to a high-energy force or if there r For other associated injuries management of selected orthopedic injuries. Emerg
is concern for spinal injury. r Critical care admission criteria: Med Clin North Am. 2007;25:763793.
r Immobilize the ipsilateral upper extremity with a 3. Lapner PC, Uhthoff HK, Papp S. Scapula fractures.
For associated life-threatening injuries
sling and swathe. necessitating mechanical ventilation or inotropic Orthop Clin North Am. 2008;39:459474.
support 4. Thompson DA, Flynn TC, Miller PW, et al. The
r Defer the scapula and shoulder exam and treat A scapula fracture alone usually does not require significance of scapular fractures. J Trauma.
intensive care admission. 1985;25:974977.
other, more life-threatening injuries 1st.
r Stabilize airway, breathing, and circulation per 5. Brown CVR, Velmahos G, Wang D, et al.
Discharge Criteria Association of scapular fractures and blunt thoracic
Advanced Trauma Life Support and Pediatric r No need for surgical repair or irrigation/debridement
r Pain is well controlled. aortic injury: Fact or fiction? Am Surg. 2005;71:
Advanced Life Support guidelines:
5457.
Immediately evaluate for and treat any r No associated injuries that require admission
life-threatening conditions (eg, severe pulmonary 6. Baldwin KD, Ohman-Strickland P, Mehta S, et al.
contusion, tension pneumothorax). Issues for Referral Scapula fractures: A marker for concomitant injury?
r Consult an orthopedic surgeon, ideally one with A retrospective review of data in the National
MEDICATION expertise in scapular fractures: Trauma Database. J Trauma. 2008;65:430435.
First Line Consult emergently or urgently for:
r Analgesia for comfort as well as to enable a good Neurologic or vascular compromise
exam Open fracture ADDITIONAL READING
r Opioids: Intra-articular fracture
Deutsch A, Craft JA, Williams GR. Injuries to the
Morphine 0.1 mg/kg IV/IM/SC q2h PRN: Fracture/Dislocation
Significantly displaced or angulated fracture glenoid, scapula, and coracoid: 1. Glenoid and scapula F
r Physical therapy eventually: fractures in adults and children. In DeLee JC, Drez D,
be repeated q1520min until pain is controlled, Miller MD, eds. DeLee and Drezs Orthopaedic Sports
then q2h PRN. Passive range of motion exercises as pain abates Medicine: Principles and Practice. 3rd ed.
Codeine or codeine/acetaminophen dosed as Active range of motion exercises later Philadelphia, PA: Saunders; 2009.
PRN See Also (Topic, Algorithm, Electronic
Hydrocodone or hydrocodone/acetaminophen FOLLOW-UP Media Element)
dosed as 0.1 mg/kg of hydrocodone component r Fracture, Clavicle
FOLLOW-UP RECOMMENDATIONS r Fracture, Humerus
PO q46h PRN
Discharge instructions: r Trauma, Chest
Second Line r Rest the shoulder.
r NSAIDs: r Trauma, Shoulder
r Wear a sling and swathe.
Consider NSAID medication in anticipation of r Take an oral analgesic for pain.
prolonged pain and inflammation: r Make follow-up appointments with the orthopedic
Some clinicians prefer to avoid NSAIDs due to CODES
theoretical concern over influence on surgeon and, eventually, a physical therapist.
coagulation and callus formation. Patient Monitoring ICD9
Animal studies have raised concerns that Follow-up immediately for: r 811.00 Closed fracture of scapula, unspecified part
NSAIDs may negatively influence bone healing; r New-onset numbness, tingling, or weakness r 811.01 Closed fracture of acromial process of
however, there is no clinical evidence in humans. r Uncontrolled pain scapula
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN r 811.02 Closed fracture of coracoid process of
Ketorolac 0.5 mg/kg IV/IM q6h PRN DIET
r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN scapula
No dietary limitations
r Nondisplaced, minimally displaced, or minimally Well-aligned scapular fractures tend to heal well: PEARLS AND PITFALLS
angulated scapular fractures are usually treated r Nonunion is rare.
r Pearls:
nonoperatively.
r Significantly displaced or angulated fractures of the COMPLICATIONS Concern for a scapula fracture should prompt a
Potential complications of intra-articular fractures thorough evaluation for more life-threatening
glenoid neck, intra-articular glenoid, acromion include: injuries.
process, or coracoid process are usually repaired via r Chronic shoulder pain If necessary, CT scan of the scapula with
open reduction with internal fixation. r Decreased range of motion 3-dimensional reconstruction can better define
r Open fractures are generally irrigated and debrided
r Premature arthritis the extent of injury.
in the operating room. r Pitfalls:
An acromion, coracoid, or scapular tip ossification
center (in a pediatric patient) or an os acromiale
(in an older individual) may be confused with a
fracture.
407
FRACTURE, SKULL
Antonio Riera
David M. Walker

BASICS r Falls
Lab
r Sporting activities Initial Lab Tests
DESCRIPTION r Motor vehicle accidents r No lab testing is routinely necessary.
r A skull fracture is a break in the bone usually caused r Nonaccidental trauma r If institution uses preoperative lab tests, consider
by direct impact to the calvaria: sending if intracranial bleed is suspected.
Can be associated with intracranial injuries COMMONLY ASSOCIATED CONDITIONS
r Skull fractures and intracranial injury are often r Intracranial injuries with possible increased Imaging
r CT indications (3):
related to high-impact closed head injuries. intracranial pressure (ICP):
r Infants are the exception, as there is increased risk Subdural hematoma Age <2 yr:
Subarachnoid hemorrhage Altered mental status
of skull fracture in setting of minor trauma (1). Nonfrontal scalp hematoma
r 4 major types: Epidural hemorrhage
r Pneumocephaly Loss of consciousness >5 sec
Linear, depressed, open, basilar Severe mechanism of injury
r Cervical spine injuries
EPIDEMIOLOGY r Facial fractures and lacerations Palpable step-off on exam
Incidence r Retinal hemorrhage: Not acting normally per parent
r Overall incidence of skull fracture during outpatient Age >2 yr:
Especially with nonaccidental trauma Altered mental status
evaluations of head trauma: 630% (2): r Cutaneous, skeletal, and visceral injuries
Children <2 yr of age (2): Vomiting
Incidence of skull fracture in children with Loss of consciousness
Severe mechanism of injury
intracranial injury: 7080% DIAGNOSIS Signs of basilar skull fracture
Incidence of intracranial injury in children with
skull fracture: 1530% HISTORY Severe headache
r Incidence of clinical deterioration for isolated linear r History of head trauma Noncontrast head CT is preferred to detect
skull fracture not requiring initial intervention: 0% r Loss of consciousness intracranial injury and skull fractures:
r Symptoms may include: Young children may require sedation.
(2)
Benefit of diagnosis of injury must be weighed
RISK FACTORS Abnormal neurologic exam
against risk of radiation (4) and sedation.
r Direct blunt trauma Seizures r Skull radiography:
r Age <2 yr Depressed mental status
Prolonged loss of consciousness Limited sensitivity (59%) and specificity (88%) as
r Highest risk for age <3 mo diagnostic test in 1 meta-analysis (5)
r Nonfrontal scalp hematoma (3) Persistent vomiting
Headache Can detect skull fracture but not intracranial
r Diseases of bone fragility (eg, osteogenesis r For children <2 yr of age, symptoms may also injury/hemorrhage
imperfecta) r US:
include irritability, change in feeding patterns, or
level of alertness: Only studied in children with open fontanelles
GENERAL PREVENTION Shown to detect dural tears (6) and intracranial
r Fall prevention (stair gates, etc.) May be asymptomatic, especially in infants
r Helmet use r Suspected nonaccidental trauma hemorrhage (7)
Possible role as screening tool, but prospective
r Car seats with appropriate restraints
PHYSICAL EXAM data are lacking
r The following features may be compatible with the
PATHOPHYSIOLOGY DIFFERENTIAL DIAGNOSIS
r A direct blunt force over the affected calvarial bone presence of an underlying skull fracture: r Diastasis
may cause a parietal, occipital, temporal, frontal, or Scalp hematoma r Hematoma
Bony step-off
basilar skull fracture. r Concussion
r Linear skull fracture: Subcutaneous crepitus
r For basilar skull fractures: r Contusion
A single fracture line that involves the thickness of
the skull: Battle sign (ecchymosis over mastoid)
Most common type (75%) Raccoon eyes (periorbital ecchymoses)
Most common site: Parietal bone Hemotympanum TREATMENT
May disrupt underlying vascular structures CSF rhinorrhea, CSF otorrhea
Cranial nerve deficits PRE HOSPITAL
Comminuted describes multiple linear fractures r Assess and stabilize airway, breathing, and
r Cushing triad (HTN, bradycardia, irregular
causing a shattered appearance circulation.
r Depressed skull fracture: respirations) if associated ICP r Administer supplemental oxygen.
r Evaluate bony cranium and cervical spine for
An uneven fracture that projects downward onto r Consider cervical spine immobilization for suspected
the dura and brain tissue evidence of injury:
Extraocular eye movement cervical spine injury or a trauma patient with altered
Often caused by a forceful blow to a small area mental status.
(eg, hammer) Orbital step-off
Increased risk of intracranial injury, seizures, and Mobility of zygoma INITIAL STABILIZATION/THERAPY
infection Palpation of temporomandibular joint in neutral r Assess and stabilize airway, breathing, and
r Open skull fracture: position and through full range of motion circulation using Advanced Trauma Life Support and
A skull fracture that communicates with injured Cervical spine tenderness Pediatric Advanced Life Support guidelines.
r Neurologic exam: r Administer supplemental oxygen.
skin or mucosa:
Fracture with overlying scalp laceration Glasgow Coma Scale r Consider cervical spine immobilization as suggested
Fracture with sinus or middle ear involvement Mental status previously if not already performed.
Increased risk of CNS infection Full exam of cranial nerves, strength, tone,
r Basilar skull fracture: coordination, reflexes
A skull fracture that involves base of the skull
Often associated with hearing loss, cranial nerve
injury (VI, VII, VIII), and CSF leaks
408
FRACTURE, SKULL
MEDICATION Issues for Referral 4. Brody AS, Frush DP, Huda W, et al. Radiation risk
r Opioids: r Skull fractures diagnosed on head CT should be
to children from computed tomography. Pediatrics.
Morphine 0.1 mg/kg IV/IM/SC q2h PRN: managed in consultation with a pediatric 2007;120(3):677682.
Initial morphine dose of 0.1 mg/kg IV/SC may neurosurgeon. 5. Dunning J, Batchelor J, Stratford-Smith P, et al. A
be repeated q1520min until pain is controlled, r Child protection specialists if concern for
meta-analysis of variables that predict significant
then q2h PRN. nonaccidental trauma intracranial injury in minor head trauma. Arch Dis
Fentanyl 12 g/kg IV q2h PRN: r Neuropsychiatric testing if prolonged concussion Child. 2004;89(7):653659.
Initial dose of 1 g/kg IV may be repeated symptoms 6. Decarie JC, Mercier C. The role of ultrasonography
q1520min until pain is controlled, then q2h in imaging of pediatric head trauma. Childs Nerv
PRN. Syst. 1999;15:740742.
Codeine/Acetaminophen dosed as 0.51 mg/kg of FOLLOW-UP 7. Trenchs V, Curcoy AI, Castillo M, et al. Minor head
codeine component PO q4h PRN trauma and linear skull fracture in infants: Cranial
Hydrocodone or hydrocodone/acetaminophen r 24-hr follow-up with primary care provider ultrasound or computed tomography? Eur J Emerg
dosed as 0.1 mg/kg of hydrocodone component r Discharge instructions and medications: Med. 2009;16(3):150152.
PO q46h PRN
r NSAIDs: Pain control
Keep child at home for 24 hr after injury.
For children <2 yr of age:
ADDITIONAL READING
prolonged pain and inflammation: Watch for poor feeding, lethargy, persistent
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN See Also (Topic, Algorithm, Electronic
Ketorolac 0.5 mg/kg IV/IM q6h PRN vomiting, irritability, seizures Media Element)
Naproxen 5 mg/kg PO q8h PRN For older children and adolescents: r Trauma, Head
r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN Watch for worsening headache, persistent r Traumatic Brain Injury
r Prophylactic antibiotics: vomiting, changes in mental status, seizures,
visual complaints, problems with balance
For open skull fractures to prevent osteomyelitis:
Cefazolin 25 mg/kg/dose IV q6h DIET CODES F
If allergic, clindamycin 10 mg/kg/dose IV q8h Resume a regular diet.
Tetanus prophylaxis 0.5 mL IM if necessary PROGNOSIS ICD9
r Excellent for isolated, linear, nondepressed skull r 803.00 Other closed skull fracture without mention
r Depressed and open skull fractures: fractures without intracranial involvement of intracranial injury, with state of consciousness
Usually require operative management r Prognosis for other skull fractures depends on the unspecified
r Basilar skull fractures: r 803.10 Other closed skull fracture with cerebral
degree and extent of associated intracranial injuries.
May require operative management laceration and contusion, with state of
COMPLICATIONS consciousness unspecified
r See Trauma, Head topic for management of r Growing skull fractures due to a tear of the
r 803.20 Other closed skull fracture with
intracranial injuries. underlying dura and subsequent bone remodeling
subarachnoid, subdural, and extradural hemorrhage,
DISPOSITION can be seen in a small number of cases of linear
with state of consciousness unspecified
skull fractures. Can present months to years after
Admission Criteria
r Ill-appearing children with persistent emesis initial injury as a skull defect or swelling.
r Depressed skull fractures:
r Symptoms suggesting neurologic injury: PEARLS AND PITFALLS
Intracranial hemorrhage, dural laceration,
Disorientation r Linear skull fractures are the most common injury
parenchymal injury, seizures
Repetitive questioning r Basilar skull fractures:
Agitation or other mental status change after blunt injury to the head.
r Intracranial injury CSF leak, meningitis, hearing loss, cranial nerve r The presence of a skull fracture is associated with an
r High suspicion of nonaccidental trauma impairment intracranial injury in 1530% of cases.
r Open skull fractures: r Isolated, linear, nondisplaced skull fractures may be
Critical care admission criteria: Nonunion, infection/meningitis managed as outpatients after consultation with a
r Admission to a critical care unit is recommended for r Developmental delay/persistent neurologic deficits pediatric neurosurgeon.
the following situations: can result from all fractures. r Depressed, open, or basilar skull fractures should be
Depressed skull fractures managed in an inpatient setting, as they often
Open skull fractures require neurosurgical intervention.
Basilar skull fractures REFERENCES r High index of suspicion for nonaccidental trauma,
Linear skull fractures associated with: especially in nonmobile younger children
Intracranial injury 1. Greenes DS, Shutzman SA. Infants with isolated
Cervical spine injury skull fracture: What are their clinical characteristics,
Depressed mental status and do they require hospitalization? Ann Emerg
Abnormal neurologic exam Med. 1997;30:253259.
Abnormal vital signs, especially development of 2. Schutzman SA, Barnes P, Duhaime AC, et al.
Cushing triad Evaluation and management of children younger
than two years old with apparently minor head
Discharge Criteria trauma: Proposed guidelines. Pediatrics. 2001;107:
r Discharge from the emergency department if patient
983993.
meets following criteria:
3. Kupperman N, Holmes JF, Dayan PS, et al.
Nondepressed linear skull fracture and >6 mo of
Identification of children at very low risk of
age
clinically-important brain injuries after head
Isolated injury
trauma: A prospective cohort study. Lancet.
Normal neurologic exam
2009;374:11601170.
Neurosurgical consultation, if obtained, agrees
Reliable follow-up
Child can tolerate PO intake without vomiting
r Possibility of nonaccidental injury reliably excluded
409
FRACTURE, SUPRACONDYLAR
Louis A. Spina
Lana Friedman
COMMONLY ASSOCIATED CONDITIONS r Gartland distinguished 3 types of supracondylar

BASICS Distal humeral fractures are frequently associated with fractures (1):
neurovascular complications, even in the absence of Type I: Nondisplaced or minimal displacement
DESCRIPTION displacement: Type II: Moderate displacement with intact
r A supracondylar fracture is a transverse fracture of r The most commonly injured structures are the posterior cortex
the distal humerus above the joint capsule in which median nerve and the brachial artery. Type III: Complete displacement with fractures of
the diaphysis of the humerus dissociates from the both cortices
condyles. r Another diagnostic aid in evaluating radiographs of
r Supracondylar fractures are subdivided based on the DIAGNOSIS suspected supracondylar fractures is to determine
position of the distal humeral segment: the carrying angle:
Extension type (posterior displacement) HISTORY The intersection of a line drawn through the
r The typical history is a fall on an outstretched arm
Flexion type (anterior displacement) midshaft of the humerus and a line through the
with hyperextension at the elbow and resultant midshaft of the ulna on the AP extension view
EPIDEMIOLOGY injury to the distal humerus.
r Supracondylar fractures account for 60% of r A 2nd mechanism involves a direct blow to the determines the carrying angle.
pediatric elbow fractures (1): Normally the carrying angle is between 0 and
elbow (direct mechanism). 12 degrees.
The vast majority (95%) of displaced
supracondylar fractures are of the extension type PHYSICAL EXAM Traumatic or asymmetric carrying angles of >12
r Recent injuries typically demonstrate mild swelling degrees are often associated with fractures.
(2).
25% of supracondylar fractures are of the with severe pain. DIFFERENTIAL DIAGNOSIS
greenstick type. r The displaced distal humeral fragment can often be r As the swelling increases, the injury can easily be
r Supracondylar fractures occur most frequently in palpated posteriorly and superiorly because of the confused with a posterior dislocation of the elbow
children between 5 and 10 yr of age. pull of the triceps muscle. resulting from the prominence of the olecranon and
r The nondominant extremity is most commonly r The involved forearm may appear shorter when the presence of a posterior concavity.
affected. compared with the uninvolved side. r Nursemaid elbow and inter- or transcondylar
r Always assume that there is neurovascular fractures should also be considered.
RISK FACTORS compromise until a physical exam has excluded this r Bursitis
r Participation in certain sports such as football,
threat: r Contusion/Sprain/Strain
hockey, and gymnastics increases the risk of Initially document the presence and strength of r Effusion
supracondylar fractures. the radial, ulnar, and brachial pulses.
r Home trampolines and playgrounds
Examine and document the motor and sensory
GENERAL PREVENTION components of the radial, ulnar, and median TREATMENT
Wearing protective equipment such as elbow guards nerves:
and pads can help reduce the risk of sustaining a Assess motor function by having the patient PRE HOSPITAL
make a thumbs up (radial nerve), a tight fist r Immobilization for transport in a long posterior
supracondylar fracture.
over the thumb (median nerve), and an OK splint without any attempt at reduction is essential
PATHOPHYSIOLOGY sign (anterior interosseous nerve). after initial triage:
r In children, the supracondylar region encompasses
Assess for adequate distal pulses.
an area of thin, weak bone located in the distal DIAGNOSTIC TESTS & INTERPRETATION r The involved extremity should be iced and elevated
humerus: Imaging to reduce swelling.
r Routine views should include AP and lateral
This region is bordered posteriorly by the r Pain control
olecranon fossa and anteriorly by the coronoid projections with comparison to the uninvolved
fossa. extremity, if necessary. INITIAL STABILIZATION/THERAPY
The medial and lateral aspects of the r AP and lateral views of the affected elbow are r Appropriate trauma exam to ensure that no other
supracondylar region extend distally to the necessary to evaluate thoroughly for injury: life-threatening injuries are present
developing medial and lateral condyles and Have the patients elbow flexed at 90 degrees on r Good neurovascular exam
epicondyles. the lateral projection for correct interpretation. r Ice and elevation of affected extremity with
r When a child falls onto an outstretched arm with r For suspected vascular insult, arteriography, Doppler administration of good pain control
the elbow in hyperextension, the force of the fall is US, or CT angiography may evaluate arterial flow r Emergent reduction by the emergency specialist is
transmitted through the olecranon to the weak and anatomy and guide treatment. Utility of these indicated only when the displaced fracture is
supracondylar region, causing a supracondylar studies is controversial (2). associated with vascular compromise, which
fracture. immediately threatens the viability of the extremity:
r Depending on the severity of the fracture, posterior Pathological Findings
r Subtle changes, such as the presence of a posterior Traction is applied with the elbow in extension
displacement of the distal fracture fragment or fat pad or an abnormal anterior humeral line, may and the forearm in supination.
anterior displacement of the proximal fracture be the only radiographic clues to the presence of a After traction has been applied and the length
fragment may occur. fracture: regained, the fracture is hyperextended to obtain
r The fracture line typically propagates transversely apposition of the fragments.
The anterior humeral line is a line drawn on the
across the distal humerus through the center of the lateral radiograph along the anterior surface of With traction being maintained, the varus or
olecranon fossa. the humerus through the elbow: valgus angulation along with the rotation of the
Normally, this line transects the middle 3rd of distal fragment is corrected.
the capitellum.
With a supracondylar extension fracture, this
line will transect the anterior 3rd of the
capitellum or pass entirely anterior to it.
410
FRACTURE, SUPRACONDYLAR
MEDICATION
r Opioids:
Admission Criteria
Morphine 0.1 mg/kg IV/IM/SC q2h PRN: All displaced supracondylar fractures require 1. Shrader MW. Pediatric supracondylar fractures and
Initial morphine dose of 0.1 mg/kg IV/SC may admission for neurovascular monitoring. pediatric physeal elbow fractures. Orthop Clin
be repeated q1520min until pain is controlled, North Am. 2008;39(2):163171.
then q2h PRN. Discharge Criteria 2. Kumar R, Trikha V, Malhotra R. A study of vascular
Fentanyl 12 g/kg IV q2h PRN: Only stable fractures with minimal swelling (usually injuries in pediatric supracondylar humeral
Initial dose of 1 g/kg IV may be repeated type I) can be safely discharged. fractures. J Orthop Surg. 2001;9(2):3740.
q1520min until pain is controlled, then q2h Issues for Referral 3. Villarin LA Jr., Belk KE, Fried R. Emergency
PRN. All displaced fractures require emergent consultation department evaluation and treatment of elbow and
Codeine or codeine/acetaminophen dosed as with an experienced orthopedic surgeon. forearm injuries. Emerg Med Clin North Am.
0.51 mg/kg of codeine component PO q4h PRN 1999;17:843.
dosed as 0.1 mg/kg of hydrocodone component FOLLOW-UP
PO q46h PRN FOLLOW-UP RECOMMENDATIONS
ADDITIONAL READING
r NSAIDs: r Discharge instructions and medications: r Baratz M, Micucci C, Sangimino M. Pediatric
Consider NSAID medication in anticipation of The affected elbow and hand should be iced and supracondylar humerus fractures. Hand Clin.
prolonged pain and inflammation: kept elevated for the 1st 23 days.
Some clinicians prefer to avoid NSAIDs due to 2006;22(1):6975.
The cast should be kept clean and dry. r Kasser JR, Beaty JH. Supracondylar fractures of the
theoretical concern over influence on Adequate pain control distal humerus. In Beaty JH, Kasser JR, eds.
coagulation and callus formation. r Activity:
Animal studies have raised concerns that Rockwood and Wilkins Fractures in Children. 5th
The child should avoid any activities that increase ed. Philadelphia, PA: Lippincott Williams & Wilkins;
NSAIDs may negatively influence bone healing; the risk of tripping or falling.
however, there is no clinical evidence in humans. 2001.
Patient Monitoring r Lins RE, Simovitch, RW, Waters PM. Pediatric elbow
r The childs fingers should be monitored often for trauma. Orthop Clin North Am. 1999;30(1): F
Naproxen 5 mg/kg PO q8h PRN restriction in movement and circulation and sensory 119132.
r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN changes for the 1st few days following surgery r Sharieff GQ. Pediatrics. In Simon RR, Koenigsknecht
and/or cast placement. SJ, Sherman SC, et al., eds. Emergency Orthopedics:
SURGERY/OTHER PROCEDURES r Monitor for signs of pin-tract infection, including The Extremities. 5th ed. Columbus, OH:
r Gartland type I fractures are treated with closed
increasing elbow pain, fever, and drainage from the McGraw-Hill; 2006.
reduction and casting. cast:
r Gartland type II fractures require closed reduction See Also (Topic, Algorithm, Electronic
3% of patients develop pin-tract infection,
and percutaneous fixation if a long arm cast does Media Element)
usually at 14 wk post-pin placement.
not adequately hold the reduction. Trauma, Elbow
r Gartland type III fractures are managed by closed COMPLICATIONS
reduction and percutaneous fixation followed by 3 Complications of supracondylar fractures include:
r Vascular injury: CODES
wk of immobilization in a long arm cast.
r Extension-type supracondylar fractures that are Occurs with posterior displacement of the distal
nondisplaced and are of <20-degrees angulation fragment stretching the brachial artery across the ICD9
fractured surface of the proximal fragment r 812.41 Supracondylar fracture of humerus, closed
are immobilized in a posterior long arm splint
extending from the axilla to a point just proximal to Vascular insufficiency or swelling may lead to r 812.51 Supracondylar fracture of humerus, open
the metacarpal heads with the elbow in >90 Volkmann ischemic contracture of the forearm,
degrees of flexion: markedly limiting function of the extremity.
r Neurologic injury: PEARLS AND PITFALLS
The splint should encircle 3/4 of the circumference
of the extremity. Occurs in up to 8% of supracondylar humeral
r Pearls:
The distal pulses should be checked; if absent, the fractures and most frequently involves the anterior
elbow should be extended 515 degrees or until interosseous branch of the median nerve: Immediate therapy consisting of pain management
the pulses return. When the anterior interosseous nerve is injured, and application of a splint for comfort with
r For nondisplaced extension fractures with there is loss of thumb interphalangeal joint expedited imaging and definitive therapy
flexion and index distal interphalangeal joint Emergent consultation with an experienced
>20-degree angulation, the emergency
flexion. orthopedic surgeon is recommended.
management includes immobilization in a posterior r Pitfalls:
long arm splint and emergent orthopedic referral for Can also see ulnar nerve palsy
r Compartment syndrome Neurovascular injuries must be a consideration
reduction under anesthesia.
r Flexion-type supracondylar fractures are also r Joint stiffness: since key structures pass through the elbow,
Diminished range of motion may be secondary to including the anterior interosseus nerve, ulnar and
immobilized in a posterior long arm splint with the
inadequate reduction or callus formation within radial nerves, and brachial artery.
elbow positioned at 35 degrees short of full
the joint. Neurovascular status must be assessed both prior
extension to avoid the development of delayed
elbow stiffness. r Cubitus varus and valgus deformities (due to to and after splinting.
r Open reduction with internal fixation is indicated malposition of the distal humeral fragment after
under the following circumstances: reduction)
Inability to achieve a satisfactory closed reduction
Complicating fractures to the forearm
Inability to maintain a closed reduction
Vascular compromise
411
FRACTURE, TIBIAL AVULSION

Deirdre D. Ryan
Robert M. Kay
GENERAL PREVENTION r Assess if patient can actively extend the leg:

BASICS r Warming up well prior to sports participation Type I: Patients may be able to actively extend the
r Quadriceps stretching knee (usually not completely).
DESCRIPTION r Resting if pain is experienced at the tibial tuberosity Types IIV: Patients will not be able to actively
r Tibial avulsion occurs when a fragment of the tibial extend the knee.
with play
tubercle is avulsed by the patellar tendon and is r Rule out compartment syndrome (3):
displaced upward. PATHOPHYSIOLOGY Palpate compartments for compressibility.
r Watson-Jones described a classification with 3 Avulsion of the tuberosity occurs when patellar tendon Check circulation and neurologic status.
fracture types, but this has been modified to traction exceeds the combined strength of the Assess pain with passive flexion/extension of the
5 types: apophysis underlying the tubercle, the surrounding toes.
Type I: A small fracture through the distal portion perichondrium, and periosteum.
of the tibial tubercle that extends proximally DIAGNOSTIC TESTS & INTERPRETATION
ETIOLOGY
through the secondary ossification center of the r Most occur during sporting or play activity Imaging
tubercle r Occurs with sudden acceleration or deceleration of AP/Lateral knee x-rays:
Type II: The fracture extends proximally and r Diagnosis is made on the lateral view.
the knee extensor mechanism
anteriorly, exiting through the area joining the r Note the size of the fragment and the degree of
tibial tubercle ossification center and the proximal COMMONLY ASSOCIATED CONDITIONS displacement.
r Osgood-Schlatter disease
tibial epiphysis.
Type III: The fracture extends upward through the r Extensor mechanism disruption (2) DIFFERENTIAL DIAGNOSIS
r Osgood-Schlatter disease
tibial epiphysis and into the knee joint. r Extensor mechanism disruption (2):
Type IV: The fracture extends from the tubercle up
to the proximal tibial physis, then traverses it DIAGNOSIS Patellar tendon avulsion
posteriorly. Quadriceps tear
HISTORY
Type V: Not a true physeal fracture, this occurs r Patients report a popping sensation.
when the periosteal sleeve of the patellar tendon r Localized pain and swelling at the tuberosity
avulses from the tibia.
TREATMENT
PHYSICAL EXAM PRE HOSPITAL
EPIDEMIOLOGY r Swelling and tenderness at the tibial tuberosity r Immobilization
Prevalence r Knee joint effusion/hemarthrosis r Application of a cold compress to the anterior knee
0.42.7% of all epiphyseal injuries r Can palpate a freely moving fragment of bone at the
RISK FACTORS anterior proximal tibia MEDICATION
r Male gender r Knee is held flexed at 2040 degrees. First Line
r Adolescents: r Patella alta: Degree correlates with the amount of r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN
Tibial tuberosity apophysis is made of cartilage at r NSAIDs:
displacement of the tibial tuberosity
this age. Consider NSAID medication in anticipation of
r Sporting activity, especially jumping activities such prolonged pain and inflammation:
as basketball (1) Ibuprofen 10 mg/kg/dose PO/IV q6h PRN
r Patella baja Ketorolac 0.5 mg/kg IV/IM q6h PRN
r Tight hamstrings Naproxen 5 mg/kg PO q8h PRN
Animal studies have raised concerns that NSAIDs
may negatively influence bone healing; however,
there is no clinical evidence in humans.
412
FRACTURE, TIBIAL AVULSION
r Opioids:
REFERENCES
Morphine 0.1 mg/kg IV/IM/SC q2h PRN: FOLLOW-UP
Initial morphine dose of 0.1 mg/kg IV/IM may 1. Hosalkar FS, Cameron DB, Cameron DB, et al.
be repeated q1520min until pain is controlled, FOLLOW-UP RECOMMENDATIONS Tibial tuberosity fractures in adolescents. Child
r Discharge instructions and medications: Orthop. 2008;6:469474.
then q2h PRN.
Codeine or codeine/acetaminophen dosed as Keep leg elevated. 2. Mosier SM, Stanitski CL. Acute tibial tubercle
0.51 mg/kg of codeine component PO q4h PRN Monitor the color, warmth, motion, and sensation avulsion fractures. J Pediatr Orthop. 2004;24:
Hydrocodone or hydrocodone/acetaminophen of the toes. 181184.
dosed as 0.1 mg/kg of hydrocodone component Keep the cast dry. 3. Pape JM, Goulet JM, Hensinger RN. Compartment
PO q46h PRN Patient should return for: syndrome complicating tibial tubercle avulsion. Clin
Increasing pain
SURGERY/OTHER PROCEDURES Orthop Rel Res. 1993;295:201204.
Numbness or tingling in the toes
r The vast majority of these fractures require open
Inability to move the toes
reduction and internal fixation followed by long leg r Activity:
cast application (1,2). CODES
r Closed treatment (with closed reduction and a long Nonweight bearing for 6 wk or until radiographic
and clinical healing occurs
leg cast) may be undertaken for those with fractures Quadriceps exercises can be started after 6 wk. ICD9
displaced <2 mm and with full active knee Return to sports: 823.00 Closed fracture of upper end of tibia
extension. Follow-up x-rays are needed to confirm After radiographically and clinically healed
anatomic reduction (1,2). When quadriceps strength is equal
When there is full range of motion of the knee
PEARLS AND PITFALLS
DISPOSITION
r Patients should be taught to sit out of any activity
Admission Criteria PROGNOSIS
r Patients with severe swelling and tense that elicits pain at the tibial tuberosity.
Good (2) r If x-rays do not show a tibial tuberosity fracture but
hemarthrosis should be admitted for observation to
COMPLICATIONS
rule out compartment syndrome.
r Patients with displaced fractures should be admitted r Compartment syndrome (3)
the patient is unable to extend the knee, refer for
MRI to look at the extensor mechanism.
F
r Genu recurvatum can result in skeletally immature
to orthopedics for surgery.
children <11 yr of age due to premature anterior
Discharge Criteria physeal closure.
r Adequate pain control r Pain can develop at screw heads after fracture
r No neurovascular compromise
fixation.
Issues for Referral
Follow up with an orthopedic surgeon.
413
FRACTURE, TODDLERS
Louis A. Spina

Initial Lab Tests
DESCRIPTION HISTORY r Lab testing is unhelpful in diagnosis of toddlers
r Toddlers fracture was originally described as an r Patients will usually present with history of an acute
fracture.
oblique spiral fracture occurring in the distal tibia of injury, inability to bear weight, and no signs or r Lab assays may be indicated if an infectious etiology
young children (1). symptoms of infection.
r Initially thought to be a unique type of fracture, r Fever should not be present, but if present, it should such as osteomyelitis or septic arthritis is suspected.
toddlers fractures are now felt to be a subset of a be unrelated to leg pain or altered gait: Imaging
Due to the mild clinical presentation, many r Radiographs of the tibia (both AP and lateral views)
more common group of injurieschildhood
accidental spiral tibial (CAST) fractures (2). children present >24 hr after the development of should be obtained if there is suspicion for a
pain, limp, or altered gait. toddlers fracture:
EPIDEMIOLOGY At times, there is history of trauma given by the Findings are often subtle but may reveal an
The mean age for CAST fractures is 50 mo, with a caregivers. In these cases, the trauma was likely oblique or spiral fracture in the distal 3rd of the
range of 1294 mo (2). unwitnessed or thought to be so minor that it tibia extending distally.
r Toddlers fractures occur more commonly in children went unnoticed. If initial views are normal, an internal oblique view
between the ages of 9 mo and 3 yr. of the tibia may be diagnostic.
PHYSICAL EXAM r If all initial imaging is normal and there is still strong
GENERAL PREVENTION r Assess vital signs with attention to temperature.
r Physical exam findings may be subtle, or the clinical suspicion, a bone scan can be used to elicit a
Avoidance of these injuries begins with general
diagnosis. However, it is also reasonable to repeat a
childhood injury prevention strategies. These can physical exam may be normal. tibial film in 10 days when a fracture, if present, is
include appropriate adult supervision, avoidance of Pain, tenderness, limp, or inability to bear weight likely to be more apparent secondary to the
dangerous activities, and adequate home safety on the affected extremity are findings that most developing periosteal reaction.
measures. commonly accompany a toddlers fracture. r If there is concern that the patients refusal to bear
PATHOPHYSIOLOGY Other notable findings are tenderness, mild
weight is due to an injury in another part of the
r External force transmitted through the tibia is the swelling, and mild warmth over the affected
extremity, those areas should be imaged as well.
common factor involved. region.
r Some fractures appear to involve only axial loading, Pain may be elicited by: DIFFERENTIAL DIAGNOSIS
Dorsiflexion of the ipsilateral ankle r Fractures of other bones:
while others may involve torque.
r The fracture remains nondisplaced due to the Transmitting force through the tibia, by applying Femur fracture
compressive force simultaneously through ankle Tibia and fibula fracture
relatively strong periosteum in young children. Pelvic fracture
and knee
ETIOLOGY With knee flexed 90 degrees and foot flat on Foot and ankle fracture
r Toddlers fractures usually occur after low-energy the floor, apply compressive force to the knee. r Sprains:
trauma: There is usually no sign of bruising or deformity Knee sprain
Tripping, twisting of the ankle, or falling from a with a toddlers fracture. Ankle sprain
low height can all cause a toddlers fracture. r Thorough exam is necessary to exclude other Foot sprain
r These low-energy actions can cause a sudden diagnoses that may have similar presentations, r Hip disorders:
twisting of the tibia, creating the spiral component including hip disorders such as polyarthritis, slipped Transient synovitis of the hip
of the fracture. capital femoral epiphysis (SCFE), Legg-Calve-Perthes SCFE
disease, or foreign body in the sole of the foot. Legg-Calve-Perthes disease
r Examine for a skin rash, which may suggest an Septic hip
alternate diagnoses.
414
FRACTURE, TODDLERS
r Rheumatologic disease DISPOSITION REFERENCES

r Bone tumor Admission Criteria
r Contusions of the lower extremity r Admission is not medically necessary. 1. Dunbar JS, Owen HF, Nogrady MB, et al. Obscure
r Muscular injuries r If there is concern about possible physical abuse and tibial fracture of infantsthe toddlers fracture.
r Infectious etiologies: there is no safe place to discharge the patient, J Can Assoc Radiol. 1964;15:136144.
admission may be the only alternative. 2. Mellick LB, Milker L, Egsieker E. Childhood
Septic arthritis
accidental spiral tibial (CAST) fractures. Pediatr
Osteomyelitis Discharge Criteria
r Once the cast has been applied and the patients Emerg Care. 1999;15(5):307309.
Cellulitis
r Trauma secondary to physical abuse caregivers have been instructed on proper care and
3. Halsey MF, Finzel KC, Carrion WV, et al. Toddlers
fracture: Presumptive diagnosis and treatment.
follow-up, the patient may be discharged home. J Pediatr Orthop. 2001;21:152156.
r If there are concerns about possible child
TREATMENT nonaccidental trauma, this should be explored and
PRE HOSPITAL
resolved prior to discharging the patient. ADDITIONAL READING
r Assess and stabilize airway, breathing, and Issues for Referral
circulation. Consider referral to a pediatric orthopedist for patients
r Determination if any acute, life-threatening injuries with confirmed or presumptive toddlers fractures. Media Element)
r American Academy of Orthopedic Surgeons:
are present. http://orthoinfo.aaos.org/topic.cfm?topic=a00161
INITIAL STABILIZATION/THERAPY FOLLOW-UP r Fracture, Femur
r Assess and stabilize airway, breathing, and r Fracture, Foot
circulation. FOLLOW-UP RECOMMENDATIONS r Limp
r Determination if any acute, life-threatening injuries r Discharge instructions and medications:
r Slipped Capital Femoral Epiphysis
are present. Parents should be instructed on proper cast r Trauma, Ankle
r Administer analgesics as needed: maintenance and instructed to seek medical care
r Trauma, Foot/Toe
Though parenteral opioids are routinely necessary
if the cast breaks or appears too tight:
Poor circulation in the toes noted by color
F
for management of other fractures, toddlers
changes (cyanosis) and being cool to the touch
fractures often may be managed with NSAIDs or CODES
are signs parents can look out for.
oral opioids such as codeine.
r Splinting: Adequate analgesia
r Activity: ICD9
Always assess neurovasculature exam pre- and
Activity is obviously limited due to the presence of 823.80 Closed fracture of unspecified part of tibia
post-splinting.
a cast.
MEDICATION Children should remain nonweight bearing on
r Ibuprofen 10 mg/kg/dose PO/IV q6h PRN: the affected extremity: PEARLS AND PITFALLS
Some clinicians prefer to avoid due to concern Most children who suffer toddlers fractures are r Toddlers fracture is a common cause of limp, and
over influence of callus formation. too young to use crutches or a cane effectively
r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN often no history of trauma is elicited.
and should not be given these, as the risk for r Some specialists recommend casting of presumed
r Codeine/Acetaminophen dosed as 0.51 mg/kg of further injury is high.
toddlers fractures even with negative radiographs
codeine component PO q4h PRN PROGNOSIS so as not to mistreat an occult fracture.
r Hydrocodone or hydrocodone/acetaminophen dosed r Any CAST fracture found in a child who is not yet
Prognosis with proper treatment is excellent.
as 0.1 mg/kg of hydrocodone component PO q46h ambulating should raise the concern about possible
PRN COMPLICATIONS
r Morphine 0.1 mg/kg IV/IM/SC q2h PRN: Casting may rarely be associated with heel ulcers and physical abuse.
Initial dose of 0.1 mg/kg IV/SC may be repeated prolonged limping after cast removal, but these are
q1520min until pain is controlled, then q2h PRN. relatively uncommon (3).
r Toddlers fractures are typically treated by casting.
r Clinician and institutional practice typically dictate
whether a short or long leg cast is chosen:
It is unclear if there is any difference in the benefit
of short leg vs. long leg casting.
Short leg weight-bearing cast
Long leg cast for up to 56 wk (2)
Patients with a limp or a history strongly
suggestive of toddlers fracture and who have no
fracture evident on tibial radiography may have a
cast or splint placed and follow-up radiographs.
415
FRACTURE, TORUS (BUCKLE)

Kevin Ching
BASICS DIAGNOSIS r Greenstick fracture
r Bowing fracture
DESCRIPTION HISTORY r Growth plate (physeal) fracture:
r Trauma resulting in longitudinal axial compression
Torus fractures are stable, nondisplaced fractures that Salter-Harris IIV fractures
commonly are sustained when axial compression of a on a long bone:
long bone causes it to buckle on itself: Usually FOOSH
r Typically involve the distal radius or ulna after a fall r Torus fractures may occur in cases of very minor TREATMENT
on outstretched hand (FOOSH) trauma or in cases with no known trauma.
r Less commonly involves the distal tibia, fibula, r Degree of pain and disability associated with torus PRE HOSPITAL
r Immobilize the injured extremity.
scaphoid, humerus, or femur fractures is typically much less severe than with
other fractures: r Ice and elevation
GENERAL PREVENTION As a result, patients with torus fractures often
Wrist guards may provide some protection against INITIAL STABILIZATION/THERAPY
present later than those with other fractures, r Immobilize the injured extremity.
wrist fractures when in-line skating, skateboarding, or which typically are brought to medical care r Provide appropriate analgesia.
roller skating (1). immediately. r Casting:
PATHOPHYSIOLOGY PHYSICAL EXAM Distal radial torus fractures are traditionally
Longitudinal forces cause the trabeculae in the r Localized pain, swelling, tenderness, and decreased managed with plaster or fiberglass short arm
transitional zone (junction between the metaphysis range of motion around site of fracture casting (below the elbow) for 24 wk.
and diaphysis) to buckle: r Assess vascular integrity of extremity. Casting practices vary by institution, but
r The cortex on 1 or both sides is compressed and r Examine motor and sensory function. placement of short arm and short leg casts is
bulges outward. r Search for concomitant injuries. within the scope of pediatric emergency medicine
r If unilateral cortical buckling occurs, there may be and emergency medicine practice.
angulation but often no appreciable deformity since DIAGNOSTIC TESTS & INTERPRETATION r Splinting:
the periosteum and cortex on the side opposite to Imaging Recent literature suggests that 3 wk of continuous
the fracture are intact. Radiographs: immobilization with a removable splint is equally
This is in contrast to a greenstick fracture, where a r Multiple views in different planes safe and effective as a cast for distal radius torus
fracture through the cortex on 1 side extends r Standard evaluation includes 23 views (depending fractures (2,3):
incompletely through to the opposite side, on site of fracture): No significant difference in clinical or radiologic
producing a plastic deformity with convex Commonly an AP and lateral view outcomes
angulation on the side of fracture. r Bilateral or unilateral outward bulging of cortex Better physical functioning
(with or without angulation) Less difficulty with daily activities
ETIOLOGY
r Sports activities (in-line skating, skateboarding, r Identify concomitant injuries (eg, Salter-Harris type II Earlier return to sports
fracture) accompanying an angulated distal radius No significant difference in pain experienced
roller skating, biking, and scooters)
r Wrist torus fractures result from pure axial loading torus fracture: Reduces the need for follow-up (4)
Consider radiographic assessment of the joint Commercially available or individually fitted
(bilateral bulging) or axial loading with
above and below the site of injury. (plaster or fiberglass) splints:
hyperextension, hyperflexion, valgus, or varus stress Volar or sugar tong splint for distal radial torus
(unilateral bulging with angulation). r When evaluating distal forearm fractures, consider
AP and lateral views of the wrist, forearm, and fracture
elbow.
416
FRACTURE, TORUS (BUCKLE)
r Opioids: FOLLOW-UP
Morphine 0.1 mg/kg IV/IM/SC q2h PRN: 1. Lewis LM, West OC, Standeven J, et al. Do wrist
Initial morphine dose of 0.1 mg/kg IV/SC may FOLLOW-UP RECOMMENDATIONS guards protect against fractures? Ann Emerg Med.
r Discharge instructions and medications: 1997;29:766769.
then q2h PRN. Rest, ice, and elevation. 2. Plint AC, Perry JJ, Correll R, et al. A randomized,
Fentanyl 12 g/kg IV q2h PRN: Adequate pain control controlled trial of removable splinting versus
Initial dose of 1 g/kg IV may be repeated Educate about the signs of tight casts/splints. casting for wrist buckle fractures in children.
q1520min until pain is controlled, then q2h Follow up with orthopedics as necessary: Pediatrics. 2006;117:691697.
PRN. Review of the literature supports the safe 3. Abraham A, Handoll HHG, Khan T. Interventions for
Codeine/Acetaminophen dosed as 0.51 mg/kg of discharge of distal radius torus fractures in treating wrist fractures in children. Cochrane
codeine component PO q4h PRN removable splints without orthopedic follow-up Database Syst Rev. 2008;(2):CD004576.
Hydrocodone or hydrocodone/acetaminophen (4). 4. May G, Grayson A. Do buckle fractures of the
dosed as 0.1 mg/kg of hydrocodone component r Activity:
paediatric wrist require follow up? Emerg Med J.
PO q46h PRN As tolerated, but restrict use of affected extremity 2009;26:819822.
r NSAIDs:
Patient Monitoring 5. Plint A, Perry JJ, Tsang JYL. Pediatric wrist buckle
Consider NSAID medication in anticipation of r Neurovascular exam fractures: Management and outcomes. Can J
prolonged pain and inflammation: r Uncontrollable pain Emerg Med. 2004;6:397401.
theoretical concern over influence on PROGNOSIS
coagulation and callus formation. Excellent if appropriately immobilized ADDITIONAL READING
Animal studies have raised concerns that
COMPLICATIONS Lawton LJ. Fractures of the distal radius and ulna. In
NSAIDs may negatively influence bone healing; r Torus fractures are generally considered stable
however, there is no clinical evidence in humans. Letts MR, ed. Management of Pediatric Fractures.
(refracture rate <1% [2,5]):
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN Philadelphia, PA: Churchill Livingstone;
Torus fractures may share a similar radiographic
appearance with nondisplaced greenstick
1994:345368. F
Naproxen 5 mg/kg PO q8h PRN fractures. See Also (Topic, Algorithm, Electronic
In 1 study, 15 children managed as torus fractures Media Element)
in the emergency department were later r All fracture/trauma of the extremity topics
DISPOSITION
rediagnosed with greenstick fractures (3). r Fracture, Greenstick/Bowing
Discharge Criteria
r No evidence of more serious injury Greenstick fractures are unstable (with a high
r Normal neurovascular exam refracture rate), necessitating closed reduction
r Provision of appropriate short arm cast or removable and casting. CODES
r Potential for unscheduled return emergency
splint
department visits for cast-related problems (eg, ICD9
Issues for Referral broken or wet cast) r 813.45 Torus fracture of radius (alone)
r Uncertainty or concern for greenstick, bowing, or
r 813.46 Torus fracture of ulna (alone)
physeal fractures requires orthopedic consultation.
r Require immediate orthopedic consultation for:
Open reduction with internal fixation
Compound fracture
PEARLS AND PITFALLS
Compartment syndrome r Pearls:
Unless reinjury occurs, torus fractures are expected
to heal fully without complication.
Casting or splinting is to provide support to
prevent a complete fracture from occurring in the
event of further trauma.
r Pitfall:
Although a torus and greenstick fracture may
share similar radiographic features, their
management is different (splinting vs. reduction
and casting).
417
FRACTURE, ZYGOMA
Usha Sethuraman
GENERAL PREVENTION r Palpation:

BASICS r Since the most common cause of zygoma fractures Feel for tenderness and crepitus.
is MVAs, effective child seat restraints are important Cheek and upper lip numbness
DESCRIPTION in preventing these injuries. Gently grasp the maxilla intraorally and rock back
r The zygomas integrity is critical to maintaining r Use of any protective device such as an airbag, seat and forth. Movement indicates Le Fort fracture.
normal facial width and cheek structure. belts, or a car seat is associated with a decreased r LeFort type I fracture:
r The zygoma consists of a body and an arch. incidence of facial injuries (5). Involves only the maxilla
r The following muscles attach to it: Zygomaticus Extends through the zygomaticomaxillary junction
PATHOPHYSIOLOGY
major and minor, masseter, and orbicularis oculi. r Structure of the facial bones is different in Causes the teeth and alveolar bone to be mobile
r The zygoma articulates with 4 bones: Frontal, r Le Fort type II fracture:
children:
sphenoid, temporal, and maxilla: More cartilage and higher proportion of Extends superiorly through the infraorbital rim and
A fracture here may involve all 4 bones: cancellous to cortical bone to the nasofrontal sutures
It may extend to involve the floor of the orbit. Causes mobility of nose and upper jaw
r Fractures occur in the following places: Irregular fractures due to indistinct medullocortical
junction Zygoma is stable.
Orbital floor and lateral orbital wall superiorly r Bones are less mineralized and more elastic: r Le Fort type III fracture:
Posterior maxillary buttress inferiorly Hence, greenstick fractures are more common. Extends through the zygomatic arch,
Arch attachment to temporal bone laterally Minimally displaced due to thicker adipose tissue, zygomaticofrontal region, orbital floor, and
The fractured bone rotates medially and elastic bones, and flexible sutures (6) nasofrontal sutures
downward into the maxillary sinus. r High rate of bone metabolism causes quicker Separates midface from skull base (craniofacial
r Le Fort fractures occur in the midface and may disassociation)
healing to occur.
include the zygoma: The entire midface or zygoma moves when the
Le Fort fractures never occur at <2 yr of age. ETIOLOGY nose or upper jaw is moved.
r Direct trauma to the zygoma can cause a fracture of r MVAs are most common, followed by sports-related Rare and asymmetric injuries
the orbital floor with intact rims. activity and falls: Usually, impact is on 1 side.
r This is a true orbital blowout fracture. MVAs double the risk of facial fractures (2). r With true orbital blowout fractures, orbital dystopia
r Facial fractures occur in 2.5% of abuse cases (2). (asymmetry of the horizontal level of the eyes) may
EPIDEMIOLOGY occur:
Incidence COMMONLY ASSOCIATED CONDITIONS
r Associated with other injuries 5060% of the time Decreased sensation of the cheek, upper gums,
r Pediatric facial fractures generally result from severe and upper lip may occur due to involvement of the
r Head injuries are most common, followed by
trauma: infraorbital nerve.
Overall frequency is lower in children due to: extremity injuries. Limitation of upward gaze due to trapping of the
Retruded position of the face relative to the skull r Associated facial soft tissue injuries occur in >50%
inferior rectus may occur.
Increased structural stability due to lack of of cases (2).
pneumatization DIAGNOSTIC TESTS & INTERPRETATION
Structural strength provided by the presence of Lab
tooth buds
DIAGNOSIS Initial Lab Tests
r Midface fractures have the lowest incidence (10%) HISTORY In case of multisystem trauma:
of all maxillofacial fractures in the general r Details of the major trauma, violence, abuse, or fall r Hemoglobin
population: should be obtained. r Liver enzymes
Of these, zygoma fractures are the most common, r History of pain and numbness in the distribution of r Urinalysis
with an incidence of 28.6% among all facial the infraorbital nerve (upper lip and side of the r Blood group and type
trauma and 52% among midfacial fractures (13). nose) may be elicited.
Le Fort fractures occur in 2.7% of cases. r Trismus may occur due to an impacted zygoma Imaging
r Plain radiographs are often ineffective due to
Prevalence impinging on the temporalis muscle. incomplete calcification and dentition.
r Lowest in infants and increases with age r Ipsilateral epistaxis may occur. r CT is the gold standard for facial injuries (6):
r Zygoma fractures following trauma occur only after
PHYSICAL EXAM Sagittal and coronal views are recommended.
pneumatization of the maxillary sinus has been r Inspection: 3-dimensional reconstruction helps define
completed, usually by age 7 yr. complex injuries.
r Usually result from lateral trauma, while Le Fort Look for asymmetry, swelling, or bruising.
Features suggestive of zygomatic fractures: r Head CT may be required if associated with head
fractures occur from anterior trauma: Periorbital hematoma injury.
Highest frequency is in the adolescent age. Flat cheek bone (malar depression)
RISK FACTORS Downward appearance of globe r Severe swelling may mask orbital injuries.
r Overall risk is lower in children. Subconjunctival hemorrhage r Mandibular fractures may often present with trismus.
r Males are at higher risk than females at all ages Inferior displacement of lateral canthus
(3:1) (4). Enophthalmos
r Alcohol consumption Facial edema may obscure above signs. TREATMENT
r Motor vehicle accidents (MVAs), sports and falls, In isolated fractures of the zygomatic arch, a
decreased temporal width may be seen. INITIAL STABILIZATION/THERAPY
and interpersonal violence among teenagers r Assess and maintain airway and breathing per
Inspect for signs of nerve deficit.
Eyebrows that cannot be raised and eyelids that Advanced Trauma Life Support protocols.
cannot be closed indicate injury to the temporal r Control of any hemorrhage
and zygomatic branch of the facial nerve. r Observation with a soft diet for:
Fractures without displacements or functional
defects (eg, diplopia) (6)
Minimally displaced arch fragments that may be
reduced intraorally and remain stable (7)
418
FRACTURE, ZYGOMA
r Displaced fractures require open fixation (8). Discharge Criteria 4. Ferreira P, Marques M, Pinho C, et al. Midfacial
r Analgesia may need to be given. r Undisplaced or greenstick fractures of the zygoma fractures in children and adolescents: A review of
r Tetanus status needs to be updated, especially for r Absence of functional defects (eg, diplopia) 492 cases. Br J Oral Maxillofac Surg.
open fractures. r Absence of other associated injuries (eg, head injury) 2004;42(6):501505.
r Antibiotics for open wounds and animal bites 5. McMullin BT, Rhee JS, Pintar FA, et al. Facial
Issues for Referral
r All nondisplaced stable fractures should be referred fractures in motor vehicle collisions:
MEDICATION Epidemiological trends and risk factors. Arch Facial
First Line to an oral and maxillofacial surgeon within 72 hr.
r Displaced fractures require urgent referrals. Plast Surg. 2009;11(3):165170.
r Opioids:
6. Hatef DA, Cole PD, Hollier LH Jr. Contemporary
Morphine 0.1 mg/kg IV/IM/SC q2h PRN: management of pediatric facial trauma. Curr Opin
Initial morphine dose 0.1 mg/kg IV/SC may be
repeated q1520min until pain is controlled,
FOLLOW-UP Otolaryngol Head Neck Surg. 2009;17:308314.
7. Evans BG, Evans GR. MOC-PSSM CME article:
then q2h PRN. FOLLOW-UP RECOMMENDATIONS Zygomatic fractures. Plast Reconstr Surg.
Fentanyl 12 g/kg IV q2h PRN: r Discharge instructions and medications:
2007;121:111.
Initial dose of 1 g/kg IV may be repeated Pain control is important in children. 8. Kaufman Y, Stal D, Cole P, et al. Orbitozygomatic
q1520min until pain is controlled, then q2h Soft diet fracture management. Plast Reconstr Surg.
PRN. Most need follow-up with surgeon. 2008;121:13701374.
Codeine/Acetaminophen dosed as 0.51 mg/kg of Close follow-up and exam every 3 days for 24
codeine component PO q4h PRN wk for nondisplaced, greenstick fractures is
Hydrocodone or hydrocodone/acetaminophen recommended. ADDITIONAL READING
dosed as 0.1 mg/kg of hydrocodone component r Activity:
PO q46h PRN Refrain from contact sports during recuperation. See Also (Topic, Algorithm, Electronic
r NSAIDs: Media Element)
Consider NSAID medication in anticipation of Patient Monitoring r Fracture, Orbital
Patients should be monitored at home for increasing r Fracture, Skull
Some clinicians prefer to avoid NSAIDs due to pain, diplopia, CSF rhinorrhea, and malocclusion. r Globe Rupture F
theoretical concern over influence on PROGNOSIS r Trauma, Dental
coagulation and callus formation. r Bony facial injuries are associated with significant r Trauma, Head
Animal studies have raised concerns that morbidity. r Trauma, Facial
NSAIDs may negatively influence bone healing; r Children with facial fractures have a 3 times longer
however, there is no clinical evidence in humans. ICU stay, 2 times longer hospital stay, and 63%
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN higher mortality:
Ketorolac 0.5 mg/kg IV/IM q6h PRN This is due to higher association with head injuries
CODES
Naproxen 5 mg/kg PO q8h PRN: (2).
Some clinicians prefer to avoid due to r However, prognosis for isolated zygoma fractures is ICD9
theoretical concern over influence on 802.4 Closed fracture of malar and maxillary bones
good.
coagulation and callus formation. r Postoperative complications are unusual.
r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN r Infections, malunions, and nonunions are less PEARLS AND PITFALLS
Second Line common in children.
r Pearls:
Antibiotics for open fractures:
r Cefazolin 2550 mg/kg IV q8h COMPLICATIONS Zygoma fractures are less common in children
r Trismus
than adults.
SURGERY/OTHER PROCEDURES r Paresthesias
Nondisplaced zygoma fractures can be managed
r Only 25% of children need operative repair (3): r Enophthalmos conservatively.
Comminuted fractures need open reduction and r Facial asymmetry Complications are rare.
fixation (6). r Ocular dystopia r Pitfalls:
In the absence of orbital entrapment, treatment is Zygoma fractures have a high association with
done after the edema has resolved, usually in 35 other major trauma.
days. REFERENCES Fractures of the zygoma may involve the orbital
Delay in orbital repair may result in higher rates of floor.
posttraumatic enophthalmos and the need for 1. Adams CD, Januszkiewcz JS, Judson J. Changing
additional surgery. patterns of severe craniomaxillofacial trauma in
r Zygomatic arch fractures, once reduced, are stable Auckland over eight years. Aust N Z J Surg.
and require no further fixation. 2000;70:401404.
r Displaced Le Fort fractures are treated by open 2. Imahara SD, Hopper RA, Wang J, et al. Patterns
reduction with rigid internal fixation. and outcomes of pediatric facial fractures in the
United States: A survey of the National Trauma
DISPOSITION Data Bank. Am Coll Surg. 2008;207:710716.
Admission Criteria 3. Haug RH, Foss J. Maxillofacial injuries in the
r Zygoma fractures associated with other severe pediatric patient. Oral Surg Oral Med Oral Pathol
cranial and extremity injuries Oral Radiol Endod. 2000;90:126134.
Severe head injuries
Hemorrhage
Tenuous airway
419
FROSTBITE
Cara Bornstein
William I. Krief

BASICS r Prolonged exposure to cold of underprotected areas
Lab
of the body r Lab tests are not necessary for diagnosis but may
DESCRIPTION r Refreezing of thawed extremities aid in management.
r Frostbite is a cold-related injury resulting from a r Urinalysis is performed to detect myoglobinuria.
variety of mechanisms. COMMONLY ASSOCIATED CONDITIONS r Gram stain and cultures from suspected frostbite
r Severity of frostbite injury is related to ambient r Hypothermia:
Children are especially susceptible due to a larger wound infections
temperature and duration of exposure.
body surface area to weight ratio. Imaging
RISK FACTORS r Alcohol and drug use r Several modalities may be effective in revealing
r Prolonged exposure to cold r Homelessness tissue perfusion and the extent of deep-tissue injury
r Alcohol or drug intoxication
and predicting tissue viability:
r Use of nicotine or vasoconstrictive drugs Technetium-99m scintigraphy can also show
r Psychiatric disorders DIAGNOSIS effects of treatment.
r Altered mental status MRI may be helpful in predicting nonviable tissue
HISTORY
r Peripheral vascular disease, diabetes mellitus r Progression of symptoms may be seen: and guiding debridement.
r High altitude Patient may complain of feeling cold, then burning Laser Doppler flowmetry can measure
r Wet and windy conditions or throbbing in the affected region microvascular RBC perfusion.
r Homelessness Numbness followed by complete loss of sensation Angiography
r Radiography for suspected fractures in the acute
r Malnutrition Loss of muscle dexterity
r Infancy or advanced age Severe joint pain setting, and osteomyelitis and growth plate injury
r Sites most susceptible include hands, feet, ears, on future presentations
GENERAL PREVENTION nose, and lips Diagnostic Procedures/Other
r Dress appropriately:
Consider ECG in any patient with hypothermia.
Protect hands and feet (waterproof shoes). PHYSICAL EXAM
r During the initial evaluation, most frostbite injuries DIFFERENTIAL DIAGNOSIS
Cover head and all parts of the face. r Pernio (chilblains/cold sores) are localized
Avoid restrictive or wet clothing. appear similar:
r Avoid smoking and alcohol use. Need to perform a careful exam that assesses for inflammatory skin lesions due to chronic repeated
r Avoid remaining in the same position for prolonged presence of necrotic tissue or compartment exposure to nonfreezing-cold temperatures.
syndrome: r Cold immersion foot (trench foot) is a peripheral
periods of time. With compartment syndrome, will see neurovascular injury due to prolonged exposure to a
PATHOPHYSIOLOGY extraordinary pain, paresthesia, pallor, poor damp nonfreezing environment.
2 components to frostbite injury: pulses and perfusion, and paralysis r Frostnip is a mild cold injury that manifests as
r During the cooling process, initial freeze injury Paresthesia is a late symptom.
redness, numbness, and swelling to affected areas.
r Classification of frostbites is applied after rewarming r Raynaud phenomenon
occurs:
Extracellular ice crystals form, causing an osmotic and can be categorized by either degree of injury or
gradient, intracellular dehydration, enzymatic by superficial (1st and 2nd degree) and deep (3rd
destruction, and cell death. and 4th degree). TREATMENT
Vascular endothelial damage leads to 1st degree:
intravascular damage and reduced blood flow. Erythema and swelling, usually no blisters PRE HOSPITAL
Patient may complain of throbbing or burning r Assess and stabilize airway, breathing, and
Vasoconstriction and arteriovenous shunting occur
at the capillary level, compounding end organ pain. circulation.
2nd degree: r Remove wet clothing.
damage.
r During rewarming, reperfusion injury occurs: Skin is red and usually has large, clear blisters. r Rewarm only if refreezing will not occur in transit.
Intracellular swelling due to the influx of fluid Pain often resolves, and the patient is numb in r Protect affected areas from mechanical trauma:
Red cell, platelet, and leukocyte aggregation the affected area. Extremities can be padded and splinted for
causes thrombosis of the microcirculation. 3rd degree: protection.
Release of free radicals and arachidonic acid Full-thickness skin injury:
Skin is waxy and hard. There may be INITIAL STABILIZATION/THERAPY
metabolites (prostaglandin and thromboxane), r Assess and stabilize airway, breathing, and
which then exacerbate vasoconstriction subcutaneous edema.
Patient may complain of numbness, throbbing, circulation.
or burning pain. r Attend to life-threatening conditions first. Address
Hemorrhagic vesicles may be present. ABCs per Advanced Trauma Life Support and
4th degree: Pediatric Advanced Life Support guidelines:
Tissue necrosis and gangrene Frostbite is primarily a condition of morbidity.
r The goal of wound care with frostbite is the
preservation of viable tissue, prevention of infection,
and return of function:
Correct hypothermia with passive and active
rewarming:
Rapid rewarming in a bath of circulating hot
water between 40 C and 42 C for 2060 min
with a mild antibacterial agent
(hexachlorophene or povidone/iodine).
Continue until distal extremity is flushed,
supple, and pliable.
Active motion may be useful.
420
FROSTBITE
Use sterile cotton between fingers and toes to DISPOSITION REFERENCES

prevent skin macerartion. Admission Criteria
Keep affected extremities elevated, with splinting Critical care admission criteria: 1. Bruen KJ, Ballard JR, Morris SE, et al. Reduction of
as indicated. r Admission recommended for deep frostbites (3rd the incidence of amputation in frostbite injury with
r Anti-inflammatory agents such as ibuprofen can thrombolytic therapy. Arch Surg. 2007;142(6):
and 4th degree)
reduce inflammation and pain. r Consider transfer of patient if medical personnel not 546551.
r Pain control to address pain associated with 2. Twomey JA, Peltier GL, Zera RT. An open-label
familiar with frostbite care:
rewarming of affected areas study to evaluate the safety and efficacy of tissue
Burn centers can often serve as the referral center
r Systemic antibiotics should be reserved for identified plasminogen activator in treatment of severe
for severe frostbites.
infections and wound sepsis. Antibiotics should not frostbite. J Trauma. 2005;59(6):13501354.
be used for prophylaxis. Issues for Referral 3. Theis FV, OConnor WR, Wahl FJ. Anticoagulants in
Superficial frostbites (1st and 2nd degree) can be acute frostbite. JAMA. 1951;146:992995.
MEDICATION followed by primary care physicians or surgeons for 4. Porter JM, Wesche DH, Rosch J, et al. Intra-arterial
r NSAIDs: development of complications: sympathetic blockade in the treatment of clinical
Consider NSAID medication in anticipation of r The hospital course will dictate follow-up of deep frostbite. Am J Surg. 1976;132(5):625630.
prolonged pain and inflammation: frostbites.
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN 5. Folio LR, Arkin K, Butler WP. Frostbite in a
Ketorolac 0.5 mg/kg IV/IM q6h PRN mountain climber treated with hyperbaric oxygen:
Naproxen 5 mg/kg PO q8h PRN FOLLOW-UP Case report. Mil Med. 2007;172(5):560563.
r Aloe vera (thromboxane inhibitor) topically q6h FOLLOW-UP RECOMMENDATIONS
r Discharge instructions and medications: ADDITIONAL READING
r Opioids:
Anti-inflammatory medication as noted in r Jurkovich GJ. Cold-induced injury. Surg Clin North
Morphine 0.1 mg/kg IV/IM/SC q2h PRN: Medication section
Initial morphine dose of 0.1 mg/kg IV/SC may Am. 2007;87:247267.
Tobacco and vasoconstrictive medications must be r Murphy JV, Banwell PE, Roberts AH, et al. Frostbite:
then q2h PRN.
withheld.
No weight bearing until edema has resolved Pathogenesis and treatment. J Trauma. F
Fentanyl 12 g/kg IV q2h PRN: May experience cold insensitivity, neuropathy, 2000;48(1):171178.
Initial fentanyl dose of 1 g/kg IV may be and/or decreased hair and nail growth See Also (Topic, Algorithm, Electronic
repeated q1520min until pain is controlled, Affected tissue at increased risk for reinjury Media Element)
then q2h PRN. Discuss with patient methods to avoid Hypothermia
Codeine or codeine/acetaminophen dosed as cold-weather injuries (see General Prevention
0.51 mg/kg of codeine component PO q4h PRN section).
Hydrocodone or hydrocodone/acetaminophen r Activity:
CODES
Encourage activity of affected extremities as soon
PO q46h PRN as possible:
r Tetanus prophylaxis as indicated Physical therapy is recommended.
ICD9
r 991.0 Frostbite of face
COMPLEMENTARY & ALTERNATIVE DIET r 991.1 Frostbite of hand
THERAPIES A high-calorie, high-protein diet will promote wound r 991.2 Frostbite of foot
r Tissue plasminogen activator (tPA) may improve
healing.
tissue perfusion and reduce amputations if
administered within 24 hr (1,2): PROGNOSIS
r Favorable prognostic factors are early sensation to PEARLS AND PITFALLS
Pediatric dosing has not been established.
Administered in conjunction with heparin infusion pinprick, clear blebs, and normal skin color after r Pearls:
Precaution: Potential for catastrophic hemorrhage rewarming. Avoid rewarming with dry heat, since temperature
r Poor prognostic factors are nonblanching skin,
if risk factors of bleeding, stroke, or gastric ulcers cannot be regulated and can cause further tissue
r Numerous medical treatments have been suggested persistent cyanotic hue, hemorrhagic blebs, and injury.
but remain investigational and should be frozen-appearing tissue. Always consider tetanus prophylaxis.
administered during inpatient management: r Pitfalls:
COMPLICATIONS
IV heparin to prevent microthrombosis (13) r Wound infections, tetanus, gangrene, and Refreezing after rewarming may worsen outcome.
Reserpine may reduce associated vasospasm (4). septicemia Compartment syndrome may develop during
r Daily hydrotherapy for 3045 min followed by r Tissue loss rewarming.
debridement r Compartment syndrome Rubbing or exercising the affected tissue does not
r Hyperbaric oxygen therapy (5) r Hyperhidrosis increase blood flow and may lead to mechanical
r Neuropathy and reflex sympathetic dystrophy trauma.
SURGERY/OTHER PROCEDURES A common error is premature termination of
r Use debridement of clear blisters; hemorrhagic r Decreased nail or hair growth
rewarming process due to reperfusion pain.
blisters should be left intact. r Premature closure of epiphyses
External rewarming of extremities in a
r Potential for compartment syndrome: r Persistent Raynaud phenomenon hypothermic patient may lead to peripheral
Measurement of compartment pressure r Squamous cell carcinoma development over areas vasodilation and intravascular volume
Emergent fasciotomy previously frostbitten redistribution (rewarming shock) and a
r Amputation and surgical debridement are often subsequent fall in core temperature (afterdrop).
delayed for 23 mo unless wound infection with
sepsis is refractory to treatment.
r Surgical sympathectomy for alleviation
vasospasm-related pain.
421
LWBK822-driver-G LWBK822-Hoffman ch210.xml April 15, 2011 13:23
GANGLION CYST
P. Micky Heinrichs
Alan L. Nager
If larger, it can compress branches of the r Small dorsal ganglions, which may be tender, may
BASICS superficial radial nerve (3). be only palpable in full wrist extension.
Volar ganglions can present with sensory or motor r Occult ganglions may not be palpable but are tender
DESCRIPTION nerve palsy involving the palmar cutaneous branch (3).
r A ganglion cyst is a benign, generally painless, of the median nerve, the median nerve itself, the r Transillumination will confirm that there is clear fluid
fluid-filled mass mainly found at the dorsum of the ulnar nerve, or the deep ulnar motor branch (3). in the ganglion cyst, unless the ganglion is very
wrist near the radiocarpal joint or the volar radial r A high percentage of ganglions resolve small and deep or the patient is dark skinned.
aspect of the wrist (1). spontaneously between 1.5 and 12 mo after
r Ganglion cysts may occur at any tendon sheath appearance. Ganglions rarely persist >2 yr (4,5). DIAGNOSTIC TESTS & INTERPRETATION
throughout the musculoskeletal system, such as the Lab
foot or the ankle (2). ETIOLOGY No lab tests are needed for a ganglion cyst.
r 70% are located at the dorsal wrist, and 75% of Unknown
Imaging
these are connected with the scapholunate joint (3). r A ganglion cyst is a clinical diagnosis, and, in
r While common in adults, wrist ganglia are unusual DIAGNOSIS general, no imaging is required.
and rare in children (4). r Imaging may be helpful in ambiguous cases,
r Colloquial term: Bible Cyst due to the use of the HISTORY
r Complaints about a spontaneously appearing, especially when ganglions cannot be easily palpated
Bible (commonly being the heaviest book in a or patients present with pain (3). US should be the
household) for forceful destruction of the cyst: usually painless, cystic growth almost always
initial imaging modality of choice for suspected
Due to the high recurrence rate and the increased located near a joint capsule or tendon sheath of the
ganglia. It is equally effective as MRI (3) but can be
likelihood of trauma to adjacent structures, this is wrist, the foot, or any other location in the
obtained more readily (although it is more operator
not a recommended procedure. musculoskeletal system
r Occasionally, a specific traumatic event can be dependent).
EPIDEMIOLOGY recalled, but usually there is none (3). DIFFERENTIAL DIAGNOSIS
r Estimated incidence of 10% in patients <20 yr of r The patient may complain of pain secondary to r Any mobile mass that moves with excursion of the
age and 2% in patients <2 yr (1). pressure on the branches of nerves (depending on extensor tendons:
r Pediatric population: Proportion of affected females Ganglion of tendon sheath
location) (3).
to males has been reported as ranging from r Pain can also occur in ganglia of the feet or ankles Tenosynovitis of inflammatory, rheumatoid, or
1.6:14.7:1 (1,2,4). when external pressure is applied (eg, wearing infectious origin
shoes) (2). Extensor digitorum brevis manus muscle belly
PATHOPHYSIOLOGY r Firm mass more radial and slightly more distal:
r Defect in 1 of the joint capsules allowing r Questioning the parent or child should reveal no
fever, erythema, pulsation, bleeding, or drainage. Osteophyte (more common in adult patients)
accumulation of synovial fluid in an outpouching of r Compressible mass: Venous aneurysm
a tendon sheath or joint capsule (1) PHYSICAL EXAM r Pulsating mass: Arterial aneurysms of the radial or
r Depending on the location of the ganglion, pain, r Firm or fluctuant, well-defined, <3 cm mass near a
sensory changes, or nerve palsy may occur when ulnar artery
joint capsule or tendon sheath without skin r Other types of tumors: Lipoma, posterior
nerves or branches of nerves are compressed by the changes, such as redness, warmth, or drainage
ganglion (3): r Most commonly found over the dorsal or volar interosseous neuroma, hamartoma, sarcoma
Dorsal ganglions can cause pain because of aspect of the wrist (3):
pressure on the branches of the posterior Volar ganglia have the highest occurrence rate (4)
interosseous nerve. with a general tendency to develop on the radial
side.
422
GANGLION CYST

Generally, no admission is needed. Thornburg LE. Ganglions of the hand and wrist. J Am
INITIAL STABILIZATION/THERAPY Acad Orthop Surg. 1999;7:231238.
r Treatment is generally not necessary for cysts with Issues for Referral
Consider referral to a surgeon.
minimal symptoms.
r Pain usually suggests pressure on a nerve and CODES
suggests the need for further workup. FOLLOW-UP
r If other structures are involved, further evaluation ICD9
should be pursued (3). FOLLOW-UP RECOMMENDATIONS r 727.41 Ganglion of joint
Follow up with a primary care physician for further r 727.42 Ganglion of tendon sheath
MEDICATION care. r 727.43 Ganglion, unspecified
r NSAIDs:
Ibuprofen 10 mg/kg/dose PO q6h PRN PROGNOSIS
Naproxen 5 mg/kg PO q8h PRN Most ganglions resolve spontaneously within 1 yr
r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN (4,5). PEARLS AND PITFALLS
COMPLICATIONS r Pearls:
Closed rupture, either by firm massage or trauma to Testing is generally not necessary for diagnosis.
THERAPIES
the area, often leads to recurrence of the ganglia. Any painful swelling that does not fit the
Injection of triamcinolone acetonide as an outpatient
has been found to reduce recurrence. description of a ganglion should trigger a more
REFERENCES extensive evaluation.
SURGERY/OTHER PROCEDURES US is the study of choice for further evaluation.
r Surgery, in general, is not required with initial r Pitfall:
1. Colberg RE, Sanchez CF, Lugo-Vincente H.
ganglion cyst presentation. Aspiration and triamcinolone acetonide injection of Ganglion cyst in a patient who has fever,
r Surgical referral can be considered for:
wrist synovial cysts in children. J Pediatr Surg. erythema, pulsation, bleeding, or drainage is
Atypical ganglions 2008;43:20872090. highly unlikely.
Ganglions that cause pain 2. MacKinnon AE, Azmy A. Active treatment of
Ganglions that do not resolve within 1 yr (6) ganglia in children. Postgrad Med J. 1977;53(621):
r Upon referral:
378381.
Surgical aspiration of the fluid can be helpful in
the short term (1), but there is a high risk of
3. Cardinal E, Buckwalter KA, Braunstein EM, et al.
Occult dorsal carpal ganglion: Comparison of US
G
recurrence (up to 43%) after aspiration (1,2). and MR imaging. Radiology. 1994;193:259262.
There is an additional risk of injury to the 4. Wang AA, Hutchinson DT. Longitudinal observation
underlying structures (radial artery or palmar of pediatric hand and wrist ganglia. J Hand Surg.
cutaneous branch of the median nerve) (4,5). 2001;26(4):599602.
Excision surgery accompanied by removal of the
5. Rosson JW, Walker G. The natural history of ganglia
tract that extends into the joint is curative.
in children. J Bone Joint Surg Br. 1989;71(4):
707708.
6. Calif E, Stahl S, Stahl S. Simple wrist ganglia in
children: A follow-up study. J Pediatr Orthop B.
2005;14(6):448450.
423
GASTRITIS
Sabina Zavolkovskaya
r Physiologic stress: DIAGNOSTIC TESTS & INTERPRETATION

BASICS Sepsis Lab
Major trauma, head injury (Cushing ulcer), surgery Initial Lab Tests
DESCRIPTION Organ failure Testing is usually not necessary. Consider the
r Gastritis is best defined as injury-induced Severe burns (Curling ulcer) following selectively:
inflammation of the gastric mucosa leading to r Drug induced: r Stool testing for blood
epithelial cell damage and regeneration. Aspirin r Hemoglobin or CBC to rule out anemia
r Gastritis is often used loosely to describe epigastric NSAIDs r H. pylori identification (46):
pain, dyspepsia, mucosal irregularity, or swelling on Steroids
radiograph images: Noninvasive:
Antibiotics Urea breath test
Gastritis is neither a clinical nor a radiologic Valproate Stool antigen testing
diagnosis. Iron
r Ethanol Serum IgG antibody
Gastritis is most accurately a histologic diagnosis
characterized by the presence of inflammatory r Caffeine Invasive:
Biopsy urease test
cells. r Allergic: Brush cytology
r Gastritis is often confused with gastropathy,
Allergic enteropathy Histologic staining with a Warthin-Starry silver
which is epithelial damage and regeneration of the Milk protein allergy stain, a modified Giemsa or a Cresyl violet stain
gastric mucosa without associated inflammation r Crohn disease Culture (recommended for refractory disease to
(1,2). r Less common causes: identify antibiotic susceptibility)
EPIDEMIOLOGY Radiation Imaging
One of most common GI diagnoses Eosinophilic gastritis r Imaging is generally not necessary.
Incidence Ingestion of corrosive agents r Abdominal upright or cross-table lateral radiographs
r True incidence is unknown. Menetrier disease (hypertrophic gastritis)
to detect free abdominal air (if perforation is
r Accounts for 1.82.1 million visits to physician Autoimmune (atrophic) gastritis
suspected)
Collagenous gastritis
offices each year Diagnostic Procedures/Other
r More common in adults than in children Zollinger-Ellison syndrome
Vascular injury Upper GI endoscopy with biopsies from different
Prevalence Direct trauma (eg, NG tube) gastric topographic zones
r 8 in 1,000 people r Idiopathic r Gold standard for diagnosis
r Increases with age (2,3) r Most sensitive test
r Helicobacter pylori (as one of the causes of COMMONLY ASSOCIATED CONDITIONS r Provides histologic evidence of mucosal
r H. pylori
gastritis): r Autoimmune diseases: inflammation
In developed countries: Isolated in <10% in
Crohn disease Pathological Findings
children <10 yr of age r Erythematous mucosa
In developing countries: As high as 80% in r Atopic mucosa
children <10 yr of age DIAGNOSIS r Ulcers or erosions
RISK FACTORS HISTORY r Mucosal petechiae or hemorrhage
r Infectious: Poor hygiene, developing nations, r Epigastric pain or discomfort, often postprandial r Enlarged gastric rugae
immunocompromised states r Decreased appetite r Nodules
r H. pylori: Poor socioeconomic conditions, bed
r Weight loss r Inflammatory cells on histologic evaluation
sharing, large sibships (3) r Bloating
GENERAL PREVENTION r Irritability DIFFERENTIAL DIAGNOSIS
r GERD
r Improving hygiene r Nausea r Peptic ulcer disease
r Stress reduction r Vomiting, often postprandial r Idiopathic (nonulcer dyspepsia)
r Avoidance of NSAIDs, caffeine, alcohol r Coffee-ground emesis or hematemesis r Functional abdominal pain
PATHOPHYSIOLOGY r Diarrhea r Inflammatory bowel disease
Imbalance between cytotoxic (acid, pepsin, certain r Melena r Biliary tract disorders
medications, bile acids, and infection) and r Midsternal chest pain r Pancreatitis
cytoprotective factors (the mucous layer, local r Genitourinary pathology (eg, renal stones, infection)
bicarbonate secretion, and mucosal bloodflow) in the PHYSICAL EXAM
r Epigastric tenderness
upper GI tract leads to injury to the gastric mucosa r Normal bowel sounds
with associated inflammation (4):
r May result from local effects at the gastric mucosa r Melena or hematochezia
r Heme-positive stool
or from systemic diseases or processes
r Pallor
ETIOLOGY
r Infectious:
Bacterial (most commonH. pylori)
Viral
Mycobacterial
Syphilitic
Parasitic
Fungal
424
GASTRITIS
Discharge Criteria 4. Oderda G, Rapa A, Bona G. Diagnostic tests for

r Normal hemoglobin or CBC if obtained
TREATMENT r Heme-positive stool with stable vital signs
childhood Helicobacter pylori infection: Invasive,
noninvasive or both? J Pediatr Gastroenterol Nutr.
General goals of treatment: r Adequate pain control 2004;39(5):482484.
r Stabilization of patient r Adequate PO intake 5. Gold BD. Current therapy for Helicobacter pylori
r Elimination of offending agents r Adequate hydration status infection in children and adolescents. Can J
r Symptomatic treatment Gastroenterol. 1999;13(7):571579.
Issues for Referral 6. Gold BD, Colletti RB. Medical position statement:
r Etiology-specific treatment (eg, Crohn disease, Gastroenterology referral for suspected H. pylori The North American Society for Pediatric
H. pylori, fungal) infection or significant/persistent symptoms Gastroenterology and Nutrition. Helicobacter pylori
PRE HOSPITAL infection in children: Recommendations for
Assess and stabilize airway, breathing, and FOLLOW-UP diagnosis and treatment. J Pediatr Gastroenterol
circulation. Nutr. 2000;31:490497.
r Fluid resuscitation in case of upper GI hemorrhage Discharge instructions:
r Pain management r Avoidance of inciting agent (eg, NSAIDs, ethanol, ADDITIONAL READING
r NPO etc.) r Agarwal K. Helicobacter pylori vaccine: From past to
r Take medications as prescribed.
r Withdrawal of offending agent future. Mayo Clin Proc. 2008;83(2):169175.
r Return if persistence or worsening of symptoms. r Chelimsky G, Czinn S. Peptic ulcer disease in
MEDICATION children. Pediatr Rev. 2001;22:349355.
Patient Monitoring
First Line r Compliance with treatment regimen r Rowland M, Bourke B, Drumm B. Gastritis. In Walker
r H. pylori gastritis (5,6):
r Symptom resolution WA, Kleinman RE, Sherman PM, et al., eds. Pediatric
Triple therapy (714 day course): Gastrointestinal Disease: Pathophysiology,
Proton pump inhibitor (PPI) plus amoxicillin (50 DIET Diagnosis, Management. 4th ed. Vol. 1. Shelton,
mg/kg/day up to 1 g b.i.d.) plus clarithromycin r Avoidance of ethanol, caffeine, tobacco
CT: PMPH; 2004.
(15 mg/kg/day up to 500 mg b.i.d.) r Bland diet with milk is no longer recommended.
PPI plus amoxicillin plus metronidazole See Also (Topic, Algorithm, Electronic
(20 mg/kg/day up to 500 mg b.i.d.) PROGNOSIS Media Element)
r There are significant relapse rates for children who r Colitis
PPI plus clarithromycin plus metronidazole
r Gastroesophageal Reflux
r Other gastritis: remain infected with H. pylori or are inadequately
treated. r Pain, Abdomen
G
H2 antagonists: r Reinfection rate is 22.4% in children >5 yr of age
Cimetidine 2040 mg/kg/day up to 400 mg
b.i.d. COMPLICATIONS
Famotidine 11.2 mg/kg/day up to 20 mg b.i.d. r Bleeding CODES
Ranitidine 24 mg/kg/day up to 150 mg b.i.d. r Anemia
Second Line r Failure to thrive ICD9
r H. pylori gastritis (4,6): r Gastric carcinoma r 041.86 H. pylori infection
r Mucosa-associated lymphoid tissue (MALT) r 535.00 Acute gastritis (without mention of
Quadruple therapy:
Bismuth subsalicylate 1 tablet (262 mg) or lymphoma hemorrhage)
15 mL (17.6 mg/mL) q.i.d. plus PPI plus r Corrosive gastritis: r 535.50 Unspecified gastritis and gastroduodenitis
metronidazole plus amoxicillin or clarithromycin Latent strictures and outlet obstruction (without mention of hemorrhage)
or tetracycline (for children 12 yr of age:
50 mg/kg/day up to 1 g b.i.d.) Pregnancy Considerations
r Treatment for H. pylori gastritis should be initiated
Ranitidine bismuth/citrate 1 tablet q.i.d. plus PEARLS AND PITFALLS
clarithromycin plus metronidazole after pregnancy and breast-feeding because some of
r Other gastritis: the recommended medications are relatively r H. pylori infects at least 50% of the worlds human
PPIs: contraindicated. population, but most people are asymptomatic.
r In most children, the presence of H. pylori infection
Lansoprazole 0.81.5 mg/kg/day up to 30 mg Some antimicrobials (clarithromycin, tetracycline)
b.i.d. have harmful effects on the fetus. does not lead to clinically apparent disease, even
Omeprazole 0.81 mg/kg/day up to 20 mg b.i.d. r H2 receptor antagonists (eg, cimetidine, ranitidine, when the organism colonizing the gastric mucosa
Cytoprotective agent: famotidine) and lansoprazole are safe for use in causes chronic active gastritis.
Sucralfate 4080 mg/kg/day up to 1 g q.i.d. r The decision to treat H. pyloriassociated gastritis
pregnancy.
without duodenal or gastric ulcer is subject to the
DISPOSITION judgment of the clinician and deliberations with the
Admission Criteria
r Inadequately controlled pain in the outpatient
REFERENCES patient and family.
r Antibiotic resistance is a growing problem that
setting 1. Hassal E. Getting to grips with gastric pathology. interferes with eradication of H. pylori.
r Persistent vomiting J Pediatr Gastroenterol Nutr. 2002;34(S1): r Noncompliance is a major cause for eradication
r Inability to tolerate PO S46S50.
failure of H. pylori.
r Critical care admission criteria: 2. Dohil R, Hassall E. Gastritis and gastropathy of
Active upper GI bleeding with unstable vital signs childhood. J Pediatr Gastroenterol Nutr. 1999;
(eg, hypotension) 29(4):378394.
3. Feidorec SC, Malaty HM, Evans DL, et al. Factors
influencing the epidemiology of Helicobacter pylori
infection in children. Pediatrics. 1991;88:578582.
425
GASTROENTERITIS
Carla Maria P. Alcid
PATHOPHYSIOLOGY
BASICS r Infection acquired through the fecaloral route by DIAGNOSIS
direct person-to-person contact or by ingestion of
DESCRIPTION contaminated food and water: HISTORY
r Gastroenteritis (GE) refers to: r Clinical spectrum ranges from asymptomatic to
Presence of preformed toxins (Bacillus cereus)
Infections of the GI tract caused by bacteria, Production of enterotoxins: Enteroinvasive severe symptoms, dehydration, and death.
viruses, or parasites r Assess the onset, frequency, and quantity of both
Escherichia coli (EIEC), enterotoxigenic Escherichia
Noninfectious causes of inflammation of the GI coli (ETEC) vomiting and diarrhea.
tract secondary to drugs and toxins Direct invasion of intestinal mucosa (villi surface r Determine the character, such as the presence of
r The majority are foodborne illnesses. destruction by viruses; wall adherence by bile, blood, or mucus.
r GE most commonly manifests as nausea, vomiting, parasites) r Note most recent oral intake, including quantifying
diarrhea, abdominal pain, and cramping. r Noninfectious: breast milk and other food or fluids.
r Usually the presence of vomiting and diarrhea, Chemical toxins most often found in food r Elicit a most recent preillness weight and amount of
together with a detailed history and physical exam (especially seafood), heavy metals, antibiotics, and urine output.
excluding other serious illnesses, constitute a other medications r Note presence of other associated symptoms such
diagnosis of acute GE. Toxins adhere to the intestinal wall, causing as fever, mental status changes, and presence of
irritation and swelling, which leads to water, rashes, as it may signify more serious disease.
EPIDEMIOLOGY mucus, or blood to leak from the wall of the r Past medical history should include any underlying
Incidence intestine. illnesses or recent medical problems.
r In the U.S., GE accounts for >1.5 million pediatric
ETIOLOGY r Include a list of medications and presence of any
outpatient visits and 200,000 hospitalizations r Viruses cause the majority of GE:
annually: immunodeficiency (HIV).
Rotavirus r Social history should include day care exposures and
There are 300 deaths per year.
r Worldwide, the WHO estimates >700 million Noroviruses and other caliciviruses presence of outbreaks in the community.
Hepatitis A r Recent travel should also be documented, including
episodes of diarrhea annually in children <5 yr of
age in developing countries (1): Astroviruses, adenoviruses, parvoviruses travel on cruise ships (noroviruses).
r Bacterial infections:
Globally, death estimates are 1.8 million deaths PHYSICAL EXAM
per year. Salmonella species, Shigella, Yersinia r Body weight and vital signs:
enterocolitica, Campylobacter species,
Prevalence Tachycardia is an early sign of dehydration.
r Accounts for 3% pediatric office visits and 10% Staphylococcus aureus, Bacillusacute food
Deep respirations suggest metabolic acidosis.
poisoning r Assess mental status for listlessness or
hospitalizations in children <5 yr of age EIEC, ETEC
r Attack rate ranges from 0.51.9 illnesses per person inconsolability.
Less commonly: Listeria, Clostridium species r Note presence or absence of tears, sunken eyes, or
annually and is higher in the 1st 23 yr of life: Vibrio cholera: Most common etiology in
2.55 illnesses per child in day care developing countries dry mucous membranes and the appearance of the
r Parasitic infections: lips, mouth, and tongue.
RISK FACTORS r Absence of bowel sounds can indicate an ileus,
r Poor hygiene Giardia lamblia, Entameoba histolytica: Mostly
r Young age (<6 mo) from uncooked foods signifying hypokalemia.
r Severe abdominal pain and tenesmus indicate
r Prematurity Toxoplasma; Cryptosporidium, Trichinella species:
r Presence of an immunodeficiency Less common involvement of the large intestines and rectum.
r Noninfectious agents: r Periumbilical pain with watery diarrhea indicates
r Malnutrition
Heavy metals small bowel involvement.
r Coexisting infection r General perfusion of the extremities helps assess the
r Lack of exclusive or predominant breast-feeding in Mushrooms (toxins)
Nitrites and pesticides level of dehydration.
small infants Fish and shellfish poisoning (scombroid, ciguatera r Delayed capillary refill and prolonged skin tenting
GENERAL PREVENTION toxins, tetrodotoxins) may be helpful clues to assess hydration.
r Strict hand hygiene with improvement in water and Antibiotics and other medications
sanitation facilities COMMONLY ASSOCIATED CONDITIONS
r Contact tracing and source identification to prevent Lab
r Poverty r Not necessary for diagnosis but may be helpful to
outbreaks from occurring r Poor environmental hygiene assess dehydration and identify etiology or
r Immunization may prevent rotavirus, some r Childs delayed developmental status complications
salmonella, and hepatitis A r Assess serum electrolytes if there is possibility of
r Proper cleaning and complete cooking of all meals,
dehydration or oral intake suggests potential
especially meats and vegetables abnormalities.
r Consider stool studies selectively:
If there is concern for acute bacterial diarrhea,
stool for WBCs may reveal >5 WBC/hpf.
Rotavirus is identified on electron microscopy or
rapid ELISA.
Stool for ova and parasites
r CBC, urine studies, and blood cultures may be
indicated in the context of sepsis.
r Clostridium difficile testing for patients with recent
antibiotic use
426
GASTROENTERITIS
r Procalcitonin has been suggested as a diagnostic r Bismuth subsalicylate (Kaopectate) (antiemetic and
REFERENCES
marker for bacterial GE but has not been helpful (2). antidiarrheal):
r C-reactive protein (CRP) has also been studied as a 100 mg/kg/day divided in 5 equal doses, max 1. King CK, Glass R, Bresee JS, et al. Managing acute
biologic marker (CRP >95 mg/L in 1st 48 hr single dose 4 g/day gastroenteritis among children: Oral rehydration,
suggests bacterial disease) and may serve as a maintenance, and nutritional therapy. MMWR
COMPLEMENTARY & ALTERNATIVE Recomm Rep. 2003;52(RR-16):116.
useful predictor of bacterial GE in children (3).
THERAPIES 2. Thia KT, Chan ES, Ling KL, et al. Role of
Imaging r Zinc supplementation reduces the incidence,
procalcitonin in infectious gastroenteritis and
Not generally warranted unless the possibility of a duration, and recurrence of diarrhea: inflammatory bowel disease. Dig Dis Sci.
surgical abdomen exists (obstruction, appendicitis, <6 mo of age: 10 mg/day 2008;53(11):29602968.
volvulus, or intussusception) >6 mo: 20 mg/day
r Probiotic (Lactobacillus, Bifidobacterium) bacteria to 3. Marcus N, Mor M, Amir L, et al. The quick-read
DIFFERENTIAL DIAGNOSIS C-reactive protein test for the prediction of
r Non-GI illnesses, including meningitis, sepsis, prevent/reduce diarrhea bacterial gastroenteritis in the pediatric emergency
pneumonia, otitis media, and urinary tract infections DISPOSITION department. Pediatr Emerg Care. 2007;23(9):
r Isolated vomiting can be the initial manifestation of 634637.
Admission Criteria
a metabolic disorder, CHF, toxic ingestions, r Severely dehydrated patients 4. Freedman SB, Adler M, Seshadri R, et al. Oral
intracranial injury, or trauma. r Moderately dehydrated patients unable to take ondansetron for gastroenteritis in a pediatric
adequate oral rehydration fluids emergency department. N Engl J Med. 2006;354:
r Consider admission for the following: 16981705.
TREATMENT 5. Rossignol JF, Abu-Zekry M, Hussein A, et al. Effect
Severe metabolic acidosis
Abnormal serum sodium (high or low) of nitazoxanide for treatment of severe rotavirus
Most GE can be effectively managed at home with diarrhea: Randomized, double-blind, placebo
oral rehydration solutions. Abnormal or changing mental status
controlled trial. Lancet. 2006;368(9530):124129.
Discharge Criteria
PRE HOSPITAL r Normal vital signs
r Ability to tolerate oral fluids ADDITIONAL READING
circulation. r Follow up with the primary care provider.
r Administer fluid bolus as necessary for dehydration.
r Reliable caregivers who can provide adequate care Salvatore S, Hauser B, Devreker T, et al. Probiotics and
INITIAL STABILIZATION/THERAPY at home zinc in acute infectious gastroenteritis in children: Are
r Initial assessment must focus on hydration status they effective? Elsevier. Nutrition. 2007;23:498506.
and presence of any toxicity. Issues for Referral
r If concern exists for other possible illnesses that may See Also (Topic, Algorithm, Electronic G
r IV rehydration with isotonic fluids boluses
complicate the clinical course Media Element)
(20 mL/kg) r Any social concerns that might prevent returning for r Dehydration
r See Dehydration topic for further management. r Diarrhea
evaluation
r Vomiting
MEDICATION
First Line FOLLOW-UP
r Expired American Academy of Pediatrics practice
guideline previously recommended no FOLLOW-UP RECOMMENDATIONS CODES
antiemetic/antidiarrheal use in children <5 yr of age. r Discharge instructions and medications:
r Ondansetron (antiemetic) (4): Early feeding with age-appropriate diet ICD9
0.15 mg/kg PO or IV r Activity: r 005.9 Food poisoning, unspecified
r Antibiotics not typically useful but may be useful for No restrictions once able to tolerate oral feeds r 009.0 Infectious colitis, enteritis, and gastroenteritis
specific pathogens: r 558.9 Other and unspecified noninfectious
Patient Monitoring
Shigellosis: Trimethoprim/Sulfamethoxazole at If patient is discharged home, strict instructions on gastroenteritis and colitis
810 mg/kg trimethoprim dosing PO divided criteria to return, such as inability to tolerate oral feeds
b.i.d., if susceptible or decreased urine output
Campylobacterif severe: PEARLS AND PITFALLS
Erythromycin 3050 mg/kg/day PO divided DIET
r Overly restricted diets should be avoided. r Obtain appropriate stool cultures early in the course
b.i.d.q.i.d. for 5 days OR
Ciprofloxacin 2030 mg/kg/day PO divided b.i.d. r Lactose-free formulas can be used in infants if of the disease in children with bloody diarrhea and
G. lamblia or E. histolytica: lactose malabsorption is of concern. suspected HUS.
Metronidazole 15 mg/kg/day PO divided t.i.d. r Avoid carbonated drinks or juices with a high r Early nutritional support is key in successful
AND concentration of simple carbohydrates. management of the majority of cases of GE.
Iodoquinol 3550 mg/kg/day PO divided t.i.d. r Breast-fed infants should nurse ad libitum. r Lower osmolality oral rehydration fluids are more
to prevent spread of the disease effective in reducing stool output.
Rotavirus GE has sometimes been effectively PROGNOSIS r The practice of withholding food for >24 hours
controlled with nitazoxanide (5). Good prognosis when early therapy is instituted and should be avoided.
no concurrent illnesses are present
Second Line
r Metoclopramide (antiemetic): COMPLICATIONS
r Bacteremia, urinary tract infection, vaginitis,
0.1 mg/kg IV/PO, max single dose 10 mg
If metoclopramide is given IV, administer as piggy endocarditis, meningitis, pneumonia, hepatitis, soft
back with normal saline over >30 min to prevent tissue infections (especially Salmonella)
akathisia. r Guillain-Barre syndrome from Campylobacter
r Loperamide (antidiarrheal): infection
68 yr (2030 kg): 2 mg PO b.i.d. r Hemolytic uremic syndrome (HUS) from Shigella
912 yr (>30 kg): 2 mg PO t.i.d. dysenteriae 1 or E. coli 0157:H7
Adolescent/Adult (>45 kg): 4 mg PO initial dose, r Hemolytic anemia from Campylobacter and Yersinia
then 2 mg/dose each stool, max single dose r Reactive arthritis and glomerulonephritis from
16 mg/day Shigella, Campylobacter, and Yersinia
427
GASTROESOPHAGEAL REFLUX
Sandra L. Grossman
r GER becomes GERD when there are disturbances in r Consider causes other than GER when the following
BASICS protective mechanisms: occur in the vomiting infant (2):
Delayed gastric emptying Forceful vomiting
DESCRIPTION Abnormal epithelial repair Bilious vomiting
r Gastroesophageal reflux (GER) is the retrograde Insufficient clearance and buffering of refluxate Onset of vomiting after 6 mo of life (GER most
passage of gastric contents into the esophagus. Decreased neural protective reflexes of commonly manifests prior to this age.)
r GER is a normal physiologic process, occurring aerodigestive tract GI bleeding (hematochezia, hematemesis)
several times per day in healthy infants, children, Failure to thrive
ETIOLOGY
and adults. r GER is a normal physiologic process. Diarrhea
r In healthy people, most episodes of GER occur in the Constipation
r GERD is due to LES incompetence as a result of loss
postprandial period, last <3 min, and cause few or Lethargy
of tone or recurrent inappropriate transient Hepatosplenomegaly
no symptoms.
r Gastroesophageal reflux disease (GERD) occurs relaxation. Seizures
when clinical symptoms result from GER. Fever
r GERD is usually minimally symptomatic but must be DIAGNOSIS Genetic/Metabolic disorders
distinguished from life-threatening causes of Micro-/Macrocephaly
r In the infant presenting before 6 mo of age with Bulging fontanelle
vomiting.
uncomplicated emesis, a thorough history and Abdominal distension/tenderness
EPIDEMIOLOGY physical should be adequate to make the diagnosis.
r This is also true for verbal older children presenting PHYSICAL EXAM
Incidence r Normal physical exam
r 4067% of healthy full-term infants (1)
with typical heartburn symptoms (substernal, r Significant GERD may lead to dental erosions.
r >50% of children with moderate to severe burning chest pain) and regurgitation. r Dystonic torso/head posturing (Sandifer syndrome)
neurologic disorders/developmental delay r There is no symptom or symptom complex in infants
is a specific manifestation of GERD.
Prevalence and toddlers that is diagnostic of GERD or predicts r Unlikely GERD if the following are present:
r 50% of infants 03 mo of age (2) response to therapy:
Appears malnourished
r 67% of infants 4 mo of age However, the presence of the bothersome
Decreased activity level
r 5% of infants 1012 mo of age signs/symptoms associated with GER often leads
Evidence of dehydration
r 1.48.2% of children 317 yr of age to the clinical diagnosis of GERD in infants and
Hypotonia
children.
Abnormal respiratory or abdominal exam
RISK FACTORS HISTORY
r Asthma DIAGNOSTIC TESTS & INTERPRETATION
r Effortless, painless vomiting is the most common
r Neurologic disorders (eg, cerebral palsy) Imaging
historical feature in healthy-appearing
r Obesity Indicated to investigate other sources of vomiting,
infants/children.
r Smoking r Vomiting, recurrent abdominal pain, and/or chest based on history and physical exam
r Caffeine use pain are more common features in adolescents and DIFFERENTIAL DIAGNOSIS
r Pregnancy adults. r Other sources of vomiting (2):
r Cystic fibrosis r Signs and symptoms associated with GER are GI obstruction (pyloric stenosis, foreign body,
r Repaired esophageal atresia or achalasia nonspecific. Not all children with GER have these malrotation/volvulus, intermittent intussusception,
r Other congenital esophageal disease symptoms, which can be caused by conditions other gastric outlet obstruction)
r Chronic lung disease than GER. Other GI (pancreatitis, cholelithiasis, appendicitis,
r Premature birth r Signs/Symptoms associated with GER: gastritis/peptic ulcer disease)
r Lung transplant Recurrent regurgitation with or without vomiting Toxins (iron, lead, caffeine, theophylline,
r Hiatal hernia Weight loss and poor weight gain medications)
Choking, gagging, arching during or after feeds Infection (gastroenteritis, Helicobacter pylori,
r Family history of GERD, Barrett esophagus, or
Feeding refusal urinary tract infection, pneumonia, hepatitis,
esophageal adenocarcinoma Irritability (infants) meningitis, sepsis)
PATHOPHYSIOLOGY Chest pain or heartburn Neurologic (intracranial bleed or mass lesion,
r Multifactorial process that involves airway Dysphagia, odynophagia intracranial injury, migraine)
responsiveness, acidity, frequency of reflux events, Cough, wheezing, stridor, or hoarseness Renal (uremia, nephrolithiasis)
and esophageal clearing mechanisms (2,3) Apnea spells Cardiac (CHF)
r Occurs during the spontaneous transient relaxation Apparent life-threatening event (ALTE) Endocrine (congenital adrenal hyperplasia,
r Other historical features associated with GER: adrenal insufficiency)
of the lower esophageal sphincter (LES)
unaccompanied by swallowing Past history of prematurity, surgery, asphyxia, Metabolic (urea cycle defects, aminoacidopathies)
r Increased intra-abdominal pressure may contribute neurologic/respiratory disease, atopic Food intolerance (celiac disease, milk/soy protein
r Vomiting associated with GER is due to stimulation dermatitis/other allergy symptoms allergy)
Tobacco, alcohol use Pregnancy
of pharyngeal sensory afferents by refluxed gastric Eating disorder
contents. Family history of GERD
r Other sources of chest pain:
Cardiac
Other GI (eosinophilic esophagitis, gastritis/peptic
ulcer disease)
428
GASTROESOPHAGEAL REFLUX
Respiratory (pneumothorax, asthma, pneumonia) Avoidance of caffeine, spicy food, high-fat food, REFERENCES
Costochondritis acid-containing food (eg, tomato sauce),
Mass carbonated beverages, chocolate, and alcohol if 1. Gold BD, Freston JW. Gastroesophageal reflux in
r If presence of dysphagia, need to consider: they provoke symptoms children: Pathogenesis, prevalence, diagnosis, and
Eosinophilic esophagitis Consume smaller, more frequent meals. roleof proton pump inhibitors in treatment. Pediatr
Stricture Avoid eating late at night. Drugs. 2002;4(10):673685.
Achalasia r Positioning therapy: 2. Vandenplas Y, Rudolph CD, Di Lorenzo C, et al.
Infants: Prone position (NOT endorsed by the Pediatric gastroesophageal reflux clinical practice
American Academy of Pediatrics [5]); upright guidelines: Joint Recommendations of the North
TREATMENT position American Society of Pediatric Gastroenterology,
Children and adolescents: Sleeping in left lateral Hepatology, and Nutrition and the European
INITIAL STABILIZATION/THERAPY decubitus position with elevation of the head of Society of Pediatric Gastroenterology, Hepatology,
r For infants who are healthy, feeding well, thriving,
the bed (2) and Nutrition. J Pediatr Gastroenterol Nutr.
and not excessively fussy, treatment is directed 2009;49(4):498547.
toward parental education and reassurance. SURGERY/OTHER PROCEDURES
r If diagnosed with GERD, consider: 3. Orenstein SR, McGowan JD. Efficacy of conservative
For children with persistent reflux refractory to
therapy as taught in the primary care setting for
Conservative management (lifestyle changes) maximal medical therapy or those with severe
symptoms suggesting infant gastroesophageal
Medication complications of GERD (1,2,4):
r Nissen fundoplication (open and laparoscopic) reflux. J Pediatr. 2008;152(3):310314.
Surgery 4. Shepherd RW, Wren J, Evans S, et al.
r Total esophagogastric dissociation (children with
MEDICATION Gastroesophageal reflux in children. Clinical profile,
Duration of therapy is variable depending on the neurologic impairment or other conditions causing course, and outcome with active therapy in 126
patient and practitioner. life-threatening aspiration during oral feedings) cases. Clin Pediatr (Phila). 1987;26(2):5560.
r Endoluminal endoscopic gastroplication
First Line 5. Task Force on Sudden Infant Death Syndrome.
r H2 blockers to reduce acid reflux, improve DISPOSITION Policy statement: The changing concept of sudden
symptoms, and aid in healing esophageal Discharge Criteria infant death syndrome: Diagnostic coding shifts,
mucosa: r Should be discharged home if the history and controversies regarding the sleeping environment,
Ranitidine (Zantac): PO: 410 mg/kg/day divided physical exam clearly suggests GER or GERD and new variables to consider in reducing risk.
b.i.d, max 300 mg/day; IV/IM: 24 mg/kg/day r For the most part, only parental education, Pediatrics. 2005;116(5):12451255.
divided q68h, max 200 mg/day; adult anticipatory guidance, and feeding modifications 6. Campanozzi A, Boccia G, Pensabene L, et al.
dosePO: 150 mg b.i.d. or 300 mg qhs; IM/IV:
50 mg/dose q68h, max 400 mg/day
(composition, frequency, and volume) are necessary Prevalence and natural history of gastroesophageal
reflux: Pediatric Prospective Survey. Pediatrics.
G
for the management of uncomplicated infant GERD
Famotidine (Pepcid): 112 yrs of age: 1 mg/kg/day (2). 2009;123:779783.
PO/IV divided b.i.d., max 80 mg/day; >12 yr:
Issues for Referral
2040 mg PO/IV b.i.d. r Uncomplicated GER can be easily managed by
Cimetidine (Tagamet): 2040 mg/kg/day PO/IM/IV
ADDITIONAL READING
general pediatricians (2). r Grossman AB, Liacouras CA. Gastroesophageal
divided t.i.d.q.i.d.; adult dose: 8001,200 mg r Consider referring to gastroenterologist if:
PO/IM/IV b.i.d.t.i.d. reflux. In: Liacouras CA, Piccoli DA, eds. Pediatric
r Proton pump inhibitors: The most effective Symptoms worsen or do not resolve by 1218 mo
of age Gastroenterology: The Requisites in Pediatrics.
medications for acid suppression; work best when Philadelphia, PA: Mosby Elsevier; 2008:7485.
Signs/Symptoms of significant GERD develop r Michail S. Gastroesophageal reflux. Pediatr Rev.
administered 1530 min before a meal. Not
approved for use in infants <1 yr of age: 2007;28:101110.
Omeprazole (Prilosec): 12 mg/kg/day PO divided FOLLOW-UP
daily b.i.d.; adult dose: 2040 mg PO daily
Lansoprazole (Prevacid): 10 kg: 7.5 mg PO daily; FOLLOW-UP RECOMMENDATIONS CODES
1130 kg: 15 mg PO dailyb.i.d.; >30 kg: 30 mg r Reassurance, parental education, anticipatory
PO daily-b.i.d.; adult dose: 1530 mg PO/IV daily guidance
r Instructions on dietary/lifestyle changes ICD9
Esomeprazole (Nexium): 111 yr of age: 10 mg
r Follow up with primary care provider. 530.81 Esophageal reflux
PO/IV daily; 12 yr: 2040 mg PO/IV daily
r Prokinetic agents: Potential adverse effects PEARLS AND PITFALLS
Resolves spontaneously in most by 1 yr of age and
outweigh the potential benefits of treatment: almost all by 2 yr of age. In full-term infants, r All that vomits is not reflux.
Metoclopramide (Reglan): 0.10.2 mg/kg/dose symptoms disappear (6): r A thorough history and physical exam is usually
PO/IM/IV q.i.d., max single dose 0.8 mg/kg/day; r In 55% by 10 mo of age
adult dose: 1015 mg PO/IM/IV qac and qhs sufficient to make the diagnosis of GER or GERD.
r In 81% by 18 mo of age r Parental education, anticipatory guidance, and
Associated with extrapyramidal reactions r In 98% by 2 yr of age
(dystonia, oculogyric crisis, tardive dyskinesia) reassurance are necessary and usually sufficient to
r Antacids PO (magnesium hydroxide, calcium COMPLICATIONS manage healthy, thriving infants with uncomplicated
carbonate, aluminum hydroxide); may be used for r Erosive esophagitis GER.
symptomatic relief but not for chronic therapy r Esophageal stricture
r Barrett esophagus
COMPLEMENTARY THERAPY
r Dietary changes (14):
Formula changes usually do not improve
symptoms in GERD.
If milk protein sensitivity/allergy: A 24 wk trial of
an extensively hydrolyzed protein formula may be
beneficial.
Thickened feeds with rice cereal (helps with visible
emesis but no measurable decrease in frequency
of esophageal reflux episodes)
429
GASTROINTESTINAL BLEEDING: LOWER

Matthew Lee Hansen
Garth Meckler
r Infants: Hirschprung disease, anal fissure, allergic PHYSICAL EXAM

BASICS colitis, intussusception, Meckel diverticulum, r Careful documentation of vital signs, especially
intestinal duplication, infectious colitis, vascular heart rate and BP will help identify life-threatening
DESCRIPTION malformations hemorrhage.
r Lower GI bleeding is defined as bleeding distal to r Children: Juvenile polyps, anal fissures, HSP, r Fever, poor skin turgor, delayed capillary refill, dry
the ligament of Treitz. infectious colitis, Meckel diverticulum, hemolytic mucous membranes, and tachycardia may indicate
r Lower GI bleeding is usually bright red in color, uremic syndrome, inflammatory bowel disease dehydration in infectious diarrhea.
though it may present with maroon or black tarry r A careful anorectal exam is essential to identify
stools (melena). COMMONLY ASSOCIATED CONDITIONS
r Food allergy fissures, which most commonly are found at the
EPIDEMIOLOGY r Eczema posterior aspect of the anus. A digital rectal exam
should be performed if stool is not available for
Incidence
inspection and occult blood testing.
Exact incidence in children is unknown; however, r Anoscopy may be useful to identify distal polyps or
lower GI bleeding is a common problem in children. DIAGNOSIS
internal hemorrhoids.
Prevalence HISTORY r Abdominal exam may reveal distention or
The prevalence is unknown. r The typical history is that of passage of bright red
tenderness, which could indicate a more serious
blood per rectum (hematochezia), though patients etiology such as perforation or volvulus. A
RISK FACTORS or parents may note maroon or black tarry stools
Constipation is a risk factor for developing anal sausage-shaped mass may be palpated on the right
(melena). side in patients with intussusception.
fissures, which may cause bleeding. r The character of the blood and stool should be r A careful skin exam may identify characteristic
GENERAL PREVENTION included in the history, as it may indicate the lesions of HSP (palpable purpura of the lower
Prevent constipation. anatomic source of bleeding: extremities and buttocks), multiple vascular
PATHOPHYSIOLOGY Stool coated in blood or blood on toilet paper malformations associated with congenital GI
r The pathophysiology varies according to etiology. suggests an anorectal source. malformations, or perioral freckling associated with
r Malrotation and intussusception are caused by Bright red liquid blood (hematochezia) suggests a hereditary polyposis syndromes.
source in the proximal colon.
twisting or sliding of bowel, which results in DIAGNOSTIC TESTS & INTERPRETATION
Bloody diarrhea usually results from a colonic
obstruction of blood flow and resultant ischemia.
r Meckel diverticulum causes bleeding from ectopic source. Lab
Maroon or tarry stool (melena) suggests a more Initial Lab Tests
gastric or pancreatic tissue, which results in local proximal sourceproximal to the illeocecal valve. r Chemical testing for occult blood (eg, Guiac smear
mucosal erosion and bleeding. r The history should also include a careful inquiry test) can be useful in confirming the presence of
r Infectious colitis is frequently caused by Escherichia
about associated symptoms (such as tenesmus, blood from stool.
coli and Salmonella, Campylobacter, or Shigella abdominal pain, vomiting, constipation, fever, r Minor bleeding that is self-limited and associated
species and can cause bleeding from local invasion diarrhea, mucus), chronic medical conditions with a normal physical exam and vital signs is likely
or through the production of toxin. (including constipation and systemic disease), the result of a benign etiology and rarely requires
r Henoch-Schonlein purpura (HSP) causes GI bleeding
medications (especially NSAIDs and steroids), and additional lab testing.
from diffuse vasculitis. familial bleeding or vascular disorders. r Patients with significant bleeding should have a CBC
r Breast-fed infants can swallow maternal blood, r Infectious diarrhea will often have a history of evaluated for hematocrit (which may be normal in
which may produce heme-positive stools (see bloody diarrhea with mucus, tenesmus, and sick acute blood loss), RBC indices that might suggest
Gastrointestinal Bleeding: Upper topic). contacts with similar symptoms or recent travel or chronic GI bleeding with microcytic anemia, and
r Formula fed infants can develop milk-protein allergy ingestion of raw foods. evaluation of the platelet count.
that may produce heme-positive stools (see r In breast-fed neonates, the mother should be asked r Patients with ongoing blood loss should have a
Gastrointestinal Bleeding: Upper topic). about cracked or bleeding nipples to identify the blood sample sent for typing and cross-matching if
ETIOLOGY potential swallowed maternal blood. transfusion is necessary.
r Neonates: Swallowed maternal blood, necrotizing r In formula-fed infants, inquire about past formula r Coagulation studies (PT, PTT, d-dimer) are indicated
enterocolitis (NEC), malrotation with volvulus, intolerance, which could signify protein allergy. for severe or ongoing bleeding or in the setting of a
Hirschprung disease, coagulopathy, vascular r Ask about ingestion of red substances, as this may suspected disorder of coagulation.
malformations, allergic colitis give the appearance of blood (eg, beets, red-dyed r If HSP is suspected, evaluate renal function by
drinks or foods). measuring creatinine, and evaluate for proteinuria
with urinalysis.
r If infectious colitis is suspected, stool should be sent
for bacterial cultures including Shigella, Salmonella,
Yersinia, Campylobacter, and E. coli 0157:H7. With
an appropriate travel or exposure history, ova and
parasite exam may be useful.
r An Apt test may be performed on rectal blood to
differentiate swallowed maternal blood from fetal
blood in breast-fed neonates.
r Inflammatory markers such as ESR and C-reactive
protein may be useful in the setting of suspected
inflammatory bowel disease.
430
GASTROINTESTINAL BLEEDING: LOWER
Imaging Second Line DIET

r Abdominal x-rays are rarely helpful but may identify r Glycerin suppositories can be used sparingly in cases r Soy-based or elemental formula may be indicated
free air, a target sign in the right upper quadrant of anal fissure if other methods do not work. for infants with milk protein allergy.
suggestive of intussusception; pneumatosis in r Prednisone 12 mg/kg/day divided b.i.d. is r Regular diet is otherwise recommended.
neonates with NEC; or paucity of bowel gas in controversial but may be considered in HSP.
malrotation with midgut volvulus (upper GI barium PROGNOSIS
SURGERY/OTHER PROCEDURES r The prognosis depends on the underlying etiology;
study with small bowel follow-through is diagnostic). r Barium or air contrast enema is often therapeutic for
r In the setting of massive painless rectal bleeding, a however, lower GI bleeding is rarely life threatening
intussusceptions. in children.
nuclear medicine Meckel scan (technetium-99m) r Immediate surgical management is indicated for r Etiologies with guarded prognoses include
is useful to evaluate for ectopic gastric mucosa in a
Meckel diverticulum. malrotation with midgut volvulus as well as malrotation with midgut volvulus, inflammatory
r Abdominal US is sensitive for intussusception but is intussusception with failed hydrostatic reduction. bowel disease, NEC, or multiple vascular
r Outpatient surgery is definitive care for Meckel malformations.
not therapeutic and should be reserved for cases in r HSP is usually self-limited and benign but may be
which the diagnosis is equivocal. diverticulum and Hirschsprung disease.
r Endoscopy is useful in the setting of suspected recurrent and associated with renal involvement in a
Diagnostic Procedures/Other vascular malformations, polyps, and inflammatory minority of cases.
r Anoscopy, sigmoidoscopy, or colonoscopy may be
bowel disease. COMPLICATIONS
useful to evaluate for vascular malformations,
inflammatory bowel disease, and polyps. DISPOSITION Intestinal ischemia and resultant intestinal necrosis
r Barium/Air contrast enema is diagnostic and Admission Criteria may develop in cases of intussusception, malrotation
frequently therapeutic in intussusception. r Critical care admission criteria: with midgut volvulus, or NEC.
r Rectal biopsy provides definitive diagnosis in Hemodynamic instability
Hirschprung disease and may be useful in Profuse and ongoing bleeding
r Inpatient admission criteria: ADDITIONAL READING
confirming suspected inflammatory bowel disease.
History of significant bleeding without r Basualdo W, Arbo A. Randomized comparison of
hemodynamic instability (eg, self-limited but azithromycin versus cefixime for treatment of
Varies depending on cause
large-volume blood loss, anemia suggestive of shigellosis in children. Pediatr Infect Dis J. 2003;22:
DIFFERENTIAL DIAGNOSIS chronic bleeding) 374377.
r Neonates: Swallowed maternal blood r Leung KC, Wong AL. Lower gastrointestinal bleeding
r Infants and children: Colored food products Discharge Criteria
r Self-limited, minor bleeding in a hemodynamically in children. Pediatr Emerg Care. 2002;18:319323.
stable patient r McCollough M, Shareiff GQ. Abdominal surgical G
r Benign etiology of lower GI bleed (eg, anal fissure, emergencies in infants and young children. Emerg
TREATMENT polyp, well-appearing child with infectious colitis) Med Clin North Am. 2003;21:909935.
r Oxygen via nasal cannula or face mask r Outpatient referrals (routine): Recurrent or chronic
r Normal saline 20 cc/kg IV or IO for patients with but self-limited lower GI bleeding of uncertain
CODES
hemodynamic compromise etiology without systemic signs should prompt
referral to a gastroenterologist for possible ICD9
INITIAL STABILIZATION/THERAPY endoscopy and further management. 578.9 Hemorrhage of gastrointestinal tract,
r Establish 2 large-bore, short-length IVs if unstable.
r Immediate referrals (within 1 wk): Congenital unspecified
r Crystalloid infusion 20 mL/kg; may repeat as
malformations of the GI tract (eg, Meckel
necessary
r Blood transfusion 10 mL/kg for life-threatening diverticulum, intestinal duplication) require referral
to a pediatric surgeon.
PEARLS AND PITFALLS
blood loss; may repeat as necessary r Consider swallowed maternal blood in
r In intussusception, barium/air contrast enema for
breast-feeding neonates, and inquire about
reduction FOLLOW-UP maternal nipple irritation.
r Malrotation with midgut volvulus is a surgical r Carefully examine the entire skin for cutaneous
emergency, and early surgical consultation is critical. FOLLOW-UP RECOMMENDATIONS
r Discharge instructions and medications: vascular malformations that may signal occult GI
MEDICATION Recurrent bleeding associated with symptoms of vascular malformations.
dizziness, light-headedness, fainting, or severe r Infants with bilious emesis should be transferred to
First Line
r In cases of anal fissure, apple juice can be titrated abdominal pain should prompt immediate medical a center with pediatric surgery available, as
PO to soften stool and warm sitz baths may provide care. malrotations with midgut volvulus are diagnostic
comfort. r Activity: considerations that represent true surgical
r In infectious colitis caused by Shigella and Normal activity is recommended for most causes emergency.
of lower GI bleeding. r Consider intussusception in children with
Campylobacter, antimicrobial therapy is
controversial but should be considered: intermittent severe abdominal pain, though lethargy
Patient Monitoring
Azithromycin 10 mg/kg/day on day 1, followed by or intermittent lethargy alone should prompt
Monitor stool color, and inform the physician if stools
5 mg/kg/day on days 25. consideration of this diagnosis.
are tarry or black or maroon in color.
r In NEC, broad-spectrum antibiotic therapy with
ampicillin (50 mg/kg/dose) and gentamycin
(2.5 mg/kg/dose) should be considered in
consultation with neonatology and pediatric surgery.
431
GASTROINTESTINAL BLEEDING: UPPER

Matthew Lee Hansen
Garth Meckler

BASICS r Neonates: Hemorrhagic disease of the newborn
Lab
(vitamin K deficiency), gastritis, esophagitis, vascular Initial Lab Tests
DESCRIPTION malformation, bleeding diatheses r Minor bleeding with a reassuring exam that is likely
Upper GI bleeding is defined as bleeding from a source r Infants: Gastritis, esophagitis, stress ulcer, the result of a benign etiology (eg, Mallory-Weiss)
within the GI tract proximal to the ligament of Treitz. Mallory-Weiss tear, vascular malformations, rarely requires lab testing.
EPIDEMIOLOGY congenital GI duplications r Chemical testing for occult blood (eg, Gastroccult
r Children: Peptic ulcer disease, gastritis, esophagitis, cards) can be useful in confirming the presence of
Incidence
r The exact incidence in children is unknown; however, foreign body, Mallory-Weiss tear, caustic or toxic blood from gastric aspirates or samples of emesis.
ingestion, esophageal varices, thrombotic r Patients with significant bleeding should have a CBC
upper GI bleeding is uncommon in children.
r The reported incidence among children in the ICU thrombocytopenia purpura, Henoch-Schonlein evaluated for hematocrit (which may be normal in
purpura acute blood loss), RBC indices that might suggest
ranges from 6.425% (1).
COMMONLY ASSOCIATED CONDITIONS chronic GI bleeding with microcytic anemia, and
RISK FACTORS evaluation of the platelet count.
r Chronic NSAID or steroid use Variceal bleeding is commonly associated with liver
r Patients with ongoing blood loss should have a
r Bleeding diatheses (eg, hemophilia) disease and portal HTN.
blood sample sent for typing and cross-matching if
r Chronic disease leading to portal HTN (eg, cystic transfusion may be necessary.
fibrosis, congenital hepatic disease) can cause DIAGNOSIS r Coagulation studies (PT, PTT, d-dimer) are indicated
varices with subsequent bleeding. for severe or ongoing bleeding or in the setting of
r Severe retching or repeated vomiting can result in HISTORY suspected disorder of coagulation.
r The typical history is vomiting of blood that is a
upper GI bleeding. r ALT and AST may be indicated in the setting of
r Inherited conditions of vascular anomalies (eg, bright red or coffee-ground color.
suspected portal HTN.
r Parents may report dark tarry stools (melena), which
Osler-Weber-Rendu) can predispose children to r The Apt test can distinguish between swallowed
upper GI bleeding. may be the result of an upper GI source of bleeding.
r The history should include a careful inquiry about maternal and neonatal blood.
r Severe head trauma (Cushing ulcers) or burns r Testing for H. pylori: Endoscopic biopsy with rapid
(Curling ulcers) associated symptoms (such as retching or recurrent
urease testing or polymerase chain reaction for
vomiting), chronic medical conditions, medications,
GENERAL PREVENTION bacterial DNA is most sensitive. Serum, saliva, and
familial bleeding, or vascular disorders.
r Closely monitor NSAID use. r In breast-fed neonates, ask about maternal cracked urine antibodies, stool antigen, or urea breath
r Prophylaxis (proton pump inhibitors) for ICU patients testing are less invasive but less sensitive.
or bleeding nipples to identify potential swallowed
maternal blood. Imaging
PATHOPHYSIOLOGY
r The pathophysiology varies according to etiology. r In formula-fed infants, inquire about formula Abdominal x-rays (kidney, ureter, bladder, and upright)
r Variceal bleeding results from hepatic venous HTN intolerance, which could signify milk protein allergy may be useful in select circumstances to identify
(seen with both cows milk and soy-based formulas). foreign bodies or free air indicative of perforation.
causing dilation of submucosal veins which may
r Inquire as to non-GI sources of blood such as cough, Diagnostic Procedures/Other
rupture.
r Nonvariceal bleeding can result from: which could indicate hemoptysis, or epistaxis, which r NG tube aspiration with instillation of normal saline
Disorders of the coagulation cascade may be swallowed blood. may be useful to identify ongoing upper GI bleeding
Loss of mucosal protective factors as a result of but is not universally indicated in self-limited or
PHYSICAL EXAM benign cases.
medications (eg, NSAIDs) r Careful documentation of vital signs, especially
r Endoscopy may be useful in cases of foreign body or
Irritation (eg, foreign body or caustic ingestion) heart rate and BP, will help identify life-threatening
Infection (eg, Helicobacter pylori) hemorrhage. variceal bleeding.
Congenital vascular malformations may be r Inspection of the nose is important to exclude this Pathological Findings
predisposed to bleeding. non-GI source of bleeding. Varies depending on the cause
r Abdominal tenderness and peritoneal signs may
suggest life-threatening GI perforation, while r Neonates: Swallowed maternal blood
hepatomegaly or splenomegaly may suggest portal r Infants and children: Epistaxis, colored food
HTN. products, hemoptysis
r A thorough exam of the skin is important to identify
stigmata of chronic liver disease and vascular
malformations.
432
GASTROINTESTINAL BLEEDING: UPPER
r Gastric or duodenal ulcers may perforate, causing
r Critical care admission criteria: peritonitis and septic shock.
PRE HOSPITAL Hemodynamic instability r Varices and arterial bleeding can result in
r Oxygen via nasal cannula or face mask Profuse and ongoing bleeding life-threatening blood loss.
r Normal saline 20 mL/kg IV or IO for patients with r Inpatient admission criteria:
hemodynamic compromise History of significant bleeding without
hemodynamic instability (eg, self-limited but REFERENCES
r Establish 2 large-bore, short-length IVs if large-volume blood loss, anemia suggestive of 1. Chawla S, et al. Upper gastrointestinal bleeding in
chronic bleeding) children. Clin Pediatr. 2007;46:1621.
tachycardia or hypotension is present.
r Crystalloid infusion 20 mL/kg; may repeat as Discharge Criteria 2. McCollough M, Shareiff GQ. Abdominal surgical
r Self-limited, minor bleeding in a hemodynamically emergencies in infants and young children. Emerg
necessary
r Blood transfusion 10 mL/kg for life-threatening stable patient Med Clin North Am. 2003;21:909935.
r Benign etiology of upper GI bleed (eg, 3. Gold BD, Colletti RB, Abbott M, et al. North
blood loss; may repeat as necessary
Mallory-Weiss tear, mild gastritis, or esophagitis) American Society for Pediatric Gastroenterology
MEDICATION and Nutrition. Helicobacter pylori infection in
First Line Issues for Referral
r Outpatient referrals (routine): Chronic or recurrent children: Recommendations for diagnosis and
r Medications for gastric acid reduction:
upper GI bleeding should prompt referral to a treatment. J Pediatr Gastroenterol Nutr. 2000;
H2 receptor antagonists 31(5):490497.
Ranitidine 12 mg/kg IV q6h, max single dose gastroenterologist for possible endoscopy and
further management.
50 mg r Immediate referrals (within 1 wk): Congenital
Proton pump inhibitors ADDITIONAL READING
Omeprazole 1 mg/kg/day PO per dayb.i.d., malformations of the GI tract (eg, Meckel
max single dose 20 mg diverticulum, intestinal duplication) require referral Molleston JP. Variceal bleeding in children. J Pediatr
Lansoprazole 1530 mg/kg/day IV/PO per to a pediatric surgeon. Gastroenterol Nutr. 2003;37:538545.
dayb.i.d. See Also (Topic, Algorithm, Electronic
Pantoprazole 1 mg/kg IV/PO per day, max single
dose 40 mg
r Gastritis
r Antibiotics for suspected or confirmed H. pylori FOLLOW-UP RECOMMENDATIONS r Pain, Abdomen
r Discharge instructions:
infection (see Additional Reading for all
recommended regimens) (3): Recurrent bleeding associated with symptoms of
G
Triple therapy (all 3 in combination): dizziness, light-headedness, fainting, or severe CODES
Amoxicillin 50 mg/kg/day PO divided abdominal pain should prompt immediate medical
b.i.d.q.i.d., max single dose 1 g PO b.i.d. care
Clarithromycin 15 mg/kg/day up to 500 mg PO r Discharge medications: ICD9
b.i.d. for 714 days 578.9 Hemorrhage of gastrointestinal tract,
Continue medications as described in medication
Proton pump inhibitor (as noted above) unspecified
section (eg, acid suppression therapy, antibiotics
Triple therapy as noted above, substituting for H. pylori)
clarithromycin with: r Activity:
Metronidazole 20 mg/kg/day up to 500 mg PO
PEARLS AND PITFALLS
Normal activity is recommended for most cases of
b.i.d. for 714 days upper GI bleeding. r Consider swallowed maternal blood in
Second Line breast-feeding neonates, and inquire about
r Octreotide (1 g/kg bolus to 50 g followed by
Patient Monitoring
r Monitor stool color, and inform the physician if maternal nipple irritation.
r Carefully examine the entire skin for cutaneous
14 g/kg/hr continuous infusion) for active stools are tarry, black, or maroon in color.
bleeding from varices r Avoid excessive use of NSAIDs in cases of suspected vascular malformations that may signal occult GI
r Fresh frozen plasma, cyroprecipitate, or specific vascular malformations.
gastritis or ulcer disease. r Consider accidental toxic ingestions in toddlers with
factor replacement for ongoing bleeding with
coagulopathy DIET upper GI bleeding (eg, iron).
r Soy-based or elemental formula may be indicated r Look for signs of portal HTN such as spider
COMPLEMENTARY & ALTERNATIVE for infants with milk protein allergy. angiomata, palmar erythema, and
THERAPIES r Regular diet is otherwise recommended. hepatosplenomegaly as a clue to possible variceal
r Licorice and zinc have been recommended as
PROGNOSIS bleeding.
alternative therapies for ulcer disease. r Gastric lavage with ice or epinephrine is no longer
r Chamomile and garlic are thought to have r The prognosis depends on the underlying etiology;
however, upper GI bleeding is rarely life threatening recommended.
antiH. pylori activity.
in children.
SURGERY/OTHER PROCEDURES r Etiologies with guarded prognoses include those
r Endoscopy is often indicated for bleeding requiring
associated with cirrhosis, portal HTN, esophageal
transfusion, chronic or recurrent bleeding, and in varices, or multiple vascular malformations.
some instances of variceal or vascular bleeding.
r Banding and sclerotherapy may be performed
endoscopically.
r Angiography may be indicated for massive bleeding
in patients too unstable for endoscopy.
r Surgical exploration is indicated for patients with
persistent bleeding of undetermined cause who
remain hemodynamically unstable.
433
GASTROINTESTINAL POLYPS
Daniel A. Green
Laura Umbrello

BASICS Mutations in tumor suppressor genes likely lead to Lab
dysregulation of cell proliferation and apoptosis in r If asymptomatic, diagnostic testing may be deferred
DESCRIPTION polyposis syndromes. to an outpatient appointment with the patients
r A GI polyp is a tissue growth protruding from the
ETIOLOGY primary care provider or a gastroenterologist.
mucosal surface into the lumen of the bowel. r If symptomatic:
r GI polyps can be solitary or multiple and neoplastic Proliferation of colonic epithelium with cystic dilation
of normal glandular elements CBC:
or nonneoplastic. Assess for anemia and thrombocytopenia.
r Classification by gross appearance: Low mean corpuscular volume associated with
Pedunculated: Attached to the mucosa by a DIAGNOSIS chronic blood loss
narrow stalk with a mushroomlike head PT/PTT/INR
Sessile: Flat lesions broadly attached to the HISTORY Type and screen for active bleeding or unstable
r Frequently asymptomatic
mucosa vital signs.
r Juvenile polyps: r Family history of polyps or polyposis syndromes
Serum electrolyte testing
Most common cause of polyps in children r Abdominal pain Stool for occult blood
Solitary in 75% of cases r Painless, bright red rectal bleeding:
Imaging
>35 juvenile polyps fulfills the criteria for the Assess amount of blood loss, if present. Imaging is usually not necessary emergently. The
diagnosis of juvenile polyposis syndrome r Diarrhea or passage of mucus
r Juvenile polyposis syndrome (1,2): following studies will help aid in the diagnosis:
r Prolapsing rectal lesion r Barium enema
Mean age of presentation between 5 and 6 yr r History of iron-deficiency anemia r Upper GI with small bowel follow-through
May be accompanied by: r Weight loss or failure to thrive r CT and MR colonography
Protein-losing enteropathy r Symptoms of obstruction such as vomiting,
Electrolyte abnormalities r Other imaging modalities depending on signs and
Failure to thrive abdominal distension, obstipation, etc. (GI polyps symptoms
r Peutz-Jeghers syndrome: may be complicated by intussusception.)
Average age of presentation is 25 yr. PHYSICAL EXAM Imaging is usually not necessary emergently. The
Hamartomatous polyps r Vital signs, especially in a patient with active or
following procedures will help aid in the diagnosis:
Increased lifetime risk of malignancy significant bleeding r Colonoscopy
r Familial adenomatous polyposis: r Complete physical exam looking for signs indicating
r Endoscopy
Colorectal and duodenal adenomas polyposis syndromes: r Capsule endoscopy may be useful to identify small
Increased lifetime risk of malignancy Juvenile polyposis syndrome (2):
Signs of failure to thrive bowel polyps.
EPIDEMIOLOGY Peutz-Jeghers syndrome: DIFFERENTIAL DIAGNOSIS
Juvenile polyposis syndrome (1,2): Hamartomatous polyps r Anal fissure
r Found in 1 in 100,000160,000 live births Black or brown freckles of the lips, buccal r Hemolytic uremic syndrome
RISK FACTORS mucosa, face, palms, and soles r Hemorrhoids
Family history of polyposis syndrome Familial adenomatous polyposis: r Henoch-Schonlein purpura
Colorectal and duodenal adenomas r Infectious enterocolitis
Cronkhite-Canada syndrome: r Inflammatory bowel disease
Hamartomatous polyps
r Intussusception
Alopecia, cutaneous hyperpigmentation, GI
r Meckel diverticulum
polyposis, onychodystrophy
r Signs of obstruction such as abdominal distension r Rectal trauma
and tenderness, etc. r Vascular malformation
r Digital rectal examination for masses
434
GASTROINTESTINAL POLYPS

TREATMENT Admission Criteria r Chow E, Macrae F. Review of juvenile polyposis
r Significant anemia for age
INITIAL STABILIZATION/THERAPY r Critical care admission criteria: syndrome. J Gastoenterol Hepatol. 2005;20:
r Address and stabilize ABCs: 16341640.
Unstable vital signs despite resuscitation r Durbin DR, Liacouras CA, Seiden JA.
Place 2 large-bore IV lines if the patient is Coagulopathy
hemodynamically unstable. Continued, significant lower GI bleeding Gastrointestinal emergencies. In Fleisher GR,
Correct volume depletion. Ludwig S, eds. Textbook of Pediatric Emergency
Transfuse as necessary for anemia.
Discharge Criteria Medicine. 6th ed. Philadelphia, PA: Lippincott
r Minor or resolved lower GI bleeding
r Correct electrolyte disturbances, if present. Williams & Wilkins; 2010:817838.
r Stable vital signs r Erdman SH, Barnard JA. Gastrointestinal polyps and
r Manage pain with analgesics.
r Stable hemoglobin
polyposis syndromes in children. Curr Opin Pediatr.
MEDICATION r Normal coagulation function 2002;14:576582.
r Analgesics are the most commonly indicated r Shilyansky J. Tumors of the digestive tract. In
medications, though most management is
Issues for Referral
r Patients suspected of having a polyp or polyposis Behrman RE, Kliegman RM, Jenson HB, eds. Nelson
supportive or surgical. Textbook of Pediatrics. 17th ed. Philadelphia, PA:
r NSAIDs: syndrome should be referred to a gastroenterologist
for evaluation. Saunders; 2004:12891292.
Ibuprofen 10 mg/kg/dose PO/IV q6h PRN r Patients with polyposis syndromes should be
referred for genetic testing.
Naproxen 5 mg/kg PO q8h PRN CODES
potential for gastritis and theoretical concern over FOLLOW-UP
influence on coagulation. ICD9
r 211.1 Benign neoplasm of stomach
r Acetaminophen 15 mg/kg/dose PO/PR q4h PRN FOLLOW-UP RECOMMENDATIONS
r Follow up with the primary care provider within r 211.2 Benign neoplasm of duodenum, jejunum, and
r Opioids:
12 days. ileum
Morphine 0.1 mg/kg IV/IM/SC q2h PRN: r 211.3 Benign neoplasm of colon
Initial morphine dose of 0.1 mg/kg IV/SC may r Referral to gastroenterology should be made as
be repeated q1520min until pain is controlled, soon as available.
then q2h PRN.
DIET PEARLS AND PITFALLS
Patients who have had bowel resection may require
special nutritional interventions, including vitamin and r Have a high index of suspicion in patients with a G
q1520min until pain is controlled, then q2h nutrient supplementation, continuous enteral family history of polyposis syndromes.
PRN. feedings, or parenteral nutrition. r Consider other organ systems in patients with GI
Codeine or codeine/acetaminophen dosed as polyps, especially in those with multiple polyps, and
0.51 mg/kg of codeine component PO q4h PRN PROGNOSIS
r With solitary polyps, usually a benign process that provide appropriate referrals.
Hydrocodone or hydrocodone/acetaminophen r Consider intussusception in the diagnosis in any
dosed as 0.1 mg/kg of hydrocodone component often requires minimal follow-up
r Increased risk of GI malignancy with many of the patient with abdominal pain, rectal bleeding, and
PO q46h PRN
either a known or unknown diagnosis of GI polyps.
polyposis syndromes, requiring the need for r Depending on the etiology, ongoing follow-up with
continued surveillance
Once stabilized, the following procedures may be a gastroenterologist may be critical to detect and
performed during admission or in follow-up with COMPLICATIONS manage malignant neoplasms.
gastroenterology: r Life-threatening GI blood loss is rare.
r Full colonoscopy with polypectomy is an essential r Polyps may act as a lead point of an intussusception.
diagnostic and therapeutic tool: r Increased lifetime risk of malignancy with several of
Removal of GI polyps can help control symptoms the polyposis syndromes
and reduce the risk of malignancy.
When adenomatous polyps are identified in
familial adenomatous polyposis, prophylactic
colectomy should be considered.
r Colectomy in other polyposis syndromes with
innumerable polyps or polyps showing premalignant
changes
435
GENITAL WARTS
Shira Yahalom
GENERAL PREVENTION ETIOLOGY

BASICS r Delaying age of 1st intercourse r HPV is a double-stranded DNA virus that has
r Condom use >100 different genotypes, with 30 that infect the
DESCRIPTION r Limiting the number of sexual partners human genital tract.
r Genital warts (condyloma acuminata) are an r Avoiding tobacco use r The 2 major groups of HPV genotypes are the
epidermal human papillomavirus (HPV) infection. r HPV vaccine is now available and offers protection low-risk genotypes (types 6, 11, and others) and the
r Lesions are papillomatous flesh to gray-brown color high-risk genotypes (types 16, 18, 31, 33, 45, and
from strains 6, 11, 16, and 18. The vaccine is
hyperkeratotic on keratinized epithelia. approved for both males and females. others).
r Can be solitary or multiple and sessile or r Screening using Pap smears should be performed r HPV types 6 and 11 account for 90% of all genital
pedunculated. Size varies from 2 mm to 2 cm. annually 3 yr from the initiation of sexual activity or warts.
r May occur anywhere below the waist: r HPV-16 is responsible for about 50% of cervical
at age 21 yr, whichever comes first.
In men: The most commonly involved area is the cancers.
penile shaft and the preputial cavity. Pregnancy Considerations
r During pregnancy, latent infections may become COMMONLY ASSOCIATED CONDITIONS
In women: The posterior introitus is most r As with all STIs, coinfection with another STI should
commonly involved. activated and present lesions may increase. The
r In younger boys and girls, warts are most common lesions will often regress postpartum. be considered.
r Genital lesions tend to bleed easily during r The presence of anogenital warts in children should
in the perianal area but may also involve the penis
or labia minora. pregnancy and depending on size and location may prompt suspicion of sexual abuse.
interfere with vaginal delivery.
EPIDEMIOLOGY r Vertical acquisition of HPV in the birth canal is
r The annual incidence of genital warts is 1%. DIAGNOSIS
r 1833% of sexually active female adolescents will causative of inoculation of the oropharynx and
respiratory tract with HPV. HISTORY
test positive for HPV. r Patients will complain of multiple painless (a single
r Prevalence of HPV infections among men seems to r Recurrent respiratory laryngeal papillomatosis
(RRLP) is a rare complication with tremendous wart is less common) raised lesions.
be lower, either due to lower incidence or shorter r Associated pruritus and discharge are common.
periods of infection. morbidity. r Postcoital bleeding may be the presenting complaint.
r The CDC estimates that 50% of sexually active r Recurrence of warts in the larynx and respiratory
r Obtain history of prior or concomitant STIs.
adults will have HPV at some point in life. tree may occur throughout the life of the child r If the patient is an infant or child, obtain the history
RISK FACTORS PATHOPHYSIOLOGY regarding HPV status of the mother and caregivers.
r Early sexual debut r HPV invades cells in the anogenital area through r History of immunodeficiency and pregnancy status
r Multiple sexual partners microabrasions in the skin and mucosa.
r Lack of condom use r Following latency of weeks to a year, viral DNA PHYSICAL EXAM
r Single or multiple lesions may be seen from a small
r Cigarette smoking particles are produced, infecting the host cells,
r Oral contraceptive use papule to cauliflower appearance.
which change their morphology to atypical r Exam of the entire anogenital area and oropharynx
r Immunodeficiency such as from HIV or koilocytosis of genital warts.
r Transmission of genital HPV infection in adolescents is warranted, as multiple areas may be involved and
chemotherapy location may vary with sexual preference.
and adults is almost always through sexual contact. r Speculum pelvic exam and cervical cultures to
r Neonates may become infected during passage
inspect for abnormal appearance of the cervix and
through the birth canal.
r Other less common forms of transmission, include check for concomitant STIs
vertical transmission, autoinoculation,
heteroinoculation (transmission from the hands of
the caretakers to the anogenital area of the child),
and transmission through fomites.
436
GENITAL WARTS
DIAGNOSTIC TESTS & INTERPRETATION r Hager WD. Human papilloma virus infection and
Lab FOLLOW-UP prevention in the adolescent population. J Pediatr
r No tests are required in the emergency department Adolesc Gynecol. 2009;22:197204.
for diagnosis of genital warts. FOLLOW-UP RECOMMENDATIONS r Middleman AB. Immunization update: Pertussis,
r Testing for other STIs such as gonorrhea, chlamydia, Discharge instructions and medications: meningococcus, and human papillomavirus. Adolesc
r Follow up with a clinician who can provide Med. 2006;17:547563.
syphilis, and HIV should be considered based on the
history and physical exam. long-term treatment as warranted. r Wellington MA, Bonnez W. Consultation with the
r Emphasize infectivity, need for evaluation, and specialist: Genital warts. Pediatr Rev. 2005;26:
DIFFERENTIAL DIAGNOSIS treatment of sexual partners. 467471.
r Neoplasm
r Nevi PROGNOSIS See Also (Topic, Algorithm, Electronic
r Vulvar neurofibromatosis r Spontaneous regression is more common with Media Element)
r Darier disease children than adults. r Herpes Simplex
r Hailey-Hailey disease r Recurrence after treatment may occur. r Sexually Transmitted Infection
r Since HPV cannot be eradicated, the risk of
malignant transformation remains despite treatment
TREATMENT of warts. CODES
COMPLICATIONS
MEDICATION r Cervical, vaginal, penile, and anal cancer ICD9
r Only symptomatic treatment is required in the
r Bleeding from lesions 078.11 Condyloma acuminatum
emergency department setting. r Obstruction of urethral meatus
r Imiquimod 5% cream applied to warts 3 times
r Transmission to sexual partners and neonates
weekly for 13 mo:
r Malignant transformation
PEARLS AND PITFALLS
May be prescribed if the emergency department
r Recurrence after treatment r Suspect abuse in children presenting with genital
clinician is comfortable with dispensing
Side effects include burning, pain, and vesicle r RRLP warts.
formation often mistakenly diagnosed as herpes r Examine and treat for concomitant STIs.
simplex virus. r Suspect immunodeficiency in a patient presenting
r Treat coexistent STIs as warranted. ADDITIONAL READING with recurrent disease.
r Do not ignore the significant psychological and
r Darville T. Genital warts. Pediatr Rev. 1999;20:
DISPOSITION
Issues for Referral 271272.
social implications of diagnosis. G
r It is advisable to avoid engaging in patients
All patients with genital warts should be referred to a r Diaz ML. Human papilloma virusprevention and
dermatologist, OB/GYN, or urology specialist for attempts to temporally implicate the contact from
treatment. Obstet Gynecol Clin North Am. 2008;
treatment and follow-up: which the infection may have been contracted.
35:199217. r In females, cervical HPV clearance typically occurs
r Treatment of genital warts includes topical r Erb T, Beigi RH. Update on infectious diseases in
within 2 yr.
applications, cryotherapy, or surgical excision. adolescent gynecology. J Pediatr Adolesc Gynecol. r Classically it was presumed that the infection
2008;21:135143.
persists for life, but the accuracy of this is unknown.
r CDC experts believe that persistent infections
actually involve re-exposure and reinfection.
437
GIARDIASIS
Sujit Iyer
GENERAL PREVENTION r Chronic giardiasis:

BASICS r Strict hand washing (especially with handling Up to 30% can develop chronic symptoms.
diapers) Loose stools
DESCRIPTION r Treatment of symptomatic children r Malabsorption of vitamins, fats, sugars, and
Giardiasis is caused by infection with the protozoan r Boiling or heating water to at least 70 C for 10 min protein:
parasite Giardia lamblia, usually with symptoms of eliminates Giardia cysts (5). Up to 40% can acquire lactose intolerance (8).
flatulence, abdominal bloating, and foul-smelling r For campers: Iodine-based water treatment for at Should consider in children with failure to thrive
diarrhea. least 8 hr (5) PHYSICAL EXAM
EPIDEMIOLOGY r Weight loss (1020% can be seen)
PATHOPHYSIOLOGY
Incidence r Incubation period of 12 wk after exposure r Abdominal distension
r Varies by state reporting. National range of <0.1 r Human and zoonotic reservoirs; dogs, cats, sheep, r Malaise, anorexia
cases (Texas) to 23.5 (Vermont) per 100,000 (1) beavers, deer, rodents r Generalized edema if chronic and there is
r The CDC estimates up to 2.1 million cases annually r Human infection can occur with ingestion of as few protein-losing enteropathy
in the U.S. (1). as 1025 cysts. Cysts survive for a long time in a r Hypersensitivity phenomenon (rare): Urticaria,
r 2-fold increase in summer and early fall (likely due
moist environment (6). reactive arthritis
to increased outdoor activities and recreational r After ingestion, trophozoites are released in the
water exposure by humans) DIAGNOSTIC TESTS & INTERPRETATION
upper small bowel and attach with an adhesive disc
Prevalence onto the mucosa of the duodenum and jejunum.
Lab
r Prevalence is directly related to the degree of r Biopsy of the small bowel shows a range from no Initial Lab Tests
r Stool sample:
sanitation and water treatment. changes to subtotal villous atrophy (severe).
r Bimodal age distribution: Children (05 yr of age) r Intestinal changes include damage to the endothelial Excretion is intermittent; the sensitivity of 1 stool
sample is 50%, while the sensitivity of
and their caretakers (3039 yr of age) brush border, enterotoxins, immunologic reactions, 3 samples approaches 90% (9).
r 3 patterns of transmission (13): and altered gut motility and fluid hypersecretion via r Diagnosis confirmed by:
Person to person: Increased prevalence related to increased adenylate cyclase activity.
r Trophozoites can revert to cysts and be excreted Cysts or trophozoites seen on microscopy of fresh
poor hygiene and among day care attendees and specimen mixed with saline or concentrated in
staff. Also increased in male homosexuals. from the stool for up to 5 mo after initial diagnosis. formalin
Waterborne: Reservoirs and surface water can r Pathogenesis of diarrhea and malabsorption is
Antigen in stool specimen detected by ELISA
lead to endemic and epidemic spread in hikers incompletely understood but may be related to
and international travelers. villous atrophy, disruption of brush border enzymes Diagnostic Procedures/Other
Foodborne: Uncommon and killed by cooking. (lactase), and parasites as a physical barrier to If high suspicion but negative stool specimens,
Occurs with uncooked food, and as few as absorption (2,3). duodenal biopsy or aspiration may be indicated for
10 cysts can establish infection. those with persistent symptoms.
ETIOLOGY
RISK FACTORS Pathological Findings
G. lamblia occurs in 2 forms: Cysts and trophozoites. r Histologic changes do not always correlate with the
r Infants, young children (not toilet trained)
r Day care attendance presence or absence of symptoms.
r Can be normal; flattening of brush border, damage
r Internationally adopted children DIAGNOSIS
r Hypo- or achlorydia (previous gastric surgery) to epithelial cells, flattening of villi, and increased
r Cystic fibrosis HISTORY goblet cells may also be seen.
r Can be asymptomatic in up to 60% (7)
r Crohn disease r 90% of symptomatic patients present with acute DIFFERENTIAL DIAGNOSIS
r Hypogammaglobulinemia/Immunodeficiency (risk r Bacterial diarrhea
diarrhea. r Viral gastroenteritis:
for chronic infection) r Acute giardiasis:
r Oralanal sexual contact Rotavirus
Watery diarrhea
r Campers exposed to contaminated surface waters Foul-smelling stools and steatorrhea
Hepatitis A
r Travel to endemic areas Norovirus
Bloating r Other protozoa:
Flatulence
Anorexia Cryptosporidia
Weight loss Microsporidia
Symptoms in young infants may mimic sprue. Cyclospora
Classic soft, foul-smelling diarrhea (52%) (2) Entamoeba
r Celiac sprue
No tenesmus or bloody diarrhea
r Cystic fibrosis
Symptoms often occur for 24 wk.
r Irritable bowel syndrome
r Lactose intolerance
438
GIARDIASIS
DIET 6. Rendtorff RC. The experimental transmission of

TREATMENT Lactose avoidance for 1 mo following treatment human intestinal protozoan parasites II. Giardia
Lamblia cysts given in capsules. Am J Hyg.
PROGNOSIS
INITIAL STABILIZATION/THERAPY 1954;59:209212.
r All symptomatic children should be treated (1). After completing appropriate treatment, symptoms
resolve within 57 days and parasites clear within 7. Pickering LK, Woodward WE, DuPont HL, et al.
r Use of empiric antibiotic therapy in children with Occurrence of Giardia lamblia in children in day
35 days.
symptoms consistent with Giardia is warranted even care. J Pediatr. 1984;104:522.
in absence of stool testing or with negative stool COMPLICATIONS 8. Singh KD, Bhasin DK, Rana SV, et al. Effect of
r Dehydration
assay. Giardia lamblia on duodenal disaccharidase levels
r People receiving treatment should avoid r Malabsorption in humans. Trop Gastroenterol. 2000;21:174.
lactose-containing foods for 1 mo after therapy (3). r Folate, vitamin B , and vitamin A deficiency 9. Hiatt RA, Markell EK, Ng E. How many stool
12
r Lactose intolerance examinations are necessary to detect pathogenic
MEDICATION r Chronic diarrhea: intestinal protozoa? Am J Trop Med Hyg.
First Line Usually caused by reinfection or drug resistance. 1995;53:36.
Metronidazole: Should retake exposure history to identify sources 10. Rossignol JF, Ayoub A, Ayers MS. Treatment of
r Not FDA approved for this indication but is
of reinfection and confirm with stool specimens. diarrhea caused by Giardia intestinalis and
commonly used as a first-line therapy Reinfection: If reinfection occurs, will respond to Entamoeba histolytica or E. dispar: A randomized,
r 15 mg/kg/day divided in 3 doses (max single dose original anti-Giardia drug. double-blind, placebo-controlled study of
250 mg) for 5 days Drug resistance: Increased with combination nitazoxanide. J Infect Dis. 2001;184:381.
Second Line regimens and with higher doses or longer courses
r Tinidazole (children 3 yr of age): of the original drug (less safe in children and
FDA approved for children >3 yr should check stool for cultures for resistance) CODES
50 mg/kg single dose (max single dose 2 g) Switch to a drug of a different class (most
r Nitazoxanide (children 1 yr of age) (10): successful option and safest in children). ICD9
r Hypersensitivity phenomenon: Urticaria, rash,
23 yr of age: 100 mg PO b.i.d. for 3 days 007.1 Giardiasis
411 yr: 200 mg PO b.i.d. for 3 days arthralgia, aphthous ulceration, reactive arthritis
r Weight loss, failure to thrive
Albendazole 1015 mg/kg/24 hr PO per day for
57 days PEARLS AND PITFALLS
r Combination therapy is indicated if treatment fails r Indolent symptomatology often results in lengthy
with single-agent therapy.
REFERENCES G
delay in diagnosis, with symptoms often wrongly
SURGERY/OTHER PROCEDURES 1. Yoder JS, Beach MJ; CDC. Giardiasis attributed to lactose intolerance or viral
r Endoscopic duodenal biopsy surveillanceUnited States, 20032005. MMWR gastroenteritis.
r String test (Entero-Test) sampling by swallowing Surveill Summ. 2007;56(7):1118. r Always consider in high-risk populations with
gelatin-coated capsule that later is retrieved. 2. Seidel J. Giardiasis. In Feigin RD, Cherry J, complaint of diarrhea.
Demmler G, et al., eds. Textbook of Pediatric r 3 stool samples are needed to maximize the yield for
DISPOSITION Infectious Diseases. 5th ed. Philadelphia, PA: WB diagnosis.
Admission Criteria Saunders; 2003:2672. r Treatment is not recommended empirically for
Indicated for severe or prolonged symptoms, especially 3. Hill DR, Nash TE. Intestinal flagellate and ciliate asymptomatic carriers unless the person is exposed
if associated with dehydration, electrolyte infections. In Guerrant RL, Walker DH, Weller PF, to pregnant women or immunocompromised
abnormalities, or failure to thrive eds. Tropical Infectious Diseases: Principles, patients or works as a food handler.
Pathogens & Practice. Oxford, UK: Churchill
Livingstone; 1999.
FOLLOW-UP
4. Brodsky RE, Spencer HC Jr., Schultz MG. Giardiasis
FOLLOW-UP RECOMMENDATIONS among American travelers to the Soviet Union. J
r Follow up with a primary care provider. Infect Dis. 1974;130:319.
r Infectious disease specialist referral if considering 5. Ongerth JE, Johnson RL, Macdonald SC, et al.
combination therapy Back-country water treatment to prevent
r Immunology referral if having recurrent infection giardiasis. Am J Public Health. 1989;79:1633.
with no identifiable repeat exposure
r Gastroenterology referral if considering other cause
of malabsorption or failure to thrive
439
GLOBE RUPTURE
Mark X. Cicero
ETIOLOGY Impaired extraocular movements and decreased

BASICS 4 mechanisms may lead to globe rupture: visual acuity should increase suspicion for a globe
r Lacerations: rupture.
DESCRIPTION Sharp objects such as knives and scissors An afferent papillary defect indicates a
r A globe rupture occurs when there is a full-thickness r Penetrating injuries: derangement in the visual axis.
laceration or puncture to the cornea or sclera. Objects with a narrow tip such as pencils, pens, When the cornea is compromised, the iris flows
r Can occur due to blunt trauma, missile, or sharp into the defect. The iris appears oblong and the
nails, and screws
object r Retained FBs: pupil appears teardrop shaped, with the narrow
r The sclera is thinnest and weakest where it meets portion of the teardrop pointing to the injury.
Metal debris, flying wood, and stone chips
the cornea anteriorly at the limbus, where the r Blunt trauma: When the sclera ruptures, the choroid of the eye
extraocular muscles insert, and posteriorly where fills the defect.
Assaults, motor vehicle collisions, sports injuries, Examiners should inspect the anterior chamber for
the optic nerve exits. and paintball injuries hyphema, ideally with a slit lamp. Because
EPIDEMIOLOGY COMMONLY ASSOCIATED CONDITIONS instilled drops may enter the globe, corneal
r In the U.S., the annual incidence of all ocular trauma r Hyphema abrasion and laceration are assessed with slit
is 15.2 per 100,000 children. r Vitreous and subconjunctival hemorrhage lamp exam alone, without fluorescein instillation.
r Specific incidence for pediatric globe rupture is
r Orbital floor fracture with or without extraocular The orbit is examined for signs of fracture,
1,600 per year (1). including bony step-offs and emphysema.
r Higher incidence in adolescent males muscle entrapment
r Retinal detachment The position of the globe in the orbit is compared
r 1/3 of childhood blindness results from ocular to the contralateral eye:
r Retrobulbar hemorrhage
trauma. Exophthalmos may indicate retrobulbar
hemorrhage, and enophthalmos may indicate
RISK FACTORS
r Male gender DIAGNOSIS loss of intraocular pressure due to globe rupture.
r Work with hand or power tools Eyelid and lacrimal injuries may occur with globe
r Sports and recreation activities, such as racquet HISTORY rupture. Their presence should prompt evaluation
r Clinicians should assess the mechanism of injury, for rupture. The Birmingham Eye Trauma
sports, baseball, and paintball including the type of object involved: Terminology Score (2) is calculated using the
r Collagen disorders may cause a thin sclera or
Consider the possibility of a retained FB: following variables and may be helpful in
cornea: Organic debris, such as wood and thorns, determining the prognosis of globe rupture:
Marfan syndrome significantly increases the risk of infection. Initial visual acuity
Osteogenesis imperfecta Assess the patients tetanus status, especially Globe rupture
r Previous eye surgery when soil or metallic etiologies are present or an Afferent papillary defect
r Myopic eyes have a longer AP axis and are more FB is suspected. Endophthalmitis
prone to rupture from blunt trauma. r It is important to ask about the timing of the injury, Retinal detachment
as delayed presentation increases the risk of Perforating injury
GENERAL PREVENTION
Safety goggles should be worn during the following enophthalmitis and other infections. DIAGNOSTIC TESTS & INTERPRETATION
r Previous visual acuity should be considered:
activities: Lab
r Working with hand and power tools Comparison to current acuity r Any routine lab assays used for patients with trauma
r Patients with collagen disorders, including
r Racquet sports or preoperatively
r Paintball osteogenesis imperfecta and Marfan syndrome, are r CBC, C-reactive protein if considering
r Target shooting with firearms prone to globe rupture.
r History of laser keratotomy or other eye surgery may endophthalmitis
PATHOPHYSIOLOGY increase risk of globe rupture. Imaging

r Sharp objects and projectiles may directly penetrate r Presence of pain r CT is the imaging study of choice in the emergency
the globe: r Diplopia indicates specific intercurrent injuries: department. Advantages include:
Small foreign bodies (FBs), such as stone chips Detection of radiopaque FBs
May be due to extraocular muscle entrapment or
and metal filings, may penetrate the globe and Detection of fractures of the bony orbit
cranial nerve injury
remain within the eye. Visualization of optic nerve injury
Monocular diplopia is possible due to lens
r Blunt trauma causes AP compression, and the Detection of retrobulbar hemorrhage
dislocation. r Plain radiographs have limited utility:
subsequent increase in intraocular pressure leads to
PHYSICAL EXAM Can be used to detect orbital fractures and
rupture, usually at one of the scleral thin points: r Once a ruptured globe is suspected or confirmed,
An analogy may be made to a crushed grape, radiopaque FBs but with less sensitivity than CT
the exam should cease and precautions to prevent r US is contraindicated since direct pressure should
which also ruptures along points of weakness or
further injury should be initiated. not be placed on the globe.
tension when subjected to blunt trauma. r Grossly visible globe rupture appears as dark tissue, r MRI may offer superior images when compared to
the iris or choroid, prolapsing through the defect. CT:
r Globe rupture is often not obvious. Several exam MRI offers excellent visualization of the soft tissue
techniques aid the diagnosis: contents of the globe.
Globe rupture may be associated with Best choice for visualizing organic FBs such as soil
subconjunctival hemorrhage. Complete or and small wood chips
near-complete subconjunctival hemorrhage Contraindicated if a metal FB is suspected
prompts suspicion for globe rupture and emergent
ophthalmologic consultation:
360-degree hemorrhage may obscure globe
ruptures that involve the sclera.
440
GLOBE RUPTURE
Diagnostic Procedures/Other r Morphine 0.1 mg/kg IV/IM/SC q2h PRN: r Sympathetic ophthalmia:
r Slit lamp Initial morphine dose of 0.1 mg/kg IV/SC may be An autoimmune response in the uninjured eye
r Fluorescein is to be avoided. repeated q1520min until pain is controlled, then weeks to months after the injury
q2h PRN. Presents with pain, photophobia, and decreased
DIFFERENTIAL DIAGNOSIS visual acuity
r Subconjunctival hemorrhage Second Line
r Corneal abrasion or laceration Lorazepam 0.1 mg/kg IV up to 2 mg hourly PRN for
r Orbital fracture agitation REFERENCES
r Lens dislocation or detached retina COMPLEMENTARY & ALTERNATIVE
r Traumatic iritis THERAPIES 1. Brophy M, Sinclair SA, Hostetler SG, et al. Pediatric
The interventions of a child life specialist can be eye injury-related hospitalizations in the United
invaluable in calming a child with globe rupture. States. Pediatrics. 2006;117(6):e1263e1271.
TREATMENT 2. Kuhn F, Morris R, Witherspoon CD, et al. The
SURGERY/OTHER PROCEDURES Birmingham Eye Trauma Terminology system
PRE HOSPITAL An ophthalmologist performs all surgical interventions. (BETT). J Fr Ophtalmol. 2004;27(2):206210.
r Apply a loose-fitting eye shield:
DISPOSITION 3. Lee CH, Lee L, Kao LY, et al. Prognostic indicators
An eye patch should not be placed on the eye. of open globe injuries in children. Am J Emerg Med.
A commercially available eye shield may be used,
Admission Criteria
All children with ruptured globe(s) are admitted to the 2009;27(5):530535.
or one may be created using the bottom of a 4. Unver YB, Kapran Z, Acar N, et al. Ocular trauma
hospital following operative management by the
paper or plastic drinking cup. score in open-globe injuries. J Trauma. 2009;66(4):
ophthalmology service:
No pressure should be applied to the eyelids. 10301032.
r Penetrating objects, such as writing instruments, are r Transfer to a referral hospital may be necessary.
left in place until the patient is in the operating
room. FOLLOW-UP ADDITIONAL READING
r The patient and caretakers are encouraged to
remain calm: FOLLOW-UP RECOMMENDATIONS Uysal Y, Mutlu F, Sobac G. Ocular Trauma Score in
Any straining and activities that increase Patients with a history of globe rupture are instructed childhood open-globe injuries. J Trauma. 2008;
intraocular pressure should be avoided. to wear eye protection in all sporting events and when 65(6):12841286.
working with tools:
INITIAL STABILIZATION/THERAPY r Patients with previous globe rupture may be prone
r If not previously done, eye shielding and securing of
to subsequent rupture.
CODES G
penetrating objects is done as outlined previously:
r Patients are monitored for endophthalmitis and
Timely consultation of ophthalmology ICD9
r IV access should be established for medication sympathetic ophthalmia. r 871.0 Ocular laceration without prolapse of
administration: PROGNOSIS intraocular tissue
In some situations, IV access is obtained after the r Blunt trauma has a better prognosis than sharp r 871.1 Ocular laceration with prolapse or exposure
patient has been sedated in the operating room injuries, as there is less risk of endophthalmitis. of intraocular tissue
using inhaled anesthetics. r Serious eye injuries regularly result in permanent r 871.2 Rupture of eye with partial loss of intraocular
Associated trauma may necessitate IV fluid visual deficit or blindness. Early, baseless optimism tissue
resuscitation. about visual outcome is to be avoided.
r No eye drops are administered for ruptured globe. r Early poor prognostic signs and symptoms include:
r Broad-spectrum IV antibiotics with good intraocular
PEARLS AND PITFALLS
penetration are indicated. The need to provide Vision loss or pupillary defect
antibiotic coverage is tempered by the risk of r Concurrent injuries may be the only sign of globe
Hyphema or vitreous hemorrhage
increased intraocular pressure due to pain from IV Retinal detachment rupture, as the globe maintains its integrity. The
catheter placement. Decreased intraocular pressure choroid and/or the iris may close the defect.
r Again, efforts should be made to keep the child r Injuries and findings that should prompt
calm: COMPLICATIONS ophthalmologic consultation include:
r Blindness and loss of visual acuity are the most
Provide analgesia (IV or PO) to decrease pain and, Hyphema
ultimately, intraocular pressure. serious consequences of globe rupture. Complete or near-complete subconjunctival
r A blind and painful eye is an indication for
Sedation with a benzodiazepine should be hemorrhage
considered: enucleation. Often, the globe may be closed and left Vision loss or blindness
Ketamine may raise intraocular pressure and in place despite blindness.
r Endophthalmitis:
should be avoided.
Antiemetics, such as ondansetron, should be An inflammatory condition of the intraocular
administered to a child with nausea or vomiting. cavities usually resulting from an infection:
Can involve aqueous or vitreous humor
MEDICATION Occurs hours to weeks later depending on the
First Line organism:
r Antibiotics with good intraocular penetration Common organisms are coagulase-negative
include: Staphylococcus epidermidis, Staphylococcus
Gram-negative coverage: aureus, and Streptococcus species.
Ceftazidime 50 mg/kg dose IV q8h OR In penetrating injuries, gram-negative organisms
Gentamicin 2.5 mg/kg IV q8h like Pseudomonas species, Escherichia coli, and
Ciprofloxacin 2030 mg/kg/day IV divided Enterococcus species are more commonly
q812h encountered.
Include ceftazidime if concerned about
Pseudomonas species
Gram-positive coverage:
Cefazolin 25 mg/kg IV q8h OR
Vancomycin 10 mg/kg IV q6h
441
GLOMERULONEPHRITIS
Colette C. Mull
r Primary GN, normal C3: r Signs of associated systemic disease:

BASICS Alport syndrome SLE: Fever, rash, arthralgia and/or arthritis
Normal serum complement level: Renal disease Alport syndrome: Corneal, lens, retinal defects
DESCRIPTION IgA nephropathy HSP, ANCA-positive disease: Purpuric rash
r Acute glomerulonephritis (AGN) is the presentation r Secondary GN, normal C3: r Genital exam must be conducted to rule out perineal
for myriad renal inflammatory disorders. HSP: 20% of patients present with nephritis or source of bleeding (eg, urethral, meatal, or introital
r Hematuria and proteinuria herald glomerular nephritic syndrome at time of diagnosis. skin trauma)
inflammationthe hallmark of glomerulonephritis ANCA-positive diseases
(GN). DIAGNOSTIC TESTS & INTERPRETATION
Wegener granulomatosis
r HTN and edema are usually present. Microscopic polyangiitis Lab
Goodpasture syndrome/disease Initial Lab Tests
EPIDEMIOLOGY r Urinalysis:
Poststreptococcal acute glomerulonephritis (PSAGN) is Presence of RBCs
one of the most common causes of GN. Incidence in DIAGNOSIS Absence of blood clots
the U.S. is sporadic and declining. Hematuria of GN produces >2+ protein.
HISTORY Presence of RBC cast is pathognomonic for
RISK FACTORS r Hematuria:
r Genetic predisposition glomerular disease.
r Autoimmune disease May be sole symptom Pyuria common
Cola-colored urine: 3050% of AGN r A urine culture helps differentiate urinary tract
r Streptococcal infection
Gross hematuria: 50% of IgA nephropathy. Pink infection from GN; both entities can have associated
PATHOPHYSIOLOGY or red urine and presence of blood clots indicate proteinuria, hematuria, and pyuria.
r Immune-mediated GN: extraglomerular source of bleeding. r Additional lab testing should be guided by the
r Pain:
Trigger: Immune complex deposition in glomerulus history and physical exam. Consultation with a
Subsequent glomerular cell proliferation and Abdominal pain: HSP and IgA nephropathy pediatric nephrologist is recommended at this
apoptosis and complement activation promote Headache: Acute malignant HTN time:
inflammation, sclerosis, and fibrosis. r Hearing loss, ocular defects:
CBC:
Examples: PSAGN, IgA nephropathy, Alport syndrome X-linked disorder Leukocytosis possible
Henoch-Schonlein purpura (HSP) nephritis, r Cough: Presence of anemia may reflect hemodilution,
systemic lupus erythematosus (SLE) nephritis Wegener granulomatosis chronicity, and/or rarely iron-deficiency
r Nonimmune-mediated or pauci-immune GN: Goodpasture syndrome secondary to pulmonary hemorrhage in
Trigger and mechanism less clear IgA nephropathy Goodpasture syndrome.
r Antineutrophilic cytoplasmic antibody r Edema Serum electrolytes, BUN, and creatinine (Cr)
(ANCA)-positive GN: r Reduced urine output levels:
Trigger: Unclear r Presentation patterns: Hyponatremia from water retention
Autoantibodies to constituents of the neutrophil PSAGN: History of pharyngitis 13 wk or history of Hyperkalemia from decreased urine output
cytoplasm induce a vasculitis of the renal pharyngitis, impetigo, or cellulitis up to 6 wk prior Elevated BUN and Cr in renal insufficiency
arterioles and glomerular capillaries. to onset of hematuria Serum C3 and C4 can be instrumental in
Other organs affected: Skin and lungs IgA nephropathy: Gross hematuria, flank pain and identifying GN etiology (see Etiology):
r Hereditary nephritis (aka Alport syndrome): low-grade fever 13 days after a viral upper A low C4 is seen only in SLE GN.
Hereditary defect of type IV collagen in the respiratory or GI illness (50%), cough and Throat culture or serum antistreptolysin O (ASO),
glomerular basement membrane (GBM) congestion ongoing antihyaluronidase (AH), (GABHS pharyngitis):
Rapidly progressive GN: CHF, acute malignant HTN ASO titers peak 1014 days post-infection
ETIOLOGY r Past medical history: AH titers peak 34 wk post-infection
r Primary GN, low complement level (C3):
High BP Anti-DNAse B titers (GABHS cellulitis)
Postinfectious GN: IgA levels high in 816% of IgA nephropathy
Most common etiology of AGN Sickle cell disease or trait
Other coagulopathy Serum ANA and antidouble-stranded DNA
Most common antecedent infecting organism: serology if suspecting SLE
r Family history:
Group A beta-hemolytic streptococcus (GABHS) ANCA and anti-GBM serology if suspecting
Less common antecedent organisms: Renal disease
vasculitis and/or Goodpasture syndrome
Staphylococcus aureus and Staphylococcus Hearing loss
epidermidis Imaging
PHYSICAL EXAM r Unnecessary in emergency department
Membranoproliferative GN (MPGN) r Abnormal vital signs:
r Secondary GN, low C3: r Consider chest radiograph in following clinical
HTN
SLE scenarios:
Tachycardia
Subacute bacterial endocarditis HTN: Cardiomegaly
Tachypnea
Ventricular shunt r Suggestive physical exam findings: CHF: Cardiomegaly, pulmonary edema
Goodpasture syndrome: Infiltrates
Change in mental status
Papilledema
Gallop, rales, hepatomegaly
Edema: Pitting, generalized or localized
442
GLOMERULONEPHRITIS
r Renal interstitial disease: Pyelonephritis, acute
ADDITIONAL READING
FOLLOW-UP r Anthony BF, Kaplan EL, Wannamaker LW, et al.
interstitial nephritis, tubulointerstitial nephritis with
uveitis r Well children with isolated microhematuria and Attack rates of acute nephritis after type 49
r Vascular pathology: Trauma, sickle cell disease and proteinuria should be referred back to their primary streptococcal infection of the skin and of the
trait, renal artery/vein thrombosis, arteriovenous care physician for repeat urinalysis, a diagnostic respiratory tract. J Clin Invest. 1969;48:16971704.
thrombosis, nutcracker syndrome, malignant HTN, workup if appropriate, and a referral to a pediatric r Barratt J, Feehally J. IgA nephropathy. J Am Soc
sports- and exercise-related hematuria, nephrologist when indicated. Nephrol. 2005;16:20882097.
hemangioma, hamartoma r All other discharged patients require initial and r Donadio JV, Grande JP. IgA nephropathy. N Engl J
r Neoplasms: Wilms tumor, renal cell carcinoma, long-term primary care provider follow-up to Med. 2002;347:738748.
uroepithelial tumors, rhabdoid tumors, congenital monitor: r Eddy A. Molecular basis of renal fibrosis. Pediatr
mesoblastic tumor, angiomyolipoma Urine output Nephrol. 2000;15:290301.
r Urinary tract pathologycystitis: Bacterial, viral Weight r Feld LG, Meyers KEC, Kaplan MB, et al. Limited
(adenovirus), parasitic (schistosomiasis), TB BP evaluation of microscopic hematuria in pediatrics.
r Medications: Cyclophosphamide cystitis Adherence to a low-sodium diet: Pediatrics. 1998;102:15.
r Other: Urethritis, urolithiasis, trauma, severe Young child: 23 mEq sodium/kg/day r Hudson BG, Reeders ST, Tryggvason K. Type IV
Older child: 2,000 mg/day
hydronephrosis, foreign body r HSP patients require weekly urinalysis for 4 wk, then collagen: Structure, gene organization, and role in
r Bleeding disorders: Hemophilia A or B, platelet human diseases. Molecular basis of Goodpasture
at 2 mo and at 3 mo following diagnosis. and Alport syndromes and diffuse leiomyomatosis.
disorders, thrombocytopenia, congenital or acquired r Pediatric nephrologist referral:
coagulopathies J Biol Chem. 1993;268:2603326036.
r Miscellaneous: Idiopathic hypercalciuria without Determines need for fluid restriction r Lau KK, Wyatt RJ. Glomerulonephritis. Adolesc Med.
urolithiasis, autosomal dominant polycystic kidney PROGNOSIS 2005;16:6785.
disease r PSAGN: r Narchi H. Risk of long term renal impairment and
Majority: Spontaneous, complete recovery duration of followup recommended for
Clinical signs resolve within weeks. Henoch-Schonlein purpura with normal or minimal
TREATMENT Hematuria resolves within 612 mo. urinary findings: A systematic review. Arch Dis Child.
Rare progression to nephrotic syndrome and/or 2005;90:916920.
INITIAL STABILIZATION/THERAPY r Pan CG. Evaluation of gross hematuria. Pediatr Clin
r Emergently stabilize patients presenting with CHF renal failure requiring dialysis
2nd cases of PSAGN in the same child have been North Am. 2006;53:401412.
and/or malignant HTN.
r Restrict sodium intake. well documented.
r IgA nephropathy:
r Seligman VA, Lum RF, Olson JL, et al. Demographic G
r Restrict fluid intake in ill patients only. differences in the development of lupus nephritis: A
r Consult a pediatric nephrologist. Variable clinical course retrospective analysis. Am J Med. 2002;112:
Remission in up to half of cases 726729.
r Treat the underlying disorder as appropriate. r Stetson CA, Rammelkamp CH Jr., Krause RM, et al.
Recurrent gross hematuria during viral respiratory
MEDICATION illnesses is common. Epidemic acute nephritis: Studies on etiology,
r There are no specific medications that are used to Chronic renal failure in <50% of cases natural history, and prevention. Medicine
r Alport syndrome and MPGN: (Baltimore). 1955;34:431450.
treat or reverse GN in the emergency department
setting. Rapidly progressive forms of AGN r Wyatt RJ, Kritchevsky SB, Woodford SY, et al. IgA
r Inpatient medication and fluid management should End-stage renal failure is common. nephropathy: Long-term prognosis for pediatric
r HSP GN: patients. J Pediatr. 1995;127:913919.
be individualized and determined in consultation
with a pediatric nephrologist: Excellent prognosis r Yoshikawa N, Ito H, Yoshiara S, et al. Clinical course
Anti-inflammatory agents: IV or oral <2%: Long-term impairment of IgA nephropathy in children. J Pediatr.
corticosteroids, cyclophosphamide, azathioprine Presentation with nephritis or nephritic syndrome 1987;110:555560.
Proteinuria-reducing agents inhibit tubular injury elevates risk of long-term impairment to close to
and fibrosis: Angiotensin-converting enzyme 20%.
inhibitors, angiotensin 2 receptor blockers, statins, r SLE GN: CODES
antioxidants. Markers of poor prognosis: Severity of histology,
Diuretics for renal failure, CHF black race ICD9
r Plasmapheresis for rapidly progressive GN r Goodpasture syndrome: Poor prognosis r 580.0 Acute glomerulonephritis with lesion of
r ANCA-positive GN: proliferative glomerulonephritis
COMPLEMENTARY & ALTERNATIVE r 580.9 Acute glomerulonephritis with unspecified
High morbidity if patient presents with renal
THERAPIES insufficiency
Fish oil supplements containing omega-3 fatty acids pathological lesion in kidney
r 583.9 Nephritis and nephropathy, not specified as
have been used to control inflammation. COMPLICATIONS
r See Prognosis. acute or chronic, with unspecified pathological
SURGERY/OTHER PROCEDURES r Most common: CHF, malignant hypertensive lesion in kidney
r Renal transplant is not always curative.
r Recurrence of GN may lead to loss of allograft. encephalopathy
DISPOSITION PEARLS AND PITFALLS

r Patients with GN and oliguria and/or HTN should be r All patients with GN require involvement of a
admitted to a monitored bed. pediatric nephrologist.
r Critical care is required for patients with rapidly r Morbidity and mortality may result from
progressive glomerulonephritis, HTN uncontrolled HTN as well as secondary infection.
encephalopathy, and/or pulmonary edema.
r Mildly ill patients may be discharged.
443
GONORRHEA
Cynthia J. Mollen
GENERAL PREVENTION r Neonates typically present with a purulent

BASICS r Use of prophylactic ophthalmic antibiotics in conjunctivitis, although scalp abscesses alone can
newborns occur.
DESCRIPTION r Limiting number of sexual partners r Ill-appearing, febrile neonates with presumed GC
r Neisseria gonorrhoeae, also called gonococcus (GC) r Consistent and correct condom use infection may have bacteremia or meningitis.
is an anaerobic gram-negative bacteria. r Routine screening of sexually active adolescents
r GC is an STI that has multiple manifestations. r Treatment of sexual partners
r GC is the 2nd most commonly reported notifiable Lab
disease in the U.S. PATHOPHYSIOLOGY Initial Lab Tests
r Incubation period is usually <1 wk. r Nucleic acid amplification technique (NAAT) testing
r Common manifestations of GC include cervicitis,
r An STI that is spread through contact with the penis, from urine or pharyngeal specimens (males and
urethritis, pelvic inflammatory disease (PID), and
vagina, mouth, or anus females), vaginal or cervical specimens (females) or
neonatal conjunctivitis:
Urethritis is the usual presentation in males. r 4 stages of infection: urethral specimens (males):
1. Attachment to the mucosal cell surface NAAT tests are highly sensitive and specific on
Cervicitis or PID is the usual presentation in
2. Local penetration or invasion endocervical, vaginal, or urine specimens from
females.
r GC can also cause pharyngitis, arthritis, epididymitis, 3. Local proliferation females and urethral and urine specimens from
4. Local inflammatory response or dissemination males.
proctitis, and disseminated disease. In the neonate, Not all NAAT tests are FDA approved for use in all
scalp abscesses, arthritis, bacteremia, meningitis, r Can also be transmitted perinatally from mother to
sites; in particular, they may not be approved for
and ophthalmia (infection of the conjunctiva and infant
r Disseminated disease may occur. pharyngeal and conjunctival specimens.
deep eye structures) can occur. r If NAAT testing is not available, GC culture using
EPIDEMIOLOGY ETIOLOGY Thayer Martin medium can be used for endocervical,
Incidence N. gonorrhoeae (GC) is an anaerobic gram-negative pharyngeal, rectal, and conjunctival specimens.
r According to CDC surveillance, there were 99.1 bacteria. r Gram stain of eye discharge in the neonate to
cases of GC per 100,000 persons in 2009. COMMONLY ASSOCIATED CONDITIONS evaluate for intracellular gram-negative diplococci
r Over 350,000 new cases of GC were reported to the r Gram stain of a male urethral specimen that
Coinfection with other STIs, particularly Chlamydia
CDC in 2009. trachomatis demonstrates polymorphonuclear leukocytes with
r Rates are highest among women and adolescents. intracellular gram-negative diplococci can be
r Although rates of GC had remained steady for 10 yr, considered diagnostic for infection with GC in
the most recent rates reported in 2009 reflect a DIAGNOSIS symptomatic men; however, because of lower
10% decrease from the 2008 rate. sensitivity, a negative Gram stain cannot rule out
HISTORY infection in this population.
Prevalence r A confidential, private interview with the adolescent
r Gram stain of endocervical, pharyngeal, or rectal
r Varies by population screened may reveal a history of sexual activity and can allow
r In 2007, the median state-specific gonorrhea test specimens are not sufficient to rule out infection.
for questioning related to contraception, number of r Culture of synovial fluid or blood cultures may be
positivity among 1524-yr-old women screened in sexual partners, and prior history of an STI, including
PID. appropriate if disseminated disease is suspected.
selected family planning clinics was 0.9%. r Testing for concurrent infection with C. trachomatis
r Also in 2007, the median positivity of women r Common complaints include dysuria, penile or
vaginal discharge, lower abdominal or suprapubic using NAAT techniques
screened in selected prenatal clinics was 0.8%. r Testing for other associated infection:
r Finally, in 2007, the median positivity for gonorrhea pain, and irregular menstrual bleeding.
r Many patients are asymptomatic (7590% in Trichomonas vaginalis
by facility in women entering selected juvenile
women; 1040% in men). HIV testing
corrections facilities was 5.3%.
r Joint pain, skin rash Serum syphilis serology
RISK FACTORS Imaging
r Female (due to prolonged contact of mucosal PHYSICAL EXAM
r Symptomatic patients may have a penile or vaginal For females with significant unilateral adnexal
surfaces with infective secretions and larger mucosal tenderness or fullness, consider obtaining US to screen
surface area of the vagina) discharge present on physical exam. for tubo-ovarian abscess (see Pelvic Inflammatory
r Adolescence (age 1519 yr): Biologic and r Females with PID may also have abdominal pain,
Disease topic).
behavioral factors cervical motion, and/or adnexal tenderness.
r Early sexual debut r Disseminated GC can present as a tenosynovitis,
r Increased number of sexual partners dermatitis and polyarthralgia syndrome, or as a
r Prior history of PID purulent arthritis without skin manifestations. The
r Infrequent use of barrier contraception rash most commonly presents as a maculopapular
r Intercourse during menstruation rash, with or without petechiae, on the hands and
feet.
444
GONORRHEA
DIFFERENTIAL DIAGNOSIS r Fluoroquinolones are not routinely recommended r Cook RL, Hutchison SL, Ostergaard L, et al.
r Patients with GC who present predominantly with for the treatment of gonococcal infections due to Systematic review: Noninvasive testing for
abdominal or pelvic pain have a broad differential increasing bacterial resistance: Chlamydia trachomatis and Neisseria gonorrhoeae.
including ovarian abscess or torsion, ectopic For patients who have severe penicillin allergies Ann Int Med. 2005;142(11):914925.
pregnancy, appendicitis, or renal calculi. and are unable to tolerate cephalosporins, r Fang J, Husman C, DeSilva L, et al. Evaluation of
r Other STIs treatment with a fluoroquinolone can be self-collected vaginal swab, first void urine, and
r Urinary tract infection considered; however, cultures rather than NAAT endocervical swab specimens for the detection of
r Vaginitis (yeast, bacterial vaginosis, other bacteria, techniques should be used in order to obtain Chlamydia trachomatis and Neisseria gonorrhoeae
contact) sensitivity data. in adolescent females. J Pediatr Adolesc Gynecol.
r For disseminated disease, consider bacterial arthritis, DISPOSITION 2008;21:355360.
r Tarr ME, Gilliam ML. Sexually transmitted infections
acute rheumatic fever, connective tissue diseases, or Admission Criteria
infective endocarditis. r Patients with disseminated disease or who are ill in adolescent women. Clin Obstetr Gynecol.
2008;51(2):306318.
appearing should be admitted for treatment.
r Neonates with GC ophthalmia need to be See Also (Topic, Algorithm, Electronic
TREATMENT
hospitalized, and clinicians should have a low Media Element)
MEDICATION threshold for obtaining blood and CSF cultures. r Pelvic Inflammatory Disease
r Urethritis
First Line Discharge Criteria
r Uncomplicated urogenital and anorectal infections: Most patients with uncomplicated GC infection can be
Ceftriaxone 250 mg IM or IV as a single dose, or discharged from the emergency department after
cefixime 400 mg PO as a single dose receiving antibiotic treatment. CODES
r Pharyngeal infections: Ceftriaxone 125 mg IM or IV
as a single dose ICD9
r Epididymitis: Ceftriaxone 250 mg IM in a single dose FOLLOW-UP r 098.0 Gonococcal infection (acute) of lower
r Neonatal conjunctivitis: Ceftriaxone 2550 mg/kg genitourinary tract
FOLLOW-UP RECOMMENDATIONS r 098.10 Gonococcal infection (acute) of upper
IV or IM in a single dose, not to exceed 125 mg, plus r In most areas, GC is reportable to health authorities.
irrigation with normal saline r Patients treated for uncomplicated GC do not genitourinary tract, site unspecified
r Disseminated GC: Ceftriaxone 1 g IV q8h r 098.11 Gonococcal cystitis (acute)
require a test of cure.
r Meningitis or bacteremia: Ceftriaxone 12 g IV q12h r Sexual partners who had contact with the patient
r Disseminated GC in neonates: Ceftriaxone 2550
mg/kg/day IV or IM in a single daily dose for 7 days,
within 60 days of the onset of symptoms should be
PEARLS AND PITFALLS G
treated empirically for C. trachomatis and N.
with a duration of 1014 days, if meningitis is gonorrhoeae. r Many cases of GC are asymptomatic.
documented; or cefotaxime 25 mg/kg IV or IM q12h r Patients should refrain from sexual activity until all r GC can present with a wide array of manifestations
for 7 days, with a duration of 1014 days, if treatment is complete. and has a low threshold for screening.
meningitis is documented. r Coinfection with other STIs is common.
r In addition, for uncomplicated documented GC
r NAAT tests are as sensitive as GC cultures.
infections of the cervix, urethra, epididymis, and ADDITIONAL READING
pharynx, the most recent CDC guidelines r CDC. Screening to detect Chlamydia trachomatis
recommend the addition of azithromycin 1 g PO
once or doxycycline 100 mg PO b.i.d. for 7 days and Neisseria gonorrhoeae infections2002.
even if Chlamydia is documented as negative. MMWR Recomm Rep. 2002;51(RR-15):138.
r CDC. Sexually Transmitted Disease Surveillance,
Second Line 2009. Atlanta, GA: U.S. Department of Health and
r For penicillin-allergic patients, azithromycin 2 g PO
Human Services; 2010.
as a single dose can be used as treatment for r CDC. Sexually transmitted diseases treatment
uncomplicated GC infection. Due to expense, a high
guidelines, 2010. MMWR Recomm Rep. 2010;
rate of side effects, and increasing bacterial
59(RR-12):1110.
resistance, azithromycin is not routinely
recommended for the treatment of GC.
445
GROIN MASS
Marie Waterhouse
Deborah R. Liu
r Hydrocele: PHYSICAL EXAM

BASICS Congenital hydrocele results from abdominal fluid r May be done with patient laying supine with hip
migrating into the scrotum via a patent processus flexed and externally rotated (frog leg) or in
DESCRIPTION vaginalis. standing position
r A groin mass is characterized as a bulge or mass Hydrocele is most commonly confined to the r Should delineate if mass is confined to scrotum/labia
noted in the groin or inguinal region, with possible scrotum, but hydrocele of the cord can be located or if it extends proximally into the inguinal canal
extension into the scrotum or labia. in the inguinal canal and mistaken for a hernia. r Always confirm presence and location of both testes.
r Most often due to: Acute hydrocele may be secondary to r Describe characteristics of the mass:
Inguinal hernia inflammatory process, viral infection, malignancy, Consistency
Hydrocele testicular torsion, or torsion of testicular Fluctuance or induration
Undescended testis appendage (3). Erythema
Inguinal lymphadenopathy or adenitis Mobility
r May rarely be caused by a variety of other conditions ETIOLOGY
r Inguinal hernia Pain
EPIDEMIOLOGY r Hydrocele Enlargement with straining or crying
Incidence r Undescended testis Bluish discoloration (concerning for ischemia or
r Inguinal hernia: r Inguinal lymphadenopathy or adenitis (see necrosis)
r Exam of inguinal canal:
Overall incidence in children 15% (1) Lymphadenopathy topic):
911% of preterm infants Lymphogranuloma venereum Invagination of scrotum with the examining finger
30% of neonates with birth weight <1,000 g (2) Granuloma inguinale toward the inguinal ring may feel a hernia bulge
Male to female ratio of 6:1 Herpes simplex with straining.
60% are right-sided (due to later descent of testis r Abscess/Cellulitis Silk glove sign describes feeling of layers of
on the right) r Hematoma patent processus vaginalis when the spermatic
r Hydrocele: 6% of term males r Localized allergic reaction cord is rolled between the index finger and pubic
r Undescended testis: 34% of term males tubercle.
r Malignancy (rare): r Transillumination does not reliably distinguish
Prevalence Lymphoma between hydrocele and incarcerated hernia (both
5% of all males will develop an inguinal hernia during Leukemia may transilluminate).
their lifetime. Germ cell tumors r Abdominal exam is important:
Rhabdomyosarcoma Rebound, guarding, or other signs of peritonitis
RISK FACTORS Neuroblastoma may metastasize to testes
r Hernia, undescended testis, and hydrocele are each could indicate a strangulated hernia.
Benign teratoma Abdominal pain and nonpalpable testis should
more common in premature infants and in those r Hematocele (rare):
with family histories of genitourinary (GU) prompt consideration of torsion of undescended
Adrenal or other retroperitoneal hemorrhage testis.
anomalies.
r Other risk factors for inguinal hernia:
Cystic fibrosis DIAGNOSIS Lab
Connective tissue disorders r Lab testing is generally not necessary for the most
Conditions of increased peritoneal fluid: HISTORY common causes of groin mass.
Ascites r Unilateral or bilateral location
r For generalized lymphadenopathy, the following
Ventriculoperitoneal shunt r Onset and duration
r Any changes in size with crying or straining tests may be helpful for diagnosis:
Peritoneal dialysis
CBC with differential, ESR, C-reactive protein
r Family history of hernias or GU anomalies
PATHOPHYSIOLOGY Lactate dehydrogenase, uric acid if suspicion for
r Inguinal hernia: r Animal or insect bites malignancy
Indirect hernias are the most common type r Trauma to lower extremities PPD placement for suspicion of TB
found in children, resulting from a congenitally r Skin disorders or inflammatory conditions Epstein-Barr virus, cytomegalovirus, toxoplasma,
patent processus vaginalis. r Systemic symptoms of malignancy: Bartonella titers
Direct hernias are more common in adults and Fever, weight loss, night sweats HIV testing
are caused by an acquired weakening of inguinal r Symptoms of incarcerated hernia: r For testicular tumor suspicious for malignancy,
floor tissues. Colicky abdominal pain serum alpha-fetoprotein and serum beta-hCG
Scrotal or labial pain should be ordered.
Vomiting
Abdominal distension
Cessation of stooling
446
GROIN MASS
Imaging
r Abdominal radiographs:
Admission Criteria
For most common causes of groin mass with a r Incarcerated hernias, if successfully reduced in the 1. Benjamin K. Scrotal and inguinal masses in the
benign abdominal exam, radiographs are emergency department, will require admission newborn period. Adv Neonatal Care. 2002;2:
generally not helpful. pending surgical repair. 140148.
May reveal loops of intestine within hernia sac r Strangulated or nonreducible incarcerated hernia 2. Brandt ML. Pediatric hernias. Surg Clin North Am.
Multiple air-fluid levels indicate small bowel will require emergent surgery. 2008;88:2743.
obstruction with incarcerated hernia. r Inguinal abscess may require IV antibiotics and 3. Kapur P, Caty MG, Glick PL. Pediatric hernias and
Free air indicates bowel perforation from surgical drainage. hydroceles. Pediatr Clin North Am. 1998;45:
strangulation. 773789.
r US: Discharge Criteria 4. Szelc CS, Kelly R. Lymphadenopathy in children.
r Well appearing with pain adequately controlled
May distinguish between hernia and hydrocele Pediatr Clin North Am. 1998;45:876888.
r Patients with hernia may be discharged from the
Poorly sensitive for locating undescended testis
emergency department if the mass is reducible and
DIFFERENTIAL DIAGNOSIS does not show signs of incarceration or bowel ADDITIONAL READING
See Etiology. obstruction.
r Klein BL, Ochsenschlager DW. Groin masses. In
Issues for Referral Fleisher GR, Ludwig S, eds. Textbook of Pediatric
TREATMENT r Referral to a pediatric surgeon for timely repair of all
Emergency Medicine. 6th ed. Philadelphia, PA:
reducible inguinal hernias. Lippincott Williams & Wilkins; 2010.
PRE HOSPITAL r Some hydrocele repairs may be postponed until after r Smith SR. Inguinal hernia reduction. In King C,
Ice or a cold pack may be applied to incarcerated age 2 yr depending on risk factors.
r Consider referral for biopsy for diagnosis of Henretig FM, King BR, et al., eds. Textbook of
inguinal hernia to decrease edema.
Pediatric Emergency Procedures. 2nd ed.
INITIAL STABILIZATION/THERAPY persistent lymphadenopathy >8 wk (4). Philadelphia, PA: Lippincott Williams & Wilkins;
Treatment depends on the etiology of the groin mass. 2008.
Refer to appropriate topics. FOLLOW-UP See Also (Topic, Algorithm, Electronic
MEDICATION Media Element)
r Analgesic agents IV, IM, or PO: FOLLOW-UP RECOMMENDATIONS r Cryptorchidism
Procedural sedation may be necessary for Discharge instructions and medications: r Hernia
r Instruct parents of children with hernias on signs r Lymphadenopathy
incarcerated inguinal hernia.
r Antibiotics: and symptoms of incarceration. r Malignancy Topics
G
r Return to emergent medical care for any signs of
Inguinal abscess or cellulitis requires antibiotics to r Scrotal Pain
cover skin flora (including MRSA, following bowel obstruction or incarceration.
regional susceptibility patterns). PROGNOSIS
Broad-spectrum IV antibiotics for strangulated r Depends on the etiology of groin mass CODES
hernia to prevent sepsis from enteric organisms r Most congenital hydroceles will resolve by age 2 yr
Adenitis from Bartonella usually self-resolves in
without surgery. ICD9
the immunocompetent host: r Inguinal hernia repair generally is safe and effective: r 550.90 Unilateral or unspecified inguinal hernia,
Consider antibiotics only for complicated cases.
1020% incidence of developing hernia on without mention of obstruction or gangrene
SURGERY/OTHER PROCEDURES contralateral side (1) r 603.9 Hydrocele, unspecified
r Incision and drainage of inguinal abscess: r 789.30 Abdominal or pelvic swelling, mass, or lump,
Presence of connective tissue disorder may
Not routinely recommended due to possibility of predispose the patient to recurrence of hernia unspecified site
formation of a permanent fistula after surgical repair.
May be attempted if abscess is superficial and the
procedure is unlikely to damage nerves, vessels, or COMPLICATIONS
r Depends on etiology of the groin mass PEARLS AND PITFALLS
other structures
r Incarceration of the hernia sac can lead to ischemic r Groin masses in children are most commonly hernia,
Consider US imaging or surgical consult if abscess
is deeper or if diagnosis is uncertain (due to risk of necrosis of involved structures (bowel, testis, ovary), hydrocele, lymphadenopathy, or undescended testis.
associated hernia, bowel perforation, and damage bowel perforation, and sepsis. r Do not incise an inguinal abscess until fully certain
to vascular or other structures). r Undescended testis can be associated with
that the bowel or other structures are not involved.
r Manual reduction of hernia increased future risk of malignancy and infertility. r Emergency department manual reduction of an
r Inguinal hernia repair: r Complication rate for hernias requiring emergent
incarcerated inguinal hernia is often successful.
Emergent for nonreducible or strangulated hernias surgery is higher than for manually reduced hernias r Strangulated or nonreducible incarcerated hernias
Elective (within 1 mo of diagnosis) for reducible repaired electively. constitute a surgical emergency.
hernias in term infants (3) r Complications of hernia repair include (2):
Testicular atrophy (12%)
Injury to vas deferens (<1%)
Iatrogenic cryptorchidism (0.62.9%)
Case reports of female infertility secondary to
fallopian tube injury
447
GROUP B STREPTOCOCCAL INFECTION

Yamini Durani
r Maternal intrapartum antimicrobial prophylaxis (IAP) PHYSICAL EXAM

BASICS is recommended if positive maternal GBS screening r Findings may include fever, tachycardia, tachypnea,
(unless planned cesarean delivery and no ROM), respiratory distress or apnea, hypotension, hypoxia,
DESCRIPTION prior infant with invasive GBS disease, maternal GBS altered mental status, irritability, and/or poor
r Group B streptococcus (GBS) is a leading cause of bacteriuria during pregnancy, or unknown maternal perfusion.
perinatal bacterial infection. GBS status AND either delivery at <37 wk or ROM r Patients with osteomyelitis or septic arthritis may
r The most important source of GBS infection in >18 hr or intrapartum fever 100.4 F (3). have decreased range of motion, swelling,
neonates is vertical transmission during delivery. r No antibiotic therapy is indicated at the time of a tenderness, or pseudoparalysis:
r Early-onset GBS infection usually occurs within 24 hr positive maternal screen; only IAP has been shown The most common site of osteomyelitis is the
of birth but can occur up until 6 days of life. to reduce early-onset GBS in the neonate (3). proximal humerus.
r Late-onset GBS infection occurs between 7 and r IV penicillin G is the drug of choice for maternal r Cellulitis and adenitis often involves the face and
89 days of life IAP: submandibular regions.
r Late, late-onset GBS infection affects children Alternatively, IV ampicillin may be given.
>3 mo of age and is the least common. Penicillin allergy: IV cefazolin or vancomycin (3)
r GBS disease occurring in children >6 mo of age is r Full-term, healthy neonates are not routinely Lab
Initial Lab Tests
uncommon and may be an indicator of an required to received prophylactic antibiotics if r In the newborn nursery, neonates who are <35 wk
underlying immunodeficiency. maternal IAP is initiated.
in gestational age or who are born to mothers who
EPIDEMIOLOGY PATHOPHYSIOLOGY received IAP <4 hr prior to delivery are
r Early-onset GBS disease most commonly causes recommended to have a limited workup including
Incidence
r The overall incidence of early-onset GBS disease is sepsis, pneumonia, or meningitis. CBC/differential and blood culture and inpatient
r Late-onset GBS disease most commonly causes observation 48 hr (3).
0.30.4 cases per 1,000 live births (1,2).
r The overall incidence of late-onset GBS disease is bacteremia without a focus or meningitis. r In the emergency department, neonates who have
r Less common GBS infections: Pneumonia, signs of sepsis (regardless of maternal IAP status)
0.30.4 cases per 1,000 live births (1,2).
r Since the introduction of maternal GBS screening osteomyelitis, septic arthritis, cellulitis and adenitis, should have a CBC/differential, blood culture, urine
and intrapartum chemoprophylaxis, there has been urinary tract infection, endocarditis, otitis media, culture, and CSF sent for cell count, protein, glucose,
an 80% decrease in the incidence of early-onset and necrotizing fasciitis (6) Gram stain, and culture (3).
r With focal GBS infections, young infants may also r If the Gram stain shows gram-positive cocci, GBS
GBS in the U.S.:
There has been no change in the incidence of have GBS bacteremia and/or meningitis (6). should be strongly suspected.
late-onset GBS disease in that same time frame ETIOLOGY Imaging
(3). r GBS is a gram-positive, aerobic diplococci and one r CXR should be considered in:
Prevalence of the -hemolytic streptococci also known as Neonates with suspected sepsis
Colonization of GBS in the genitourinary or lower GI Streptococcus agalactiae. Patients with GBS infection, especially if there are
tract occurs in up to 30% of pregnant women and in r GBS serotype III is implicated in the majority of cases respiratory signs or symptoms
the absence of maternal chemoprophylaxis, 50% of r If osteomyelitis is suspected, consider MRI or bone
of early-onset meningitis and most late-onset
infants acquire GBS colonization, and 12% develop infections (3). scan.
invasive disease (4). r Prior to discontinuing antibiotics in infants with GBS
COMMONLY ASSOCIATED CONDITIONS meningitis, head CT with contrast should be
RISK FACTORS Persistent pulmonary HTN of the newborn is a
r Early-onset GBS disease: Heavy maternal performed to rule out cerebritis, ventriculitis,
condition that may be associated with early-onset GBS
subdural empyema, and intracranial abscess (6).
colonization with GBS, prolonged rupture of disease.
membranes (ROM), intrapartum fever, DIFFERENTIAL DIAGNOSIS
chorioamnionitis, prematurity, maternal bacteriuria r Other causes of neonatal sepsis: Escherichia coli and
during pregnancy, and delivery of a previous infant DIAGNOSIS herpes simplex virus
who developed GBS disease (4) r Hyaline membrane disease
r GBS virulence factors and low levels of maternal
HISTORY
r In early-onset GBS disease, the clinical signs and r Congenital heart disease
GBS type-specific IgG at delivery symptoms most commonly occur within the 1st r Metabolic disorders
r Late-onset GBS disease: Vertical or horizontal 24 hr of life: r Intracranial hemorrhage (7)
transmission (ie, newborn nursery, home, or other History often nonspecific: Irritability, lethargy,
community sources) difficulty breathing, apnea, poor feeding
GENERAL PREVENTION Fever may or may not be present.
r Potential GBS vaccines for pregnant women are r Neonates with meningitis may or may not have
being researched and developed. localizing symptoms or signs of infection.
r As per the CDC (5), all pregnant women should be r In late-onset GBS disease, complaints may include
screened for GBS colonization at 3537 wk of fever, irritability, apnea, seizures, or lethargy.
gestation via culture swabs of the lower vagina and
rectum.
448
GROUP B STREPTOCOCCAL INFECTION
6. Baker CJ. Streptococcus agalactiae (group B

TREATMENT FOLLOW-UP streptococcus). In Long SS, Pickering LK, Prober
CG, eds. Principles and Practice of Pediatric
INITIAL STABILIZATION/THERAPY FOLLOW-UP RECOMMENDATIONS Infectious Diseases. 3rd ed. Philadelphia, PA:
r Assess and stabilize airway, breathing, and Discharge instructions and medications: Churchill Livingstone; 2003:711716.
circulation. r Neonates may be discharged once the antibiotic 7. Gotoff SP. Group B streptococcal infections. Pediatr
r Critically ill patients with GBS infection may require course has been completed and they are judged to Rev. 2002;23:381385.
endotracheal intubation, IV fluid resuscitation, be stable and accept PO intake without emesis. 8. Edwards MS, Nizet V, Baker CJ. Group B
and/or inotropic support. PROGNOSIS streptococal infections. In Remington JS, Klein JO,
r Some patients may also need treatment of r The case fatality rate of early-onset GBS disease in Wilson CB, et al., eds. Infectious Diseases of the
disseminated intravascular coagulation, seizures, term infants is 35% and up to 20% in preterm Fetus and Newborn Infant. 6th ed. Philadelphia,
and increased intracranial pressure and electrolyte neonates (3). PA: Elsevier Saunders; 2006:403464.
disturbances. r The case fatality rate of late-onset GBS disease is
MEDICATION 12% in term infants and 56% in preterm infants ADDITIONAL READING
First Line (2,8).
r Broad-spectrum IV antibiotics initially r Recurrent GBS disease occurs in 13% of treated See Also (Topic, Algorithm, Electronic
r Ampicillin and cefotaxime are common choices: neonates (3). This is thought to occur due to Media Element)
persistent colonization or reinfection. r Arthritis, Septic
Ampicillin 50 mg/kg/dose q6h; if meningitis,
r Infants may continue to be colonized with GBS for r Cellulitis
100 mg/kg/dose q6h
Cefotaxime 50 mg/kg/dose q8h; if meningitis several months after birth and after treatment for r Fever topics
100 mg/kg/dose q8h systemic infection (3). r Meningitis
r Once GBS has been isolated, then IV penicillin G r Osteomyelitis
COMPLICATIONS
alone is preferred: r Patients with GBS meningitis are at risk for r Sepsis
GBS is universally sensitive to penicillin; no long-term neurologic sequelae such as deafness and
penicillin resistance occurs. motor delays.
Penicillin G 100,000 units/kg/dose IV q6h r Up to 30% of those with meningitis may have CODES
Duration of therapy for bacteremia, sepsis, and cortical blindness, spasticity, and mental retardation
pneumonia is 10 days: (7).
For meningitis, consider repeating a lumbar ICD9
puncture after 2448 hr to ensure CSF is sterile
r 041.02 Streptococcus infection in conditions G
classified elsewhere and of unspecified site,
prior to narrowing therapy to penicillin G alone. REFERENCES streptococcus, group b
GBS meningitis should be treated for 1421 days. r 771.89 Other infections specific to the perinatal
1. CDC. Trends in perinatal group B streptococcal
Second Line diseaseUnited States, 20002006. MMWR Morb period
For suspected sepsis in neonates <3 wk old, consider Mortal Wkly Rep. 2009;58:109.
empiric acyclovir therapy:
r 20 mg/kg/dose IV q8h 2. Phares CR, Lynfield R, Farley MM, et al.
Epidemiology of invasive group B streptococcal PEARLS AND PITFALLS
COMPLEMENTARY & ALTERNATIVE disease in the United States, 19992005. JAMA. r GBS infection is a leading cause of neonatal sepsis.
THERAPIES 2008;299:2056. r Incidence of early-onset GBS has declined with
There is no current evidence to support the routine use 3. American Academy of Pediatrics. Group B
universal screening during pregnancy.
of corticosteroids in GBS meningitis. streptococcal infections. In Pickering LK, Baker CJ, r In addition to screening, maternal IAP is a key factor
Kimberlin DW, et al., eds. Red Book: 2009 Report
DISPOSITION of the Committee on Infectious Diseases. 28th ed. in preventing early-onset GBS infection.
Admission Criteria r Early-onset GBS infection typically causes sepsis,
Elk Grove Village, IL: Author; 2009:628634.
r All neonates and infants with suspected GBS pneumonia, or meningitis, while late-onset GBS
4. Lachenauer CS, Wessels MR. Group B
infection should be admitted to the hospital. streptococcus. In Kliegman RM, Behrman RE, infection typically causes bacteremia without a focus
r Critical care admission criteria: or meningitis.
Jenson HB, et al., eds. Nelson Textbook of r All neonates suspected of having sepsis should have
Patients with respiratory or hemodynamic Pediatrics. 18th ed. Philadelphia, PA: WB Saunders;
instability 2007:11451150. broad-spectrum antibiotic coverage. If GBS has been
Consider for any neonate with suspected GBS 5. CDC. Prevention of perinatal group B streptococcal confirmed by culture, then antibiotic treatment may
meningitis. disease. Revised guidelines from CDC. MMWR be narrowed to penicillin G alone to complete the
Recomm Rep. 2002;52(RR-11):122. treatment.
Discharge Criteria r Even in the presence of focal late-onset GBS
From newborn nursery: Neonates whose mothers
received adequate IAP may be discharged home 24 hr infection such as cellulitis and adenitis, many infants
after birth if they are 38 wk of gestation, are healthy may have concurrent bacteremia.
appearing, will be observed reliably at home, and
there is access to telephone and immediate transport
to a health care facility:
r All others should be observed in the hospital for at
least 48 hr.
449
GUILLAIN-BARRE SYNDROME
Christopher J. Russo
r During the infection, complement-fixing IgG PHYSICAL EXAM

BASICS antibodies that arise to attack infection also bind to r Autonomic dysfunction may be seen, manifested by
peripheral nerve gangliosides, inducing autoimmune tachycardia or HTN.
DESCRIPTION injury: r Weakness is generally greatest in distal extremities;
r Guillain-Barre syndrome (GBS) is an acquired, AIDP: Multifocal mononuclear cell infiltration proximal weakness may occur. Weakness is usually
inflammatory, peripheral polyradiculoneuropathy. throughout peripheral nervous system. symmetrical.
r Characterized by rapidly progressive, symmetric Macrophages invade myelin sheaths; r Areflexia occurs in most within 1 wk of onset.
weakness and areflexia demyelination occurs. r Sensory examination is often normal.
r GBS is usually preceded by a triggering event such AMAN: Macrophages invade nodes of Ranvier, r Cranial nerve involvement is common; facial
as an infection, which may be minor. leaving myelin sheath intact. Axonal damage
weakness may occur in up to 50% of patients.
r GBS is the most common peripheral neuropathy occurs; may cause axonal degeneration. r Respiratory difficulty results in the need for
affecting children. AMSAN: Similar to AMAN, but dorsal and ventral
mechanical ventilation in 1 in 3 patients.
r Several clinical subtypes are described: roots are affected.
MFS: Pathogenesis is unclear. Impending respiratory failure can often be
Sporadic GBSalso termed acute inflammatory unpredictable.
demyelinating polyneuropathy (AIDP)is the ETIOLOGY
most common subtype (8590%). AIDP is an r Preceded by infection in many cases: DIAGNOSTIC TESTS & INTERPRETATION
immune attack on the myelin or myelin sheaths. Viral infections include cytomegalovirus, Lab
Acute motor-sensory axonal neuropathy (AMSAN): Epstein-Barr, influenza, and varicella zoster. Initial Lab Tests
Clinical presentation similar to AIDP but has a r Lab tests may be used to rule out other causes of
Bacterial infections include Campylobacter jejuni
worse prognosis. Pathophysiology involves axonal and Mycoplasma pneumoniae. weakness.
degeneration rather than demyelination; there are r Surgery, childbirth, and some immunizations such as r The hallmark of GBS is the finding of elevated CSF
no inflammatory features, as seen in AIDP. tetanus toxoid and rabies vaccine have been protein levels in the absence of pleocytosis and
Acute motor axonal neuropathy (AMAN): Similar associated normal opening pressure.
to AMSAN; however, electrophysiologic studies r Often, no precipitating event can be identified. r Consider other testing as indicated:
show normal sensory nerve conduction velocities. Botulinum assay
Miller-Fisher syndrome (MFS): Symptoms include COMMONLY ASSOCIATED CONDITIONS Serum electrolyte levels (hypokalemia)
r Certain systemic illnesses such as systemic lupus
external ophthalmoplegia, ataxia, and areflexia. Heavy metals and toxins (lead, mercury, arsenic)
Chronic inflammatory demyelinating erythematosus, sarcoidosis, or HIV infection are Organophosphates
polyneuropathy (CIDP): Evolution of symptoms is associated with GBS. Porphyria screen
slower. r Muscle atrophy, joint contractures, and pressure Acetylcholine receptor antibodies (myasthenia
ulcers may be associated with immobility. gravis)
EPIDEMIOLOGY
Creatine kinase (myositis)
Incidence HIV or other assays to assess for infection
Overall incidence of 0.52 per 100,000 per year in DIAGNOSIS
those <18 yr of age Imaging
HISTORY MRI of the brain and spine may be used to rule out a
RISK FACTORS r Typical presentation includes a history of mimic of GBS (myelopathy, cord compression). MRI
r Genetics: Most investigations have failed to reveal
progressive, symmetric weakness of muscles and may also reveal engagement of involved nerve roots or
any association with certain HLA types. areflexia: cranial nerves (supporting the diagnosis of GBS).
r Male to female ratio of 1.5:1
A hallmark of the weakness is that it is usually Diagnostic Procedures/Other
r Increasing incidence with increased age ascending from lower to upper parts of the body. r Lumbar puncture:
r Associated with antecedent infection with Weakness progresses rapidly (most reach clinical Elevated CSF protein without pleocytosis suggests
Campylobacter jejuni, Mycoplasma pneumoniae, nadir by 2 wk, and almost all reach it by 4 wk). GBS.
and certain immunizations such as quadrivalent r Other common initial presentations include difficulty
CSF may be normal within 7 days of onset of
meningococcal vaccine ambulating, facial weakness, and extremity pain. symptoms.
r Dysarthria and dysphagia may be seen.
PATHOPHYSIOLOGY CSF glucose level is normal.
r GBS is an autoimmune disorder that is often r Some patients complain of sensory deficits. Opening pressure is normal.
preceded by an otherwise trivial infection. r Many patients will have a history of antecedent r Electrodiagnostic testing:
r Weakness is typically most severe several weeks to illness within the prior 23 wk. Nerve conduction studies and electromyography
1 mo into the process. r Absence of fever is the rule. may be employed in the diagnosis of GBS. These
r Weakness can lead to respiratory compromise in 1 may be helpful when clinical findings, imaging, or
in 3 patients. lumbar puncture fail to clarify the diagnosis. Early
r Miller-Fisher variant involves descending weakness electrodiagnostic studies may be abnormal in
that initially involves the facial/bulbar musculature. 85% of patients.
450
GUILLAIN-BARRE SYNDROME
DIFFERENTIAL DIAGNOSIS SURGERY/OTHER PROCEDURES Pregnancy Considerations

r Acute myelopathy (transverse myelitis, cord r Plasmapheresis: r Parturition is associated with GBS.
compression) Removal of antibodies and immunoglobins from r Plasmapheresis may be safely carried out during
r Spinal cord tumor/compression the blood pregnancy.
r Epidural abscess Patients with rapid disease progression are most
r Vasculitic infarct likely to benefit.
r Myasthenia gravis r Physical therapy:
ADDITIONAL READING
r West Nile encephalomyelitis, Lyme neuroborreliosis, May help to avoid contractures by splinting lower
extremities and proceed with early passive range r Agrawal S, Peake D, Whitehouse WP. Management
tick paralysis
r Acute myelitis of motion exercises. of children with Guillain-Barre syndrome. Arch Dis
Physical and occupational therapy may improve Child Educ Pract Ed. 2007;92:161168.
r Poliomyelitis r Burns TM. Guillain-Barre syndrome. Semin Neurol.
outcomes.
r Heavy metal toxicity (lead, mercury, arsenic)
2008;28(2):152167.
r Acute intermittent porphyria DISPOSITION r Hughes RAC, Cornblath DR. Guillain-Barre
r Diphtheria Admission Criteria syndrome. Lancet. 2005;366:16531666.
r HIV r Most children with newly diagnosed GBS require
r Korinthenberg R, Schessl J, Kirschner J, et al.
r Hypokalemia, hypophosphatemia hospitalization, especially those who are
nonambulatory, whose symptoms are rapidly Intravenously administered immunoglobulin in the
r Myositis, rhabdomyolysis treatment of childhood Guillain-Barre syndrome: A
progressive, or whose diagnosis remains in doubt.
r Botulism r Critical care admission criteria: randomized trial. Pediatrics. 2005;116:814.
r Lawn ND, et al. Anticipating mechanical ventilation
Admission to the critical care unit should be
anticipated for those who demonstrate the in Guillain-Barre syndrome. Arch Neurol. 2001;58:
TREATMENT 893898.
potential for respiratory compromise. r Nachamkin I, Barbosa PA, Ung H, et al. Patterns of
INITIAL STABILIZATION/THERAPY Signs of autonomic dysfunction may be a poor
prognostic factor. Guillain-Barre syndrome in children. Neurology.
Identify potential for respiratory failure immediately:
r Look for shallow, rapid breathing suggesting 2007;69:16651671.
Discharge Criteria r Vajsar J, Fehlings D, Stephens D. Long-term outcome
impending respiratory failure; may often be r Patients can be safely discharged from the hospital
in children with Guillain-Barre syndrome. J Pediatr.
unpredictable. upon completion of immunotherapy if their 2003;142:305309.
r Monitor vital capacity; may require tracheal symptoms have stabilized. r Winer JB. Guillain-Barre syndrome. BMJ. 2008;337:
intubation and mechanical ventilation. r Inpatient rehabilitation may be necessary for
r Forced vital capacity (FVC) <20 mL/kg is severe, and optimal outcome.
227231. G
FVC <15 mL/kg warrants endotracheal intubation. See Also (Topic, Algorithm, Electronic
Issues for Referral
Anticipate referral to a specialist (pediatric neurology) Media Element)
MEDICATION r GBS/CIDP Foundation International (in the U.S.):
First Line to optimize the medication regimen and establish an
ongoing relationship with the patient and family. http://www.gbs-cidp.org
Intravenous immunoglobulin (IVIG): r Guillain-Barre Syndrome Support Group (in the UK):
r Dosing is institution dependent, with a max of http://www.gbs.org.uk
2 g/kg divided over 25 days. FOLLOW-UP r Weakness
400 mg/kg/day for 5 days or 1 g/kg/day for
2 days, or 2 g/kg as a single dose FOLLOW-UP RECOMMENDATIONS
IVIG and plasmapheresis are equally effective. PROGNOSIS CODES
Complications are less common with IVIG. r Most children (9095%) demonstrate good recovery
Second Line within 312 mo. ICD9
r Corticosteroids have not been shown to be r Overall mortality is <5%. 357.0 Acute infective polyneuritis
beneficial and are therefore not recommended. r The need for mechanical ventilation is a poor
r Pain remains a common symptom and can be prognostic indicator.
controlled with different medications: r Results of electrodiagnostic studies may help with PEARLS AND PITFALLS
NSAIDs and acetaminophen are not often helpful. the prognosis. r The absence of back pain helps to distinguish GBS
IV morphine 0.1 mg/kg/dose from other spinal cord pathology resulting in lower
r Antiepileptic drugs (carbamazepine, gabapentin) are COMPLICATIONS
r Respiratory failure with the need for tracheostomy extremity weakness.
well tolerated and effective: for prolonged mechanical ventilation r Elevation of CSF protein without pleocytosis
Oral carbamazepine: Initial doses range from r Complications related to mechanical ventilation, suggests GBS.
100200 mg b.i.d. depending on the childs age. r Respiratory failure may occur rapidly.
including aspiration, pneumonia, and other infection
Oral gabapentin: Initial doses are 5 mg/kg/day r Autonomic dysregulation (HTN and/or hypotension) r Reflexes may be preserved early.
divided t.i.d. r Urinary retention r Proximal weakness may predominate early.
r Pain syndromes
r Deep venous thrombosis
r Decubitus ulcers
r Muscle wasting
451
GYNECOMASTIA
Maria Carmen G. Diaz
r Exogenous estrogen administration:

BASICS Occupational DIAGNOSIS
Dietary
DESCRIPTION Percutaneous absorption HISTORY
r Gynecomastia is enlargement of the male breast r Deficiency in serum androgens: Detailed history should be obtained to rule out serious
due to glandular proliferation. Primary hypogonadism underlying systemic or endocrine disease in patients
r May be unilateral or bilateral Klinefelter syndrome with suspected pathologic gynecomastia. Patients
r May be asymmetric Medications: with physiologic gynecomastia should have a benign
r May be physiologic or pathologic (associated with Ketoconazole history. Key questions to ask include:
Spironolactone r Onset, rate of development, and duration of
underlying organic disease)
r Physiologic gynecomastia may be seen in newborns Metronidazole gynecomastia
Infection: r Associated breast pain/tenderness
due to normal stimulation by maternal hormones.
r Physiologic gynecomastia may also be seen in males Mumps r Nipple discharge
Orchitis r Weight loss/gain
from early to mid puberty (Tanner stages 24).
r Prepubertal gynecomastia outside of the newborn Secondary hypogonadism: r Symptoms of liver/kidney disease
Pituitary/Hypothalamic disease r Symptoms of thyroid disease
period requires further investigation. Castration
r Pathologic gynecomastia requires further r Hypogonadism
r Altered serum androgen/estrogen ratio:
investigation. r Medication use
Chronic liver or kidney disease r Illicit drug use
EPIDEMIOLOGY r Decreased androgen action:
r Anabolic-androgenic steroid use
Incidence Complete and partial androgen insensitivity r Use of herbal products:
r Peak incidence is in preteen and early teenage syndromes
prepubertal patients. Medications: Skin and hair care products containing lavender
r 3% incidence of testicular tumors in all men with Spironolactone and tea tree oil
Cimetidine (2) r Occupational/Dietary/Accidental estrogen exposure
gynecomastia
r Family history:
Prevalence ETIOLOGY Male relatives with gynecomastia
r 40% of all pubertal males develop transient r Physiologic:
gynecomastia during puberty. Newborn: PHYSICAL EXAM
r 6090% of newborns (1) Transient elevation of estrogen levels r Degree of virilization:
r 5070% of pubertal males (2) Tanner stage 24 male: Voice, facial/body hair, muscular development
r 2/3 of adolescent patients have bilateral Estrogen androgen imbalance r Breast exam:
Estrogen levels rise sooner than testosterone Place patient in supine position with hand behind
gynecomastia.
r 50% of all adolescents with gynecomastia have a levels. head.
Later in puberty when estrogenandrogen Examiner should grasp breast between thumb and
positive family history of gynecomastia.
r >50% of patients with Klinefelter syndrome have balance is restored, symptoms resolve. forefinger and gradually move toward nipple.
r Pathologic: With gynecomastia, the patient will have a
gynecomastia (3).
Exogenous estrogen discrete rubbery, mobile subareolar mass or
RISK FACTORS Congenital virilizing adrenal hyperplasia diffusely tender breast (4).
r Altered estrogen androgen balance Leydig cell tumors of the testis Compare subareolar tissue with adjacent
r Increased net effect of estrogen action relative to Sertoli cell tumor subcutaneous fat to distinguish true gynecomastia
androgen action Feminizing tumors of the adrenal gland from pseudogynecomastia.
Hermaphroditism Look for signs of cancer:
PATHOPHYSIOLOGY Klinefelter syndrome Firm asymmetric breast mass
r Estrogen excessendogenous estrogen
Prolactinoma Nipple discharge
overproduction: Hyperthyroidism Axillary lymphadenopathy
Leydig cell tumors Chronic liver or kidney disease r Genitalia:
Feminizing adrenocortical tumors Breast cancer Testicular size
hCG-secreting tumors Medications Masses
Hyperthyroidism
Phallus size and development
Drugs: COMMONLY ASSOCIATED CONDITIONS
Androgens r Milk production (witchs milk) in neonates Pubic hair
Ethanol r Obesity Palpate thyroid and look for stigmata of thyroid
r Puberty disease.
Stigmata of liver or kidney disease
r Neoplasm
452
GYNECOMASTIA
DIAGNOSTIC TESTS & INTERPRETATION SURGERY/OTHER PROCEDURES

r Areolar incision or axillary incision to access breast
REFERENCES
Lab
Initial Lab Tests may be used. 1. Cakan N, Kamat D. Gynecomastia: Evaluation and
r If physiologic gynecomastia (neonatal or pubertal r Liposuction is a newer method. treatment recommendations for primary care
gynecomastia) is strongly suspected after history r Consider surgery if: providers. Clin Pediatr. 2007;46:487490.
and physical exam, no lab workup is necessary. Affected breast measures >4 cm (rarely 2. Singh Narula H, Carlson HE. Gynecomastia.
r If pathologic gynecomastia is suspected (eg, spontaneously resolves) (4) Endocrinol Metab Clin North Am. 2007;36:
prepubertal age, presence of undervirilization, Breast enlargement persists for >2 yr (rarely 497519.
eccentric breast mass, nipple discharge, adenopathy, spontaneously resolves due to the development of 3. Nordt CA, DiVasta AD. Gynecomastia in
rapid progression of breast enlargement, testicular stromal fibrous tissue). adolescents. Curr Opin Pediatr. 2008;20:375382.
mass, persistence of symptoms >2 yr), consider Associated with pain/discomfort 4. Arca MJ, Caniano DA. Breast disorders in the
obtaining: Severe emotional or psychological reaction (6) adolescent patient. Adolesc Med. 2004;15:
BUN/Creatinine 473485.
DISPOSITION
Hepatic enzyme tests 5. Ma NS, Geffner ME. Gynecomastia in prepubertal
Thyroid function tests Admission Criteria and pubertal boys. Curr Opin Pediatr. 2008;20:
r Admission usually is not required for pathologic
Serum testosterone, luteinizing hormone, 465470.
follicle-stimulating hormone, prolactin gynecomastia.
r Consider admission for significant kidney/liver 6. Graydanus DE, Matytsina L, Gains M. Breast
Serum estrogens disorders in children and adolescents. Prim Care
Adrenal androgens disease.
r Consider admission if malignancy is the likely Clin Office Pract. 2006;33:455502.
Beta-hcG
Alpha-fetoprotein etiology of gynecomastia.
Karyotype to rule out Klinefelter syndrome (2) Discharge Criteria CODES
Imaging Most children with either physiologic (neonatal or
r Testicular US for suspected testicular neoplasm in pubertal) or pathologic gynecomastia may be treated ICD9
pathologic gynecomastia as outpatients. r 611.1 Hypertrophy of breast
r Breast US is usually not recommended unless a Issues for Referral r 778.7 Breast engorgement in newborn
pathologic etiology is suspected. r Prepubertal males with gynecomastia beyond the
r Consider CT of abdomen/adrenal glands. neonatal period should be referred to an
r Consider cranial CT or MRI to rule out pituitary endocrinologist. PEARLS AND PITFALLS
tumor. r Refer to an endocrinologist if there is evidence of an
r Patients with gynecomastia require a thorough G
r Mammography and fine-needle aspiration are not underlying pathologic condition in adolescent males
with gynecomastia. testicular exam.
recommended in the diagnostic evaluation of r Breast exam in physiologic gynecomastia:
adolescent breast enlargement (3). r Consult with a surgeon and oncologist if the breast
or testicular exam is suspicious for malignancy or Discrete, mobile subareolar mass
DIFFERENTIAL DIAGNOSIS Diffusely enlarged, painful breast
r Pseudogynecomastiaalso known as other mass. r Breast exam in pseudogynecomastia:
lipomastiais fat deposition without glandular No discrete mass palpable
proliferation. FOLLOW-UP r Do not overlook a medication-related cause.
r Breast cancer r Breast exam concerning for malignancy:
r Breast abscess FOLLOW-UP RECOMMENDATIONS
Discharge instructions and medications: Firm asymmetric breast mass
r Lipoma/Hemangioma/Lymphangioma/Dermoid cyst Eccentric location
r Physiologic (neonatal and pubertal):
r Hyperprolactinemia Fixation to skin or underlying structures
r Hypogonadism Reassurance Ulceration
r Klinefelter syndrome Follow up with primary care provider. Nipple retraction or discharge
r Pathologic:
Axillary lymphadenopathy
Discontinue offending medications. r Assess for stress level and depression in pubertal
TREATMENT Consider referral to an endocrinologist. patients.
Referral for further testing
INITIAL STABILIZATION/THERAPY PROGNOSIS
r Pseudogynecomastia:
Most gynecomastia resolves spontaneously:
Reassurance r 75% of pubertal gynecomastia resolves within 2 yr;
Recommend weight loss, as pseudogynecomastia
90% resolves within 3 yr.
occurs due to deposition of adipose tissue. r Neonatal gynecomastia usually resolves in the 1st yr.
r Physiologicneonatal:
Reassurance COMPLICATIONS
Symptoms will resolve in a few weeks. r Psychological stress and embarrassment
r Physiologicpubertal: r Skin erosion of nipple due to rubbing inside clothing
Reassurance r Breast cancer
Symptoms will resolve within a few months to 2 yr.
Rarely persist beyond 2 yr (5).
Pathologic
Treat underlying disorder
Refer to an endocrinologist if needed.
Refer to a surgeon and/or oncologist if needed.
453
LWBK822-driver-H LWBK822-Hoffman ch226.xml April 15, 2011 17:38
HAIR-THREAD TOURNIQUET
Mark R. Zonfrillo

BASICS r Hair-thread tourniquets are almost exclusively r Infection (eg, cellulitis, paronychia, felon)
accidental. r Dactylitis
DESCRIPTION r Thread tourniquets in infants are typically caused by r Dermatitis
A hair-thread tourniquet occurs when a hair or an mittens or booties. r Insect bite
artificial thread fiber wraps around fingers, toes, or r Intentional fiber wrapping should be considered, r Trauma:
genitalia, possibly leading to tissue strangulation, since abuse by hair tourniquet has been reported (1). Inflicted
necrosis, or amputation.
Accidental
EPIDEMIOLOGY r Ainhum (dactylolysis spontanea) involves only the
r In a review of 66 cases of hair or thread tourniquet DIAGNOSIS 5th toe.
syndrome in children: HISTORY r Pachyonychia congenita (1,2)
43% involved the toe r History of pain, redness, or swelling of a digit or
24% involved the finger genitalia.
33% involved the genitalia r Irritability or inconsolable crying may be the only TREATMENT
r The median age for various body parts is as follows
symptoms. r If the hair or thread is visualized, the provider can
(1): r Inquiries regarding fever, trauma, recent insect bite,
Finger: 3 wk attempt unwrapping the fiber.
or a history of sickle cell anemia may reveal an r For a hair tourniquet, a chemical depilatory (such as
Toe: 4 mo alternative diagnosis.
Penis: 2 yr the hair-removal cream Nair [Church & Dwight
Clitoris or labia: 8 yr PHYSICAL EXAM Co., Inc.]) can be used:
r Inflammation of a digit or the penis, labia, or clitoris
RISK FACTORS This should be applied for only 35 min. Chemical
r The tissue may be strangulated or necrotic.
r Maternal telogen effluvium (hair loss after depilatories are contraindicated for severely
r The hair or thread fiber may not always be visible if inflamed or broken skin (2,3).
pregnancy) r The affected structures are highly sensitive, with
r Mitten and glove use there is significant edema or skin reepithelialization.
increased pain secondary to edema and
PATHOPHYSIOLOGY strangulation:
r Tissue constriction leads to lymphatic obstruction, While hair-thread tourniquet is a clinical diagnosis,
Therefore, instrumented removal of tourniquets
other conditions should be considered and individually
edema, venous outflow obstruction, and subsequent requires adequate analgesia with topical
evaluated when appropriate.
arterial flow restriction. preparations or regional nerve blocks.
r In severe cases, tissue necrosis, bony erosion, or r For looser fibers that cannot be unwrapped, a blunt
amputation may occur. probe can be used to expose the tourniquet, which
is then cut with a scalpel or fine-tip scissors.
454
HAIR-THREAD TOURNIQUET
r For tight finger or toe fibers, an incision can be

ADDITIONAL READING
made on the lateral or dorsal aspects of the digit (3). FOLLOW-UP r Barton DJ, Sloan GM, Nichter LS, et al. Hair-thread
r For any tightly wrapped fibers refractory to removal
attempts, particularly genital tourniquets, prompt FOLLOW-UP RECOMMENDATIONS tourniquet syndrome. Pediatrics. 1988;82(6):
surgical consultation is warranted (eg, urology or Caregivers should closely observe the affected area, 925928.
plastic surgery), and procedural sedation or general and patients should be re-evaluated within 24 hr or r Carlson DW, DiGiulio GA, Givens TG, et al.
anesthesia may be necessary (1,3). sooner if symptoms persist or worsen. Illustrated techniques of pediatric emergency
PROGNOSIS procedures. In Fleisher GR, Ludwig S, Henretig F,
SURGERY/OTHER PROCEDURES et al., eds. Textbook of Pediatric Emergency
Manual cutting of the hair thread: Usually, prompt relief and full recovery occur:
r Prolonged constriction and strangulation may result Medicine. 5th ed. Philadelphia, PA: Lippincott
r Usually, significant swelling makes this difficult.
Williams & Wilkins; 2005.
r Local anesthetic administration or procedural in necrosis or loss of digit.
sedation may be necessary. COMPLICATIONS
r Incision at the 3 oclock and/or 9 oclock position is r Secondary infection CODES
safest. r Bleeding
r Consider a urology consultation. r Necrosis ICD9
r Amputation r 607.89 Other specified disorders of penis
DISPOSITION
r Since constricting bands may not always be visible r 729.81 Swelling of limb
after fiber removal, observing edema improvement
and reperfusion is necessary prior to discharge.
REFERENCES
r Even with successful tourniquet release, admission 1. Mat Saad AZ, Purcell EM, McCann JJ. Hair-thread PEARLS AND PITFALLS
may be necessary for wound care. tourniquet syndrome in an infant with bony erosion: r A high index of suspicion, careful physical exam,
Admission Criteria A case report, literature review, and meta-analysis. and prompt removal of the fiber are critical in
r Patients requiring treatment under anesthesia Ann Plast Surg. 2006;57(4):447452. preventing tissue necrosis or amputation.
r Patients with tissue breakdown or necrosis 2. Sylwestrzak MS, Fischer BF, Fischer H. Recurrent r Unlike inflammation caused by a hair-thread
clitoral tourniquet syndrome. Pediatrics. tourniquet, that due to dactylitis typically involves
2000;105:866. multiple digits.
3. Pantuck AJ, Kraus SL, Barone JG. Hair strangulation r Neurovascular status should be documented before
injury of the penis. Pediatr Emerg Care. and after tourniquet removal.
1997;13:423. r Although rare, the provider must consider
intentional wrapping from ethnic beliefs,
superstitions, or deliberate physical or sexual abuse.
r Caregivers should be given anticipatory guidance
about not leaving their infants hands and feet
covered for extended periods of time.
H
455
HALLUCINOGEN POISONING
Robert J. Hoffman
r Sympathomimetic syndrome may result from r HEENT:

BASICS adrenergic agonism. This includes HTN, tachycardia, Miosis or mydriasis may be present depending on
hyperthermia, and possibly end organ injury such as the hallucinogen involved.
DESCRIPTION stroke, myocardial dysrhythmia, or MI. Nystagmus is very common with ketamine and
r Hallucinogens are substances whose primary effects r Synesthesia is a common effect of hallucinogens in dextromethorphan use.
are alteration of sensory perception. which sensory modalities are crossed, mixed, or r CNS: Depressed mental status or coma may be
r These are drugs of abuse, though some are legal. blended: present.
r LSD is the prototypical hallucinogen, others include During synesthesia, patients may sense that they r Choreoathetosis, odd movements, and muscle
PCP, mescaline, peyote (cactus button) psilocybin can see sounds, etc. stiffness or rigidity may be present with
(mushrooms), Salvia divinorum, ketamine, dextromethorphan or ketamine.
ETIOLOGY r Psychiatric:
dextromethorphan in cough suppressants, and r Marijuana
others. r LSD Patients will typically have hallucinations, some of
r Though the drug is typically taken volitionally, users which may be very disturbing or frightening. Other
r PCP
may unknowingly be given the drug or may receive r Mescaline significant cognitive impairment may also be
it unknowingly in an adulterated drug, such as present.
r Peyote
marijuana laced with PCP or pills purported to Patients may be catatonic.
contain Ecstacy (MDMA) that also contain r S. divinorum
Patients may be a threat to themselves or others.
dextromethorphan. r Dextromethorphan r Diaphoresis may be present.
r Altered perception and cognition is the effect sought r Ketamine
by users, but adverse experiences, called a bad r Ecstacy (MDMA) DIAGNOSTIC TESTS & INTERPRETATION
trip, often result in the patient being brought to Lab
medical care. COMMONLY ASSOCIATED CONDITIONS Initial Lab Tests
r Vomiting r Assess serum glucose in any patient with altered
EPIDEMIOLOGY r Depressed consciousness consciousness.
Incidence r Anxiety, agitation, or fear r Serum electrolytes
r Hallucinogens are widely used, though precise r Drug of abuse screening typically only detects
numbers are unknown. marijuana and no other hallucinogens:
r Marijuana is the most widely used drug of abuse in DIAGNOSIS Such testing is not recommended because it
the U.S. cannot be used for clinical management.
HISTORY
PATHOPHYSIOLOGY A history is typically available from the patient or Attempting to use such results for clinical
r Hallucinogens act by a variety of mechanisms, others who have brought the patient to medical care. management often results in misinterpretation of
including agonism at serotonin receptors, sigma the assay and mismanagement.
opioid receptors, kappa opioid receptors, PHYSICAL EXAM Urinalysis and/or creatine phosphokinase to
r Assess vital signs and pulse oximetry:
cannabinoid receptors, and NMDA receptor screen for rhabdomyolysis may be indicated in
antagonism. Tachycardia and HTN are common as direct results cases of psychomotor agitation.
r Serotonin syndrome may rarely result from of drug use as well as secondary to anxiety.
Slight elevation of temperature may result from
serotonergic agonism. This includes severe,
psychomotor agitation.
hyperthermia, muscle rigidity, and altered mental
status.
456
HALLUCINOGEN POISONING
Imaging r Lorazepam 0.05 mg/kg IV, max single dose 2 mg,

CT of the brain may be indicated if an intracranial may be repeated q1520min. FOLLOW-UP
lesion is suspected: r Antipsychotics are not recommended in treatment of
r This is not routinely indicated. hallucinogen toxicity. The psychotic effects typically PROGNOSIS
resolve very quickly after the responsible drug has Patients usually recover fully without sequelae.
been metabolized: COMPLICATIONS
Obtain ECG. r Injury secondary to psychomotor agitation
Unlike patients with ongoing psychiatric problems,
DIFFERENTIAL DIAGNOSIS hallucinogen toxicity fully resolves with no need r End organ injury secondary to sympathomimetic
r Sympathomimetic poisoning for further treatment. effect of amphetamine-like hallucinogens
r Ethanol intoxication r Serotonin syndrome
Second Line
r Other drug intoxication r Seizure
Ondansetron:
r Psychosis r 0.15 mg/kg IV, max single dose 8 mg; may repeat
r Schizophrenia
q45min to a max total dose 0.6 mg/kg
r For uncommon cases of severe vomiting ADDITIONAL READING
r DOnofrio G, McCausland JB, Tarabar AF, et al. Illy:
TREATMENT COMPLEMENTARY & ALTERNATIVE
THERAPIES Clinical and public health implications of a street
PRE HOSPITAL Placing patient in a darkened, quiet room with drug. Subst Abus. 2006;27:45.
Assess and stabilize airway, breathing, and circulation: minimal sensory stimulation is often practiced and r Lange JE, Reed MB, Croff JM, et al. College student
r Protect patients from themselves; restraint may seems to be helpful to minimize agitation, fear, and use of Salvia divinorum. Drug Alcohol Depend.
sometimes be necessary. degree of medication and nursing care required. 2008;94:263.
r Richardson WH 3rd, Slone CM, Michels JE. Herbal
INITIAL STABILIZATION/THERAPY DISPOSITION
r The main goals of therapy are ensuring that no other drugs of abuse: An emerging problem. Emerg Med
Admission Criteria Clin North Am. 2007;25:435.
causes of symptoms, such as hypoglycemia, head r Patients with prolonged symptoms, such as might
r Spain D, Crilly J, Whyte I, et al. Safety and
trauma, etc., are etiologic. occur with those who have ingested peyote or
r Once a diagnosis is established, supportive care and effectiveness of high-dose midazolam for severe
another long-acting drug, may need admission for
behavioural disturbance in an emergency
maintaining a safe environment are needed. ongoing care until there is return to a safe baseline
r Sedation with benzodiazepines is sometimes department with suspected psychostimulant-
mental function.
r Admit for concomitant injury or medical issues. affected patients. Emerg Med Australas. 2008;20:
necessary. 112.
MEDICATION Discharge Criteria See Also (Topic, Algorithm, Electronic
First Line After resolution of hallucinations or psychosis, patients
r Benzodiazepines: First-line therapy and typically the
Media Element)
may be safely discharged.
Sympathomimetic Poisoning
only medication needed to treat hallucinogen Issues for Referral
r Refer all patients for drug counseling.
poisoning
Diazepam: r If patients have persistent psychiatric symptoms,
H
First-line medication for any cocaine-intoxicated
CODES
psychiatric consult may be needed:
patient Patients with schizophrenia often are substance
Administer for agitation, chest pain, or ICD9
abusers, and it is common that the drug use has 969.6 Poisoning by psychodysleptics (hallucinogens)
HTN/tachycardia simply unmasked an underlying psychiatric
Initial dose 0.1 mg/kg IV, which may be disease.
repeated q5min PEARLS AND PITFALLS
After administering a given dosage 3 times,
increase the dose by doubling. r It is critical to evaluate for alternate etiologies of
symptoms, such as hypoglycemia or head trauma.
r Most patients with hallucinogen toxicity require only
supportive care.
r If medication is required, benzodiazepines are
preferred and usually provide excellent sedation.
r Most patients may be discharged from the
emergency department within 412 hr.
457
HAND-FOOT-AND-MOUTH DISEASE
Esther Maria Sampayo
r A primary or minor viremia results in spread to r Cutaneous lesions are present in 2/3 of patients:
BASICS distant parts of the reticuloendothelial system, The exanthem may be macular, maculopapular, or
including the liver, spleen, bone marrow, and distant papulovesicular and may be petechial.
DESCRIPTION lymph nodes. Typically, the dorsal, interdigital aspect of the
r Hand-foot-and-mouth disease (HFMD) is a viral r The host immune response may curtail replication at hands and feet are involved.
illness characterized by: this point, resulting in a subclinical infection with The lesions are usually elliptical in shape with the
Fever and malaise only fever, sore throat, and malaise. long axis of the lesion along the skin lines and
Vesiculoulcerative enanthem in the mouth r A secondary major viremia usually occurs to target start as a 210-mm erythematous macule on
Macular, papular, or vesicular exanthem on the organs such as the pharynx, the skin, the which a gray, oval vesicle develops.
distal extremities myocardium, and the meninges. It can also involve The exanthem may also occur on the proximal
r The most common causative agent is Enterovirus. extremities, buttocks, and genitalia.
the adrenal glands, pancreas, liver, pleura, and
lungs. r Some patients may also exhibit a mild
EPIDEMIOLOGY
r HFMD is seen in children <10 yr of age, but most r Tropism to target organs is determined by the lymphadenopathy of the cervical or submandibular
commonly is seen in children <5 yr. infecting Enterovirus serotype. glands.
r In temperate climates, most commonly summer and r The minor and major viremia may correlate with the
fall biphasic appearance of fever and symptoms Lab
r Highly contagious and afflicts up to 50% of those commonly seen with Enterovirus. r The diagnosis can be made clinically.
r Antibody production in response to enteroviral r Routine lab tests are not indicated.
exposed
r Infection results in immunity to the specific virus infections occurs within the 1st 710 days, and r Although most children will not require culturing to
that caused the illness; however, a 2nd illness may viremia ceases with antibody production.
establish the diagnosis, viral cultures from the
occur to a different strain of Enterovirus. ETIOLOGY lesions, throat, CSF, urine, or stool may be sent to
r Infected persons are most contagious during the 1st r Enterovirus is the causative agent, of which classify the virus.
2 wk of the illness with respiratory viral shedding coxsackievirus A16 and enterovirus 71 are the most r Polymerase chain reaction assay is more rapid and
but may be carriers for a month after the initial common. more sensitive than cell culture and can detect
infection with fecal viral shedding. r Sporadic cases of HFMD may also be caused by Enterovirus.
r It is not transmitted to or from pets or other animals. coxsackieviruses A5, A7, A9, A10, B2, and B5. Pathological Findings
RISK FACTORS r Classic histopathologic findings of HFMD include an
r Contact with oral and respiratory secretions, blister intradermal vesicle containing neutrophils and
DIAGNOSIS
fluid, fecal material or aerosolized droplets in a eosinophilic cellular debris.
fecaloral or oraloral route HISTORY r The adjacent epidermis is characterized by
r Risk factors for infection include diaper changing, r The disease usually begins with a low-grade fever, intracellular and intercellular edema called reticular
poor sanitation, crowded living conditions, and low poor feeding and appetite, malaise, and often a sore degeneration.
socioeconomic status. throat or mouth. r The dermis has a mixed infiltrate in which
r Children <5 yr of age are the most susceptible to r Occasionally, patients may have high fever, diarrhea, eosinophilic intranuclear inclusions can be visualized
infection due in part to a lack of prior immunity; cough, and arthralgias. with an electron microscope (1).
HFMD is extremely uncommon in adults. r The enanthem is composed of painful lesions in the r Neuropathology in fatal cases of enterovirus 71
mouth, on the tongue, and in gingival and buccal have demonstrated features of acute encephalitis
GENERAL PREVENTION
r Good hand hygiene mucosa that develop 1 or 2 days after the onset of involving the brain stem and spinal cord.
r Cleaning dirty surfaces and soiled items such as toys symptoms.
r The exanthem is composed of a nonpruritic rash DIFFERENTIAL DIAGNOSIS
with soap and water initially, then disinfecting them r The characteristic findings of HFMD are seldom seen
located on the hands and feet that also develops in other diseases. However, early in the disease,
with a dilute solution of chlorine-containing bleach.
r Avoiding close contact with persons with the disease over 12 days. when only the exanthem or enanthem occur, the
r A person may only have the rash or only the mouth
r Standard and contact precautions in the differential diagnosis includes:
lesions, but both may occur simultaneously. r Herpetic gingivostomatitis
hospitalized patient r Mucosal lesions heal in 57 days.
r Breast-feeding reduces risk of infection. r Herpangina
r Cutaneous lesions are usually present for 510 days. r Aphthous stomatitis
PATHOPHYSIOLOGY r Stevens-Johnson syndrome
r Enterovirus infection is acquired initially via the oral PHYSICAL EXAM
r Most patients with HFMD will be febrile. r Boston exanthem:
or respiratory route with viral implantation in the r Oral lesions begin as erythematous macules that
buccal and ileal mucosa. The causative organism is echovirus 16.
r The incubation period for most enteroviral infections evolve into 23-mm vesicles on an erythematous Mild febrile illness with macular rash on the face,
base, appearing as a halo: trunk, palms, and soles accruing at the time or
ranges from 310 days.
r Initial replication in the pharynx and intestine is Vesicles are rarely observed because they rapidly after defervescence
become ulcerated. Oral lesions absent
followed by invasion of the lymphatic system within Lesions are usually located on the palate, buccal r Varicella
24 hr. mucosa, gingival, and tongue.
The tongue is involved in 44% of cases and is
usually tender and edematous.
The total number of ulcers averages from 510.
458
HAND-FOOT-AND-MOUTH DISEASE
DIET
r Avoid spicy foods. CODES
TREATMENT r Avoid acidic foods such as orange juice.
INITIAL STABILIZATION/THERAPY r Encourage cool fluids such as popsicles in frequent, ICD9
r Assess and stabilize airway, breathing, and small aliquots. 074.3 Hand, foot, and mouth disease
circulation.
r Severe cases may require administration of IV fluid PROGNOSIS
HFMD is self-limited and generally has

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P1: OSO/OVY P2: OSO/OVY QC: OSO/OVY T1: OSO

LWBK822-FM LWBK822-Hoffman April 19, 2011 8:53

Fleisher & Ludwigs

EDITORS ASSOCIATE EDITORS

Fleisher & Ludwigs

Vincent J. Wang, MD, MHA

Senior Acquisitions Editor: Frances DeStefano

Two Commerce Square

Library of Congress Cataloging-in-Publication Data

Tzvi Aaron, MD Carla Maria P. Alcid, MD Bhawana Arora, MD

Michael D. Baldovsky, DO, MBA Robert A. Belfer, MD Stuart A. Bradin, DO

Kerry Caperell, MD Lauren S. Chernick, MD Ilene A. Claudius, MD

Barbara Csanyi, MD Naomi Dreisinger, MD Ara Festekjian, MD, MS

Marianne Gausche-Hill, MD Sandip A. Godambe, MD, PhD, MBA Ewa Grochowalska, MD

Matthew Lee Hansen, MD Jeffrey Hom, MD, MPH Nazreen Jamal, MD

Allison A. Keller, MD In K. Kim, MD, MBA William I. Krief, MD

Karen Y. Kwan, MD Kerry Leupold, DO Frank LoVecchio, DO

D. Richard Martini, MD Lilit Minasyan, MD Brent W. Morgan, MD

Joshua Nagler, MD Kevin C. Osterhoudt, MD Pinaki N. Patel, DO

Mary Jane Piroutek, MD Juliette Quintero-Solivan, MD Lilia Reyes, MD

Michael D. Rosen, MD Mary T. Ryan, MD Kalyani Samudra, MD

Cindy Ganis Roskind, MD Sunil Sachdeva, MD Genevieve Santillanes, MD

Emily Schapiro, MD Hanan Sedik, MD Adhi Sharma, MD

Donna M. Simmons, MD Kai M. Sturmann, MD Jennifer Thull-Freedman, MD, MSc

Michael E. Valente, MD Vincent J. Wang, MD, MHA Derek A. Wong, MD

Preface v Apparent Life-Threatening Event 70

Carpal Tunnel Syndrome 144 Cystic Hygroma 230

Epiglottitis/Supraglottitis 314 Fracture, Pelvic Avulsion 400

Hepatic Encephalopathy 486 Irritable Bowel Syndrome 572

Neoplasm, Brain 658 Pertussis 742

Salicylate Poisoning 828 Testicular Torsion 912

Urinary Retention 998 Ventriculoperitoneal Shunt Malfunction 1020

TOPICAL TABLE OF CONTENTS

Cardiovascular Emergencies Abscess, Rectal 20

xxxiv r r r TOPICAL TABLE OF CONTENTS

Poison Ivy/Oak/Sumac 760 Drowning 272

TOPICAL TABLE OF CONTENTS r r r xxxv

Gastroenteritis 426 Groin Mass 446

xxxvi r r r TOPICAL TABLE OF CONTENTS

Trauma, Vaginal 980 Stomatitis 874

TOPICAL TABLE OF CONTENTS r r r xxxvii

Dermatomyositis 244 Epiglottitis/Supraglottitis 314

xxxviii r r r TOPICAL TABLE OF CONTENTS

Osteomyelitis 688 Upper Respiratory Infection 992

TOPICAL TABLE OF CONTENTS r r r xxxix

Neurologic Emergencies Subdural Hematoma 886

xl r r r TOPICAL TABLE OF CONTENTS

Eye, Red 332 Trauma, Knee 966

TOPICAL TABLE OF CONTENTS r r r xli

Hemoptysis 480 Panic Attack 716

xlii r r r TOPICAL TABLE OF CONTENTS

Surgical Emergencies Calcium Channel Blocker Poisoning 134

TOPICAL TABLE OF CONTENTS r r r xliii

Dislocation, Knee 260 Pericardial Effusion/Tamponade 732

Fleisher & Ludwigs

ETIOLOGY r Chronic isolated abdominal distention in otherwise

ABSCESS, BARTHOLIN GLAND

BASICS DIAGNOSIS TREATMENT

ABSCESS, BARTHOLIN GLAND

PATHOPHYSIOLOGY DIAGNOSTIC TESTS & INTERPRETATION

r Other pathogens: DIAGNOSTIC TESTS & INTERPRETATION

ABSCESS, LUDWIG ANGINA

r Diagnostic criteria: DIAGNOSTIC TESTS & INTERPRETATION

ABSCESS, LUDWIG ANGINA