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S E V E N T H E D I T I O N
Clinical
Anesthesia
LWBK1137-FM_i-xxii.indd 1 12/01/13 2:14 AM

S E V E N T H E D I T I O N
Clinical
Anesthesia
Edited By
Paul G. Barash, md Michael K. Cahalan, md

Professor Professor and Chair
Department of Anesthesiology Department of Anesthesiology
School of Medicine School of Medicine
Yale University School of Medicine The University of Utah
Attending Anesthesiologist Salt Lake City, Utah
Yale-New Haven Hospital
New Haven, Connecticut M. Christine Stock, md
Professor and Chair
Bruce F. Cullen, md Department of Anesthesiology
Feinberg School of Medicine
Emeritus Professor
Northwestern University
Department of Anesthesiology
Chicago, Illinois
School of Medicine
University of Washington
Seattle, Washington
Rafael Ortega, md
Professor
Vice-Chairman of Academic Affairs
Robert K. Stoelting, md Department of Anesthesiology
Emeritus Professor and Past Chair School of Medicine
Department of Anesthesia Boston University
School of Medicine Boston, Massachusetts
Indiana University
Indianapolis, Indiana

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Library of Congress Cataloging-in-Publication Data

Clinical anesthesia/edited by Paul G. Barash . . . [et al.]. – 7th ed.
p. ; cm.
Includes bibliographical references and index.
ISBN 978-1-4511-4419-2 (alk. paper)
I. Barash, Paul G.
[DNLM: 1. Anesthesia. 2. Anesthesiology. 3. Anesthetics. WO 200]

617.9′6–dc23 2012050848
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10 9 8 7 6 5 4 3 2 1

F or A ll S tudents of A nesthesiology

C ont r i b u tin g A u tho r s
Saint Adeogba, MD Honorio T. Benzon, MD

Senior Research Fellow Professor of Anesthesiology
Department of Anesthesiology and Pain Medicine Department of Anesthesiology
School of Medicine Feinberg School of Medicine
University of Washington Northwestern University
Seattle, Washington Attending Staff
Shamsuddin Akhtar, MD Northwestern Memorial Hospital
Associate Professor Chicago, Illinois
School of Medicine Christopher M. Bernards, MD*
Yale University Professor
New Haven, Connecticut Department of Anesthesiology
School of Medicine
Virginia Mason University
Michael L. Ault, MD, FCCP, FCCM Seattle, Washington
Associate Professor
Departments of Anesthesiology, Neurological Surgery and Surgery
Marcelle E. Blessing, MD
Assistant Professor
Medical Director
School of Medicine
Departments of Blood Gas Laboratory and Emergency Response Teams
Yale University
Northwestern Memorial Hospital
New Haven, Connecticut
Chicago, Illinois
Michelle Y. Braunfeld, MD
Douglas R. Bacon, MD, MA Professor and Chair
Professor and Chair Department of Anesthesiology
Department of Anesthesiology David Geffen School of Medicine
School of Medicine University of California Los Angeles
Wayne State University Greater Los Angeles VA Hospital
Detroit, Michigan Los Angeles, California
Chair
Saint Joseph Mercy Oakland
Ferne R. Braveman, MD
Professor
Pontiac, Michigan
School of Medicine
Gina C. Badescu, MD Yale University
Assistant Professor New Haven, Connecticut
School of Medicine Brenda A. Bucklin, MD
Division of Cardiothoracic Anesthesiology Professor
Duke University Hospital Department of Anesthesiology
Durham, North Carolina School of Medicine
University of Colorado
Dalia Banks, MD, FASE Aurora, Colorado
Associate Professor
School of Medicine Asokumar Buvanendran, MD
University of California San Diego Professor
Division of Cardiothoracic Anesthesiology Chief Department of Anesthesiology
Clinical Director for Sulpizio CVC and PTU Rush University Medical Center
San Diego, California Senior Attending Staff
Paul G. Barash, MD Rush University Medical Center
Professor Chicago, Illinois
School of Medicine
Yale University
Attending Anesthesiologist
Yale-New Haven Hospital
New Haven, Connecticut *Deceased
vii

viii Contributing Authors
Michael K. Cahalan, MD Marie Csete, MD, PhD

Professor and Chair Division Director
Department of Anesthesiology Center for Cellular Therapies
School of Medicine AABB
University of Utah Bethesda, Maryland
Salt Lake City, Utah Adjunct Faculty
Levon M. Capan, MD USCD Medical Center
Professor San Diego, California
School of Medicine
New York University Bruce F. Cullen, MD
Associate Director Emeritus Professor
Bellevue Hospital School of Medicine
New York, New York University of Washington
Seattle, Washington
Louanne M. Carabini, MD
Assistant Professor Anthony Cunningham, MD
Department of Anesthesiology Professor
Feinberg School of Medicine Foundation Dean
Northwestern University Pu-RCSI School of Medicine
Chicago, Illinois Malaysia
C. Richard Chapman, PhD Armagan Dagal, MD, FRCA

Professor
Assistant Professor
Department of Anesthesiology and Pain Medicine
School of Medicine
School of Medicine
University of Utah
Pain Research Center University of Washington
Salt Lake City, Utah Chief of Spine and Orthopedic Anesthesia Services
Harborview Medical Center
Amalia Cochran, MD Seattle, Washington
Associate Professor
Department of Surgery
School of Medicine Albert Dahan, MD
University of Utah Professor
Salt Lake City, Utah Department of Anesthesiology
Leiden University Medical Center
Edmond Cohen, MD Leiden, The Netherlands
Professor
Department of Anesthesiology Steven Deem, MD
Director of Thoracic Anesthesia Professor
Mount Sinai School of Medicine Department of Anesthesiology and Pain Medicine
New York, New York School of Medicine
Christopher W. Connor, MD, PhD Director
Assistant Professor Department of Neurocritical Care
Departments of Anesthesiology, and Harborview Medical Center
Biomedical Engineering Seattle, Washington
School of Medicine
Boston University
Boston, Massachusetts Timothy R. Deer, MD
Clinical Professor
C. Michael Crowder, MD, PhD
School of Medicine
Dr. Seymour and Rose T. Brown Professor
West Virginia University
School of Medicine President and CEO
Washington University Center for Pain Relief, Inc.
St. Louis, Missouri Charleston, West Virginia

Contributing Authors ix
Stephen F. Dierdorf, MD John H. Eichhorn, MD

Professor and Vice Chair Professor
Department of Anesthesia Department of Anesthesiology
School of Medicine College of Medicine
Indiana University University of Kentucky
Indianapolis, Indiana University of Kentucky Medical Center
Lexington, Kentucky
Karen B. Domino, MD, MPH
Professor James B. Eisenkraft, MD
Department of Anesthesiology and Pain Medicine Professor
School of Medicine Department of Anesthesiology
University of Washington Mount Sinai School of Medicine
University of Washington Medical Center New York, New York
Seattle, Washington
Matthew R. Eng, MD
Resident
François Donati, MD, PhD, FRCPC Department of Anesthesia
Professor
Cedars-Sinai Medical Center
Los Angeles, California
Université de Montréal
Department of Anesthesiology Alex S. Evers, MD
Hôpital Maisonneuve-Rosemont Henry Mallinckrodt Professor and Chair
Montréal, Québec, Canada Department of Anesthesiology
School of Medicine
Washington University
Michael B. Dorrough, MD Anesthesiologist-in-Chief
Staff Anesthesiologist Department of Anesthesiology
United Medical Center Barnes-Jewish Hospital
Cheyenne, West Virginia St. Louis, Missouri
Randal O. Dull, MD, PhD Ana Fernandez-Bustamante, MD, PhD

Vice Head for Research Assistant Professor
College of Medicine School of Medicine
University of Illinois at Chicago University of Colorado, Denver
Chicago, Illinois Aurora, Colorado
Thomas J. Ebert, MD, PhD Lynne R. Ferrari, MD

Professor, Vice Chair for Education Chief, Division of Perioperative Anesthesia
Residency Program Director Department of Anesthesia
Department of Anesthesiology The Children’s Hospital
School of Medicine Boston, Massachusetts
Medical College of Wisconsin
Staff Anesthesiologist Scott M. Fishman, MD
Department of Anesthesiology Chief
Zablocki VA Medical Center Division of Pain Medicine
Milwaukee, Wisconsin Professor of Clinical Anesthesiology
School of Medicine
Jan Ehrenwerth, MD University of California, Davis
Professor
Sacramento, California
School of Medicine
Yale University Lee A. Fleisher, MD
Attending Staff Robert Dunning Dripps Professor of Anesthesiology
Department of Anesthesiology and Critical Care
Yale-New Haven Hospital Chair
New Haven, Connecticut Department of Anesthesiology and Critical Care
University of Pennsylvania Health System
Philadelphia, Pennsylvania

x Contributing Authors
Michael A. Fowler, MD, MBA Jay S. Grider, DO, PhD

Assistant Professor Associate Professor
Virginia Commonwealth University University of Kentucky
Medical Director Division Chief
Post Anesthesia Care Unit Regional Anesthesia and Pain Medicine
Department of Anesthesia Department of Anesthesiology
VCU Health Systems University of Kentucky Chandler Medical Center
Richmond, Virginia Lexington, Kentucky
Kevin Friede, BA Dhanesh K. Gupta, MD

Research Fellow Associate Professor
Perioperative Genomics Program Departments of Anesthesiology and Neurological Surgery
Division of Cardiothoracic Anesthesia and Critical Care Feinberg School of Medicine
Department of Anesthesiology Northwestern University
Duke University Medical Center Director
Durham, North Carolina Neuroanesthesia Research
Departments of Anesthesiology and Neurological Surgery
J. Sean Funston, MD Northwestern Memorial Hospital
Assistant Professor Chicago, Illinois
School of Medicine Steven C. Hall, MD
University of Texas Medical Branch Professor
Galveston, Texas Department of Anesthesiology
Tong J. Gan, MD Northwestern University
Professor Anesthesiologist-in-Chief
Department of Anesthesiology Ann and Robert H. Lurie Children’s Hospital
Duke University Medical Center Chicago, Illinois
Durham, North Carolina
Matthew R. Hallman, MD
Steven I. Gayer, MD, MBA Assistant Professor
Professor Department of Anesthesiology and Pain Medicine
Department of Anesthesiology and Ophthalmology School of Medicine
Bascom Palmer Eye Institute University of Washington
School of Medicine Harborview Medical Center
University of Miami Seattle, Washington
Miami, Florida
J. Steven Hata, MD, FCCP, MSc
Kevin J. Gingrich, MD Director, Center for Critical Care
Professor Departments of Cardiac Anesthesiology,
Department of Anesthesiology and Pain Management General Anesthesiology and Outcomes Research
College of Medicine Anesthesiology Institute
University of Texas Southwestern Medical Center Cleveland Clinic
Dallas, Texas Cleveland, Ohio
Kathryn E. Glas, MD, MBA Tara M. Hata, MD

Associate Professor Staff Anesthesiologist
Department of Anesthesiology Department of Pediatric Anesthesia
School of Medicine Anesthesia Institute
Emory University Cleveland Clinic
Co-Director Cleveland, Ohio
Cardiothoracic Anesthesiology
Crawford Long Hospital Laurence M. Hausman, MD
Atlanta, Georgia Associate Professor
Director Ambulatory Anesthesia
Loreta Grecu, MD Department of Anesthesia
Assistant Professor Mount Sinai School of Medicine
Department of Anesthesiology New York, New York
School of Medicine
Yale University

Contributing Authors xi
Jeana E. Havidich, MD Michael P. Hutchens, MD, MA

Associate Professor Assistant Professor
Department of Anesthesiology Department of Anesthesiology and Perioperative Medicine
Dartmouth-Hitchcock Oregon Health and Science University
Lebanon, New Hampshire Portland, Oregon
Thomas K. Henthorn, MD Adam K. Jacob, MD

Professor and Chair Assistant Professor
School of Medicine Mayo Clinic College of Medicine
University of Colorado Mayo Clinic
Aurora, Colorado Rochester, Minnesota
Simon C. Hillier, MB, ChB Girish P. Joshi, MBBS, MD, FFARCSI

Professor Professor
Departments of Anesthesia and Pediatrics Department of Anesthesiology and Pain Management
Dartmouth Hitchcock Medical Center University of Texas Southwestern Medical Center
Lebanon, New Hampshire Dallas, Texas
Robert S. Holzman, MD John P. Kampine, MD, PhD

Professor of Anesthesia Professor and Chair Emeritus
School of Medicine Department of Anesthesia
Harvard Medical School College of Medicine
Senior Associate in Perioperative Anesthesiology Medical College of Wisconsin
Department of Anesthesiology, Perioperative and Pain Medicine Milwaukee, Wisconsin
Boston Children’s Hospital
Boston, Massachusetts
Jonathan D. Katz, MD
Clinical Professor
Harriet W. Hopf, MD Department of Anesthesiology
Professor and Vice Chair School of Medicine
Department of Anesthesiology Yale University
School of Medicine New Haven, Connecticut
University of Utah Attending Anesthesiologist
Salt Lake City, Utah Department of Anesthesia
St. Vincent Medical Center
Terese T. Horlocker, MD Bridgeport, Connecticut
Professor of Anesthesiology and Orthopaedics
Mayo Clinic College of Medicine Sandra L. Kopp, MD
Mayo Clinic Associate Professor
Rochester, Minnesota Department of Anesthesiology
Mayo Clinic College of Medicine
Anesthesiologist
Lucy S. Hostetter, MD Mayo Clinic
Staff Anesthesiologist Rochester, Minnesota
Physician’s Anesthesia Service
Swedish Medical Center
Seattle, Washington Catherine Kuhn, MD
Associate Professor
Robert W. Hurley, MD, PhD School of Medicine
Chief Duke University Medical Center
Division of Pain Medicine Durham, North Carolina
Departments of Anesthesiology, Neurology, Psychiatry, Orthopaedics
and Rehabilitation
School of Medicine Arthur M. Lam, MD, FRCPC
University of Florida Clinical Professor of Anesthesiology and Pain Medicine
Chest Pain Medicine School of Medicine
UF & Shands Hospital University of Washington
Gainesville, Florida Medical Director of Neuroanesthesia and Neurocritical Care
Swedish Medical Center, Cherry Hill Campus
Seattle, Washington

xii Contributing Authors
Jerrold Lerman, MD, FRCPC, FANZCA David A. Lubarsky, MD, MBA

Clinical Professor CEO
Department of Anesthesiology UHealth Physician Practice
School of Medicine Emanuel M. Papper Professor and Chair
State University of New York Department of Anesthesiology, Perioperative Medicine, and
Women and Children’s Hospital Pain Management
Buffalo, New York Miller School of Medicine
University of Rochester University of Miami
Strong Hospital Department of Anesthesiology
Rochester, New York Jackson Memorial Hospital
Miami, Florida
Jerrold H. Levy, MD, FAHA, FCCM
Professor Stephen M. Macres, PharmD, MD
Department of Anesthesiology Clinical Professor of Anesthesiology
School of Medicine Department of Anesthesiology and Pain Medicine
Duke University School of Medicine
Durham, North Carolina University of California, Davis
Director
Postoperative Pain and Regional Anesthesia Service
Adam D. Lichtman, MD Sacramento, California
Assistant Professor of Anesthesiology
Department of Anesthesiology Gerard Manecke, MD
Weill Cornell Medical Center Clinical Professor and Chair
New York Presbyterian Hospital Department of Anesthesiology
New York, New York UCSD Medical Center
San Diego, California
J. Lance Lichtor, MD
Professor Joseph P. Mathew, MD
Department of Anesthesiology Professor
Yale University Duke University Medical Center
New Haven, Connecticut Durham, North Carolina
Yi Lin, MD, PhD Michael S. Mazurek, MD

Clinical Instructor of Anesthesiology Associate Professor of Clinical Anesthesia
Department of Anesthesiology Department of Anesthesia
Weill Medical College School of Medicine
Cornell University Indiana University
Assistant Attending Anesthesiologist Division of Pediatric Anesthesia
Hospital for Special Surgery Riley Hospital for Children
New York, New York Indianapolis, Indiana
Larry Lindenbaum, MD Kathryn E. McGoldrick, MD

Assistant Professor of Anesthesiology
Professor and Chair
and Critical Care Medicine
School of Medicine
School of Medicine
New York Medical College
Medical College of Wisconsin
Director of Anesthesiology
Froedtert Memorial Lutheran Hospital
Westchester Medical Center
Milwaukee, Wisconsin
Valhalla, New York
Spencer S. Liu, MD
Attending Anesthesiologist Sanford M. Miller, MD
Department of Anesthesiology Clinical Associate Professor
Hospital for Special Surgery Department of Anesthesiology
New York, New York School of Medicine
NYU School of Medicine
Assistant Director
Bellevue Hospital Center
New York, New York

Contributing Authors xiii
Timothy E. Miller, MBChB, FRCA Charles W. Otto, MD, FCCM

Assistant Professor Professor of Anesthesiology
Department of Anesthesiology Associate Professor of Medicine
Duke University Medical Center University of Arizona
Durham, North Carolina Tucson, Arizona
Peter G. Moore, MD, PhD Frank J. Overdyk, MSEE, MD

Professor and Chair Professor
University of California, Davis Hofstra North Shore-LIJ
Sacramento, California Hempstead, New York
Michael J. Murray, MD, PhD, FCCM, FCCP Nathan Leon Pace, MD, MStat
Colonel Professor
US Army Medical Corp Department of Anesthesiology
Professor of Anesthesiology School of Medicine
Mayo Clinic College of Medicine University of Utah
Mayo Clinic Salt Lake, Utah
Jacksonville, Florida
Paul S. Pagel, MD, PhD
Charles D. Nargozian, MD Professor and Director of Cardiac Anesthesia
Assistant Professor Department of Anesthesiology
School of Medicine Clement J. Zablocki Veterans Affairs Medical Center
Harvard Medical Center Milwaukee, Wisconsin
Senior Associate in Anesthesia
Department of Anesthesiology, Perioperative and Ben Julian Palanca, MD, PhD
Pain Medicine Assistant Professor
Boston Children’s Hospital Department of Anesthesiology
Boston, Massachusetts School of Medicine
Washington University
Steven M. Neustein, MD St. Louis, Missouri
Professor
Department of Anesthesiology Albert C. Perrino, Jr., MD
Mount Sinai School of Medicine Professor
Attending Staff Department of Anesthesiology
Department of Anesthesiology School of Medicine
Mount Sinai Hospital Yale University
New York, New York New Haven, Connecticut
Chief
Marieke Niesters, MD Department of Anesthesiology
Department of Anesthesiology VA Connecticut
Leiden University Medical Center West Haven, Connecticut
The Netherlands
Andrew J. Pittaway, FRCA
Erik Olofsen, MSc Assistant Professor
Research Associate Department of Anesthesiology and Pain Medicine
Department of Anesthesiology School of Medicine
Leiden University Medical Center University of Washington
The Netherlands Attending Staff
Rafael Ortega, MD Seattle Children’s Hospital
Professor Seattle, Washington
Vice-Chairman of Academic Affairs
Department of Anesthesiology Mihai V. Podgoreanu, MD
School of Medicine Associate Professor
Boston University Department of Anesthesiology
Boston, Massachusetts Director
Perioperative Genomics Program
School of Medicine
Duke University
Durham, North Carolina

xiv Contributing Authors
Wanda M. Popescu, MD Richard W. Rosenquist, MD

Associate Professor Chairman
Department of Anesthesiology Department of Pain Management
Yale University Cleveland Clinic
Attending Physician Cleveland, Ohio
Yale New Haven Hospital
New Haven, Connecticut Aaron Sandler, MD, PhD
Associate Professor
Karen L. Posner, PhD Department of Anesthesiology
Research Professor School of Medicine
Department of Anesthesiology and Pain Medicine Duke University Medical Center
School of Medicine Durham, North Carolina
Seattle, Washington
Barbara M. Scavone, MD
Associate Professor
Donald S. Prough, MD Departments of Anesthesia & Critical Care and Obstetrics &
Professor and Chair Gynecology
Department of Anesthesiology Pritzker School of Medicine
The University of Texas Medical Branch University of Chicago
Galveston, Texas Section Chief, Obstetric Anesthesia
Clinical Director, Labor and Delivery
Glenn Ramsey, MD The University of Chicago Medical Center
Professor Chicago, Illinois
Department of Pathology
Northwestern University Katie Schenning, MD, MPH
Medical Director Fellow
Blood Bank Departments of Anesthesiology and Perioperative Medicine
Northwestern Memorial Hospital College of Medicine
Chicago, Illinois Oregon Health and Science University
Portland, Oregon
Kevin T. Riutort, MD, MS
Anesthesiologist Jeffrey J. Schwartz, MD
South Denver Anesthesiologists, P.C. Associate Professor
Denver, Colorado Department of Anesthesiology
School of Medicine
G. Alec Rooke, MD, PhD Yale University
Professor Attending Physician
School of Medicine Yale New Haven Medical Center
University of Washington New Haven, Connecticut
Seattle, Washington
Harry A. Seifert, MD, MSCE
Stanley H. Rosenbaum, MA, MD Adjunct Assistant Professor of Clinical Anesthesiology
Professor Department of Anesthesiology and Critical Care
Departments of Anesthesiology, Internal Medicine, and Surgery The Children’s Hospital of Philadelphia
School of Medicine Philadelphia, Pennsylvania
Yale University
New Haven, Connecticut Aarti Sharma, MD
Assistant Professor
Meg A. Rosenblatt, MD Department of Anesthesiology
Professor School of Medicine
Department of Anesthesiology and Orthopaedics Weill Cornell Medical Center
Mount Sinai School of Medicine New York Presbyterian Hospital
Mount Sinai Medical Center New York, New York
New York, New York
Andrew Shaw, MB, FRCA, FCCM
William H. Rosenblatt, MD Associate Professor
Professor Department of Anesthesiology
Departments of Anesthesia and Surgery School of Medicine
Department of Anesthesiology Duke University Medical Center
School of Medicine Durham, North Carolina
Yale University

Contributing Authors xv
Benjamin M. Sherman, MD Mark Stafford-Smith, MD, CM, FRCPC

Assistant Professor Professor
Yale University School of Medicine
VA Medical Center Duke University Medical Center
Department of Cardiothoracic Anesthesiology Durham, North Carolina
West Haven Connecticut
Andrew F. Stasic, MD
Nikolaos J. Skubas, MD, FASE Associate Professor
Director, Cardiac Anesthesia Department of Anesthesia
Associate Professor of Anesthesiology School of Medicine
School of Medicine Indiana University
Weill Cornell Medical College Indianapolis, Indiana
Associate Attending of Anesthesiology
New York Hospital—Weill Cornell Medical Center
New York, New York Randolph H. Steadman, MD
Professor and Vice Chair
Todd J. Smaka, MD Chief, Anesthesia of Liver Transplant
Assistant Professor David Geffen School of Medicine
Department of Anesthesiology, Perioperative Medicine and University of California, Los Angeles
Pain Management Los Angeles, California
School of Medicine
University of Miami Miller
Jackson Memorial Hospital M. Christine Stock, MD
Miami, Florida Professor and Chair
Hugh M. Smith, MD Northwestern University
Assistant Professor Chicago, Illinois
Mayo Clinic College of Medicine
Mayo Clinic Robert K. Stoelting, MD
Rochester, Minnesota Emeritus Professor and Past Chair
Department of Anesthesia
School of Medicine
Terry Smith, PhD Indiana University
Department of Anesthesiology Indianapolis, Indiana
Leiden University Medical Center
The Netherlands
David F. Stowe, MD, PhD
Professor
Karen J. Souter, MB, BS, MSc, FRCA Department of Anesthesiology
Associate Professor College of Medicine
Vice Chair for Education and Residency Program Medical College of Wisconsin
Director Milwaukee, Wisconsin
School of Medicine
University of Washington Wariya Sukhupragarn, MD
University of Washington Medical Center Assistant Professor
Seattle, Washington Department of Anesthesiology
Chiang Mai University
Maharaj Nakorn Chiang Mai
Bruce D. Spiess, MD, FAHA Chiang Mai, Thailand
Professor
Departments of Anesthesiology and Emergency Medicine
Director of Virginia Commonwealth University Santhanam Suresh, MD
Reanimation Engineering Shock Center Professor of Anesthesiology and Pediatrics
Virginia Commonwealth University Medical Center Chair, Department of Pediatric Anesthesiology
Richmond, Virginia Feinberg School of Medicine
Anesthesiologist-in-Chief
Ann and Robert H. Lurie Children’s Hospital of Chicago
Chicago, Illinois

xvi Contributing Authors
Christer H. Svensén, MD, PhD, DEAA, MSc Mary E. Warner, MD

Professor of Anesthesiology, and Intensive Care Associate Professor
Department of Clinical Science and Education, Section of Department of Anesthesiology
Anestheseiology and Intensive Care Mayo Clinic College of Medicine
Karolinska Institutet/Stockholm Mayo Clinic
South General, Stockholm, Sweden Rochester, Minnesota
Denise J. Wedel, MD
Paul C. Tamul, DO Professor
Assistant Professor Department of Anesthesiology
Department of Anesthesiology and Mayo Clinic College of Medicine
Neurological Surgery Mayo Clinic
Feinberg School of Medicine Rochester, Minnesota
Medical Director
Post-Anesthesia Care Unit Paul F. White, MD, PhD, FANZCA
Northwestern Memorial Hospital Director of Research and Education
Chicago, Illinois Department of Anesthesia
Cedars-Sinai Medical Center
Los Angeles, California
Stephen J. Thomas, MD Visiting Scientist
Topkin-Van Poznak Professor and Vice-Chairman Research Unit of Anesthesia and Intensive Care
Department of Anesthesiology Rizzoli Orthopedic Institute
Weill Medical College University of Bologna
Cornell University Italy
New York Presbyterian Hospital Scott W. Wolf, MD
New York, New York Assistant Professor
Miriam M. Treggiari, MD Feinberg School of Medicine
Professor of Anesthesiology and Neurological Surgery Northwestern University
School of Medicine Northwestern Memorial Hospital
University of Washington Chicago, Illinois
Harborview Medical Center
Seattle, Washington Cynthia A. Wong, MD
Professor and Vice Chair
Ban C.H. Tsui, MSc, MD, FRCP(C) Section Chief, Obstetric Anesthesiology
Pediatric and Adult Anesthesiologist Department of Anesthesiology
Professor and Vice Chair (Research) Feinberg School of Medicine
Department of Anesthesiology and Pain Management Northwestern University
Stollery Children’s Hospital Chicago, Illinois
University of Alberta Hospital
Edmonton, Alberta James R. Zaidan, MD, MBA
Professor and Past Chair
J. Scott Walton, MD Department of Anesthesiology
Associate Professor Emory University Hospital
Department of Anesthesia and Perioperative Medicine Atlanta, Georgia
School of Medicine
Medical University of South Carolina
Charleston, South Carolina

PREFACE
Seminal editions are an intrinsic part of the life cycle of textbooks. electronic media in education, Dr. Ortega incorporated electronic
Certainly the first edition of Clinical Anesthesia in 1989 was deci- materials throughout the 7th Edition of Clinical Anesthesia, a
sive in shaping the goals and objectives that continue today. That Herculean task. Drs. Michael Cahalan and Christine Stock con-
goal was to create a single volume, comprehensive, yet clinically tinue to bring new and fresh ideas and have been instrumental in
focused textbook that supports efficient and rapid acquisition of shaping its future.
knowledge and meets the educational and clinical needs of all In addition to being published in an electronic version, this
anesthesia providers including those with decades of experience edition of Clinical Anesthesia contains a new chapter on Lapa-
and those just embarking on their careers. roscopic and Robotic Surgery. Also, the Appendices on Elec-
The development of the Clinical Anesthesia series is designed to trocardiography and Pacemakers/Implantable Defibrillators are
fulfill the more specific needs of our readers. First, the Handbook presented in a new graphic interface to improve reader com-
of Clinical Anesthesia meets the requests of the health care provid- prehension of these important subjects. Finally, approximately
ers to have the essential information contained in the parent text- twenty percent of the Chapters are written by new contributing
book in a more ‘portable format’. Even with advent of personal authors who are leading authorities in their respective areas.
computers, smart phones and tablets, the Handbook continues We wish to express our appreciation to all our contributors
to have a vital role. Subsequently, a guided study book Review whose knowledge, hard work, dedication and timely submissions
of Clinical Anesthesia edited by Drs. Neil Connelly and David allowed us to maintain quality while working with a tight produc-
Silverman facilitated integrated study of subject matter in the tion schedule. Our readers also provided comments instrumental
textbook. However, the hallmark of the series has been the con- to the editors’ continual improvement of Clinical Anesthesia. We
tinuous launching of electronic products to enhance the reader are also grateful to our administrative assistants—Gail Norup,
experience. As technology has evolved, so has Clinical Anesthesia. Ruby Wilson, Deanna Walker, and Mary Wynn. We would like
Clinical Anesthesia was one of the first textbooks in medicine to to thank our editors at Lippincott Williams & Wilkins-Wolters
have an ‘app’ for a hand held electronic device, the Palm. This app Kluwer, Brian Brown and Lisa McAllister, for their commit-
was awarded the prestigious Folio Award for the Best Electronic ment to excellence. Finally, we owe a debt of gratitude to Nicole
Media in Science, Medicine and Technology. Using this as the Dernoski—Managing Editor at LWW, Chris Miller—Production
electronic foundation, the Lippincott-Raven Interactive Anesthesia Manager at Aptara, Lisa Lawrence—Marketing Manager at LWW
Library was developed and was highly successful as a study guide whose day-to-day management of this endeavor resulted in a
for Board examinations. Finally, in the previous edition, Clinical publication that exceeded the Editor’s expectations.
Anesthesia introduced Podcasts as enhancements to the educa- The discovery and application of anesthesia is the single most
tional process. important contribution of American medicine to mankind. The
This brings us to Clinical Anesthesia 7th Edition, which has major achievements of modern surgery could not have taken
turned out to be a seminal edition and perhaps of even greater place without the accompanying vision of the pioneers in Anes-
importance than the first. This is the first anesthesia textbook thesiology. This statement is echoed by surgeon-author Atul
of the 21st Century to be designed from the ‘ground up’ as an Gawande, who in the article Two Hundred Years of Surgery (New
electronic edition. In essence, we have created two distinct books, England Journal of Medicine) stated
which share material. Previously, we and others have scanned
the textbook pages to create an e-media version of a book. This “The crucial spark of transformation—the moment that
not only results in a sub-optimal reader experience, but more changed not just the future of surgery but of medicine as a
importantly does not capture the strengths of e-publications, whole—was the publication on November 18, 1846, of Henry
e.g. video clips, animation and updating etc. So for the book- Jacob Bigelow’s groundbreaking report, ‘Insensibility during
lover, the printed textbook is still available with access to a com- Surgical Operations Produced by Inhalation’.”
pletely enhanced and innovative digital experience powered by The Editors hope that every page of Clinical Anesthesia evokes
Inkling. Viewable through a browser or as a download to your the pride of being a part of the specialty of Anesthesiology and its
smartphone or tablet, the electronic version has three hundred achievements for the betterment of mankind.
videos, animated tables, an enhanced search and navigation style
and regular content updates. The readers will recognize that they Paul G. Barash, MD
are no longer reading an electronic version of the printed stan- Bruce F. Cullen, MD
dard page, rather the presentation of information in a new and Robert K. Stoelting, MD
enhanced style. Michael K. Cahalan, MD
This publication marks the addition of Dr. Rafael Ortega M. Christine Stock, MD
to the editorial board. Known internationally for the use of Rafael Ortega, MD
xvii

CONTENTS
SECTION I 14 Fluids, Electrolytes, and

Acid–Base Physiology 327
Introduction to Anesthesiology Donald S. Prough, J. Sean Funston, Christer H. Svensén,
and Scott W. Wolf
1 The History of Anesthesia 3
Adam K. Jacob, Sandra L. Kopp, Douglas R. Bacon, 15 Autonomic Nervous System: Physiology
and Hugh M. Smith and Pharmacology 362
2 Scope of Practice 28 Loreta Grecu
John H. Eichhorn and Jay S. Grider 16 Hemostasis and Transfusion Medicine 408
3 Occupational Health 61 Louanne M. Carabini and Glenn Ramsey
Jonathan D. Katz and Robert S. Holzman
4 Anesthetic Risk, Quality Improvement,

and Liability 90 SECTION IV
Karen L. Posner, Saint Adeogba, and Karen B. Domino
Anesthetic Agents, Adjuvants,
SECTION II and Drug Interaction
17 Inhaled Anesthetics 447
Scientific Foundations of Anesthesia Thomas J. Ebert and Larry Lindenbaum
5 Mechanisms of Anesthesia and
Consciousness 107 18 Intravenous Anesthetics 478
Paul F. White and Matthew R. Eng
C. Michael Crowder, Ben Julian Palanca, and Alex S. Evers
6 Genomic Basis of Perioperative Medicine 130 19 Opioids 501

Kevin Friede, Joseph P. Mathew, and Mihai V. Podgoreanu Albert Dahan, Marieke Niesters, Erik Olofsen,
Terry Smith, and Frank Overdyk
7 Basic Principles of Clinical Pharmacology 156
Dhanesh K. Gupta and Thomas K. Henthorn 20 Neuromuscular Blocking Agents 523
François Donati
8 Electrical and Fire Safety 189
Jan Ehrenwerth and Harry A. Seifert 21 Local Anesthetics 561
Yi Lin and Spencer S. Liu
9 Experimental Design and Statistics 219
Nathan Leon Pace
SECTION III SECTION V
Anatomy and Physiology Preanesthetic Evaluation and

10 Cardiac Anatomy and Physiology 239 Preparation
Paul S. Pagel, John P. Kampine, and David F. Stowe 22 Preoperative Patient Assessment and
11 Respiratory Function in Anesthesia 263 Management 583
Paul C. Tamul and Michael L. Ault Tara M. Hata and J. Steven Hata
12 The Allergic Response 287 23 Rare Coexisting Diseases 612

Jerrold H. Levy Stephen F. Dierdorf, J. Scott Walton,
and Andrew F. Stasic
13 Inflammation, Wound Healing, and
Infection 304 24 The Anesthesia Workstation and Delivery
Harriet W. Hopf, C. Richard Chapman, Amalia Cochran, Systems for Inhaled Anesthetics 641
Michael B. Dorrough, and Randal O. Dull Kevin T. Riutort and James B. Eisenkraft
xix

xx Contents
SECTION VI 4 0 Obstetrical Anesthesia 1144

Ferne R. Braveman, Barbara M. Scavone,
Anesthetic Management Marcelle E. Blessing, and Cynthia A. Wong
25 Commonly Used Monitoring Techniques 699 41 Neonatal Anesthesia 1178

Christopher W. Connor Steven C. Hall and Santhanam Suresh
26 Echocardiography 723 4 2 Pediatric Anesthesia 1216

Albert C. Perrino Jr, Wanda M. Popescu, Jerrold Lerman
and Nikolaos J. Skubas 43 Anesthesia for Laparoscopic
27 Airway Management 762 and Robotic Surgeries 1257
William H. Rosenblatt and Wariya Sukhupragarn Girish P. Joshi and Anthony Cunningham
28 Patient Positioning and Potential Injuries 803 4 4 Anesthesia and Obesity 1274
Mary E. Warner Brenda A. Bucklin and Ana Fernandez-Bustamante
29 Monitored Anesthesia Care 824 45 The Liver: Surgery and Anesthesia 1294
Simon C. Hillier, Michael S. Mazurek, Randolph H. Steadman and Michelle Y. Braunfeld
and Jeana E. Havidich
46 Endocrine Function 1326
30 Ambulatory Anesthesia 844 Jeffrey J. Schwartz, Shamsuddin Akhtar,
J. Lance Lichtor and Stanley H. Rosenbaum
31 Office-Based Anesthesia 860 47 Anesthesia for Otolaryngologic Surgery 1356

Laurence M. Hausman and Meg A. Rosenblatt Lynne R. Ferrari and Charles Nargozian
32 Nonoperating Room Anesthesia (NORA) 876 48 Anesthesia for Ophthalmologic Surgery 1373
Karen J. Souter and Andrew J. Pittaway Kathryn E. Mcgoldrick and Steven I. Gayer
33 Anesthesia for the Older Patient 891 49 The Renal System and Anesthesia for
G. Alec Rooke Urologic Surgery 1400
Mark Stafford-Smith, Andrew Shaw, Aaron Sandler, and
34 Epidural and Spinal Anesthesia 905 Catherine Kuhn
Christopher M. Bernards and Lucy S. Hostetter
50 Anesthesia for Orthopedic Surgery 1440
Terese T. Horlocker and Denise J. Wedel
SECTION VII 51 Transplant Anesthesia 1459

Marie Csete, Dalia Banks, Gerard Manecke, and Kathryn Glas
Anesthesia for Surgical 52 Trauma and Burns 1490
Subspecialties Levon M. Capan, Sanford M. Miller, and Kevin J. Gingrich
35 Peripheral Nerve Blockade 937 53 Emergency Preparedness for and Disaster

Ban C.H. Tsui and Richard W. Rosenquist Management of Casualties from Natural
36 Anesthesia for Neurosurgery 996 Disasters and Chemical, Biologic,
Armagan Dagal and Arthur M. Lam Radiologic, Nuclear, and High-Yield
Explosive (CBRNE) Events 1535
37 Anesthesia for Thoracic Surgery 1030 Michael J. Murray
James B. Eisenkraft, Edmond Cohen,
and Steven M. Neustein
38 Anesthesia for Cardiac Surgery 1076

Nikolaos J. Skubas, Adam D. Lichtman, Aarti Sharma,
SECTION VIII
and Stephen J. Thomas
Perioperative and Consultative
39 Anesthesia for Vascular Surgery 1112
Todd J. Smaka, Timothy E. Miller, Michael P. Hutchens, Services
Katie Schenning, Lee A. Fleisher, Tong J. Gan, and 54 Postanesthesia Recovery 1555
David A. Lubarsky
Michael A. Fowler and Bruce D. Spiess

Contents xxi
55 Critical Care Medicine 1580 Appendix 1 Atlas of Electrocardiography 1701

Matthew R. Hallman, Miriam M. Treggiari, ina C. Badescu, Benjamin Sherman, James R. Zaidan,
G
and Steven Deem and Paul G. Barash
56 Acute Pain Management 1611 Appendix 2 Pacemaker and Implantable

Stephen M. Macres, Peter G. Moore, Cardiac Defibrillator Protocols 1721
and Scott M. Fishman Gina C. Badescu, Benjamin Sherman, James R. Zaidan,
and Paul G. Barash
57 Chronic Pain Management 1645
Honorio T. Benzon, Robert W. Hurley, Timothy Deer, and
Asokumar Buvanendran
Index 1731
58 Cardiopulmonary Resuscitation 1672
Charles W. Otto

C H A PT E R
36 Anesthesia for Neurosurgery

ARMAGAN DAGAL • ARTHUR M. LAM
NEUROANATOMY Transfusion Therapy

NEUROPHYSIOLOGY Glucose Management
Anesthetic Influences Emergence
PATHOPHYSIOLOGY COMMON SURGICAL PROCEDURES
MONITORING Surgery for Tumors
Central Nervous System Function Pituitary Surgery
Cerebral Perfusion Arteriovenous Malformations
Cerebral Oxygenation/Metabolism Monitors Cerebral Aneurysm Surgery and Endovascular
CEREBRAL PROTECTION Treatment
Ischemia and Reperfusion Carotid Surgery
Hypothermia Epilepsy Surgery and Awake Craniotomy
Medical Therapy for Cerebral Protection ANESTHESIA AND TRAUMATIC BRAIN INJURY
Glucose and Cerebral Ischemia Overview of Traumatic Brain Injury
Promising Areas of Research Anesthetic Management
A Practical Approach ANESTHESIA FOR SPINE TRAUMA AND COMPLEX
ANESTHETIC MANAGEMENT SPINE SURGERY
Preoperative Evaluation Spinal Cord Injury
Induction and Airway Management Comorbid Injuries
Maintenance of Anesthesia Initial Management
Ventilation Management Intraoperative Management
Fluid and Electrolytes Complications of Anesthesia for Spine Surgery
Ke y Points
1 Anatomically, blood flow to the normal brain is supplied by the 6 Anesthetic management of the patient with neurologic disease
two carotid arteries and vertebral arteries. Collateral circulation mandates a thorough preoperative assessment as there are
is provided via the Circle of Willis. often multisystem manifestations.
2 Physiologically, blood flow to the brain is tightly regulated. The 7 Anesthetic techniques may influence brain relaxation condi
homeostatic mechanisms include flow–metabolism coupling, tions. In general, intravenous agents cause more cerebral
pressure autoregulation, and CO2 reactivity. vasoconstriction than inhalation agents. There are no outcome
3 These homeostatic mechanisms are affected by diseases as well studies demonstrating the superiority of any particular
as anesthetic drugs and techniques. anesthetic agent. The use of intraoperative monitoring of
4 Multiple monitoring modalities are available to monitor brain evoked potentials impacts the choice of anesthetic technique.
function, perfusion, and oxygenation/metabolism. These include 8 Movement of water into the brain is primarily determined
the electroencephalogram, somatosensory evoked potentials, by the osmotic gradient, which in turn is determined by
motor evoked potentials, electromyogram, intracranial pressure, serum osmolarity. Outcome studies do not provide guidance
transcranial Doppler ultrasonography, brain tissue oxygenation, regarding the choice of crystalloids versus colloids. In patients
and jugular venous oximetry. Although most are applicable for with brain trauma the use of albumin for resuscitation is
monitoring in the neurointensive care unit, many are useful in the associated with increased mortality.
operating room to increase patient safety and improve outcome. 9 Common neurosurgical procedures requiring special under
5 Definitive cerebral protective therapy remains elusive, but many standing and expertise include tumor excision, transsphenoidal
techniques have been investigated and some are frequently or transcranial removal of pituitary lesions, extirpation of
used in the operating room on theoretical grounds. These arteriovenous malformation, repair or clipping of aneurysms,
include the use of hypothermia, control of blood glucose, and carotid endarterectomy, and craniotomy for traumatic brain
maintenance of adequate perfusion. The anemia threshold for lesions including epidural and subdural hematomas.
blood transfusion remains controversial.
996
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Chapter 36 Anesthesia for Neurosurgery 997
Mult imedia
1 Intracranial Compliance 3 Neurosurgery Tumor Excision
2 Cerebral Blood Flow 4 Mayfield Clamp
Neuroanatomy Neurophysiology
A basic knowledge of neuroanatomy is essential for all anesthesi Cerebral metabolic rate is directly related to the number of stimu
ologists, particularly those caring for patients with disease of the lated neurons and rate of depolarization. Therefore, any activ
central nervous system (CNS). Components of the CNS, the brain ity or stimulation raises the metabolic rate. Cerebral blood flow
and spinal cord, are protected by the bony structures that surround (CBF) is tightly coupled to metabolism, on a regional as well on
them. Yet by virtue of their protective nature, these structures are a global level. As an example, while visual stimulation may raise
nondistensible. The intracranial volume is fixed, thereby provid blood flow to the occipital cortex, mild hyperthermia, which raises
ing little room for anything other than the brain, cerebrospinal global cerebral metabolic rate, increases flow to the entire brain.
fluid (CSF), and blood contained in the cerebral vasculature. Even The CSF occupies the subarachnoid space, providing a pro
the space in the spinal column, although not as restrictive as the tective layer of fluid between the CNS and the tissue that sur
cranium, is quickly exhausted by a space-occupying lesion such rounds it. CSF is produced by the choroid plexus in the ventricles
as an expanding hematoma or abscess. It is in the context of the at about 0.3 mL/min. CSF circulation follows the path from the
restrictive nature of the cranium and vertebral column in which lateral ventricles into the third ventricle via the interventricular
the CNS is housed that all interventions must be considered. foramina (foramina of Monro). It subsequently transits through
1 Both the brain and spinal cord have unique blood supply. The the cerebral aqueduct of Sylvius into the fourth ventricle, and then
carotid artery in the neck bifurcates into the external and internal into the space around the brain via the foramina of Magendie
carotid arteries at the level of the third cervical vertebra, sending
the internal branch through the base of the skull, giving seven
branches including the ophthalmic artery, and ultimately bifur Anterior Anterior cerebral
cating into the anterior and middle cerebral arteries. These vessels communicating artery
define the anterior cerebral circulation. The posterior circulation artery
results from the vertebral arteries, which ascend in the posterior Ophthalmic artery
aspect of the neck through foramina in the cervical vertebral bod
ies before exiting, coursing around the brainstem, and joining the
contralateral vessel to form the basilar artery. The basilar artery
Anesthesia for Surgical

ascends along the brainstem before dividing into the posterior Middle Anterior
cerebral arteries. The anterior and posterior circulations anasto cerebral choroidal artery
Subspecialties
mose through the posterior communicating arteries to provide artery Internal
collateral flow; collateral circulation can also occur through the carotid artery
Posterior
anterior communicating artery connecting the bilateral anterior Posterior
communicating
cerebral arteries. This system of collateralization, named the circle artery cerebral artery
of Willis (Fig. 36-1), was described by Thomas Willis (1621–1675)
with the recognition of its purpose “ . . . that there may be a mani
fold way, and that more certain, for the blood about to go into Superior
divers Regions of the Brain.” Pontine cerebellar artery
The spinal column is the bony structure made up of the arteries
7 cervical, 12 thoracic, 5 lumbar vertebrae, 5 fused sacral and 3 to
5 fused coccygeal vertebrae. It is about 70 cm long in the adult Basilar artery
male with cervical and lumbar regions which convex forward
and thoracic and sacral regions that are concave. The spinal cord
exits the skull through the foramen magnum and enters the canal Anterior inferior
formed by the vertebral bodies. In the adult, the cord typically cerebellar
artery
ends at the lower aspect of the first lumbar vertebral body. It is
around 45 cm long in men and 43 cm long in women.
Blood supply to the cord is provided by several sources. The Vertebral artery
anterior spinal artery, which arises from the vertebral arteries, sup
plies the anterior two-thirds of the spinal cord. This vessel runs the
length of the cord, receiving contributions from radicular arter Posterior inferior
ies via intercostal vessels. The artery of Adamkiewicz is the most cerebellar artery
important radicular vessel, typically joining the anterior spinal Anterior spinal
artery in the lower thoracic region and providing blood to the tho artery
racolumbar cord. The posterior third of the cord is supplied by two
Figure 36-1. The circle of Willis, and other blood supply to the brain
posterior spinal arteries, which arise from the vertebral arteries and and spinal cord.
also receive contributions from radicular arteries (Fig. 36-2).
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998 SECTION ViI Anesthesia for Surgical Subspecialties
Basilar trunk
Vert. art. 1 Ant. spinal artery

2
Intracranial pressure
3
4 Radicular art. C3–C4
5
6 Radicular art. C5–C6
7
Radicular art. C7–C8
1
2
3
Radicular art. T3–T4
4
5 Intracranial mass
6
Figure 36-3. Intracranial compliance (elastance) curve. The brain has
Postspinal art. minimal compensatory capacity, and any increase in mass from hema-
7
and radicular toma or brain swelling will result in an inordinate increase in intracra-
8 supply nial pressure.
9
10
11 thecal sac, but only to a small extent. A further increase, as with
Art. Adamkiewicz significant cerebral edema or accumulation of an extradural
12 (rad. art. T11–T12) hematoma, will quickly lead to a marked increase in ICP due to
1 1 limited intracranial compliance (Fig. 36-3).
2
As mentioned earlier, blood flow to the brain is tightly coupled
2 to cerebral metabolism. As such, many factors affect CBF because
3 of their effect on metabolism. Stimulation, arousal, nociception,
4 Radicular lumbo- and mild hyperthermia elevate metabolism and flow, while seda
sacral art. tive–hypnotic agents and hypothermia decrease both metabolism
5 2 and flow. A number of other factors govern CBF directly with
out changing metabolism. A potent determinant of CBF is the
arterial CO2 tension (Paco2). Within physiologic range, CBF has
an approximately linear relationship with Paco2. CBF changes
by approximately 3% of baseline for each 1 mm Hg change in
Paco2 (Fig. 36-4). As CBF changes, so does cerebral blood vol
ume (CBV), which is why hyperventilation can be used for short
periods of time to relax the brain or decrease the ICP. How
Figure 36-2. Blood supply to the spinal cord. Both the single ante- ever, this effect is thought to be short-lived. CSF pH normalizes
rior spinal artery and the paired posterior spinal artery arise from the
vertebral arteries. The radicular arteries and particularly the artery of
Adamkiewicz are important contributors. The anterior spinal artery sup-
plies the anterior two-thirds of the spinal cord, with the posterior spinal
artery supplying the rest. (vert., vertebral; art., artery; ant., anterior)
Cerebral blood flow
(midline posteriorly) and Luschka (laterally). It bathes both

the spinal cord and the brain. Absorption into the dural venous
sinuses occurs through the arachnoid granulations. Although
CSF volume is approximately 150 mL, more than three times this
amount is produced in a 24-hour period. This continuous flow of
CSF from the source to sink allows it to participate in many func
tions in addition to cushioning the brain. It maintains a milieu in
which the brain can function by regulating pH and electrolytes,
carrying away waste products, and delivering nutrients.1,2
Intracranial pressure (ICP) is low except in pathologic states.
The Monro–Kellie doctrine states that in the setting of a non
distensible cranial vault, the volume of blood, CSF, and brain Arterial carbon dioxide partial pressure
tissue must be in equilibrium. An increase in one of these three Figure 36-4. Cerebrovascular response to change in Paco2 partial
elements, or the addition of a space-occupying lesion, can be pressure. The change is linear between Paco2 of 25 and 65 mm Hg.
accommodated initially through displacement of CSF into the
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Autoregulatory plateau
Cerebral blood flow
Cerebral blood flow

Approximately
50 mm Hg
Arterial oxygen partial pressure Cerebral perfusion pressure

Figure 36-5. Cerebrovascular response to change in Pao2 partial Figure 36-6. Cerebral autoregulation. It is generally accepted that
pressure. The response of cerebral blood flow to change in Pao2 is flat cerebral blood flow is maintained constant between 60 and 160 mm
until Pao2 falls below 50 mm Hg. Hg. However, these are average values, and there is considerable varia-
tion in both the lower and the upper limit of cerebral autoregulation
among normal individuals.
over time, and vessel caliber returns to baseline. The exact dura
tion of hypocapnic vasoconstriction is uncertain; a period of min Other factors affect CBF as well. Anemia increases CBF via
utes to hours has been found in different patient populations.3 higher cardiac output, CPP and lower blood viscosity, as well
Because the decrease in CBF occurs without a change in cerebral as induced cerebral vasodilatation.8–10 Proposed mechanisms
metabolic rate, the risk of ischemia is a theoretical concern. How underlying this dilatation may include upregulation of nitric
ever, the significance of this concern is uncertain. We have no oxide (NO) production, sympathetic β2-receptor stimulation
evidence of harm of moderate hyperventilation to the normal and upregulation of vascular endothelial growth factor, hypoxia-
brain under general anesthesia. Early hyperventilation in trau inducible factor 1α, and erythropoietin that contributes to vaso
matic brain injury (TBI) is associated with poor outcome, and the dilatation and maintenance of CBF. Although it seems likely that
consequence of hyperventilation in TBI after the initial 24 hours these mediators are neuroprotective, it remains possible that they
is uncertain.4–6 could also have harmful pathophysiologic effects.11–13
In contrast to CO2, O2 has little effect on CBF except at abnor

mally low levels (Fig. 36-5). When Pao2 falls below 50 mm Hg,
CBF begins to increase sharply. A teleologic explanation for this Anesthetic Influences
Subspecialties
phenomenon is that CBF needs to increase only when the O2 con
tent of the blood begins to decrease significantly. Anesthetic agents have variable influence on CBF and metabolism,
CBF remains approximately constant despite modest swings CO2 reactivity, and autoregulation.14 Inhalation anesthetics tend
in arterial blood pressure. The mechanism by which CBF is to cause vasodilation in a dose-related manner, but do not per se
maintained, originally described by Lassen,7 is called autoregu- uncouple flow and metabolism. Thus the vasodilatory influence is
lation of CBF, or at times, pressure autoregulation of CBF. As opposed by metabolism-mediated decrease in flow. The resultant
cerebral perfusion pressure (CPP), defined as the difference of effect is that during low doses of inhalation anesthesia, CBF is either
mean arterial pressure (MAP) and ICP, changes, cerebrovas unchanged or slightly increased. Higher doses result in dominance
cular resistance adjusts to maintain stable flow. The resistance of the vasodilatory effect and an increase in CBF. Compared to
is varied at the arteriolar level. The range of CPP over which other inhaled agents, sevoflurane in clinically relevant doses does
autoregulation is maintained is termed the autoregulatory pla- not increase CBF, although propofol at comparable doses results
teau. Although this range is frequently quoted as a MAP range of in more profound cerebral vasoconstriction, and sevoflurane does
60 to 150 mm Hg, there is significant variability between individ not appear to impair cerebrovascular autoregulation.15,16 Further
uals, and these numbers are only approximate. At the low end of more, sevoflurane anesthesia is associated with profound regional
the plateau, cerebrovascular resistance is at a minimum, and any and global reduction in cerebral metabolic rate.17 Intravenous
further decrease in CPP will compromise CBF. At the high end agents including thiopental and propofol cause vasoconstriction
of the plateau, cerebrovascular resistance is at a maximum, and coupled with a reduction in metabolism.18 Ketamine, on the other
any further increase in CPP will result in hyperemia (Fig. 36-6). hand, increases flow and metabolism.19 CO2 reactivity is a robust
Various mechanisms have been proposed to account for auto mechanism and is preserved under all anesthetic conditions.
regulation, including myogenic, neurogenic, and local metabolic Dexmedetomidine is a pure α2 agonist that is increasingly uti
mediators. However, the exact mechanism remains undefined. lized to provide a state of “conscious sedation” associated with
There is interaction between CO2 reactivity and pressure auto minimal respiratory depression and some analgesia. It may cre
regulation, although the molecular mechanism is likely different ate an ideal state to facilitate procedures such as awake craniot
for these two homeostatic processes. When blood pressure is low, omy, carotid endarterectomy (CEA) under regional anesthesia,
CO2 reactivity is reduced. In contrast, under hypercapnic condi carotid angioplasty and stenting, and other neurointerventional
tions, autoregulatory capacity is lost because of the concurrent procedures. It appears to preserve flow–metabolism coupling in
vasodilation. healthy volunteers,20 although its effects on the injured brain still
LWBK1137-C36_p996-1029.indd 999 11/01/13 7:52 PM

need to be determined. It has been reported to have little effect the depolarization of cortical neurons that can be detected by
on static cerebrovascular autoregulation (sCA) in healthy vol surface electrodes placed on the scalp. Typically the activity is
unteers (unpublished observation), but it may weaken dynamic measured between two points on the scalp (bipolar), as there is
cerebrovascular autoregulation (dCA) and delay restoration of no electrically neutral place from which to reference the signal.
CBF velocity to normal with reduction in blood pressure.21 Other sources of electrical activity, such as that from the heart and
muscles, must be filtered from the signal, otherwise they would
overwhelm the small voltages generated by the cortical activity.
Common-mode rejection, that is, rejection of signals common
Pathophysiology to both electrodes, allows interference from cardiac and muscle
activity to be minimized.
3 The homeostatic mechanisms that ensure protection of the brain The EEG can be used for intraoperative monitoring (IOM)
and spinal cord, removal of waste, and delivery of adequate O2 and diagnosis. Monitoring provides information regarding func
and substrate to the tissue can be interrupted through a multi tional assessment of the brain, the occurrence of ischemia, seizure
tude of mechanisms. Traumatic insults may result in contusion activity, burst-suppression pattern, and potentially, depth of anes
with subsequent edema formation, direct injury from depressed thesia. Several standardized systems of electrode placement have
skull fractures or spine fractures, diffuse injury to neurons from been developed to facilitate reliable and consistent EEG moni
rapid deceleration, and disruption of the vasculature, resulting in toring, the most common of which is the International 10–20
ischemia or hemorrhage. All of these insults may ultimately com System. In brief, artificial meridians are generated on the scalp
promise CNS perfusion. running front to back and side to side, where the 10 to 20 refers
Mass lesions, such as tumors, may compress adjacent struc to the percentage of the distance across the scalp, either from the
tures, raise ICP, and obstruct normal flow of CSF. Hemorrhage tragus to tragus or the nasion to inion, that defines the meridian
may be spontaneous or traumatic. Depending on its location, this (Fig. 36-7). Electrodes can be placed at the intersection of each
may cause a mass effect, impair CSF circulation, or, in the case of meridian. Each such intersection or point is given a name—either
subarachnoid blood, breakdown of the blood may lead to further a combination of letters and a number or two letters, where the
ischemic injury by causing cerebral vasospasm. final letter is Z. The letters are F for frontal, C for central, P for
Hydrocephalus is caused by an imbalance between CSF pro parietal, T for temporal, O for occipital, A for auricular, and Fp
duction and removal. It frequently results in the elevation of ICP. for frontal pole. A letter followed by an odd number is a point on
Hydrocephalus is commonly divided into two categories: Com- the left hemisphere, while a letter followed by an even number is a
municating hydrocephalus and obstructive hydrocephalus. The for point on the right hemisphere. Two letters, with the second letter
mer is characterized by a failure to absorb CSF, typically because a Z, indicate a point along the midline.
of dysfunctional arachnoid granulations. The latter may be caused Although sophisticated EEG monitoring for epilepsy evalua
by any direct obstruction or extrinsic compression of a passage tion may require recording of multiple channels, providing infor
way through which CSF must pass, such as the cerebral aqueduct. mation on the activity between numerous points, EEG monitor
This obstruction, for example, may result from a clot within the ing during anesthesia frequently uses a broad montage with fewer
space or from a tumor adjacent to it. Depending on the circum channels (two or four) to evaluate hemispheric activity. Once
stances, hydrocephalus can have a subtle or dramatic presenta the signal is recorded, it can be evaluated in several ways. View
tion. For example, acute hydrocephalus following an intraventric ing raw EEG may be appropriate at times, but subtle changes are
ular hemorrhage may result in a rapidly progressive obtundation difficult to detect, particularly for the infrequent user. However,
that improves dramatically with external ventricular drainage. In the EEG can be processed to yield readily interpretable informa
contrast, normal pressure hydrocephalus may evolve over years, tion. A common method used is frequency domain analysis. Using
resulting in barely perceptible changes in cognition and gait. Fourier analysis, the apparent random activity of raw EEG can be
broken down into a series of wave frequencies, the summation
Monitoring Nasion
4 Anesthesia for neurosurgery and spine surgery requires the stan

dard American Society of Anesthesiologists monitoring for physi Fp1 Fp2
ologic parameters. However, the risk imposed to the CNS by these
surgical procedures may warrant more extensive monitoring. For F7 F8
F3 Fz F4
many procedures, adequate oxygenation, ventilation, and sys L Rolandic R
sulcus
temic blood pressure do not ensure the well being of the brain A1 A2
and spinal cord. Instead, the integrity of the CNS needs to be T3 C3 Cz C4 T4
Central
evaluated intraoperatively with monitors that specifically detect sulcus
CNS function, perfusion, or metabolism. At times, the monitor P3 Pz P4
T5 T6
ing modalities can be combined to provide greater information
regarding the well being of the CNS.
O1 O2
Inion
Central Nervous System Function
Figure 36-7. The international 10–20 system for electroencephalo-
Electroencephalogram gram electrode montage. The odd numbers denote the left (L) hemi-
sphere whereas the even numbers represent the right (R) hemisphere.
The electroencephalogram (EEG) is the quintessential cerebral See text for details.
function monitor. It records the electrical activity generated by
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Table 36-1. Electroencephalogram Table 36-2. Indications for

Frequencies Electroencephalogram
Monitoring
Range
Wave (Hz) Description During 1. Carotid endarterectomy
anesthesia 2. Cardiopulmonary bypass procedures
Delta 0–3 Low frequency, high amplitude; present
3. Cerebrovascular surgery
in deep coma, encephalopathy, and
a. Aneurysm surgery involving
deep anesthesia
temporary clipping
Theta 4–7 Not prominent in adults, although may
b. Vascular bypass procedures
be seen in encephalopathy
4. When burst suppression is desired for
Alpha 8–12 Prominent in the posterior region
cerebral protection
during relaxation with eyes closed
In the intensive 1. Barbiturate coma for patients with
Beta >12 High frequency, low amplitude; the
care unit traumatic brain injury
dominant frequency during arousal
2. When subclinical seizures are
suspected
of which gives the overall EEG pattern. The range of frequencies

seen in EEG is described in Table 36-1. The power (amplitude optimal for the prevention of intraoperative awareness. However,
squared) at each frequency can then be plotted as a spectral array, a recent study failed to demonstrate the superiority of a BIS proto
whereby the effect of various influences such as anesthetic agents col over a protocol based on end-tidal anesthetic agent concentra
or an ischemic insult can be detected by how they modify the tion monitoring in the prevention of intraoperative awareness.22
spectral analysis. A common parameter to include in the analysis
of EEG is the spectral edge frequency, which is the frequency below
Evoked Potential Monitoring
which 95% of the power resides.
A progressive reduction in CBF will produce a reliable pattern Although EEG is a cerebral function monitor that detects spon
change in the EEG, consisting of a loss of high-frequency activ taneous activity, evoked potential (EP) modalities detect signals
ity, a loss of power, and the eventual progression to EEG silence. that are the result of specific stimuli applied to the patient. These
The monitor is therefore useful when surgical procedures jeop include somatosensory evoked potential (SSEP), brainstem audi
ardize perfusion to the brain, such as when the carotid artery is tory evoked potential (BAEP), visual evoked potential (VEP), and
cross-clamped during CEA. The EEG is particularly useful in this motor evoked potential (MEP).
setting because the spectral analysis on the at-risk side can be The proposed benefit of EP monitoring is to identify the dete
compared in real time with the unaffected side, thus facilitating rioration of neuronal function, thus enabling the opportunity to

detection of ischemia by the resultant asymmetry of the spectral correct offending factors before becoming irreversible. Such fac
edge frequency. tors include positioning of the patient (e.g., neck position, shoulder
Subspecialties
However, the changes in the EEG spectrum seen with ischemia position), hypotension, hypothermia, and surgical intervention.
can occur as a result of other influences. Intravenous anesthetic In elective spinal surgery without EP monitoring, iatrogenic
agents such as propofol and thiopental, as well as inhaled agents neurologic injuries have been estimated to be 0.46% for anterior
such as isoflurane, will cause a similar decrease in the spectral cervical discectomy, 0.23% to 3.2% with scoliosis correction, and
edge frequency, with eventual progression to a drug-induced iso between 23.8% and 65.4% with intramedullary spinal cord tumor
electric EEG in a dose-related manner. During certain surgical resection. A recent systematic review indicated that, although
procedures, such as extracranial-to-intracranial arterial bypass there is a high level of evidence that multimodal neurophysiologic
procedures, maximal suppression of cerebral metabolic rate is monitoring is sensitive and specific for detecting intraoperative
desirable to protect the brain during an ischemic insult. Under neurologic injury during spine surgery, there is very little evi
such circumstances, the anesthetic agent can be titrated against dence that an intraoperative response to a neuromonitoring alert
the EEG until the desired effect is achieved. Typically, instead of reduces the rate of perioperative neurologic deterioration. Con
an isoelectric EEG, the goal is a state called burst suppression. In sequently there is a low level of evidence that it reduces the rate of
this state, periods of isoelectric EEG are punctuated by “bursts” new or worsening perioperative neurologic deficits.23,24
of EEG activity. When burst suppression is the goal, a suppression
ratio can be calculated as the percentage of an epoch in which
Somatosensory Evoked Potential
the patient’s EEG is isoelectric. The suppression ratio allows one
to achieve near-complete suppression (>90%) of EEG activity, SSEP is a signal that is detectable on EEG and is generated in
while remaining certain that regular EEG activity will return in a a time-locked fashion in response to a specific applied sensory
short while with cessation of administration of the drug. In con input, typically a cutaneous electrical stimulation (i.e., of a
trast, when complete isoelectric EEG is achieved, time to arousal peripheral sensory nerve, but also of a cranial nerve with a sen
becomes unpredictable. Other settings in which EEG monitoring sory pathway). As a result, an intact neural pathway from the
and burst suppression may be useful are listed in Table 36-2. periphery to the cerebral sensory cortex is essential for a signal
Using a proprietary algorithm based on probabilistic analysis, to be generated. This monitoring modality has application in any
a computer-processed EEG has been used to derive a dimension surgical procedure that may jeopardize this pathway. Specifically,
less number to monitor the degree of hypnosis or the “depth of spine surgery in which the dorsal column of the spinal cord may
anesthesia.” The most commonly used monitor is the Bispectral be placed at risk is a particularly appropriate application, but it
index (BIS) where a number between 40 and 60 is considered may also be used during other procedures such as craniotomy
LWBK1137-C36_p996-1029.indd 1001 11/01/13 7:52 PM

and carotid surgery where any part of the pathway may be sub Brainstem Auditory Evoked Potential
jected to ischemia or surgical retraction.
BAEP is a specialized type of sensory evoked potential. Instead of
Because of the presence of spontaneous EEG activity, a single
an electrical stimulus applied to a somatosensory nerve, a stan
peripheral stimulus, which generates cortical activity of relatively
dardized sound (click) is applied to the eighth cranial nerve via
low amplitude, would not be detectable amidst the background
the auditory apparatus. A recognized series of peaks are generated
noise. Summation followed by signal averaging of repetitive stim
with this technique, where the latency of each peak has signifi
uli is therefore necessary in order to extract meaningful signals.
cance with respect to the integrity of various parts of the auditory
Stimulation is typically done in the regions of the median
pathway. Although this monitoring modality is specific to cranial
nerve, ulnar nerve, and posterior tibial nerve to generate predict
nerve VIII, and is particularly useful in acoustic neuroma surgery,
able and reliable signals. However, in theory, any sensory nerve
it may be used during any surgical procedure around the brain
could be used to generate SSEP. The SSEP is described by its
stem to infer its integrity, although such use is associated with
polarity (the direction of the wave deflection) and its latency (the
both low sensitivity and specificity.
time required for a signal to be detected after the stimulus has
been applied), and is quantified by both the amplitude of that
signal and its latency. For example, N20 is the SSEP generated via Visual Evoked Potential
stimulation of the median nerve that is expected to have a latency VEP signals are generated via light stimulation of the retina.
of approximately 20 ms and a negative displacement (Fig. 36-8). Typically, goggles that emit LED lights are worn. Although this
Disruption of the neural pathway at any point will result in modality is particularly appealing to monitor the integrity of
complete loss of SSEP. More commonly, ischemia, not mechani the optic nerve in settings in which visual loss is a concern,
cal disruption, is the intraoperative insult. As a result of ischemia, such as in prone spine surgery, the signals are not robust. They
the amplitude of the signal decreases and the latency increases. A are difficult to record in a consistent fashion during anesthe
50% decrease in signal amplitude is generally accepted as clini sia, although it appears to be more stable during propofol
cally significant, as is a 10% increase in latency. compared to inhalation anesthesia. Research is ongoing with
respect to its intraoperative use, particularly with regard to its
interpretation.
V

IV Motor Evoked Potential
I III 0.5 V
MEP monitoring is different from the other evoked potential
II
modalities described thus far. Whereas SSEP, BAEP, and VEP
VI provide information about ascending sensory neural pathways
(i.e., from the periphery to the cerebral cortex), MEP evaluates
descending motor pathways (i.e., from the cerebral cortex, past the
neuromuscular junction, to peripheral muscle groups). This differ
0 2 4 6 8 10
ence allows MEP to complement SSEP, particularly in the setting
ms
BAEP
of spine surgery, in which the two modalities provide information
about the integrity of anatomically different areas of the spinal cord.
With MEP, the stimulus is applied in a transcranial fashion over
P57 the motor cortex. The deflection, essentially an electromyographic
P40 signal, is then detected by electrodes embedded in the muscle belly.

1 V Although theoretically the stimulus can be delivered with either a
magnetic or electrical source, transcranial magnetic stimulation is
obliterated under anesthesia. The transcranial electrical signal is
N35 N45 usually delivered as a rapid train of four or more stimuli, the voltage
N20 of which is adjusted to achieve adequate signals in both the upper
0 60 120 0 15 30 and lower extremities. The MEP is typically detected at the thenar
ms ms
eminence and the abductor hallucis muscle. Transcranial electrical
SSEP-Posttibial n SSEP-Median n
MEP is of substantially greater magnitude compared with SSEP, and
signal averaging with repetitive stimuli is therefore not required.
However, it is very sensitive to anesthetic agents, particularly inha
P109 lation anesthetics. Its amplitude can be augmented by increasing

the transcranial voltage, or the number of stimuli in the train. The
5 V
stimulus can cause patient movement, so MEP signals are typically
obtained intermittently at points during the surgery when slight
patient movements are not problematic. A bite block is mandatory
to prevent injury to the tongue during transcranial stimulation.
0 100 200 With MEP, latency of the signal is somewhat unreliable, and
ms not typically used to make clinical decisions. Decision making is
VEP-Goggles based on amplitude alone, where a 50% decrease is considered
significant (Fig. 36-9). Although MEP can be used during any
spine or intracranial surgical procedure, it is becoming increas
Figure 36-8. Representative tracings of multiple modalities of sen- ingly used during cervical spine surgery.
sory evoked potential. BAEP, brainstem auditory evoked potential; ms, MEP signals are much more sensitive to volatile anesthesia
millisecond; n, nerve; SSEP, somatosensory evoked potential; VEP, visual
evoked potential.
than SSEP. Although there is some evidence that MEP signals
are adequate during desflurane anesthesia, more research on
LWBK1137-C36_p996-1029.indd 1002 11/01/13 7:52 PM

MEP from stimulation of left cranium instance, the quality of signals obtained with SSEP monitoring
depends on the anesthetic agents used. Signals are obtainable
under volatile anesthesia, but the anesthetic is typically kept at
500 µV
sub-MAC (minimum alveolar concentration) doses to avoid
degradation in quality (increase in latency and decrease in ampli
tude), as amplitude of SSEP signals are depressed by volatile
agents in a dose-related manner; they are recordable during low
dose and obliterated with high doses. Potent volatile anesthetics
should not be combined with nitrous oxide, as this technique will
Rt Thenar–Hypothenar further compromise quality. The signals are unaffected by opi
oids, and opioid infusions are frequently used to facilitate low-
dose volatile anesthesia. Signal quality is also excellent under
intravenous anesthesia with propofol. Ketamine has been shown
to enhance evoked potential monitoring. Dexmedetomidine
infusion has also been used as an adjunct, allowing a reduction in
propofol dose, but its effects on MEP remain controversial, with
some studies reporting a lack of effect while some reports suggest
a deleterious effect.27,28
To summarize the influence of anesthetic agents on evoked
potential monitoring, general statements can be made.
Figure 36-9. Representative tracing of motor evoked potential
(MEP) recorded from the thenar muscles in response to transcranial 1. Inhalation agents including nitrous oxide generally have
electrical stimulation. more depressant effects on EP monitoring than intravenous
agents.
2. Cortical EP with long latency involving multiple synapses are
exquisitely sensitive to the influence of anesthetic while short
the efficacy of this technique is required, and total intravenous latency brainstem and spinal components are resistant to anes
anesthesia is the preferred technique when MEP monitoring is thetic influence. Thus, BAEP can be recorded under any anes
required.25 Some centers use partial neuromuscular blockade, but thetic technique, whereas VEP and SSEP are very sensitive.
most centers avoid muscle relaxants altogether with MEP in order 3. Monitoring of MEP and cranial nerve EMG in general pre
to avoid compromise of the signal.26 clude the use of muscle relaxants, although the use of a short-
acting neuromuscular blocking agent for the purpose of
Spontaneous Electromyography tracheal intubation is not contraindicated as its effect usually
wears off before monitoring and surgery begins.
Spontaneous electromyography (EMG) is different from other 4. MEP is exquisitely sensitive to the depressant effects of inha
evoked potentials in that a signal is not intentionally generated lation anesthetics including nitrous oxide. Although it can

through stimulation at some point in a known neural pathway. be recorded with low-dose agents, the signals are so severely
Instead, it is a continuous recording of EMG activity in the muscle attenuated that this practice is generally not advisable. Total
of regions innervated by nerve roots around which surgeons are
Subspecialties
intravenous anesthesia without nitrous oxide is the ideal
working. Its purpose is to detect injury to those nerve roots by the anesthetic technique for monitoring of MEP. Ketamine may
surgical procedure. Impingement on a nerve root by an instru enhance the amplitude of MEP, while dexmedetomidine may
ment will cause immediate motor activity that is easily detectable, have either negligible or some depressant effects.
which may allow the surgeon to modify his or her technique. 5. Opioids and benzodiazepines have negligible effects on
Although spontaneous EMG is a robust signal that is tolerant of recording of EP.
various anesthetic techniques, muscle relaxant must be avoided. 6. Propofol and thiopental attenuate the amplitude of virtu
Spontaneous EMG is frequently used during cervical and lumbar ally all modalities of EP but do not obliterate them. SSEP
spine surgery where the brachial plexus and lumbosacral plexus and MEP can be monitored even during burst suppression
are encountered. induced by these agents. BAEP can be recorded with any
anesthetic technique.
Cranial Nerve Monitoring 7. During crucial events in which part of the central neural
pathway is specifically placed at risk by surgical manipula
Surgery in the posterior cranial fossa and adjacent to the brain
tion, as in placement of a temporary clip during aneurysm
stem places the surgeon in close proximity to cranial nerves.
surgery, change in “anesthetic depth” should be minimized to
Although cranial nerve VIII can be monitored with BAEP as
avoid misinterpretation of the changes in EP recorded.
discussed earlier, several other cranial nerves can be monitored
8. Ketamine and etomidate have been reported to enhance the
as well. Generally, only the integrity of nerves with motor com
quality of signals in patients with weak baseline SSEP signals,
ponents can be detected, either through spontaneous EMG
although the clinical significance and interpretation of signals
or through EMG evoked by local electrical stimulation. These
obtained under these circumstances remain unclear.
include cranial nerves V, VII, IX, X, XI, and XII. Cranial nerve X
is usually monitored via special monitoring endotracheal tubes
embedded with electrodes near the cuff.
Cerebral Perfusion
Influence of Anesthetic Technique
Although adequate CBF does not guarantee the well being of
As mentioned previously, anesthetic agents can have a profound the CNS, it is one factor that is essential to its integrity. Mea
influence on the amplitude and latency of evoked potentials. For suring CBF is therefore an attractive method of monitoring the
LWBK1137-C36_p996-1029.indd 1003 11/01/13 7:52 PM

CNS. Currently available techniques for quantitative measure bral artery, posterior cerebral artery, ophthalmic artery, vertebral
ment of CBF are not practical as an intraoperative monitor, but artery, and basilar artery, not all of these vessels can be monitored
other methods for looking at relative changes in CBF do lend continuously during surgical procedures. Many of these vessels
themselves to use in the operating room. Transcranial Doppler can only be evaluated with a hand-held TCD probe, which is use
ultrasonography (TCD) and laser Doppler flowmetry are exam ful for providing a brief snapshot of flow velocity in that vessel.
ples. Furthermore, as adequate CBF depends on an appropriate A commercially available device for fixation of the TCD probe
CPP, measuring ICP may be useful in certain patients to ensure is essential for continuous monitoring. These devices are avail
conditions are adequate for sufficient CBF. Finally, numerous able either as a headband or as a rack that remains attached via
other modalities that evaluate CBF and that may not be practi fixation points on the bridge of the nose and in bilateral auditory
cal in the operating room are used commonly in the periopera canals. With these devices, flow velocity in the middle cerebral
tive setting. artery can be continuously evaluated.
In addition to the measurement of flow velocity, TCD is useful
for detecting emboli. Microembolic signals can be generated by
Laser Doppler Flowmetry
the passage of either gas or particulate matter (Fig. 36-11). The
Laser Doppler flowmetry is a technique that measures corti former is likely to occur as a result of venous air embolism (VAE),
cal blood flow in a small region of the brain adjacent to the particularly if the patient has a patent foramen ovale, while the
placement of the device. Although it is useful for detecting latter may occur during the manipulation of an atheroma in a
relative changes in CBF, its utility is limited by several factors. neck vessel or as the result of thrombus formation and dislodge
First, it requires a burr hole for placement, which prevents its ment on a vascular dissection.
use in most patients. Second, it measures flow in only a small Specific applications for intraoperative use of TCD include
region of the brain; it could miss hypoperfusion in any area CEA, nonneurologic surgery in patients with TBI, and surgical
of the brain not directly monitored. Accuracy is also affected procedures requiring cardiopulmonary bypass. There are also
by movement and the presence of underlying major vessels. numerous indications for TCD in the perioperative setting.
Because of these limitations, laser Doppler flowmetry has Perhaps the most important use of TCD is in the neurocritical
found limited applications. care unit, where it is used to monitor the development of vaso
spasm in patients who have suffered a subarachnoid hemorrhage.
It has also been used for the measurement of cerebral autoregula
Transcranial Doppler Ultrasonography
tion in patients with TBI, vasomotor reactivity in patients with
TCD is a noninvasive monitor for evaluating relative changes in occlusive vascular disease, noninvasive measurement of ICP,
flow through the large basal arteries of the brain (i.e., the circle of determination of intracranial circulatory arrest and confirmation
Willis). TCD does not measure flow directly, and therefore can of brain death.30–33
not provide information regarding absolute CBF. TCD measures
flow velocity (Fig. 36-10), which is directly proportional to the
Intracranial Pressure Monitoring
flow if the diameters of these large vessels are constant. Except in
well-known circumstances such as cerebral vasospasm following Although monitoring ICP does not provide direct information
aneurysmal subarachnoid hemorrhage, these vessels are thought about CBF, it allows the derivation of CPP, which must be in an
to be conductance vessels, where diameters of the basal arteries are appropriate range in order for CBF to be adequate. CPP is defined
stable.29 Pressure autoregulation and CO2 reactivity of CBF occurs as the difference between MAP and ICP. In other words, it is the
via changes in arteriolar diameter distal to these large vessels. net pressure acting to move blood through the cerebral vascula
Although the vessels that can be evaluated with TCD include ture (assuming ICP is greater than right atrial pressure). CPP and
the middle cerebral artery, internal carotid artery, anterior cere CBF are not expected to be proportional, as there are other factors
Figure 36-10. Transcranial Doppler tracing with CM/S MedaSonics//CDS

release of cross-clamp during carotid endarterec- MedaSonics//CDS 50
tomy. The resultant hyperemia is accompanied 100
with evidence of air emboli (vertical streaks on the Depth
12:39
tracing). MCA, middle cerebral artery; ICA, internal
carotid artery.
25
ID# Peak
Ref DR : None
Vessel : RMCA
18
Power : 700%
Probe : PW 2 MHZ Mean
0
Gain : 8 dB
Range : 19 dB RT. MCA
Angle : 0 deg
Sample : 13 mm RT. ICA Released
Flow :
Cursor
LWBK1137-C36_p996-1029.indd 1004 11/01/13 7:52 PM

9:50:18 AM 9:54:46 AM
MCA L 56 mm 2 MHz PW MCA R 50 mm 2 MHz PW
cm/s cm/s
33 1.83 0.83 33 1.83 0.88
TIC PI TIC PI
100 100
96 63 96 54
Power Mean Power Mean

0 0
56 94 50 84
Depth Sys Depth Sys

100 100
10 42 10 37
9 SV Dia 9 SV Dia
9:57:28 AM 9:58:02 AM
MCA R 50 mm 2 MHz PW MCA R 50 mm 2 MHz PW
cm/s cm/s
33 1.83 0.93 33 1.83 1.0
TIC PI TIC PI
100 100
96 49 96 44
Power Mean Power Mean

0 0
50 78 50 71
Depth Sys Depth Sys

100 100
10 32 10 28

9 SV Dia 9 SV Dia
Subspecialties
Figure 36-11. Particulate emboli seen on transcranial Doppler in a patient with symptoms of transient ischemic attacks
consistent with right carotid artery territory embolization. The emboli are denoted by the arrows. MCA, middle cerebral artery;
PW, pulse wave.
determining CBF (discussed elsewhere). In fact, within a physi volume, drainage of CSF, removal of brain water with osmotic
ologic range of CPP, CBF should remain approximately constant. agents such as mannitol, and if absolutely essential, mild-to-
However, a CPP that is too low will result in cerebral ischemia moderate hyperventilation to further decrease CBV. MAP is
and CPP that is too high will cause hyperemia. raised via adequate intravascular resuscitation and with a vaso
ICP monitoring is recommended in all salvageable patients pressor as needed. The goal CPP in TBI is >50 to 60 mm Hg.34
with severe TBI (GCS ≤ 8) and an abnormal CT scan (hemato
mas, contusions, swelling, herniation, or compressed basal cis
Other Modalities
tern), and in patients with severe TBI with a normal CT scan if
two or more of the following features are noted at the admission: Although seldom employed in the intraoperative setting, CT per
Age >40 years, unilateral or bilateral motor posturing, or SBP fusion, single-photon emission computed tomography, positron
<90 mm Hg. However, patients who present to the operating emission tomography, and cerebral angiography all have roles,
room in the acute stage of injury will seldom have an ICP monitor experimental or clinical, in the evaluation of CBF. However, these
in place, and the presence of elevated ICP must be inferred from techniques are frequently used preoperatively and postopera
the medical history, physical examination, and CT scan. tively in neurosurgical patients. On the other hand, intraopera
When ICP is high and CPP is low, interventions can target tive angiography is frequently used during neurovascular surgery
either ICP or MAP in order to restore a favorable balance of the to confirm placement of an aneurysm clip or to verify complete
two. Ideally, ICP should be maintained under 20 mm Hg. Inter obliteration of an arteriovenous malformation (AVM). More
ventions to lower ICP include suppression of cerebral metabolic recently, this has been superseded by indocyanine green videoan
activity, positional changes to decrease cerebral venous blood giography, as this obviates the need for radiation.35
LWBK1137-C36_p996-1029.indd 1005 11/01/13 7:52 PM

Interventions to raise the Pbto2 must either target oxygen

Cerebral Oxygenation/Metabolism Monitors delivery or oxygen consumption. In order to improve oxygen
delivery, Fio2-inspired oxygen can be increased, but treating ane
A number of invasive and noninvasive monitors provide insight mia makes more sense from a physiologic perspective. Decom
into the metabolic state of the brain and the level of tissue oxy pressive craniectomy may improve perfusion. Decreasing oxygen
genation of the brain, both of which reveal the balance between requirements can be accomplished by metabolic suppression with
blood supply and metabolic demands. propofol or a barbiturate, as well as by treating hyperthermia with
external cooling, acetaminophen, and when appropriate, nonste
roidal anti-inflammatory medications.
Near-infrared Spectroscopy
Near-infrared spectroscopy (NIRS) is a noninvasive method of
Jugular Venous Oximetry
detecting the oxygenation of cerebral tissue. It is based on reflec
tance spectroscopy; it measures the light reflected from chromo Although Pbto2 gives a local view of the balance of oxygen sup
phobes in the brain (hemoglobin) to derive the regional oxygen ply and demand, jugular venous oximetry provides that same
saturation. In this manner, it provides an indication of the bal information for a larger portion, if not the complete, brain. For
ance between flow and metabolism. Typically, a sensor is applied this monitor, a catheter is inserted into the jugular vein in a ret
to the forehead (over hairless skin). A light signal is transmitted rograde fashion so that its tip sits at the base of the skull in the
through the skin, skull, and meninges into the cerebral cortex. jugular bulb. This allows continuous pressure monitoring as well
A complex analysis of the reflected light allows calculation of as intermittent withdrawal of a jugular venous blood sample for
the oxygenation of blood in the cortex, which is a mix of venous gas analysis. Continuous monitoring can be achieved using an
and arterial blood. Falling saturation indicates a decline in cere oximetry catheter inserted via a conduit sheath. Confirmation of
bral perfusion. Exact thresholds for concern relate to the specific location can be made with a lateral cervical spine film.
device used for this purpose. For best representation of the metabolic state of the brain, the
Bilateral monitoring is particularly attractive for procedures catheter should be placed in the dominant jugular vein, most com
that place a single hemisphere at risk for ischemia, such as CEA monly the right side. In patients who have had a cerebral angio
carotid surgery. In this setting, the development of significant gram, the venous phase of the study will provide information
asymmetry in cerebral oxygenation could be used as an indicator on dominant venous drainage. Often the intra-arterial contrast
for the need for a shunt. will drain almost exclusively through one jugular vein, regard
Individual variations in extracranial tissue (hence contamina less of the side of injection. Side dominance can also be predicted
tion), arterial to venous blood volume ratio, systemic blood pres using ultrasound where the dominant vein may be larger. In the
sure, Paco2, hematocrit, and regional CBV are factors that can absence of this information, the right side is preferred.
influence cerebral tissue oxygenation, and this creates potential Pressure transduction of the jugular bulb catheter allows
difficulties when attempting to establish a consensus value for comparison with the central venous pressure to rule out poten
NIRS-derived “thresholds” for ischemia/hypoxia.36 It is generally tial venous obstruction. In a supine patient with a neutral neck
accepted that normal range varies between 60% and 75%, with a position, there should be no pressure gradient between the tip of
coefficient of variation of almost 10%.36,37 the jugular bulb and the central venous catheter. Although rare, a
The applicability of NIRS in brain injury monitoring is as yet significant gradient (>4 mm Hg) can occasionally develop during
to be defined and there are no data to support the widespread positioning if there is significant twisting or bending of the neck.
application of NIRS to monitor cerebral oxygenation routinely This gradient indicates venous obstruction, potentially causing
during anesthesia and surgery. Ironically NIRS has found most brain edema, or ischemia. The head should be repositioned until
acceptance in cardiac anesthesia, where access to the forehead for the gradient resolves.
placement of the sensor is less of a problem than in neuroanes Blood gas analysis of the sample provides several useful
thesia. Nevertheless, it is a promising technology that, as advances parameters. The saturation of jugular venous blood (Sjvo2) dem
in design are made, may find increasing application in the field of onstrates whether CBF is sufficient to meet the cerebral meta
neuroanesthesia. bolic rate for oxygen (CMRO2) of the brain. A normal value is
in the 65% to 75% range. In TBI, Sjvo2 below 50% for more than
10 minutes is undesirable and associated with poor outcome.41
Brain Tissue PO2
However, it has low sensitivity, and a study using PET scan indi
The brain tissue PO2 (Pbto2) monitor is an invasive probe that cates that a relatively large volume of tissue must be affected,
is inserted through a burr hole into the brain parenchyma, typi approximately 13%, before Sjvo2 levels decreased below 50%.42
cally in conjunction with a fiberoptic ICP monitor. As a result, Intraoperative hyperventilation will lower Sjvo2 as it decreases
this monitor is used most commonly in patients with TBI. It CBF. In the setting of a nontraumatized brain that is exposed
measures oxygen tension in the surrounding brain. An adequate to moderate hyperventilation for the duration of a neurosurgi
CPP in such a patient is encouraging, but it does not guarantee cal procedure, the acceptable level for Sjvo2 is unknown. In the
adequate blood supply to meet the metabolic needs of the brain. absence of other demands, it is reasonable to guide intraoperative
Pbto2 complements ICP information in that it provides insight hyperventilation by maintaining Sjvo2 >50%. It is essential that
into oxygen delivery. A low Pbto2 is indicative of inadequate oxy blood samples from the retrograde catheter be drawn slowly to
gen delivery to that area of brain. A level of 15 mm Hg is concern avoid contamination from noncerebral venous blood.43
ing for cerebral hypoxia, and warrants intervention in TBI.38,39 In Measurement of simultaneous arterial and jugular venous
patients with TBI, Pbto2 has been shown to correlate well with the samples allows the determination of lactate output from the
treatment effects and outcome.40 brain, the presence of which indicates occurrence of anaerobic
Its major limitation is that the information it provides reflects metabolism. The obvious disadvantage to jugular venous oxim
oxygenation at the local level—in proximity to the probe—meaning etry is precisely the opposite of the shortcoming for Pbto2, in that
that an adequate Pbto2 at that location may not guarantee ade it is a global monitor that could easily miss small areas of regional
quate oxygen delivery to other regions of the brain. ischemia. The two monitors may be complementary in the setting
LWBK1137-C36_p996-1029.indd 1006 11/01/13 7:52 PM

of TBI. Intraoperatively, jugular venous oximetry is used rou these pathways as well to provide protection. A shift in the focus
tinely in some centers that specialize in neurosurgical procedures. of neuroprotection from metabolic suppression to targeting isch
emic cascades has recently been advocated.46
Cerebral Protection Hypothermia

5 Cerebral ischemia and/or hypoxia leads to neuronal death in It is important to distinguish mild/moderate and profound hypo
multiple settings. For example, ischemic stroke, TBI, and cerebral thermia, as they have very different practical considerations and
vasospasm following subarachnoid hemorrhage. Efforts to avert they likely modify cerebral function in different ways.
neurologic insult, using medications or through the manipula Profound hypothermia is well known for its neuroprotec
tion of physiologic parameters, have met with meager results. In tive effects. Anecdotes of successful resuscitation of hypothermic
the setting of ischemic stroke, for example, thrombolysis may drowning and avalanche victims with good neurologic recovery
restore perfusion and decrease infarct size, but it may also lead to have been reported.47,48 Furthermore, extensive use of deep hypo
expansion of the infarct, edema, and even hemorrhage as a result thermia with circulatory arrest has been used intraoperatively
of ischemia-reperfusion injury. In general, a protective strategy for the repair of aneurysms of the thoracic aorta and for cere
that is effective in experimental cerebral ischemia has not been bral aneurysms.49,50 When core body temperature is <20°C, and
found to be useful in the clinical setting. Of recent advances the brain is <15°C, circulatory arrest of <30 minutes appears to
that are intriguing and controversial, none matches that gener be well tolerated. This level of hypothermia not only decreases
ated by the concept of cerebral protection by mild or moderate cerebral activity, but it also decreases the energy required for cel
hypothermia. lular housekeeping. The practical constraints against using deep
Persons suffering out-of-hospital cardiac arrest have been hypothermia in settings in which cerebral ischemia is antici
shown to have improved neurologic outcome if they are made pated are numerous. Foremost is the need for cardiopulmonary
mildly hypothermic following resuscitation.44,45 Therefore, it bypass during the cooling and warming portion of the procedure.
would seem that mild hypothermia is protective against global Hypothermia-induced coagulopathy is another concern during
ischemia/hypoxia at least in the setting of cardiac arrest. surgical procedures in the cold patient. Despite the drawbacks to
One problem with most settings in which cerebral ischemia is this technique, it remains a reasonable anesthetic option to pro
encountered is that the therapeutic intervention can be applied vide protection for the brain and other organs when the surgical
only after the insult has occurred, that is, during the reperfusion procedure necessitates circulatory arrest.
phase. Little opportunity exists to intervene before the ischemic Mild hypothermia (33° to 35°C) not only decreases cerebral
event. However, the operating room is a unique environment metabolism, but likely modulates the immune and inflammatory
in this respect. Many ischemic insults that patients suffer in the response to ischemia, thus affecting the reperfusion portion of the
operating room are iatrogenic and anticipated. A temporary injury as well. Animal studies have shown improved neurologic
aneurysm clip on the middle cerebral artery is an example of a function following resuscitation from arrest.51 This promising
focal ischemic insult that could be predicted, and a brief period of result in animals was later confirmed by two independent stud
circulatory arrest induced with adenosine to facilitate clipping of a ies in humans, demonstrating that induction of hypothermia in

basilar artery aneurysm is an example of a global insult. The value cardiac arrest patients improved the outcome.44,45
of anticipating such events is that it allows the anesthesiologist Although mild hypothermia is clearly beneficial in the setting
Subspecialties
to intervene in advance. of cardiac arrest, cerebral ischemia due to an arrest is an uncom
Despite the luxury of planning the intervention for the isch mon occurrence in patients under anesthesia. In contrast, the
emic insult, the options anesthesiologists have for cerebral pro cerebral ischemia frequently encountered by the anesthesiologist
tection are few and the evidence for benefit is modest; much of is focal in nature because of the temporary occlusion of a cerebral
this evidence has been extrapolated from animal research. Each vessel. Although there is considerable evidence in rats that mild
technique will be examined in detail here. hypothermia is beneficial here too, there is a paucity of evidence
in humans. In fact, a large multicenter study (IHAST II—Intra
operative Hypothermia for Aneurysm Surgery Trial) evaluating
Ischemia and Reperfusion patients undergoing cerebral aneurysm surgery found no ben
efit with mild intraoperative hypothermia.52 However, the study
Ischemic insult to the brain results in energy failure. The brain was not designed to study patients at the highest risk—that is,
depends on a continuous supply of glucose and O2 to support aer those who had undergone temporary occlusion for more than
obic metabolism, generation of adenosine triphosphate (ATP), 20 minutes. Although the sample size is small, a post-hoc analy
and maintenance of cellular function. When this nutrient supply sis of these at-risk patients suggest that there is a trend for either
is interrupted, ATP is depleted. Cellular processes, such as those hypothermia or metabolic suppression to improve outcome.53
that maintain cellular membrane integrity, fail. It is reasonable Nevertheless, hypothermia remains our most promising inter
then to attempt to minimize ischemic insult by lowering cere vention for cerebral protection. There is a compelling physiologic
bral metabolic rate, thus decreasing the likelihood of exhausting rationale for its use, a clearly demonstrated effect in animals,
ATP reserves during the period of ischemia. This has been the and human data showing benefit in the setting of cardiac arrest.
traditional paradigm for approaching the subject of intraopera Unfortunately, inadequate evidence exists in humans outside
tive neuroprotection. cardiac arrest to recommend its routine use in the neurosurgical
Unfortunately, further damage occurs as a result of processes patient.
that are initiated during the reperfusion stage. The reperfusion Despite the lack of evidence to support hypothermia in
injury may be mediated via the generation of toxic oxygen spe humans for cerebral protection, there is ample evidence that
cies, release of excitotoxic amino acids such as glutamate, up- hyperthermia is associated with worse outcome in the setting of
regulation of nitric oxide synthase, and initiation of cellular ischemic stroke, subarachnoid hemorrhage, cardiac arrest, and
apoptosis. Further therapeutic interventions would need to target TBI.54–57 A common extrapolation from these studies is the belief
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that concomitant hyperthermia and cerebral ischemia is deleteri recognition of its association with worse outcome in many set
ous. However, it is important to consider that these studies dem tings, including acute coronary syndrome, stroke, TBI, and critical
onstrate an association, not a causation, of poor outcome from illness, forced the medical community to reconsider the burden
fever. Nevertheless, it would seem reasonable to avoid hyperther of hyperglycemia.81–86 Furthermore, animal studies suggested
mia and treat fever aggressively in any setting in which the brain that hyperglycemia in the setting of both cerebral and myocardial
is at risk.58 ischemia increased infarct size.87,88
In the operating room, during neurosurgical procedures in Although considerable evidence accumulated suggesting
which the brain is at risk for ischemic insult, a goal temperature harm associated with hyperglycemia, evidence for benefit with
of 35° to 36°C is reasonable. Mild hypothermia (33° to 35°C) normalization of serum glucose using insulin has been somewhat
may be appropriate in many patients with a planned period of controversial. The most influential literature is from the inten
temporary focal ischemia (as in temporary occlusion for aneu sive care unit (ICU) setting, not the operating room. A prospec
rysm clipping) even recognizing that there is currently a lack of tive study in surgical ICU patients (predominantly after cardiac
solid evidence to support this therapy. Finally, deep hypothermia surgery) showed that mortality and morbidity benefit with tight
(<20°C) is appropriate in any situation in which a prolonged car glycemic control (80 to 110 mg/dL).89 This study spurred an
diac arrest is required. unfettered enthusiasm for aggressive treatment of hyperglycemia,
changing practice not only in the surgical ICU but the medical
ICU, and in many cases, the operating room. However, a sub
Medical Therapy for Cerebral Protection sequent study evaluating this therapy in a much sicker medical
ICU population showed no overall mortality benefit.90 In fact,
Volatile and intravenous anesthetic agents decrease cerebral subgroup analysis revealed increased mortality in patients who
metabolism, and thus seem like appropriate candidates for cere stayed in the ICU <3 days, with an improvement only in those
bral protection. However, evidence that the level of metabolic who had a longer ICU stay. In the heterogeneous patient popula
suppression does not correlate with the degree of protection has tion who present for neurologic surgery, with operative times of
eroded the traditional belief in the mechanism of protection.59 several hours, not several days, it is inappropriate to extrapolate
Nevertheless, numerous animal studies have found protective conclusions from a body of controversial ICU literature to the
effects of volatile anesthetics, particularly isoflurane, in mitigat anesthetic environment, particularly when there is evidence for
ing mild-to-moderate ischemic insult, although this effect may harm with short durations of therapy. Furthermore, a prospective
only be short-lived.60–63 This effect may exist when applied during study of intraoperative insulin therapy in cardiac surgery patients
the insult, but also may be effective when administered prior to further eroded the basis for translating this ICU literature to the
the insult as a preconditioning therapy.64,65 operating room; the insulin group had a higher incidence of
Barbiturates, such as thiopental, have been extensively death and stroke.91
researched in regard to cerebral protection. They have been Despite our reluctance to embrace intraoperative tight glycemic
shown to have at least short-term benefit on focal cerebral isch control given the current literature, it is worthwhile to consider
emia, while benefit in global ischemia remains controversial.66–74 the patient undergoing cerebrovascular surgery in particular.
This effect may be mediated through a reduction in glutamate Given the preponderance of evidence that hyperglycemia and
activity and intracellular calcium, an increase in γ-aminobutyric cerebral ischemia in combination are harmful, changing practice
acid (GABA) activity, as well as N-methyl-d-aspartate (NMDA) in these patients may be warranted. Hyperglycemia on the day of
antagonism.75,76 Propofol likely has similar protective effects surgery for CEA is associated with worse outcome.92 And, patients
through its action on GABA receptors, as well as via free radical who suffer from an ischemic stroke have an improved outcome if
scavenging and limiting lipid peroxidation.77,78 Again, the dura their glucose is treated aggressively.93 Therefore, it may be appro
bility of this protection is unknown. priate to treat neurosurgical patients who will have a period of
Current opinion is that anesthetic neuroprotection is pri cerebral ischemia due to temporary vascular occlusion differ
marily mediated through prevention of excitotoxic injury, not ently from other neurosurgical patients. Better glycemic control
through termination of apoptotic pathways; it thus delays neu is a reasonable goal in these patients, aiming for a range of 140 to
ronal death and leaves a greater temporal window for interven 180 mg/dL however, we cannot state at this time that this inter
tion.61 Without other therapeutic options to prevent eventual vention is neuroprotective.
cell death, outcome is unlikely to be improved, save for perhaps
the setting of mild ischemic insult in which apoptotic pathways
are not initiated. Sufficient evidence in humans to guide clinical Promising Areas of Research
interventions, apart from modest hypothermia in cardiac arrest,
is difficult to obtain.45,79 Clinically, barbiturates and propofol Continued research in the various excitotoxic and apoptotic path
are used intraoperatively to achieve metabolic depression as evi ways that lead to cell death with cerebral ischemia is essential to
denced by a burst suppression EEG pattern, and although not sta bring promising interventions to the clinical arena. It is likely that
tistically significant, results from IHAST II suggest that patients only a multimodality approach will create durable meaningful
undergoing temporary occlusion for >20 minutes may benefit cerebral protection.61 Mild to moderate hypothermia continues
from metabolic suppression therapy.53 to hold promise, given its efficacy in experimental focal ischemia.
Several additional medical interventions show potential as well.
Statins, which inhibit 3-hydroxy-3-methylglutaryl-coenzyme A
Glucose and Cerebral Ischemia (HMG-CoA) reductase, have nonlipid lowering effects such as
improved endothelial function, as well as antithrombotic and
Although hyperglycemia has long been recognized as a frequent anti-inflammatory activity, which may be neuroprotective.94 Fur
occurrence in critically ill patients, it was commonly viewed as thermore, the nonhematopoietic effects of erythropoietin include
benign or even beneficial.80 Hyperglycemia could facilitate cel mitigation of lipid peroxidation and prevention of apoptosis.95
lular uptake of glucose through noninsulin-dependent mecha Whether these medications will offer any benefit to neurosurgical
nisms, and thus may benefit cellular metabolism. A subsequent patients remains to be determined.
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of patients undergoing intermediate-risk surgical procedures:

A Practical Approach Those already receiving a beta-blocker, and those who are at high
risk for perioperative myocardial infarction due to documented
In the absence of compelling evidence in humans regarding the reversible ischemia from a noninvasive study.99,100 Furthermore,
benefit of one practice over another, it is difficult to present firm patients previously receiving a statin should continue their statin
guidelines with respect to the prevention of intraoperative isch in the perioperative period.
emic insult. Maintaining optimal systemic and cerebral hemody Further considerations in the preoperative visit should include
namics, as well as oxygenation, remain the most important prin issues that will affect choice of medications and anesthetic agents.
ciples. Beyond these, for patients undergoing surgical procedures Many patients presenting for spine surgery have weakness or
with an anticipated period of temporary focal cerebral ischemia paralysis that may present a contraindication to the use of suc
such as cerebral aneurysm surgery or cerebrovascular bypass pro cinylcholine. In addition, some neurosurgical patients may have
cedures, either volatile anesthesia or an intravenous technique suffered from a stroke resulting in a similar contraindication.
can be used. It is reasonable to administer additional propofol or Finally, many neurosurgical patients have been exposed to anti
thiopental prior to vessel occlusion. Optimally this intervention epileptic medications, which are known to induce liver enzymes
should be guided by EEG monitoring with the goal of achieving and alter drug metabolism. Previous allergies or reactions to these
burst suppression nearing a 50% ratio. A total intravenous anes medications, especially phenytoin, should be elucidated.
thetic technique is preferred when maximal brain “relaxation” is
desired. Euglycemia, or near euglycemia prior to vessel occlusion
is desirable (140 to 180 mg/dL), but frequent glucose checks are Induction and Airway Management
essential throughout the anesthetic to avoid episodes of hypogly
cemia if insulin is administered. Finally, hyperthermia should be With the exception of some minimally invasive spine surgery
avoided during this time, with the temperature kept at or below procedures and awake craniotomies, placement of an endotra
36°C. cheal tube is essential for most surgical procedures of the brain
and spinal cord.
During induction of anesthesia, hypotension, hypertension,
Anesthetic Management and prolonged apnea should be avoided. A brief period of mild
hypotension is frequently encountered following induction of
anesthesia. Although most patients tolerate this transient phe
Preoperative Evaluation nomenon well, it should be aggressively avoided and/or treated
in patients with brain injury in which any episode of hypoten
6 Risk stratification is indicated for neurologic or spine surgery sion may be associated with unfavorable outcome.101 Hyper
to assess the patient’s neurologic condition, as well as the inher tension due to laryngoscopy, in contrast, is poorly tolerated by
ent risk of the surgical procedure. For a smooth transition from patients following aneurysmal subarachnoid hemorrhage, as
patient referral to surgical intervention, dynamic communica systolic hypertension is thought to be a cause of recurrent hemor
tion between neurosurgeons, anesthesiologists, the preanesthesia rhage from the aneurysm.102 Finally, apnea results in a predict
clinic, neurophysiologists, and the laboratory is essential.96,97 able increase in Paco2, and corresponding cerebral vasodilation.

Preoperative assessment allows identification of modifiable Although most patients tolerate the increase in CBV, patients
risk factors, optimization of the patient’s condition, explana with poor intracranial compliance may develop severe intracra
Subspecialties
tion of the risks and formulating the best possible anesthetic nial hypertension and decompensate from apnea, as well as suffer
plan to improve patient safety, optimize resource utilization and a decrease in cerebral perfusion.
increased patient satisfaction. A thorough history may be difficult TBI patients in particular are frequently intolerant of apnea.
to obtain from patients whose disease has resulted in a neurologic Unfortunately, many of these patients require a rapid-sequence
decline, such as those obtunded from TBI. Prior medical records, induction. To further complicate matters, the presence of a cervi
discussion with family physicians and family members are both cal collar for known or suspected cervical spine injury may make
helpful in this context. intubation more difficult. Careful preparation for a difficult air
Perioperative cardiac outcome is influenced by urgency, way is essential. Furthermore, these patients may have concomi
magnitude, type, duration of surgery, associate blood loss, fluid tant injuries with significant blood loss that may predispose to
shifts, and change in body temperature. The 2007 American Col systemic hypotension. Vigorous resuscitation with isotonic fluid
lege of Cardiology/American Heart Association guidelines has and/or blood should be administered prior to induction and con
a simplified algorithm for considering whether a patient needs tinued until the patient is euvolemic. A conservative dose of thio
preoperative cardiac testing, such as stress echocardiography, or a pental, propofol, or etomidate is appropriate for induction, with
nuclear medicine evaluation of myocardial perfusion.98 Spine and succinylcholine a reasonable choice as the muscle relaxant in the
neurosurgical surgery fall into the intermediate-risk procedure setting of acute injury.
category. The decision to perform a noninvasive cardiac test in Because patients with subarachnoid hemorrhage are at risk of
patients with risk factors for coronary disease and poor functional rebleeding from hypertension, it is reasonable to place an arterial
status hinges on whether findings from that evaluation will affect catheter for hemodynamic monitoring prior to induction. Unac
management of the patient in the time before surgery. For neuro ceptable increases in blood pressure during laryngoscopy should
logic patients with significant cardiac disease, current guidelines result in discontinuing the attempt, returning to mask ventila
include delaying surgery for at least 2 weeks following simple bal tion, and deepening the anesthesia. The latter can be accom
loon angioplasty, 1 month for a bare metal stent, and a full year plished either with a higher concentration of inspired volatile
for a drug-eluting stent. However, it is generally not feasible to anesthetic, or a bolus of an intravenous agent such as propofol or
delay most of the spine and neurosurgical procedures. For these remifentanil. In addition, esmolol (0.5 mg/kg) can be given prior
patients joint consultation with cardiologists is essential. As for to laryngoscopy to blunt the hypertensive response.
beta-blockers, the results of the POISE trial indicated that peri Most intravenous anesthetic agents (propofol, thiopental,
operative beta-blockade is recommended primarily in two types and etomidate) are indirect cerebral vasoconstrictors, reducing
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cerebral metabolism (CMR) leading to a corresponding reduc The use of intraoperative muscle relaxant is controversial for
tion of CBF while preserving autoregulation and CO2 reactivity. neurosurgical procedures. It should be avoided during MEP,
In contrast, ketamine has sympathomimetic properties. Its cere spontaneous EMG, or cranial nerve monitoring (except the
bral effects include an increase in CBF and ICP, but these are usu VIIIth). However, it may be used during isolated SSEP monitor
ally attenuated by the actions of other concurrently administered ing. Some anesthesiologists are more comfortable managing a
drugs.103–105 Etomidate decreases the cerebral metabolic rate, CBF, patient whose head is held in rigid fixation with muscle relax
and ICP. At the same time, because of minimal cardiovascular ant, but adequate anesthesia and avoidance of stimulating airway
effects, CPP is well maintained. However, it has been reported to manipulations are far more important and should prevent unin
reduce brain tissue oxygen tension, but the mechanism is unclear. tended patient movement.
Although changes in the EEG resemble those associated with bar Dexmedetomidine, a highly selective α2-adrenoreceptor ago
biturates, etomidate enhances SSEPs and causes less reduction nist, provides sedation without causing respiratory depression,
of MEP amplitudes than thiopental or propofol.106,107 The major does not interfere with electrophysiologic mapping and provides
limitation of etomidate is its known adrenal suppression effects. hemodynamic stability. It has been found to be particularly useful
Even after a single induction dose etomidate has been shown to for implantation of deep brain stimulators in patients with Par
prolong hospital and ICU length of stay.108–110 kinson’s disease and for awake craniotomies, when sophisticated
The choice of muscle relaxant for use during induction neurologic testing is required.117,118
deserves some consideration. Succinylcholine is contraindicated
in patients with muscle denervation from stroke, myelopathy,
or spinal cord injury (SCI) which results in up-regulation of Ventilation Management
acetylcholine receptor isoforms on myocyte membranes.111 In
these patients, profound hyperkalemia may result from the use Hypocapnic cerebral vasoconstriction provides the anesthesiolo
of succinylcholine which has the potential to lead to a cardiac gist with a powerful tool for manipulating CBF and CBV. Hyper
arrest.112 However, it is generally safe to use succinylcholine in ventilation is routinely employed to provide brain relaxation and
the first 24 to 72 hours after an injury, as well as, although contro optimize surgical conditions. Because hyperventilation decreases
versial, after the spasticity is well established in about 9 months. CBF, it has the theoretical potential for causing or exacerbating
In general a nondepolarizing muscle relaxant is appropriate for cerebral ischemia. Clinically it has been associated with harm
most neurosurgical patients to achieve acceptable conditions for only in the early period of TBI, but it is still recommended to be
tracheal intubation. Duration of action should be considered if avoided in all patients with TBI except when necessary for a brief
MEP, spontaneous EMG, or cranial nerve monitoring is planned period to manage acute increases in ICP.119,120 In the nontrauma
when adequate reversal is not possible. When used in appropri population, it is not clear whether there is harm in mild-to-
ate doses, rocuronium (1.2 mg/kg) is comparable to succinylcho moderate hyperventilation, particularly for the duration of a typi
line (1 mg/kg) for rapid sequence induction.113 When available, cal anesthetic. As it appears to be well tolerated, it is reasonable
profound neuromuscular blockade from rocuronium can be during neurosurgical procedures to maintain a Paco2 between 30
reversed with sugammadex, which currently awaits approval in and 35 mm Hg. Further brain relaxation should be accomplished
the United States.114,115 with other modalities, such as mannitol, hypertonic saline (HTS),
or intravenous anesthesia. Should hyperventilation to a Paco2
below 30 mm Hg be required, it might be appropriate to guide
Maintenance of Anesthesia this therapy with jugular venous oximetry when available.
The duration of effectiveness of hyperventilation is also con
7 The primary considerations for maintenance of anesthesia troversial as normalization of CBF, and consequently CBV, has
include the type of neuromonitoring planned for the procedure, been reported to occur within minutes. Clinically, the effects of
optimal brain relaxation, and the balance between adequate anal CBV appear to be sustained during most neurosurgical proce
gesia and the ability to assess neurologic function at the end of the dures of modest duration.
surgical procedure.
Most neurosurgical and spine procedures can be performed
using a balanced anesthetic with volatile agents and judicious Fluid and Electrolytes
doses of opioids to reduce volatile anesthetic requirements. For
both SSEP monitoring and brain relaxation, less than one MAC 8 To maintain adequate cerebral perfusion, adequate intravas
of volatile anesthetic is desired. When selecting an opioid, an cular volume should be maintained. With perhaps the excep
infusion of remifentanil, fentanyl, sufentanil, or alfentanil are all tion of healthy patients with an AVM, the aim should always be
reasonable options. Because of its short context half-life, remi euvolemia or slight hypervolemia. For the care of the neurosur
fentanil is most appropriate for neurosurgical procedures in gical patient, a large volume of hypotonic fluids including lac
which tracheal extubation is planned at the end of the surgery tated Ringer’s solution should not be used. Colloid has no proven
and minimal residual effect is desired to facilitate neurologic advantage over crystalloid. Moreover, hetastarch can result in
examination.116 Other opioids with a longer duration of action coagulopathy, and although low doses in healthy individuals is
are appropriate for spine surgery in which more durable analge well tolerated, this may not be the case with patients undergoing
sia following the procedure may be required. However, in most intracranial procedures as the brain is rich in thromboplastin, the
instances administration must be tapered toward the end of the release of which may initiate coagulation abnormalities.
procedure to avoid excessive analgesia and sedation that may Both mannitol and HTS are effective in the treatment of intra
interfere with prompt neurologic assessment. cranial hypertension.121–124 Hypertonic saline (3%) administra
Replacement of the volatile anesthetic with a continuous infu tion results in less dehydration and electrolyte disturbance, and
sion of propofol is desirable in two settings. First, MEP monitor may have anti-inflammatory actions with reduction in leukocyte
ing virtually requires it to obtain optimal signal quality. Second, adhesion and endothelial cell edema.125–127 With high-dose manni
when brain relaxation is inadequate with a volatile anesthetic, tol (2 g/kg), hyperkalemia can occur and serum potassium should
propofol will provide better relaxation by further decreasing CBV. be monitored.128 Because of the presence of the blood–brain
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barrier, movement of water into the intracellular and interstitial with a high PLT:RBC ratio (platelet to red blood cell) experienced
compartments of the brain from the vascular compartment is pri improved 30-day survival.147 A proposed mechanism may involve
marily dependent on the osmotic pressure, and not on the oncotic improved blood–brain barrier healing with activation of oligo
pressure. Consequently, to minimize brain edema, it is important dendrocytes and repair of demyelination.148
to maintain serum tonicity. The most important osmotic species
in blood is sodium, so it is prudent to check the serum sodium
level on a regular basis in prolonged surgical procedures during Glucose Management
which mannitol has been given. In addition to osmotic dehydra
tion of the brain interstitium, other proposed benefits of hyper As discussed earlier, the combination of hyperglycemia and
tonic solutions include a reduction in blood viscosity, increasing cerebral ischemia appears to be particularly deleterious.149–151
erythrocyte deformability, and improved cardiac output and Although there is a paucity of evidence addressing the topic of
microcirculatory flow.129–135 intraoperative glucose management, logic would dictate that glu
cose should be normalized prior to periods of iatrogenic ischemia.
Tight glycemic control (80 to 110 mg/dL) with intensive insu
Transfusion Therapy lin therapy has been shown to improve morbidity and mortality
in critically ill patients.152,153 More recently, however, the find
There has been an increasing effort to conserve the limited ings of the NICE-SUGAR (Normoglycemia in Intensive Care
resource of banked blood. While anemia is associated with Evaluation-Survival Using Glucose Algorithm Regulation) have
increased in-hospital mortality, lower hospital discharge GCS suggested the use of intensive insulin therapy is associated with
score and discharge Glasgow outcome score, paradoxically RBC higher 90-day mortality.154 With regard to the neurosurgical
transfusion to maintain a higher hemoglobin (10 gm/dL vs. population, intensive insulin treatment may result in increased
7 gm/dL) is associated with more acute lung injury, longer ICU variability in blood glucose leading to cerebral osmotic shifts
and hospital stay, and increased mortality.136 The lower limit of and higher incidences of hypoglycemia, leading to worse out
acceptable hemoglobin or hematocrit has not been well defined. come.155–160 Patients with neurologic injury may have poor corre
The TRICC trial demonstrated that liberal transfusion targets in lation of systemic glucose with brain tissue glucose concentration.
intensive care patients had higher mortality rates.136 Even though In this specific group, intensive insulin treatment may result in
this study has been criticized for various reasons, including the significantly lower brain tissue glucose concentration and the pre
poor representation of neurosurgical patients, it remains the best cipitation of brain energy crises. This risk is potentially greater in
evidence to support avoidance of transfusion down to a hemato an anesthetized patient than an ICU patient, as the signs of hypo
crit of approximately 21% except in the context of ongoing hem glycemia are masked by the anesthetic. Therefore, intraoperative
orrhage and possibly the early phase of resuscitation for septic glucose management with insulin requires frequent assessment of
patients.137 Despite the lack of evidence to support the practice, the serum glucose level. Patients who present for cerebrovascular
many who care for neurosurgical patients have advocated for surgery should have a preoperative glucose check. Those who are
more liberal transfusion practices to optimize oxygen delivery hyperglycemic should be started on an insulin infusion. Continu
to the CNS.138,139 However, there is evidence to support a simi ous closed-loop glucose control systems composed of pumps for
lar conservative transfusion threshold in both TBI and spine the infusion of appropriate amounts of insulin and a glucose sen

patients.140,141 sor for the detection and/or monitoring of glucose levels regu
Unfortunately, most of the evidence available on transfu lated by computerized algorithms, is an emerging method that
Subspecialties
sion thresholds relates to critically ill but euvolemic patients. In could assist in the management of perioperative and inpatient
the operating room with patients undergoing neurosurgical and hyperglycemia.
spine procedures, ongoing hemorrhage may necessitate transfu Intraoperative hyperglycemia is found to be common in
sion well before the hemoglobin falls to 7 g/dL (or a hematocrit adults undergoing urgent/emergent craniotomy for TBI and was
of 21%). predicted by severe TBI, the presence of subdural hematoma, pre
A practical approach is to consider the rate of surgical blood operative hyperglycemia, and age ≥65 years.161 A target of 140 to
loss. If it is slow, then it may be appropriate simply to maintain 180 mg/dL is adequate in most patients to achieve this goal.
a normal intravascular volume with isotonic crystalloid solution
or with an appropriate colloid, recognizing that albumin should
be avoided in patients with TBI.142 Autologous predonation of Emergence
blood, erythropoietic support, acute normovolemic hemodilu
tion, intraoperative cell salvage, induced hypotension and the use The decisions that need to be made with respect to emergence
of pharmacologic agents such as tranexamic acid, in addition to from anesthesia of neurosurgical and spine surgery patients
meticulous surgical hemostasis, have all been utilized with mod hinge on whether the patient is an appropriate candidate for tra
est reductions in allogeneic blood transfusion rates during intra cheal extubation. To determine this, one must evaluate what has
cranial and spine surgery.143–145 However, such practice has not changed over the duration of the procedure with respect to the
been widespread, as the benefits are marginal. patient’s airway, oxygenation, ventilation and metabolic status.
Monitoring of regional and/or global cerebral oxygenation In addition, one must consider whether this patient will tolerate
may help determine the transfusion needs, and brain tissue oxy the hemodynamic changes that occur with extubation. Finally,
gen tension as well as NIRS have been utilized for this purpose. postoperative plans, such as cerebral angiography, should be
Currently available evidence supports a hemoglobin threshold taken into account.
level of 8 to 9 g/dL. In the context of ongoing bleeding, lower lev For extensive prone spine surgeries, significant dependent
els (e.g., 7 g/dL) may result in brief periods of profound anemia, edema frequently occurs. Although the predictive value of a cuff
which may be linked to inadequate brain perfusion.146 leak from the endotracheal tube is poor in general, the combi
Coagulopathy of trauma in patients with severe TBI has been nation of pronounced facial edema and an absent cuff leak fol
noted to resolve more quickly than coagulopathy in patients lowing prone surgery should make one suspicious for upper air
without severe TBI. In trauma, patients with TBI when transfused way edema.162–164 Delaying extubation of the trachea under these
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circumstances is prudent. In addition, intraoperative adminis transpulmonary passage of air has been described and its risk may
tration of intravenous steroids have not been found to be useful be higher with volatile than intravenous anesthesia.168–170 Patients
in prevention of airway edema and delayed extubation.165 Other to be placed in the sitting position should be evaluated for a patent
factors that may delay extubation in these patients include the foramen ovale, either preoperatively or intraoperatively, and an
development of pulmonary edema and hypoxemia from fluid alternate position should be considered for those who have one.
administration, as well as persistent hemodynamic instability. The structures in the posterior fossa, most notably the brain
For neurosurgical cases, usually the desire is to allow the stem and cranial nerves, are particularly vulnerable and intoler
patient to emerge from anesthesia and extubate the trachea as ant of surgical invasion. BAEP and cranial nerve monitoring are
soon as possible after completion of the procedure. This path appropriate when the surgical procedure places the cranial nerves
way provides for an immediate neurologic examination and may or brainstem at risk. SSEP and MEP monitoring can be used
obviate the need for postoperative CT scans. To facilitate emer for any tumor resection, whether supra or infratentorial; these
gence and extubation in the operating room, minimal use of modalities may be particularly useful in surgeries that place spe
opioids other than remifentanil is appropriate. Whether to give cific tracts at risk.171,172
a longer-acting opioid, such as fentanyl or morphine, prior to The brainstem is intimately involved in systemic hemody
emergence to treat postoperative pain is controversial. Opioids namics, and surgery in that region may affect rapid changes in
administration may delay emergence in a patient population that blood pressure and heart rate. Hemodynamic lability should be
usually requires a relatively small amount of postoperative opioid anticipated and treated during surgery in this region. Bradycardia
for pain control.166 The antitussive properties of opioids may be can be treated with atropine, but it should also prompt commu
desirable during emergence. nication with the surgeon, as its development may suggest a need
Avoidance of coughing and the hemodynamic changes associ to alter surgical technique.
ated with emergence is important for all neurosurgical patients, Adequate brain relaxation is typically achieved with a stan
and particularly those at high risk for postoperative hemorrhage, dard anesthetic including sub-MAC volatile anesthesia, an opioid
such as patients who have just had resection of an AVM. Cough infusion, mild-to-moderate hyperventilation, and mannitol. In
ing due to irritation of trachea can be minimized with intrave addition, minimizing tumor edema may be accomplished with
nous lidocaine (1 to 1.5 mg/kg). Instillation of 4% lidocaine in the the administration of dexamethasone.173 Further relaxation can
cuff of the endotracheal tube for the duration of the procedure be achieved with discontinuation of the volatile anesthetic and
may achieve equivalent results.167 Labetalol, hydralazine, and initiation of a propofol infusion. HTS is a reasonable alterna
nicardipine are all reasonable options for controlling hyperten tive to mannitol, particularly in the setting of anuric renal failure
sion on emergence. when mannitol is contraindicated. A randomized trial showed
that 3% saline and mannitol have equivalent brain relaxation
effects, but with the former having less electrolyte and vascular
volume sequelae.125 A brain that remains “full” may be the result
Common Surgical Procedures of venous congestion. This problem can be mitigated with head-
up tilt, but is best prevented by positioning the patient so as to
minimize excessive rotation or angulation of the neck. The cen
Surgery for Tumors tral venous pressure and jugular bulb venous pressure (if avail
able) can be transduced to confirm the absence of a pressure
9 The fundamental anesthetic considerations in tumor surgery gradient across the neck.
are proper positioning of the patient to facilitate the surgical Vascular tumors such as meningioma may benefit from pre
approach, providing adequate relaxation of the brain to optimize operative embolization. Surgical removal of large ones or ones
surgical conditions, and avoiding well-known devastating com that could not be embolized represents a high risk for significant
3 plications, such as VAE. In addition, patients with large tumors operative blood loss. Coagulopathy can develop as a consequence
resulting in significant intracranial hypertension are at risk of of massive transfusion. It is important to perform frequent coag
cerebral ischemia as well as herniation. Preoperative review ulation studies and administer clotting products and platelets
of the level of consciousness and the CT scan should always be promptly.
performed and the results taken into consideration in the anes
thetic plan.
Patient positioning can be very challenging for any neurosur Pituitary Surgery
gical procedure, particularly for surgery in the posterior fossa.
Lateral, park-bench, prone, and sitting positions are all used for Masses in the region of the sella turcica most commonly are of
surgical procedures in this region. When placing a patient in a pituitary origin, although other benign (meningioma, craniopha
complicated position for surgery, it is essential for the safety of the ryngioma) and malignant (germ cell tumor, lymphoma) tumors
patient that all catheters and the endotracheal tube are secured may occur in this region. These tumors are typically recognized
particularly well. Ample help should be available at the time of as a result of the neurologic changes they effect as they compress
positioning, particularly for obese patients. Padding adequately adjacent structures, such as visual changes with impingement of
to avoid pressure necrosis is also essential. The head is typically the optic chiasm, or through the systemic effects they exert via a
4 secured in a Mayfield apparatus. Nothing should impinge on the change in hormone secretion.
nose, eyes, or chin. Although many patients with sellar tumors may undergo sur
As the sitting position confers the greatest risk for VAE, plans gical resection with an uncomplicated general anesthetic, there
should be made for treating it, should it occur. The overall inci are several preoperative considerations that will affect the man
dence of VAE is about 39% in posterior fossa surgery and 11% in agement of the patient. Patients should undergo a preoperative
cervical spine procedures. A multiorifice catheter can be placed evaluation of their hormonal function to detect hypersecretion
in the right atrium to evacuate air. Its location can be confirmed of pituitary hormones, common in pituitary adenomas, as well as
either with the ECG or with echocardiography. A patent fora panhypopituitarism. The hormones that may be secreted by pitu
men ovale increases the risk of paradoxical embolism. However, itary tumors include prolactin, growth hormone, corticotropin,
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and thyroid-stimulating hormone. Patients with excess growth anesthesiologist to allow emergence and tracheal extubation,
hormone eventually will develop acromegaly. The anesthesiolo aggressive management of blood pressure should be instituted,
gist should be prepared for a difficult airway, as well as postopera and coughing should be avoided. Intravenous labetalol and
tive respiratory complications in the acromegalic patient. Patients hydralazine may be adequate, but a nicardipine infusion may
with a corticotropin-secreting adenoma will develop Cushing dis be most appropriate for blood pressure control. Blood pressure
ease. These patients may have a typical “Cushingoid” habitus that control needs to be conducted using an anticipated and prophy
may make airway management challenging. In addition, venous lactic approach rather than a reactive one, as the delay in treating
access may be difficult, and intraoperative hyperglycemia is likely. hypertension may be detrimental. Intravenous lidocaine can be
Patients with thyroid-stimulating hormone hypersecretion will used to blunt coughing.
exhibit signs of hyperthyroidism (e.g., tachycardia, weight loss).
These patients should be managed in the preoperative period
with antithyroid medications and beta-blockade. Close hemody
namic monitoring during surgery is essential. Cerebral Aneurysm Surgery and
Patients with panhypopituitarism will need hormone replace Endovascular Treatment
ment including cortisol, levothyroxine, and possibly DDAVP
(1-desamino-8-D-arginin vasopressin). These medications should Cerebral aneurysms are relatively prevalent vascular abnormali
be continued in the perioperative period. ties (approximately 5% incidence at autopsy) that arise from
Small to medium pituitary tumors can be resected from a congenital weakness of the vessel wall as well as extrinsic influ
transsphenoidal approach. Larger tumors may require a crani ences such as hypertension and cigarette smoking. They are more
otomy. IOM of glucose and electrolytes is essential, particularly prevalent in women than in men. Some aneurysms become clini
if the patient has pre-existing diabetes insipidus, or if the patient cally significant when they rupture, resulting in arterial bleeding
develops signs of diabetes insipidus during the surgery. Diabetes into the subarachnoid space. This event typically causes severe
insipidus is a common complication of pituitary surgery due to headache, and may also cause focal neurologic deficit, lethargy,
the loss of antidiuretic hormone production. It may be tempo and coma. For patients who survive their hemorrhage, surgical
rary or permanent, and may occur either in the intraoperative or endovascular intervention to secure the aneurysm is essen
or postoperative period. It is initially suspected on the basis of tial to prevent further hemorrhage. In addition, many patients
copious urine output, as well as rising serum sodium. A urine are incidentally found to have cerebral aneurysms, and they may
specific gravity of <1.005 is confirmatory. Although infusions of need intervention to decrease the risk of an initial subarachnoid
intravenous fluids containing free water may mitigate the electro hemorrhage. Intervention for a cerebral aneurysm may include a
lyte changes, replacement of antidiuretic hormone with DDAVP craniotomy and surgical clipping, or endovascular coiling.
(0.5 to 1 μg intravenously or subcutaneously) is an effective ther Anesthetic considerations for cerebral aneurysm surgery are
apy for diabetes insipidus. Volume replacement therapy may be somewhat different in those patients who have experienced a sub
guided with the use of central venous pressure monitoring as well arachnoid hemorrhage as compared with those who present for
as the observation of systolic variation in blood pressure. elective repair. Patients with aneurysmal subarachnoid hemor
rhage are at risk for numerous complications that may affect the
anesthetic plan. These include cardiac dysfunction, neurogenic or

Arteriovenous Malformations cardiogenic pulmonary edema, hydrocephalus, as well as further
hemorrhage from the aneurysm. This last complication is per
Subspecialties
A cerebral AVM is an abnormal vascular connection between the haps the most devastating and requires intensive treatment (see
arterial and the venous circulation. The absence of an interven also Chapter 55).
ing capillary bed results in a low-resistance path for blood flow. Careful attention to hemodynamics, particularly during
Patients may present with hemorrhage, seizure, or focal neuro stimulating procedures, is essential to avoid recurrent hemor
logic deficit. Cerebral angiography remains the gold standard rhage. Laryngoscopy and placement of the head in the Mayfield
for AVM diagnosis. Although preoperative embolization of the device are two points at which transient hypertension is likely and
AVM is commonly performed, either radiosurgery or an open the anesthesiologist must be particularly vigilant about maintain
surgical procedure is typically required subsequent to the embo ing an adequate depth of anesthesia.
lization to cure the lesion. Although these lesions may be adjacent Following subarachnoid hemorrhage, cardiac dysfunction,
to vital structures, and an immediate postoperative neurologic and pulmonary edema commonly resolve over time. The cardiac
examination may be desirable, emergence from anesthesia fol dysfunction may be severe, resulting in ECG changes, elevated
lowing resection of an AVM requires particular care. Because troponin, and even cardiogenic shock. Echocardiography may
of local hemodynamic changes as a result of the AVM, the adja reveal hypokinesis in a distribution not consistent with an ana
cent vessels must chronically vasodilate to preserve perfusion. tomic vascular territory. Unfortunately, the need to secure the
When the low-resistance AVM has been occluded or resected, aneurysm in a timely fashion may require the anesthesiologist to
the adjacent vessels are exposed to higher pressures than to provide anesthesia despite ongoing cardiac and pulmonary issues.
which they were previously accustomed. These vessels may not Hemodynamic support with carefully titrated vasopressors may
be able to autoregulate appropriately within the normal blood be necessary, recognizing the risk of elevating the blood pres
pressure range, and “normal perfusion pressure breakthrough” sure too much. Hypoxemia can often be managed with increased
may occur. This phenomenon is defined by regional hyperemia Fio2 and positive end-expiratory pressure. With the exception of
at a normal systemic blood pressure. Normal perfusion pressure a hemodynamically unstable patient, surgical clipping of a rup
breakthrough may result in vasogenic edema and hemorrhage. It tured aneurysm should rarely be postponed.
can be minimized with careful blood pressure control; preopera Once the aneurysm is secured with an aneurysm clip, the
tive embolization likely decreases its incidence as well. Following risk of recurrent hemorrhage from the aneurysm is removed.
resection of large AVMs or those in the posterior fossa, taking the Although careful attention to hemodynamics as well as coughing
patient to the ICU in a ventilated and sedated state may be appro during emergence is still important, the concern of devastating
priate. Should the decision be made between the surgeon and hemorrhage from the aneurysm is diminished.
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The patient presenting for an elective aneurysm procedure will agreeable to this anesthetic technique. General anesthesia with
typically have good brain conditions, with easily achievable relax an endotracheal tube is therefore a more common technique for
ation using mannitol (0.5 to 1 g/kg), mild-to-moderate hyperven CEA. A multicenter, randomized controlled trial, GALA, involving
tilation, and sub-MAC volatile anesthetic in combination with 3,526 patients, compared general anesthesia versus local anesthe
an opioid infusion. Following subarachnoid hemorrhage, brain sia for carotid surgery, and did not show a significant difference
relaxation may be more difficult to achieve; intravenous anesthe between the two groups regarding quality of life, length of hos
sia may be required. Drainage of CSF via a lumbar drain or exter pital stay, and perioperative complications of stroke, myocardial
nal ventricular drain can be used at the discretion of the surgeon. infarction, and death.181 Both techniques are therefore similarly
In contrast to aneurysm surgery, endovascular treatment of efficacious.
aneurysms is a minimally invasive procedure performed in the Patients undergoing carotid surgery are nevertheless at
interventional radiology suite. The interventional neuroradiolo increased risk for perioperative complications, given their high
gist or neurosurgeon accesses the aneurysm via an intra-arterial prevalence of coronary artery disease, hypertension, chronic
catheter and typically deploys coils into the aneurysm that cause obstructive pulmonary disease, diabetes mellitus, and chronic
it to thrombose. This technique requires a favorably shaped aneu kidney disease. Continuation of beta-blockers and statins is
rysm that will retain the coils once they are deployed. Increasingly appropriate for patients who are receiving these medications
sophisticated techniques, such as placing a stent in the adjacent preoperatively. Blood pressure should be maintained as close to
vessel and coiling through the stent, have increased the range of baseline as possible throughout the surgery. Without evidence
aneurysms that are amenable to endovascular therapy. to support it, some advocate raising the blood pressure during
Despite the less invasive nature of this procedure, it can have carotid cross-clamp to improve flow through collateral vessels.
equally severe complications as surgery, including further hemor This practice presupposes that collateralization is marginal and
rhage, stroke, and vessel dissection. will be helped by the elevation in pressure. Collateral flow may
Although the procedure is not particularly stimulating, the be marginal, but it may also be absent or entirely adequate. In
general anesthetic needs to be performed with great care. Obvi the latter two situations, elevation in blood pressure through
ously, hypertension with laryngoscopy should be avoided. Fur the use of phenylephrine will only increase myocardial oxygen
thermore, any patient movement during the procedure can incur demand. However, evidence of hypoperfusion ipsilateral to the
devastating consequences because it may result in deployment cross-clamp is reason to consider blood pressure elevation. The
of coils in a vessel rather than the aneurysm itself. Hyperventila decision to raise blood pressure is facilitated by the concurrent
tion should be avoided, as it will decrease CBF and make access use of CNS monitors.
to the aneurysm more challenging. Heparin is commonly admin Several CNS monitors may be used during CEA under general
istered during this procedure. It is meant to decrease the risk of anesthesia. EEG allows for easy detection of a decline in spectral
thromboembolic complications associated with the intra-arterial power on the hemisphere ipsilateral to the surgery, which would
catheter. Protamine must be available should arterial rupture and be concerning for ischemia. NIRS is also promising for its abil
extravasation occur. In addition, prompt transfer to an operating ity to demonstrate relative changes between the ipsilateral and
room for neurosurgical intervention should also be possible. contralateral hemispheres, but it has not come into common use
as yet. TCD is particularly attractive, as it allows determination
of changes in flow during carotid cross-clamp, and detection of
Carotid Surgery emboli, as well as diagnosis of postoperative hyperemia. The hypo
perfusion during cross-clamp can be avoided with a shunt during
Carotid stenosis is a common cause of transient ischemic attack the surgical procedure, but at the increased risk of embolization. A
and ischemic stroke. It is amenable to surgical intervention and decrease in flow velocity of up to 60% of baseline is generally well
endovascular stenting. In older studies, CEA was found to be ben tolerated in the anesthetized patient during this procedure. Should
eficial in reducing stroke rate in symptomatic patients (ipsilat a shunt be needed, the development of microembolic signals can
eral transient ischemic attack or nondisabling stroke) with ≥70% provide feedback to the surgeon if there is a modifiable technique
internal carotid artery stenosis and, to a lesser extent, in patients to the surgical procedure. At the end of the endarterectomy, dur
with 50% to 69% internal carotid artery stenosis.174,175 In asymp ing surgical closure, continued presence of a good flow velocity
tomatic carotid stenosis, the benefit of surgical intervention over waveform on TCD provides confirmation of stability of the graft
medical therapy appears to be somewhat smaller, and it depends and lack of an intimal flap, or thrombosis. Although each moni
on the incidence of perioperative stroke.176,177 In addition, sur tor has attractive features, ultimately user familiarity and comfort
gery is associated not only with a risk of stroke, but also myocar will determine its utility.182 Postoperatively, sustained elevation of
dial infarction, wound infection, and cranial nerve dysfunction. flow velocity exceeding 100% of baseline values is highly sugges
At the time of the NASCET trial,174 medical therapy consisted tive of the development of hyperperfusion syndrome, and should
primarily of daily aspirin. With advances in medical therapy, prompt lowering of systemic blood pressure.
including more aggressive lipid-lowering drugs as well as other Rapid emergence and tracheal extubation at the end of the
effective antiplatelet agents and better antihypertensive therapy, procedure is desirable because it allows immediate neurologic
the margin of benefit of surgery may be even less.178 Appropriate assessment. Hemodynamic changes can occur in the postopera
candidate selection for surgery has therefore become extremely tive period from denervation of the carotid baroreceptor. In addi
important. Preoperative evaluation of the asymptomatic patient tion, headache, obtundation, and/or focal neurologic deficit in
depends on assessment of the risk for progression to stroke and the postoperative period should prompt one to consider hyper
weighing that risk against the morbidity of the procedure. emia, hemorrhage, or ischemic stroke.
Both general and regional anesthesia may be used for CEA. Carotid artery stenting (CAS) may be used to treat carotid ste
Regional anesthesia is accomplished with a superficial cervical nosis as well. It is an attractive procedure in that it is minimally
plexus block, or a combination of superficial and deep block.179,180 invasive and can be performed under sedation. However, noninfe
This technique allows continuous neurologic assessment during riority studies have not supported stenting as compared with CEA
the surgery, which is particularly useful at the time of carotid in symptomatic patients.183,184 Yet the SAPPHIRE trial has indi
cross-clamp. However, some patients and surgeons may not be cated that stenting may be a reasonable option in asymptomatic
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patients with tight stenosis; currently, most centers reserve stent operating table for maximal comfort and cooperativeness. Direct
ing for patients who are poor surgical candidates.185,186 A clinical visual and verbal contacts with the patient should be maintained
trial in 2010, comparing CAS and CEA did not show a difference throughout the procedure. The environment should be made
in the primary outcome of stroke, MI, or death among symptom quiet, calm, and comfortable with an appropriate room tempera
atic and asymptomatic patients.187 However, the patients who ture and humidity.
underwent CEA had a lower stroke rate, whereas patients who
had CAS had a lower rate of myocardial infarction.
Conscious Sedation (CS) Technique
Anesthetic considerations for this procedure are important,
even though it is typically performed under sedation. These The goal of sedation is to allow the patient to have a minimally
patients tend to have significant medical comorbidities. Conver depressed level of consciousness but remain able to maintain
sion to general anesthesia may incur significant risk. Further his/her own airway and respond to verbal stimulation. Only the
more, the procedure itself may induce significant hemodynamic administration of supplemental O2 via nasal prongs or cannula,
changes, most notably bradycardia or asystole during balloon or a facemask is required. Sedation may be given throughout
angioplasty of the internal carotid artery. Although pretreatment the procedure or can be utilized intermittently for the surgically
with atropine may prevent this complication, a brisk tachycardia stimulating part of the procedure. Frequently used drugs for CS
is generally not desirable in these patients. include propofol, opioids such as fentanyl or remifentanil, and
dexmedetomidine.192–194 Generally, benzodiazepines are avoided.
Propofol is one of the most frequently used drug either alone,
Epilepsy Surgery and Awake Craniotomy or in combination with remifentanil. Propofol can be titrated to
provide adequate sedation and a rapid, smooth recovery. How
Some intracranial neurosurgical procedures are performed on ever, it can decrease the incidence of seizures. At least 15 to
“awake” (i.e., sedated and pain free, with local anesthesia, yet 30 minutes is required for discontinuation of the propofol infu
able to respond to verbal or visual command) patients in order sion prior to electrocorticographic recording. Retrospective anal
to facilitate monitoring of the region of the brain on which the ysis of an AAA (asleep–awake–asleep) sequence using propofol
surgeon is operating. These procedures require particular atten and remifentanil showed that adequate conditions are obtained
tion on the part of the anesthesiologist to provide patient comfort in 98% of patients, with a median wake-up time of 9 minutes at
and safety. Typically these surgeries are for tumors adjacent to the mean infusion rates of 50 μg/kg/min.195–197
eloquent cortex or for resection of an epileptic focus. Frequently There is growing evidence suggesting that dexmedetomidine
the decision to perform the procedure awake has been made by may be the ideal sedative for awake procedures with low-dose
the neurosurgeon prior to the patient meeting the anesthesiolo infusion rates (0.3 to 0.6 μg/kg/hr).119,198 Dexmedetomidine is a
gist. It is the role of the anesthesiologist to determine whether central-acting α2 agonist that offers sedation and anxiolysis, helps
the patient is an appropriate candidate for an awake procedure, maintain hemodynamic stability (through its central α-agonist
to coordinate with the neurosurgeon the anesthetic plan, and to activity) and has analgesic properties. Dexmedetomidine also causes
support and reassure the patient through the process. minimal respiratory depression and has an anesthetic-sparing
Although the patient with a difficult airway, obstructive effect, even with infusions at the higher end of the dose range.
sleep apnea, or orthopnea may present a relative contraindica

tion to an awake craniotomy, it is the patient with severe anxi
“Asleep Awake Asleep” (AAA) Technique
ety, claustrophobia, or other psychiatric disorder who may be
Subspecialties
particularly inappropriate for this type of procedure. On the The AAA pathway is often the preferred method for epilepsy sur
other hand, patients with neurodegenerative disorders are often gery and tumor resection. This anesthetic plan involves general
elderly and may have respiratory, cardiovascular, and autonomic anesthesia for the skin incision (supplemented by scalp blocks or
system compromise. Potential drug interactions and adverse local anesthetic infiltration), initial craniotomy, and then for the
effects from anti-Parkinson’s medications may also occur during closure in the end, while the patient is allowed to emerge from
anesthesia.188 Patients with dystonia or torticollis may present dif anesthesia for the middle portion of the surgery in which the sur
ficulties in airway management. Patients with psychiatric, epilep geon is working around the eloquent areas of the brain. Intraop
tic, and chronic pain disorders will present with their own set of erative mapping of cortical functions in the awake patient helps
challenges and will need special consideration in the management to identify the precise location of epileptic focus. During such
of their medications perioperatively.189–191 mapping, the neurosurgeon applies electrical stimulation to the
Preoperative evaluation should be comprehensive and should exposed brain cortex of the awake patient, which allows the neu
include a thorough airway examination. Conversion to a general rophysiologist to report any sensory, motor, and speech effects
anesthetic remains a possibility at any point during the proce as well as any effects on more complex cognitive functions. Such
dure. Extensive discussion with the patient regarding the plan is mapping can also be performed during resection of the tumor,
essential to prepare him or her for the experience in the operating thereby allowing for maximal tumor resection while minimizing
room. neurologic deficits (the resection is stopped if symptoms emerge).
This gives the patient better postoperative quality of life, better
chance of survival.
Intraoperative Management
The asleep portions of the procedure may be performed with
Standard anesthesia monitors including an ECG, noninvasive out an airway, with a laryngeal mask airway (LMA), or with an
arterial blood pressure, oxygen saturation, and end-tidal CO2 endotracheal tube in place. For suitable candidates, spontaneous
are minimum requirements. Where tight control of blood pres ventilation with propofol anesthesia is an attractive option, as it
sure is required, invasive blood pressure monitoring should be allows straightforward emergence with minimal coughing, gag
employed. O2 is provided through variable or fixed rate oxygen ging, or straining. In addition, propofol provides a nice anesthetic
delivery devices with end-tidal CO2 monitoring capability in for these patients because of its low incidence of nausea and vom
order to verify airway patency and track respiratory rate. Atten iting during the awake period. An LMA is a suitable alternative to
tion should be given to the positioning of the patients on the an endotracheal tube as it can frequently be removed with little
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movement of the patient as he or she emerges from anesthesia. settings, including the initial resuscitation in the emergency
Topical application of lidocaine to the airway prior to insertion department, anesthetic management in the operating room, and
of the LMA supplemented with lidocaine jelly on the LMA may ongoing care in the ICU (see also Chapter 55).
improve patient tolerance during emergence. Primary injury is the result of the initial, mechanical forces on
An endotracheal tube provides the most secure airway, but it the brain tissue and skull, resulting in skull fracture, brain con
is also the most difficult to remove during the procedure, particu tusion and/or intracranial hematoma as a result of shearing and
larly with the patient’s head secured in rigid fixation. If this path compression of neuronal, glial, and vascular tissues. The conse
way is chosen, several options exist to minimize coughing as the quences of the initial TBI include physical disruption of cell mem
patient emerges. Prior to placement of the endotracheal tube, the branes and infrastructure, and disturbance of ionic homeostasis
larynx and trachea may be anesthetized with lidocaine. In addi secondary to increased membrane permeability. This in turn may
tion, the cuff of the endotracheal tube can be filled with 4% lido lead to astrocytic and neuronal swelling, relative hypoperfusion,
caine rather than air. Finally, allowing the patient to emerge on perturbation of cellular calcium homeostasis, increased free radi
an infusion of low-dose remifentanil or dexmedetomidine may cal generation and lipid peroxidation, mitochondrial dysfunc
facilitate extubation with little movement. tion, inflammation, apoptosis, and diffuse axonal injury. These
During the awake portion of the procedure, all sedatives are mechanisms result in irreversible damage.34 Secondary injury is
typically withheld. For particularly stimulating events (e.g., drill the progression of the pathologic insults, such as ischemia, reper
ing) and in coordination with the surgeon, small boluses of pro fusion and hypoxia starting immediately after the initial TBI.
pofol may be given. Antiemetics may be given for nausea and Systemic insults such as hypotension (systolic BP <90 mm Hg),
small doses of fentanyl for discomfort. hypoxemia (Pao2 <60 mm Hg), hypoglycemia, hyperglycemia,
Following this critical portion of the surgery, the patient may hypocarbia, and hypercarbia are major contributors to secondary
be fully anesthetized for the surgical closure. Initiating a propofol injury. The initial approach to patients with TBI should be similar
infusion and continuing with spontaneous ventilation is again a to that of any trauma patient, as outlined in Advanced Trauma
good option; otherwise, manipulation of the airway to place an Life Support (ATLS) by the American College of Surgeons and fol
LMA or endotracheal tube will be necessary while avoiding the lowed by limitation of secondary insults. Although delayed brain
sterile field. ischemia appears to be the major common pathway of secondary
brain damage, reperfusion hyperemia may also occur.
Airway and breathing are obviously of paramount impor
General Anesthesia (GA)
tance in any critically ill patient but even more so in patients with
Patient groups more likely to require GA includes infants and head injuries, given the sensitivity of the brain to hypoxemia and
children, patients with learning difficulties, certain seizure or hypercapnia. Prehospital tracheal intubation of the patient with
continuous movement disorders, severe pain, claustrophobia, TBI may be associated with worse outcomes.199–205 If the patient
and those patients who are critically ill (e.g., with high ICP). arrives in the emergency department intubated, one must con
GA may create several problem areas during surgery. For epi firm proper placement of the endotracheal tube with a CO2 detec
lepsy surgery, if intraoperative localization of the epileptic focus tor and chest radiograph.200,202–205 If the patient is not intubated,
is needed in order to provide good conditions for electrocorti immediate attention should focus on assessing the airway and
cography and for motor testing, the influence of anesthetic agents making preparations for intubation. Patients with TBI usually
should be kept at a minimum, while concomitantly avoiding long have several indications for intubation including: Decreased level
periods of potential awareness on the part of the patient. Specific of consciousness, increased risk of aspiration, as well as concern
preoperative preparation should include informing the patients for hypoxemia and hypercarbia. Sometimes these patients must
of the possibility that awareness and recall may occur at the time be intubated and sedated simply to allow further diagnostic stud
of electrocorticographic recording, but reassuring them that this ies. SCI occurs in up to 2% to 5% of all major trauma cases and
will be brief and painless. All anesthetics will affect electrocor at least 14% of these cases have the potential to have an unstable
ticography but the use of the shorter-acting anesthetic agents, spine. Techniques to minimize cervical spine (C-spine) move
either inhalation agents and/or intravenous agents will allow ment should be employed during airway management, while
for faster decrease in the depth of anesthesia. During the time of considerations should be given to other potential injuries.
recording, all or most of the anesthetic agents are discontinued. Patients with TBI have up to a 10% incidence of an unstable
Long-term anticonvulsant therapy may lead to increased dosage cervical spine injury.206,207 Risk factors include a motor vehicle
requirements for opioids and neuromuscular blocking agents. accident and Glasgow Coma Scale (GCS) score <8. Therefore, all
Nitrous oxide should be avoided to prevent complications from attempts at intubation should include in-line neck stabilization
a pneumocephalus. Complications that may occur during epi to decrease the chance of worsening a neurologic injury.208 This
lepsy surgery are similar to those for any craniotomy. However, maneuver may worsen the view of the glottis, making intubation
severe bradycardia is a common occurrence with resection of the more difficult.209 Therefore, one must always have a backup plan
amygdala–hippocampus. and device in mind when performing an emergency intubation,
including but not limited to LMAs and fiberoptic or videolaryn
goscope technology. Patients with TBI should generally be intu
bated orally, as the potential presence of a basilar skull fracture
Anesthesia and Traumatic could increase the risk associated with a nasal intubation. A sur
Brain Injury gical airway remains an appropriate procedure for patients with
severe facial trauma and an expected difficult airway.
Minimizing the risk of aspiration of gastric contents dur
Overview of Traumatic Brain Injury ing airway procedures is essential. The effectiveness and correct
application of cricoid pressure (CP) in this setting has been ques
The presence of TBI is the primary determinant in the quality tioned.210,211 New evidence suggests that the alimentary canal at
of outcome for patients suffering from trauma.34 Anesthesiolo the level of cricoid ring is the postcricoid hypopharynx and not
gists are involved in the care of these patients in many different the esophagus.212 Rice et al.213 define the concept of “cricoid
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pressure unit” and discredit the logic of ineffectiveness of the CP monitoring and optimization of blood pressure and CPP are
due to previously reported displacement of the esophagus in rela essential. It is worth noting that there is a lack of information
tion to the trachea. Incorrectly applied CP may displace cervical on what the optimal intraoperative hemodynamic goals should
fractures, whereas bimanual application may help to reduce this be. Cerebral autoregulation may be impaired after TBI. This
displacement.214,215 has two possible consequences: (a) when blood pressure is low,
Another important consideration is the choice of drugs to cerebral ischemia may result, (b) in the presence of high blood
facilitate intubation. As discussed previously, hypotension is pressures, cerebral hyperemia and hemorrhage may ensue. The
extremely detrimental to the injured brain; therefore, the choice overwhelming evidence of harm from hypotension necessitates
of drugs must be tailored to each individual patient. Sodium thio restoration of intravascular volume.101 Isotonic crystalloid solu
pental in a dose of 3 to 6 mg/kg is a useful drug in euvolemic tions should be used to accomplish this goal; note that lactated
hemodynamically stable patients, but is no longer available in Ringer solution is slightly hypotonic (Table 36-3). The goal is to
the United States. Through its depressant effect on cerebral maintain CPP in the range of 50 to 70 mm Hg, as recommended
metabolism, thiopental decreases CBF, CBV, and ICP,216,217 but by the guidelines from the Brain Trauma Foundation in 2007.221
may cause profound hypotension. Propofol and etomidate are Glucose-containing solution should definitely be avoided. The
suitable alternatives, with the latter causing less hypotension at role of colloids is controversial. According to the Saline versus
the expense of adrenal suppression. In doses of 1.5-mg/kg lido Albumin Fluid Evaluation (SAFE) study, resuscitation with albu
caine blunts the effects of laryngoscopy and intubation on ICP min is associated with higher mortality rate and unfavorable out
with minimal hemodynamic effects. Finally, although controver come in TBI patients.142 In regards to synthetic colloids, recently
sial, succinylcholine is not contraindicated in patients with TBI, published studies indicate that administration of hydroxyethyl
as the effects on ICP are clinically insignificant. Succinylcholine starch in patients with severe TBI may be relatively safe, but con
may be the relaxant of choice when intubation needs to be estab firmation is needed.222–224 A multicenter, clinically randomized
lished quickly.218–220 On the other hand, rocuronium is a suit control trial to determine whether out-of-hospital administra
able alternative when no difficulty with the airway or intubation tion of hypertonic fluids would improve neurologic outcome fol
is anticipated. Once the trachea is intubated, the initial ventila lowing severe TBI has been terminated early due to futility. The
tion parameters should include 100% O2; arterial CO2 should be investigators concluded that initial fluid resuscitation of patients
maintained in the lower normal range (35 mm Hg), and the sub with severe TBI with either HTS/dextran or HTS was not supe
sequent ventilation regimen should be guided by arterial blood rior to 0.9% saline with respect to 6-month neurologic outcome
gas analysis. or survival.225
The goal of resuscitation in any trauma patient should be to Vasopressors and inotropes may be needed after fluid resusci
establish adequate circulation, with oxygenated blood, so that tation to achieve the desired CPP, or to treat hypotension while
cerebral perfusion may be maintained. Blood pressure and CPP volume restoration is ongoing. They should be used judiciously,
are often low after TBI. Several studies have documented wors as they are thought to increase the incidence of acute respiratory
ened outcome in TBI patients who have experienced episodes distress syndrome.226 Currently there are no recommendations
of hypotension (SBP < 90 mm Hg) after TBI. Thus, continuous regarding the choice of vasopressors to achieve optimal CPP.

Subspecialties
Table 36-3. Intravenous Fluids
Oncotic
Osmolality Pressure Na+ Cl− K+ Ca2+/Mg2+ Glucose
Fluid (mOsm/kg) (mm Hg) (mEq/L) (mEq/L) (mEq/L) (mEq/L) (g/L)
Plasma 289 21 141 103 4–5 5/2 —
Crystalloid
0.9% NS 308 0 154 154 — — —
0.45% NS 154 0 77 77 — — —
3% NS 1,030 0 515 515 — — —
7.5% NS 2,400 0 1,200 1,200 — — —
LR 273 0 130 109 4 3/0 —
D5LRa 527 0 130 109 4 3/0 50
D5Wa 252 0 — — — — 50
D5 NSa 586 0 154 154 — — 50
D50.45% NSa 406 0 77 77 — — 50
Plasma-Lyte 148 294 0 140 98 5 0/3 —
Normosol-R 294 0 140 98 5 0/3 —
Mannitol (20%) 1,098 0 — — — — —
Colloid — — — — —
Hetastarch (6%) 310 31 154 154 — — —
Albumin (5%) 290 19 145 145 — — —
a
In dextrose-containing solutions, it is important to distinguish between osmolality and tonicity.
NS, normal saline; LR, lactated Ringer solution; D5W, 5% dextrose in water.
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should be established to maintain Pao2 >60 mm Hg or oxygen

Table 36-4. Glasgow Coma Scale saturation >90%. Hyperventilation causes cerebral vasoconstric
tion, primarily in the small resistance arterioles in the brain;
this vasoconstriction rapidly reduces the CBV and therefore the
Eyes 1. No eye opening ICP. The reduction in CBV; however, is achieved at the expense
2. Opens to painful stimulus of reduction in CBF and may exacerbate cerebral ischemia. The
3. Opens to voice current guidelines for managing TBI indicate that prophylactic
4. Spontaneous eye opening hyperventilation (Paco2 ≤ 25 mm Hg) is not recommended and
Verbal 1. No sounds hyperventilation should be avoided during the first 24 hours after
2. Incomprehensible sounds TBI. Hyperventilation is recommended as a temporizing measure
3. Inappropriate words for the reduction of elevated ICP and may be utilized briefly dur
4. Confused conversation ing emergent evacuation of an expanding intracranial hematoma.
5. Normal speech When hyperventilation is required because of failure of other
agents to control ICP, monitoring of Pbto2, Sjvo2, and the arte
Motor 1. No movement
riovenous lactate gradient has been advocated.230
2. Extension to painful stimulus
Induced moderate hypothermia has been considered as a
3. Abnormal flexion to painful stimulus
therapeutic modality in head injury for many years. Several
4. Withdrawal from painful stimulus
mechanisms have been proposed for the beneficial effects of
5. Localization of painful stimulus
hypothermia on brain protection; reduction in brain metabolic
6. Follows commands
rate, attenuation of blood–brain barrier permeability, reduction
of the critical threshold for oxygen delivery, calcium antagonism,
blockade of excitotoxic mechanisms, preservation of protein syn
thesis, reduction of intracellular acidosis, modulation of the inflam
Norepinephrine is probably the most commonly used agent to matory response, a decrease in edema formation, suppression of
achieve these goals in adults.227 free radicals and antioxidants and modulation of apoptotic cell
Patients with TBI are typically described by their localized death.234–236 Furthermore, hypothermia lowers the cerebral meta
GCS score (Table 36-4). This simple test facilitates communica bolic rate by 6% to 7% for every 1°C decrease in core tempera
tion between providers, and it provides prognostic information. ture, which consequently improves oxygen supply to the areas of
Mild head injury is represented by a score of 13 to 15, moderate ischemic brain and decreases ICP.
head injury by a score of 9 to 12, and severe head injury by a A 2009 Cochrane review concludes that there is no evidence
score of <8. The score should be determined on postresuscita that hypothermia is beneficial in the treatment of head injury.235
tion information, as hypotension may depress mental status in A multicenter trial published in 2011, on the use of early hypo
any patient, even those without TBI. Younger age, lower ICP on thermia for TBI: The National Acute Brain Injury Study: Hypo
presentation, and the presence of reactive pupils were identified thermia II trial (NABIS:HII) was terminated early due to the
as the main prognostic factors in severe head injury patients. The lack of efficacy during an intermediate analysis.236 Similarly, or
pupil examination is particularly useful. The presence of a uni perhaps unexpectedly, a clinical trial in pediatric head injury
lateral dilated pupil suggests uncal herniation, and is a surgical observed that the hypothermia group had a higher mortality
emergency, whereas the presence of bilateral fixed and dilated rate than the normothermia group.237 In addition, hypothermia
pupils portends a poor prognosis. Quantitative pupillary mea increases the risk of pneumonia and wound infection, and may
surements have been introduced to facilitate monitoring and may cause electrolyte and coagulation abnormalities.238 Because of
help to diagnose increased ICP. Using automated pupil index, a the demonstrated efficacy of hypothermia in experimental brain
trend was identified to indicate an inverse relationship between injury, and the perceived flaws in the clinical trials conducted
decreasing pupil reactivity and increasing ICP.228 thus far, the pursuit of therapeutic hypothermia for TBI remains
Intracranial hypertension predisposes patients to poor out vigorous, and there are ongoing clinical trials in both pediatric
comes, and elevated ICP refractory to therapy is associated with and adult TBI. (e.g., POLAR-RCT: Prophylactic Hypothermia Trial
a worse prognosis. Some controversy exists regarding what con to Lessen Traumatic Brain Injury – Randomised Controlled
stitutes the optimal ICP and CPP. The current accepted recom Trial based in Australia/New Zealand, and the Eurotherm
mendation is to maintain CPP between 60 and 70 mm Hg, and 3235 Trial based in the United Kingdom).239,240 While the value
ICP <20 to 25 mm Hg.221 Reduction of ICP in patients with head of hypothermia remains to be established, it is important to note
injuries can be accomplished effectively using osmotic diuretics. that hyperthermia is detrimental to the injured brain and should
Mannitol, given at 0.25 to 1 g/kg, is the most commonly used be prevented and/or treated.
agent. The general guideline is that it can be repeatedly given, Barbiturates may be used as an adjunct to other therapy for
provided that serum osmolality does not exceed 320 mOsm, but controlling ICP. As discussed earlier, they lower ICP via their
there is no data to support this threshold. The mechanism of ICP effect on cerebral metabolism. As long as the MAP is maintained,
reduction by mannitol may be related to its osmotic effect in CPP will improve. Barbiturate therapy is appropriate only in
shifting fluid from the brain tissue compartment to the intravas patients who are hemodynamically stable and who have been
cular compartment as well as its ability to improve blood rheol adequately resuscitated. It should not be employed if MAP and
ogy by decreasing blood viscosity leading to reflex vasoconstric CPP cannot be maintained. Some patients with refractory eleva
tion. In addition, mannitol, like other hypertonic fluids, decreases tions in ICP have sustained extensive neurologic injury, and their
production of CSF. HTS (3% or 7.5%) is increasingly being used cerebral metabolic rate may already be low; failure to respond
to treat elevated ICP instead of mannitol. Patients refractory to to barbiturates carries with it an ominous prognosis.241 Propofol
mannitol treatment may respond to HTS therapy. There is also is a reasonable alternative to barbiturates for ICP management,
less fluid loss from osmotic diuresis with HTS. with the added advantage of shorter duration of action. Pro
Hypoxia, hypercarbia, and hypocapnia should be avoided as longed use of high-dose propofol is not recommended as it may
they cause secondary injuries after TBI. Adequate oxygenation cause propofol infusion syndrome, which is characterized by the
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time. These patients may have other injuries that will affect their
Table 36-5. Interventions for Inadequate care. The neurologic condition of the patient can be determined
rapidly by obtaining the GCS score, examining the pupils, and
Cerebral Perfusion Pressure reviewing the CT scan. The hemodynamic status of the patient is
also extremely important. Patients may demonstrate the Cush
Reduce brain water 1. Mannitol ing response of hypertension and bradycardia, which signifies
2. Hypertonic saline brainstem compression from raised ICP. However, these clas
3. Furosemide sic findings may be masked by hypovolemia, and their absence
Remove cerebrospinal 1. External ventricular drain does not rule out brainstem compression. An estimation of vol
fluid 2. Lumbar drain ume status is appropriate. Other important information includes
3. (Hypertonic fluid) oxygenation, which may be compromised because of pulmonary
contusion; hematocrit, which may be low in the presence of addi
Decrease cerebral 1. Head-up tilt tional injuries; and the extent of the evaluation obtained prior to
blood volume 2. Neutral neck position the decision to proceed to the operating room. An incomplete
3. Metabolic suppression evaluation, radiographic or otherwise, should leave one highly
(propofol or barbiturate) suspicious for missed injuries, such as pneumothorax or intra-
4. Mild-to-moderate abdominal hemorrhage.
hyperventilation Appropriate monitoring must be established rapidly so as
Elevate mean arterial 1. Adequate intravascular not to delay surgical intervention. Standard monitors should be
pressure volume resuscitation applied including ECG, pulse oximetry, capnography, and nonin
2. Support with vasopressor vasive blood pressure measurement. Two large-bore intravenous
catheters are required at a minimum. Delay for placement of a
central venous catheter should occur only if adequate peripheral
access cannot be obtained. Consideration for a femoral venous
catheter should be made, as it can be placed while preparation of
development of lactic acidosis, cardiac failure, lipemia, and is the head for surgery is ongoing. An arterial catheter is desirable,
associated with a high mortality rate.242,243 but it is a secondary priority after venous access.
Both barbiturates and propofol can be used in a dose-response These patients usually do not have ICP monitors in place but
manner to provide ICP control, ranging from mild sedation to one can assume the presence of intracranial hypertension in the
induced coma. If maximal metabolic suppression is desired, the setting of an acute space-occupying lesion. The presence of mid
infusion rate can be guided by EEG to achieve burst suppression. line shift on CT scan and pupillary abnormalities on physical
Decompressive craniectomy is another management option examination reinforce this diagnosis. Moderate hyperventilation
for refractory intracranial hypertension in TBI. Although this should be used in these patients until the dura is opened, as the
intervention decreases ICP and improves Pbto2, definitive elevation in ICP is likely more detrimental than the short-term
demonstration of outcome improvement in TBI remains elu hyperventilation.
sive.244–248 The recently published Australian multicenter DECRA Blood pressure management in these patients is critical. They

Trial reported on 155 adults with severe diffuse TBI and refrac may arrive in the operating room in a hypertensive state. The
tory ICH. According to this study, early bifrontotemporoparietal hypertension is often a response to the stress of the injury as well
Subspecialties
decompressive craniectomy lowers ICP and the length of stay as the elevated ICP. Unfortunately, this hypertension may mask
in the ICU but leads to more unfavorable outcomes.249 Rates of an underlying volume deficit due to hemorrhage or high urine
death were found to be similar in both the craniectomy group output from mannitol administered prior to arrival in the operat
(19%) and the standard-care group (18%) at 6 months. The ing room. Profound hypotension may quickly follow anesthesia
United Kingdom initiated (RESCUEicp) prospective multicenter induction, or more likely, after the craniectomy when the intrin
randomized trial is currently ongoing (Table 36-5). sic stimulus for blood pressure elevation diminishes. Risk fac
tors for postdecompressive hypotension include low GCS score,
absence of basal cisterns on CT, and bilateral dilated pupils.250
Anesthetic Management To avoid hypotension, intravenous volume loading in the early
stages of the anesthetic is essential, particularly in patients with
Patients with TBI requiring surgery can be subdivided into two
other injuries and significant blood loss.
major groups with different perioperative concerns. These groups
The choice of anesthetic agents should be based on the clinical
include those who require emergent surgery and those who
condition of the patient. The anesthetic requirement for patients
require nonemergent surgery. The emergent group can also be
with a traumatized CNS is lower; adequate anesthesia should be
subdivided into neurosurgical procedures and nonneurosurgical
administered without compromising hemodynamics. Volatile
procedures. The anesthetic management of these groups will be
anesthesia is acceptable as it is easily titratable, whereas intrave
discussed here.
nous agents have the benefit of a greater reduction in CBV and
ICP. Nitrous oxide should be avoided as it increases CMRO2,
Emergent Surgery CBF, and ICP in head-injured patients.251–253 Narcotics can be
used safely in these patients as long as blood pressure is not com
Neurosurgical
promised and the patient is mechanically ventilated.
These patients commonly arrive in the operating room with
an endotracheal tube in place. If their airway has not yet been
Nonneurosurgical
secured, then the same principles that were discussed in the air
way section should be applied. Often there is little time allotted for Trauma patients presenting for emergent surgical management
the preoperative assessment; one’s approach must be concise and of noncranial injuries who also have a concurrent TBI are com
focused to obtain the pertinent information in a brief amount of plex to manage. The most immediately life-threatening condition
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Figure 36-12. Transcranial Doppler

tracing illustrating the characteristic
changes associated with increasing in-
tracranial pressure. The occurrence of
biphasic or oscillating flow signifies the
onset of intracranial circulatory arrest.
Transcranial Doppler is accepted as a con-
firmatory test for brain death. (Reprinted
from Hassler W, Steinmetz H, Gawlowski
J. Transcranial Doppler ultrasonography Normal Decreasing diastole Systolic peaks
in raised intracranial pressure and in in-
tracranial circulatory arrest. J Neurosurg.
1988;68:745, with permission.)
No signal
Biphasic flow (oscillating flow) Systolic spikes Zero

Cerebral circulatory arrest
must take priority but the presence of TBI should be considered, going to the operating room, particularly for longer surgeries
particularly in someone with a depressed level of consciousness and those taking place in the first 48 hours after injury. When
or an abnormal pupil examination. If the history and examina available, advanced neuromonitoring, including TCD, jugular
tion are consistent with TBI, and a complete evaluation was not bulb oximetry, and brain tissue oxygenation should be used for
possible prior to emergent management in the operating room, intraoperative management.
obtaining an intraoperative neurosurgical consult for institution
of ICP monitoring is reasonable. The presence of dilated pupils
bilaterally may suggest a devastating brain injury. TCD, if avail
able, could be used to assess for nonviable CBF patterns.33 A well- Anesthesia for Spine Trauma
characterized progression of TCD waveform morphology has and Complex Spine Surgery
been described for increasing ICP with a corresponding decrease
in CPP (Fig. 36-12).33,254 Increasing pulsatility of the waveform
Surgery on the spinal column has become increasingly complex
is suggestive of high ICP. Appropriate intervention should be
and lengthy, with multilevel fusions, combined anterior and pos
implemented when this morphology is seen (e.g., head-up and
terior approaches to the spine, as well as staged procedures. The
neutral neck position, elevation of MAP, administration of man
anesthetic plan for these procedures is made more complicated
nitol, conversion to intravenous anesthesia).
by the increasing age of patients requiring spine surgery and the
concomitant increase in comorbid disease, as well as the need
Nonemergent Surgery for sophisticated monitoring of the spinal cord. In addition, SCI
often requires surgical intervention either for decompression of
Patients with TBI frequently have other injuries, especially frac
the spinal cord in patients with neurologic impairment and/or
tures requiring operative fixation. The timing of surgery in these
to restore the spinal column alignment and spinal stability to
patients remains a controversial issue.255 One must balance the
facilitate early patient mobilization and eventual rehabilitation.
need for operative fixation of these fractures to decrease the inci
The anesthesiologist encounters many patients with disease of the
dence of complications related to immobility, such as atelectasis,
spinal column, both in and out of the operating room. There are
pneumonia, and venous thromboembolism, with the risks of per
several aspects of their care, including airway management, resus
forming surgery in patients with head injuries. These patients have
citation, and intraoperative management, that require a particu
altered physiologic mechanisms, such as cerebral autoregulation,
lar understanding of their disease. The focus of this section will
and they are at risk for secondary injury, especially that from hypo
be on anesthesia and SCI, but the anesthetic management will be
tension.256 Early fixation of major orthopedic injuries are safe and
relevant to all complex spine surgery.
associated with fewer complications and ICU stay.257 On the other
hand, delayed fixation may allow the brain to recover in a more sta
ble hemodynamic environment.258 Consequently, clear definitions Spinal Cord Injury
for resuscitation parameters are needed to better define the opti
mal time for surgery in patients with multiple-system trauma.257 Primary Injury
In the absence of definitive evidence to guide management,
we offer several conservative recommendations. In the setting SCI is analogous to TBI in that there is both a primary and second
of refractory elevations in ICP or very labile ICP, only emergent ary component. Initial traumatic injury typically results in dam
surgery should be performed. Because patients with TBI cannot age to the bones and ligaments of the spinal column. Although
be examined clinically during anesthesia, there should be a low SCI can occur without radiographic abnormality, which is
threshold for placing an ICP monitor in someone who will be referred to as SCIWORA, this phenomenon is more common in
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children than adults. Damage to the spinal column may occur

without injury to the cord, or it can cause SCI through various Table 36-6. American Spinal Injury
insults, including compression, hemorrhage, and traumatic vaso
spasm, all which can result in cord ischemia and/or infarction. Association (Asia)
The nature of the bony injury is important, as it will guide Classification for Spinal
further management of the patient irrespective of the SCI. The Cord Injury
purpose of the spinal column is to provide support to the individ
ual while protecting the spinal cord and nerve roots. An unstable
injury puts the neural elements at risk, and will necessitate some Classification Description
intervention to provide stability, which may be the application of A Complete cord injury. No motor or
a brace or surgical intervention. sensation in sacral nerve roots S4 and
S5.
Secondary Injury B Incomplete cord injury. Sensory
preserved below the level of the injury,
Secondary injury to the spinal cord is mediated through a cascade including S4–S5.
of deleterious events similar to that seen in TBI, and begins within C Incomplete cord injury. Motor function
minutes following initial trauma. Pathologic mechanisms induce preserved below the level of the injury,
cord edema, and as a result of the rigid confines of the vertebral but with strength of less than three in
canal, increased pressure within that canal. This reaches its maxi half the major muscle groups.
mum between 4 and 6 days after the injury, with a consequent D Incomplete cord injury. Motor function
risk of ischemia. Pathologic consequences include induction of preserved below the level of the injury,
nitric oxide synthase, release of excitotoxic amino acids, cellular with strength of three or more in at
influx of calcium, oxidative stress, and lipid peroxidation.259 Sec least half the major muscle groups.
ondary injury may be exacerbated by hypotension due to hemor E No cord injury. Motor and sensory intact.
rhage or neurogenic shock.
Central, Anterior, Brown-Séquard, and

Cauda Equina Injuries
lesion, including S4–S5. ASIA C indicates an injury where more
Although a complete cord transection will result in disruption of than half the important muscle groups below the injury have
afferent and efferent signals, many injuries damage only a por motor scores of <3. ASIA D is an injury where more than half
tion of the spinal cord. The nature of this injury will determine its the muscles groups have motor scores >3. ASIA E indicates a neu
clinical manifestation. Several syndromes are well described for rologically intact individual.
their classic cord lesion and corresponding signs.
Central cord syndrome is characterized by greater severity of
paresis in the upper extremities than the lower, as well as bladder Comorbid Injuries

dysfunction and variable loss of sensation below the lesion. It is
probably caused by a cervical spine lesion via hemorrhage into SCI occurs in up to 2% to 5% of all major trauma cases and at
Subspecialties
the cord following trauma. It is more common in elderly patients least 14% of these patients have the potential to have an unstable
with pre-existing arthropathy. spine. Cervical spine trauma is associated with blunt cerebro
Anterior cord syndrome is generally due to disruption of blood vascular injury, TBI, and facial fractures.207,260,261 Between 20%
flow through the anterior spinal artery at the level of the injury. and 60% of SCI are associated with a concurrent TBI. Thoracic
The anterior portion of the cord becomes ischemic, disrupting trauma is also associated with vascular injury; in addition, one
motor function below the level, with a variable effect on sensa must consider the possibility of pneumothorax, myocardial con
tion. Pain and temperature tracts are typically interrupted as well, tusion, pulmonary contusion, and so forth, with trauma to the
but two-point discrimination and proprioception remains intact. thorax.262 Lumbar spine fractures may be associated with bowel
Brown-Séquard syndrome is characterized by the interruption and solid organ injury.263
of a lateral half of the spinal cord, typically through penetrating
trauma. Although a patient may not display all the classic find
ings of the Brown-Séquard syndrome, these would include loss of
motor and touch sensation ipsilateral to the lesion, with pain and
Initial Management
temperature sensation loss contralateral to the lesion.
Urgent Airway Management
Cauda equina syndrome is the result of injury below the level
of the conus, or caudal end of the cord, typically below L2. Com Initial management of the patient with spine trauma follows the
pression of the cauda equina results in perineal anesthesia, uri standard practices of care for trauma patients in general, with ini
nary retention, fecal incontinence, and lower extremity weakness. tial emphasis on airway, breathing, and circulation (as outlined
in ATLS). Endotracheal intubation can be particularly difficult
in the patient with SCI, especially if the lesion is in the cervical
American Spinal Injury Association Classification
spine. In addition, intubation frequently needs to be accom
In an effort to categorize the nature of the injury, the American plished before the presence or location of an injury can be con
Spinal Injury Association (ASIA) classification was developed in firmed. As a result, cervical spine injury should be presumed in
1982 (Table 36-6). This system rates cord injuries with a letter all trauma patients requiring intubation prior to complete physi
from A through E. ASIA A is a complete cord lesion in which cal and radiographic evaluation. Intubation should proceed with
no motor or sensory function is preserved in the sacral segments little movement of the cervical spine. A rapid-sequence induc
S4–S5. ASIA B is incomplete, with only sensory spared below the tion, with or without cricoid pressure (see discussion above), and
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manual in-line stabilization (MILS) of the neck is appropriate, injury to the cord. Management of the patient with SCI frequently
unless a difficult airway is anticipated. requires intervention for comorbid life-threatening trauma, such
as intra-abdominal or pelvic hemorrhage. With the exception
of patients requiring immediate surgical reduction of fractures
Hemodynamic Stabilization
compromising neurologic function, decompression of the spinal
Traumatic SCI is frequently complicated by systemic hypoten cord with fixation of the spinal column generally must wait until
sion and reduced spinal cord perfusion pressure (SCPP). This in the patient is clinically appropriate for the procedure. Persistent
turn may contribute to secondary ischemic neurologic injury and hemodynamic instability or severe acute respiratory distress syn
should be avoided. SCPP is determined by the difference in MAP drome may impose a significant delay on surgical intervention.
and cerebrospinal fluid pressure (CSFP) [SCPP = MAP − CSFP]. However, there is increasing interest in early fixation and mobili
Spinal cord perfusion is autoregulated over a range of systemic zation. The Surgical Treatment of Acute Spinal Cord Injury Study
BP in the same fashion as CBF. Systemic vasodilation from loss (STASCIS) showed 24% of patients who received decompressive
of sympathetic tone occurs in increasing severity with ascending surgery within 24 hours of their injury experienced a 2-grade or
levels of SCI above L2, leading to hypotension. Bradycardia com greater improvement on the ASIA scale, compared with 4% of
plicates the picture with injuries above T6 due to compromise of those in the delayed-treatment group.267
the sympathetic cardiac accelerator fibers.
Restoration of intravascular volume is the first step in the treat
ment of hypotension in the patient with SCI. Conversely, exces
sive fluid administration can be associated with significant edema
Intraoperative Management
(including airway edema), cardiac failure, electrolyte abnormali
Anesthetic Induction and Airway Management
ties, coagulopathy and prolonged duration of postoperative ICU
stay. The use of albumin has become debatable, similar to the Airway interventions may be required during the hospital course
concerns of increased mortality in TBI. Goal-directed treatment of the patient with known or suspected traumatic SCI. The spine
using cardiac output monitoring devices should be considered to should be immobilized in all trauma victims with suspected SCI
help with intraoperative fluid administration. until radiographically and/or clinically “cleared” with applica
Higher cord lesions result in greater sympathectomy, vasodi tion of a cervical collar, plus immobilization with lateral head
lation, and thus vascular capacitance. Although volume is ben supports and straps. Increasingly CT scans have replaced radi
eficial in this setting, a pure α-agonist such as phenylephrine is a ography for clearance of cervical spine injury. Attention should
reasonable choice to restore vascular tone. It also has the potential be given to minimize C-spine movement during airway manage
to induce a reflex bradycardia. Patients with higher lesions, in the ment. It has been clinically shown that in the normal spine, direct
upper thoracic or cervical spine, with concomitant hypotension laryngoscopy leads to extension of the C-spine, predominantly at
and bradycardia should receive an agent such as dopamine or the atlantooccipital junction, and to a lesser extent at the C1 to
norepinephrine, which will restore cardiac inotropy and chro C2 joint. The subaxial cervical segments (C4–C7) are minimally
notropy, as well as peripheral vascular tone. Vasopressin has a displaced but additional flexion occurs at the cervicothoracic
vasoconstrictive and catecholamine sparing effect, that may be junction. Instability of the occiput–atlas–axis complex may lead
useful in hypotension. However, its antidiuretic effects may lead to anterior movement of the atlas during direct laryngoscopy,
to increased water retention and hyponatremia, with potential thereby reducing the space available for the spinal cord.
exacerbation of intracellular edema after injury. Thus, its role in Several methods of tracheal intubation in this scenario exist,
SCI is not well defined, and it should be used with some caution. but no one technique has been proven superior to others. Exces
Dobutamine is predominantly an inotropic agent and its use in sive jaw thrust and chin lift should be avoided and early employ
SCI is limited because of its vasodilatory effects. Persistent brady ment of an oral or nasal airway helps to reduce the force required
cardia may be seen in high cervical (C1 to C5) lesions in the first for airway maintenance. Generally, a rapid sequence induction
2 weeks after traumatic SCI and requires the use of anticholinergic with direct or indirect laryngoscopy with MILS is the preferred
agents or application of cardiac pacemakers. practice. MILS provides better cervical stability but impairs the
view of the vocal cords during conventional laryngoscopy. Nev
ertheless, when MILS is utilized, the incidence of neurologic
Role for Steroids
impairment due to endotracheal intubation is extremely rare.
Methylprednisolone has become a common therapy for patients Elective fixation of confirmed cervical spine or associated injuries
with neurologic deficit resulting from SCI following large clinical requires careful planning for safe airway intervention. The patient
studies from the 1990s, which showed important improvement may present in cervical traction or a “halo” frame, which impedes
in the motor function of patients with SCI.264 However, these access to the airway. If the airway is potentially difficult and the
studies have subsequently been criticized, on the grounds that patient has an existing neurologic deficit with C-spine instability,
the benefits are marginal, while there is a significantly increased an alternative technique should be considered. Awake fiberoptic
risk of serious side effects associated with the use of high-dose intubation has not been shown to be superior to an asleep proce
steroids, including pulmonary complications, wound infections, dure. Awake fiberoptic intubation allows a neurologic examina
steroid myopathy, and gastrointestinal hemorrhage.265,266 Cur tion to be performed after intubation and positioning. However, it
rent guidelines published by the American Association of Neuro requires patient cooperation, and may increase stress, discomfort
logical Surgeons recommend the use of methylprednisolone only and disability in acutely injured patients. Provided that there is no
as a treatment option (while considering the risks and benefits airway patency or respiratory compromise, fiberoptic intubation
associated with glucocorticoid use) and not as a standard of care. in an anesthetized or deeply sedated patient provides the optimal
conditions for success without causing excessive movement of the
unstable spine, although some anesthesiologists might be uncom
Timing of Surgical Intervention
fortable with the potentially increased legal liability.
The purpose of surgical intervention is to decompress the neu The decision whether or not to extubate the trachea at the end
ral structures and stabilize the spinal column to prevent further of the surgical procedure is influenced by many factors. These
LWBK1137-C36_p996-1029.indd 1022 11/01/13 7:53 PM

include the ease of intubation, extent and duration of surgery, sur Although the use of IOM has never been validated by ran
gical complications (e.g., recurrent laryngeal nerve injury), prone domized controlled trials, it is now considered standard practice,
positioning, blood loss and subsequent fluid balance. The absence with the primary potential benefit being identification of a dete
of a cuff leak in the spontaneously breathing patient has not con rioration of spinal cord function during the surgical procedure.
sistently been shown to predict subsequent airway obstruction, Contributing factors include incorrect patient position (e.g., neck
but the presence of a cuff leak generally indicates a patent airway position, shoulder position), hypotension, hypothermia, and sur
after extubation. When in doubt, extubating the patient’s trachea gical retraction/injury. Identification and correction of reversible
with an airway exchange catheter in situ can facilitate emergent factors may help preserve spinal cord function. A recent system
reintubation if necessary. Good clinical judgment is paramount, atic review indicated that although there is a high level of evi
and if there is concern, it would be prudent to delay extubation. dence that multimodal IOM is sensitive and specific for detecting
As in most trauma situations, adequate neuromuscular block intraoperative neurologic injury during spine surgery, there is a
ade is required for successful intubation. Succinylcholine is the low level of evidence that IOM reduces the rate of new or wors
preferred agent for emergent intubation, but should be avoided ening perioperative neurologic deficits and there is very low evi
between 2 days and 9 months following SCI due to the risk of dence that an intraoperative response to a neuromonitoring alert
induced hyperkalemia caused by denervation hypersensitivity. reduces the rate of perioperative neurologic deterioration.24 Nev
Rocuronium is an acceptable alternative. ertheless, most spine surgeons are of the opinion that IOM allows
a more aggressive surgical approach to complex spine pathology
without increasing the risk of neurologic injury.272
Anesthetic Technique
Complex spine and trauma surgery imposes a significant risk of
Patient Positioning
blood loss. An arterial catheter is essential for continuous hemo
dynamic monitoring and intermittent arterial blood gas and The prone position provides multiple challenges to the anes
hematocrit analysis. In addition, the respiratory variation of the thesiologist with respect to both physiologic considerations and
arterial line, or reversed pulsus paradoxus, is a useful indicator of practical considerations. The former includes hemodynamic sta
volume responsiveness.268 bility that can be compromised by high intrathoracic pressure and
Several large-bore peripheral intravenous catheters are appro tamponade of the heart in thin individuals. The latter includes
priate for volume and blood product administration. In extensive difficulty with venous access (if the arms are tucked), and more
thoracic or lumbar spine surgeries, particularly in the prone posi importantly, adequate protection of pressure points. Areas at par
tion, central venous access may be appropriate. In addition to pro ticular risk include the eyes, and face, the breasts, genitals, knees,
viding more access for volume resuscitation, it enables easier access and toes. Whether using the Mayfield device to hold the head in
to venous circulation when arms are not accessible, helps to guide pins or a prone foam pillow, pressure on the eyes and nose must
the resuscitation with mixed venous oxygen saturation determina be avoided. Frequent confirmation that the eyes are free from
tion, provides appropriate access when vasopressor drugs are used, contact is important, as the pillow may move over time. In addi
and when advanced in to the heart may be used to aspirate air in the tion, slight reverse Trendelenburg position may facilitate venous
event of an air embolism. However, the value of the central venous drainage from the head and reduce congestion and intraocular
pressure is controversial. It is neither a good indicator of end- pressure.273 Padding on the chest should not compress the neck,

diastolic volume nor a predictor of volume responsiveness in hypo as this too may obstruct venous drainage. The breasts and male
tension.269 Although there is some literature suggesting a benefit genitals should be checked to ensure that they are free of undue
Subspecialties
to managing older patients with trauma with a pulmonary artery pressure. Lower extremities must be padded adequately to pre
catheter (PAC), its use is not routinely recommended.270 Devel vent excess weight resting on the knees and toes.
opment of less invasive and perhaps superior approach to hemo
dynamic monitoring has increasingly become available. Dynamic
Hypothermia
indicators of preload include respiratory variation in systolic pres
sure and pulse pressure, both of which can be derived from the Transportation, stabilization, investigation (particularly radio
analysis of the waveform generated by a peripherally placed arte logic), and organization of surgery necessitates delays of minutes
rial catheter.271 In addition, techniques for deriving stroke vol to hours. The ability to delay ongoing secondary injury to the spi
ume, cardiac output, and intrathoracic blood volume have been nal cord in the interim would be of great benefit in limiting ulti
introduced. These methods are all dependent on a quality arterial mate neurologic dysfunction. As with the brain, there has been a
waveform without dampening. Nevertheless, when functioning wide range of reported enthusiastic research into the biochemi
properly, these techniques provide support for goal-directed fluid cal, histologic, and physiologic effects attributed to the applica
management and have been shown to improve outcome. tion of cooling. These include a reduction in the initial rate of
ATP depletion, alteration of gene expression and protein syn
thesis, reduction in the release of excitotoxic neurotransmitter,
Neuromonitoring
changes to intracellular messengers, inhibition of inflammatory
Since the wake up test (in which the level of general anesthesia is responses, and a decrease in the excitatory postsynaptic potential
transiently reduced intraoperatively to enable the patient to move slope in a temperature-dependent manner. Utilization of intra
an extremity in response to a verbal command) provides only a vascular cooling catheters allows achievement of moderate sys
single time point of assessment of neurologic function, sophisti temic hypothermia more rapidly and precisely during abdominal
cated neuromonitoring techniques are now used intraoperatively aortic aneurysm repair and other procedures that require aortic
to continually assess the functional integrity of the spinal cord. clamping. In animal models, moderate hypothermia increases
Generally SSEP and MEP with or without nerve root monitoring the tolerable spinal cord ischemia duration as much as 2.5 times
are utilized, and these modalities as well as the anesthetic tech and the effect is longer with lower temperatures in humans.274
niques required to allow optimal acquisition of signals had been There is conflicting data on whether it affords any protection in
previously discussed. When used collectively, these are referred to circumstances of significant ongoing cord compression. Safety
as multimodal IOM. and efficacy of intravascular hypothermia for acute SCI have been
LWBK1137-C36_p996-1029.indd 1023 11/01/13 7:53 PM

encouraging.275 Important determinants are cooling technique ment of a compartment syndrome of the optic nerve. Both types
(surface or intravascular), timing, rate, duration, and degree of of ION have poor potential for recovery of vision, and are indis
temperature depression, and importantly, rewarming and its tinguishable in the later stages with both showing optic nerve
associated complications such as infection.276,277 However, a pro atrophy.
spective randomized trial of hypothermia for acute SCI is yet to Cortical blindness is typically associated with states of pro
be undertaken.278 And despite the heightened recent interest in found hypotension such as cardiac arrest or cardiac bypass proce
temperature modulation for spinal function preservation and dures where emboli are common. Of the four causes of visual loss,
recovery, the American Association of Neurological Surgeons, cortical blindness has the best chance for recovery.
and the Congress of Neurological Surgeons, published a state Currently there is no proven method to prevent periopera
ment in November 2007, concluding that there is insufficient tive blindness associated with spine surgery, nor is there a reliable
scientific evidence to support or oppose systemic or local hypo method to monitor visual function during these procedures. A
thermia for traumatic spine injury.279 number of investigators have focused on monitoring of intraop
erative intraocular pressure, which is unlikely to yield meaning
ful results. On the other hand, monitoring of VEP may provide
Complications of Anesthesia for more useful information. Careful and frequent eye checks in
Spine Surgery the prone position with documentation are recommended, but
direct compression is not the cause of PION. A Mayfield head
Autonomic Hyperreflexia rest with pins is being used increasingly to obviate any possibility
of direct compression to the globe. Hence virtually all cases of
Patients with a chronic spinal cord lesion above the level of T7 PION occur while the patient’s head is in Mayfield pins. A recent
may develop autonomic hyperreflexia when stimulated below case control study comparing the index cases in the POVL reg
the site of lesion. This is a condition characterized by intense istry with controls suggest that the risk factors for ION include
vasoconstriction below the site of the lesion, accompanied by obesity, male gender, the use of Wilson frame, long surgical dura
cutaneous vasodilation above the site, hypertension, and brady tion, greater estimated blood loss, and decreased percent colloid
cardia. This is the result of reflex sympathetic stimulation below replacement of blood (as a percent of overall fluid administra
the lesion unmodulated by supraspinal influence from above. In tion).280 Of note, there was no association with the level of blood
severe cases, cerebral hemorrhage and myocardial ischemia can pressure or hematocrit.
occur. To reduce the incidence of this complication, suppression Given the increasing recognition of POVL, and the frequency
of the afferent pathway by “deepening” the level of general anes of subsequent litigation, the patient should be informed preop
thesia is necessary. Alternatively, the use of a spinal anesthetic eratively about the potential risk of blindness with complex spine
which blocks the reflex stimulation may be the ideal anesthetic. surgery, and vision documented immediately upon emergence
from anesthesia. Unfortunately, even with prompt diagnosis and
Postoperative Visual Loss appropriate consultation, currently there is no effective treat
ment once the complication occurs. Staging of a complex spine
Postoperative visual loss (POVL) is of particular concern in procedure to minimize the duration of the procedure, to reduce
prone spine surgery, although it can occur in other settings. It the amount of blood loss, and to decrease the quantity of fluid
is estimated to occur as often as 1:1,000 following spine opera administered, may be the most effective means of preventing this
tions. Central retinal artery occlusion (CRAO); anterior ischemic devastating complication.
optic neuropathy (AION); posterior ischemic optic neuropathy
(PION); and cortical blindness encompass the majority of the
perioperative vision losses. Though an uncommon cause of
blindness in general, PION is by far the most common cause of References
POVL from a spine operation. Alarmed by the apparent increase 1. Emerich DF, Vasconcellos AV, Elliott RB, et al. The choroid plexus: Function,
in incidence, the American Society of Anesthesiology established pathology and therapeutic potential of its transplantation. Expert Opin Biol Ther.
a POVL registry to examine common factors shared by the index [Review]. 2004;4(8):1191–1201.
cases. Early reports from the POVL registry indicate that, while 2. Praetorius J. Water and solute secretion by the choroid plexus. Pflugers Arch.
[Review]. 2007;454(1):1–18.
all of the CRAO cases were unilateral, a majority of ION cases 3. Steiner LA, Balestreri M, Johnston AJ, et al. Sustained moderate reductions in
were bilateral. These findings are consistent with the proposed arterial CO2 after brain trauma time-course of cerebral blood flow velocity and
etiology of CRAO resulting from direct compression of the globe intracranial pressure. Intensive Care Med. 2004;30(12):2180–2187.
when the head slipped off the headrest, and the dependent eye 4. Diringer MN, Yundt K, Videen TO, et al. No reduction in cerebral metabolism
as a result of early moderate hyperventilation following severe traumatic brain
was left resting on the hard edge. In contrast, ION is ischemic injury. J Neurosurg. 2000;92(1):7–13.
in origin. AION results from ischemia to the anterior segment of 5. Coles JP, Minhas PS, Fryer TD, et al. Effect of hyperventilation on cerebral blood
the optic nerve, and PION from ischemia to the posterior seg flow in traumatic head injury: Clinical relevance and monitoring correlates. Crit
ment of the optic nerve behind the optic disc. AION is the most Care Med. 2002;30(9):1950–1959.
6. Warner KJ, Cuschieri J, Copass MK, et al. The impact of prehospital ventilation
common cause of blindness in the community, usually resulting on outcome after severe traumatic brain injury. J Trauma. 2007;62(6):1330–1336.
from systemic hypotension secondary to gastrointestinal hemor 7. Lassen NA. Cerebral blood flow and oxygen consumption in man. Physiol Rev.
rhage in an elderly patient. The prevalence of PION secondary to 1959;39(2):183–238.
spine surgery cannot be easily explained etiologically. 8. Bruder N, Cohen B, Pellissier D, et al. The effect of hemodilution on cerebral
blood flow velocity in anesthetized patients. Anesth Analg. 1998;86(2):320–324.
Suggested risk factors for ION may include hypovolemia, 9. van Bommel J, Trouwborst A, Schwarte L, et al. Intestinal and cerebral oxygen
hypotension, anemia, venous congestion, edema, adverse drug ation during severe isovolemic hemodilution and subsequent hyperoxic ventila
effects, and individual patient variation in anatomy and physiol tion in a pig model. Anesthesiology. 2002;97(3):660–670.
ogy of the optic nerve blood flow. There has been no association 10. Rebel A, Ulatowski JA, Kwansa H, et al. Cerebrovascular response to decreased
hematocrit: Effect of cell-free hemoglobin, plasma viscosity, and CO2. Am
demonstrated with direct pressure or embolic events. A plausible J Physiol Heart Circ Physiol. 2003;285(4):H1600–H1608.
mechanism is the development of venous congestion in the optic 11. Hare GM, Tsui AK, McLaren AT, et al. Anemia and cerebral outcomes: Many
nerve secondary to the prone position and subsequent develop questions, fewer answers. Anesth Analg. 2008;107(4):1356–1370.
LWBK1137-C36_p996-1029.indd 1024 11/01/13 7:53 PM

12. Hare GM, Mazer CD, Hutchison JS, et al. Severe hemodilutional anemia 42. De Georgia MA, Deogaonkar A. Multimodal monitoring in the neurological
increases cerebral tissue injury following acute neurotrauma. J Appl Physiol. 2007; intensive care unit. Neurologist. [Review]. 2005;11(1):45–54.
103(3):1021–1029. 43. Matta BF, Lam AM. The rate of blood withdrawal affects the accuracy of jugular
13. Todd MM, Farrell S, Wu B. Cerebral blood flow during hypoxemia and hemo venous bulb. Oxygen saturation measurements. Anesthesiology. 1997;86:806.
dilution in rabbits: Different roles for nitric oxide? J Cereb Blood Flow Metab. 44. Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-
1997;17(12):1319–1325. of-hospital cardiac arrest with induced hypothermia. N Engl J Med. 2002;346:557.
14. Dagal A, Lam AM. Cerebral autoregulation and anesthesia. Curr Opin Anaesthe- 45. Hypothermic after Cardiac Arrest Study Group. Mild therapeutic hypothermia to
siol. [Review]. 2009;22(5):547–552. improve the neurologic outcome after cardiac arrest. N Engl J Med. 2002;346:549.
15. Kaisti KK, Metsähonkala L, Teräs M, et al. Effects of surgical levels of propofol 46. Koerner IP, Brambrink AM. Brain protection by anesthetic agents. Curr Opin
and sevoflurane anesthesia on cerebral blood flow in healthy subjects studied Anaesthesiol. 2006;19:481.
with positron emission tomography. Anesthesiology. 2002;96(6):1358–1370. 47. Fritz KW, Kasperczyk W, Galaske R. [Successful resuscitation in accidental hypo
16. Summors AC, Gupta AK, Matta BF. Dynamic cerebral autoregulation dur thermia following drowning]. Anaesthesist. 1988;37:331.
ing sevoflurane anesthesia: A comparison with isoflurane. Anesth Analg. 1999; 48. Oberhammer R, Beikircher W, Hormann C, et al. Full recovery of an avalanche
88(2):341–345. victim with profound hypothermia and prolonged cardiac arrest treated by extra
17. Schlunzen L, Juul N, Hansen KV, et al. Regional cerebral glucose metabolism corporeal re-warming. Resuscitation. 2008;76(3):474.
during sevoflurane anaesthesia in healthy subjects studied with positron emission 49. Kunihara T, Grun T, Aicher D, et al. Hypothermic circulatory arrest is not a risk
tomography. Acta Anaesthesiol Scand. 2010;54:603–609. factor for neurologic morbidity in aortic surgery: A propensity score analysis. J
18. Schlunzen L, Juul N, Hansen KV, et al. Regional cerebral blood flow and glucose Thorac Cardiovasc Surg. 2005;130:712.
metabolism during propofol anaesthesia in healthy subjects studied with posi 50. Mack WJ, Ducruet AF, Angevine PD, et al. Deep hypothermic circulatory arrest
tron emission tomography. Acta Anaesthesiol Scand. 2012;56:248–255. for complex cerebral aneurysms: Lessons learned. Neurosurgery. 2007;60:815.
19. Langsjo JW, Kaisti KK, Aalto S, et al. Effects of subanesthetic doses of ketamine 51. Leonov Y, Sterz F, Safar P, et al. Mild cerebral hypothermia during and after
on regional cerebral blood flow, oxygen consumption, and blood volume in cardiac arrest improves neurologic outcome in dogs. J Cereb Blood Flow Metab.
humans. Anesthesiology. 2003;99(3):614–623. 1990;10:57.
20. Drummond JC, Dao AV, Roth DM, et al. Effect of dexmedetomidine on cerebral 52. Todd MM, Hindman BJ, Clark WR, et al. Intraoperative hypothermia for aneu
blood flow velocity, cerebral metabolic rate, and carbon dioxide response in nor rysm surgery trial (ihast) investigators. Mild intraoperative hypothermia during
mal humans. Anesthesiology. 2008;108(2):225–232. surgery for intracranial aneurysm. N Engl J Med. 2005;352:135.
21. Ogawa Y, Iwasaki K, Aoki K, et al. Dexmedetomidine weakens dynamic cere 53. Hindman BJ, Bayman EO, Pfisterer WK, et al. No association between intraop
bral autoregulation as assessed by transfer function analysis and the thigh cuff erative hypothermia or supplemental protective drug and neurologic outcomes
method. Anesthesiology. 2008;109(4):642–650. in patients undergoing temporary clipping during cerebral aneurysm surgery:
22. Avidan MS, Jacobsohn E, Glick D, et al. Prevention of intraoperative awareness in Findings from the Intraoperative Hypothermia for Aneurysm Surgery Trial.
a high-risk surgical population. N Engl J Med. 2011;365(7):591–600. Anesthesiology. 2010;112(1):86–101.
23. Costa P, Bruno A, Bonzanino M, et al. Somatosensory- and motor-evoked potential 54. Reith J, Jorgensen HS, Pedersen PM, et al. Body temperature in acute stroke: Rela
monitoring during spine and spinal cord surgery. Spinal Cord. 2007;45(1):86–91. tion to stroke severity, infarct size, mortality, and outcome. Lancet. 1996;347:422.
24. Fehlings MG, Brodke DS, Norvell DC, et al. The evidence for intraoperative neu 55. Oliveira-Filho J, Ezzeddine MA, Segal AZ, et al. Fever in subarachnoid hemor
rophysiological monitoring in spine surgery: Does it make a difference? Spine rhage: Relationship to vasospasm and outcome. Neurology. 2001;56:1299.
(Phila Pa 1976). 2010;35(9 suppl):S37–S46. 56. Zeiner A, Holzer M, Sterz F, et al. Hyperthermia after cardiac arrest is associated
25. Lo YL, Chih HW, Yeh CY, et al. Intraoperative monitoring study of ipsilateral with an unfavorable neurologic outcome. Arch Intern Med. 2001;161:2007.
motor evoked potentials in scoliosis surgery. Eur Spine J. 2006;15(suppl 17):656. 57. Jiang JY, Macchiarelli G, Miyabayashi K, et al. Early indicators of prognosis in 846
26. Kakimoto M, Kawaguchi M, Yamamoto Y, et al. Tetanic stimulation of the cases of severe traumatic brain injury. J Neurotrauma. 2002;19:869.
peripheral nerve before transcranial electrical stimulation can enlarge amplitudes 58. Aiyagari V, Diringer MN. Fever control and its impact on outcomes: What is the
of myogenic motor evoked potentials during general anesthesia with neuromus evidence? J Neurol Sci. 2007;261:39.
cular blockade. Anesthesiology. 2005;102:733. 59. Warner DS, Takaoka S, Wu B, et al. Electroencephalographic burst suppression is
27. Bala E, Sessler DI, Nair DR, et al. Motor and somatosensory evoked potentials are not required to elicit maximal neuroprotection from pentobarbital in a rat model
well maintained in patients given dexmedetomidine during spine surgery. Anes- of focal cerebral ischemia. Anesthesiology. 1996;84:1475.

thesiology. 2008;109(3):417–425. 60. Elsersy H, Sheng H, Lynch JR, et al. Effects of isoflurane versus fentanyl-nitrous
28. Mahmoud M, Sadhasivam S, Salisbury S, et al. Susceptibility of transcranial elec oxide anesthesia on long-term outcome from severe forebrain ischemia in the rat.
tric motor-evoked potentials to varying targeted blood levels of dexmedetomi Anesthesiology. 2004;100:1160.
Subspecialties
dine during spine surgery. Anesthesiology. 2010;112(6):1364–1373. 61. Kawaguchi M, Furuya H, Patel PM. Neuroprotective effects of anesthetic agents.
29. Huber P, Handa J. Effect of contrast material, hypercapnia, hyperventilation, J Anesth. 2005;19:150.
hypertonic glucose and papaverine on the diameter of the cerebral areteries. 62. Kawaguchi M, Kimbro JR, Drummond JC, et al. Isoflurane delays but does not
Angiographic determination in man. Invest Radiol. 1967;2:17. prevent cerebral infarction in rats subjected to focal ischemia. Anesthesiology.
30. Martin KK, Wigginton JB, Babikian VL, et al. Intraoperative cerebral high-inten 2000;92:1335.
sity transient signals and postoperative cognitive function: A systematic review. 63. Soonthon-Brant V, Patel PM, Drummond JC, et al. Fentanyl does not increase
Am J Surg. 2009;197(1):55–63. brain injury after focal cerebral ischemia in rats. Anesth Analg. 1999;88:49.
31. Kincaid MS. Transcranial Doppler ultrasonography: A diagnostic tool of increas 64. Blanck TJ, Haile M, Xu F, et al. Isoflurane pretreatment ameliorates postischemic
ing utility. Curr Opin Anaesthesiol. 2008;21(5):552–559. neurologic dysfunction and preserves hippocampal Ca2+/calmodulin-dependent
32. Rigamonti A, Ackery A, Baker AJ. Transcranial Doppler monitoring in sub protein kinase in a canine cardiac arrest model. Anesthesiology. 2000;93:1285.
arachnoid hemorrhage: A critical tool in critical care. Can J Anaesth. 2008;55(2): 65. Kapinya KJ, Lowl D, Futterer C, et al. Tolerance against ischemic neuronal injury
112–123. can be induced by volatile anesthetics and is inducible NO synthase dependent.
33. Sharma D, Souter MJ, Moore AE, et al. Clinical experience with transcranial Stroke. 2002;33:1889.
ultrasonography as a confirmatory test for brain death: A retrospective analysis. 66. Drummond JC, Cole DJ, Patel PM, et al. Focal cerebral ischemia during anes
Neurocrit Care. 2011;14(3):370–376. thesia with etomidate, isoflurane, or thiopental: A comparison of the extent of
34. Chestnut RM. Care of central nervous system injuries. Surg Clin North Am. cerebral injury. Neurosurgery. 1995;37:742.
2007;87:119. 67. Michenfelder JD, Milde JH, Sundt TM Jr. Cerebral protection by barbiturate
35. Snyder LA, Spetzler RF. Current indications for indocyanine green angiography. anesthesia. Use after middle cerebral artery occlusion in Java monkeys. Arch
World Neurosurg. 2011;76(5):405–406. Neurol. 1976;33:345.
36. Highton D, Elwell C, Smith M. Noninvasive cerebral oximetry: Is there light at 68. Selman WR, Spetzler RJ, Roski RA, et al. Barbiturate coma in focal cerebral isch
the end of the tunnel? Curr Opin Anaesthesiol. [Review]. 2010;23(5):576–581. emia. Relationship of protection to timing of therapy. J Neurosurg. 1982;56:685.
37. Thavasothy M, Broadhead M, Elwell C, et al. A comparison of cerebral oxygen 69. Smith AL, Hoff JT, Nielsen SL, et al. Barbiturate protection in acute focal cerebral
ation as measured by the NIRO 300 and the INVOS 5100 Near-Infrared Spectro ischemia. Stroke. 1974;5:1.
photometers. Anaesthesia. 2002;57(10):999–1006. 70. Bleyaert AL, Nemoto EM, Safar P, et al. Thiopental amelioration of brain damage
38. Valadka AB, Gopinath SP, Contant CF, et al. Relationship of brain tissue PO2 to after global ischemia in monkeys. Anesthesiology. 1978;49:390.
outcome after severe head injury. Crit Care Med. 1998;26:1576. 71. Gisvold SE, Safar P, Hendrickx HH, et al. Thiopental treatment after global brain
39. Maloney-Wilensky E, Gracias V, Itkin A, et al. Brain tissue oxygen and outcome ischemia in pigtailed monkeys. Anesthesiology. 1984;60:88.
after severe traumatic brain injury: A systematic review. Crit Care Med. [Review]. 72. Snyder BD, Ramirez-Lassepas M, Sukhum P, et al. Failure of thiopental to modify
2009;37(6):2057–2063. global anoxic injury. Stroke. 1979;10:135.
40. Spiotta AM, Stiefel MF, Graciaas VH, et al. Brain tissue oxygen-directed manage 73. Steen PA, Milde JH, Michenfelder JD. No barbiturate protection in a dog model
ment and outcome in patients with severe traumatic brain injury. J Neurosurg. of complete cerebral ischemia. Ann Neurol. 1979;5:343.
2008;108:943–949. 74. Todd MM, Chadwick HS, Shapiro HM, et al. The neurologic effects of thiopen
41. Robertson CS, Gopinath SP, Goodman JC, et al. SjvO2 monitoring in head- tal therapy following experimental cardiac arrest in cats. Anesthesiology. 1982;
injured patients. J Neurotrauma. 1995;12:891. 57:76.
LWBK1137-C36_p996-1029.indd 1025 11/01/13 7:53 PM

75. Zhan RZ, Fujiwara N, Endoh H, et al. Thiopental inhibits increases in [Ca2+]i 105. Schmittner MD, Vajkoczy SL, Horn P, et al. Effects of fentanyl and S(+)-ketamine
induced by membrane depolarization, NMDA receptor activation, and ischemia on cerebral hemodynamics, gastrointestinal motility, and need of vasopressors
in rat hippocampal and cortical slices. Anesthesiology. 1998;89:456. in patients with intracranial pathologies: A pilot study. J Neurosurg Anesthesiol.
76. Zhu H, Cottrell JE, Kass IS. The effect of thiopental and propofol on NMDA- and 2007;19(4):257–262.
AMPA-mediated glutamate excitotoxicity. Anesthesiology. 1997;87(4):944. 106. Sloan TB, Ronai AK, Toleikis JR, et al. Improvement of intraoperative
77. Rodriguez-Lopez JM, Sanchez-Conde P, Lozano FS, et al. Laboratory investiga somatosensory evoked potentials by etomidate. Anesth Analg. [Case Reports].
tion: Effects of propofol on the systemic inflammatory response during aortic 1988;67(6):582–585.
surgery. Can J Anaesth. 2006;53:701. 107. Taniguchi M, Nadstawek J, Langenbach U, et al. Effects of four intravenous anes
78. Young Y, Menon DK, Tisavipat N, et al. Propofol neuroprotection in a rat model thetic agents on motor evoked potentials elicited by magnetic transcranial stimu
of ischaemia reperfusion injury. Eur J Anaesthesiol. 1997;14:320. lation. Neurosurgery. 1993;33(3):407–415.
79. Fukuda S, Warner DS. Cerebral protection. Br J Anaesth. 2007;99:10. 108. Hildreth AN, Mejia VA, Maxwell RA, et al. Adrenal suppression following a sin
80. Mizock BA. Alterations in carbohydrate metabolism during stress: A review of gle dose of etomidate for rapid sequence induction: A prospective randomized
the literature. Am J Med. 1995;98:75. study. J Trauma. 2008;65(3):573–579.
81. Capes SE, Hunt D, Malmberg K, et al. Stress hyperglycaemia and increased risk 109. Vinclair M, Broux C, Faure P, et al. Duration of adrenal inhibition following
of death after myocardial infarction in patients with and without diabetes: A sys a single dose of etomidate in critically ill patients. Intensive Care Med. 2008;
tematic overview. Lancet. 2000;355:773. 34(4):714–719.
82. Capes SE, Hunt D, Malmberg K, et al. Stress hyperglycemia and prognosis of 110. den Brinker M, Hokken-Koelega AC, Hazelzet JA, et al. One single dose of etomi
stroke in nondiabetic and diabetic patients: A systematic overview. Stroke. 2001; date negatively influences adrenocortical performance for at least 24h in children
32:2426. with meningococcal sepsis. Intensive Care Med. 2008;34(1):163–168.
83. Gore DC, Chinkes D, Heggers J, et al. Association of hyperglycemia with 111. Martyn JA, Richtsfeld M. Succinylcholine-induced hyperkalemia in acquired
increased mortality after severe burn injury. J Trauma. 2001;51:540. pathologic states: Etiologic factors and molecular mechanisms. Anesthesiology.
84. Krinsley JS. Association between hyperglycemia and increased hospital mortality in [Review]. 2006;104(1):158–169.
a heterogeneous population of critically ill patients. Mayo Clin Proc. 2003;78:1471. 112. Gronert GA, Theye RA. Pathophysiology of hyperkalemia induced by succinyl
85. O’Neill PA, Davies I, Fullerton KJ, et al. Stress hormone and blood glucose choline. Anesthesiology. 1975;43(1):89–99.
response following acute stroke in the elderly. Stroke. 1991;22:842. 113. Perry JJ, Lee JS, Sillberg VA, et al. Rocuronium versus succinylcholine for
86. Rovlias A, Kotsou S. The influence of hyperglycemia on neurological outcome in rapid sequence induction intubation. Cochrane Database Syst Rev. 2008;(2):
patients with severe head injury. Neurosurgery. 2000;46:335. CD002788.
87. Chew W, Kucharczyk J, Moseley M, et al. Hyperglycemia augments ischemic 114. Magorian T, Flannery KB, Miller RD. Comparison of rocuronium, succinyl
brain injury: in vivo MR imaging/spectroscopic study with nicardipine in cats choline, and vecuronium for rapid-sequence induction of anesthesia in adult
with occluded middle cerebral arteries. AJNR Am J Neuroradiol. 1991;12:603. patients. Anesthesiology. 1993;79(5):913–918.
88. Marfella R, D’Amico M, DiFilippo C, et al. Myocardial infarction in diabetic rats: 115. Jones RK, Caldwell JE, Brull SJ, et al. Reversal of profound rocuronium-induced
Role of hyperglycaemia on infarct size and early expression of hypoxia-inducible blockade with sugammadex: A randomized comparison with neostigmine. Anes-
factor 1. Diabetologia. 2002;45:1172. thesiology. 2008;109(5):816–824.
89. van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in the 116. Aouad MT, Al-Alami AA, Nasr VG, et al. The effect of low-dose remifentanil on
critically ill patients. N Engl J Med. 2001;345:1359. responses to the endotracheal tube during emergence from general anesthesia.
90. Van den Berghe G, Wilmer A, Hermans G, et al. Intensive insulin therapy in the Anesth Analg. 2009;108(4):1157–1160.
medical ICU. N Engl J Med. 2006;354:449. 117. Mack PF, Perrine K, Kobylarz E, et al. Dexmedetomidine and neurocognitive
91. Gandhi GY, Nuttell GA, Abel MD, et al. Intensive intraoperative insulin therapy testing in awake craniotomy. J Neurosurg Anesthesiol. 2004;16(1):20–25.
versus conventional glucose management during cardiac surgery: A randomized 118. Rozet I, Muangman S, Vavilala MS, et al. Clinical experience with dexmedeto
trial. Ann Intern Med. 2007;146:233. midine for implantation of deep brain stimulators in Parkinson’s disease. Anesth
92. McGirt MJ, Woodworth GF, Brooke BS, et al. Hyperglycemia independently Analg. 2006;103(5):1224–1228.
increases the risk of perioperative stroke, myocardial infarction, and death after 119. Davis DP, Dunford JV, Poste JC, et al. The impact of hypoxia and hyperventila
carotid endarterectomy. Neurosurgery. 2006;58:1066. tion on outcome after paramedic rapid sequence intubation of severely head-
93. Gentile NT, Seftchick MW, Huynh T, et al. Decreased mortality by normalizing injured patients. J Trauma. 2004;57(1):1–8.
blood glucose after acute ischemic stroke. Acad Emerg Med. 2006;13:174. 120. Bratton SL, Chestnut RM, Ghajar J, et al. Guidelines for the management of
94. Cimino M, Gelosa P, Gianelli A, et al. Statins: Multiple mechanisms of action in severe traumatic brain injury. XIV. Hyperventilation. J Neurotrauma. [Practice
the ischemic brain. Neuroscientist. 2007;13:208. Guideline]. 2007;24 (suppl 1):S87–S90.
95. Maiese K, Li F, Chong ZZ. New avenues of exploration for erythropoietin. JAMA. 121. Oddo M, Levine JM, Frangos S, et al. Effect of mannitol and hypertonic saline on
2005;293:90. cerebral oxygenation in patients with severe traumatic brain injury and refractory
96. Conway JB, Goldberg J, Chung F. Preadmission anaesthesia consultation clinic. intracranial hypertension. J Neurol Neurosurg Psychiatry. 2009;80(8):916–920.
Can J Anaesth. 1992;39(10):1051–1057. 122. Vialet R, Albanese J, Thomachot L, et al. Isovolume hypertonic solutes (sodium
97. Hepner DL, Correll DJ, Beckman JA, et al. Needs analysis for the development chloride or mannitol) in the treatment of refractory posttraumatic intracranial
of a preoperative clinic protocol for perioperative beta-blocker therapy. J Clin hypertension: 2 mL/kg 7.5% saline is more effective than 2 mL/kg 20% mannitol.
Anesth. 2008;20(8):580–588. Crit Care Med. 2003;31(6):1683–1687.
98. Fleisher LA, Beckman JA, Brown KA, et al. ACC/AHA 2007 Guidelines on Peri 123. Schwarz S, Schwab S, Bertram M, et al. Effects of hypertonic saline hydroxyethyl
operative Cardiovascular Evaluation and Care for Noncardiac Surgery: Execu starch solution and mannitol in patients with increased intracranial pressure after
tive Summary: A Report of the American College of Cardiology/American Heart stroke. Stroke. 1998;29(8):1550–1555.
Association Task Force on Practice Guidelines (Writing Committee to Revise the 124. Rozet I, Tontisirin N, Muangman S, et al. Effect of equiosmolar solutions of man
2002 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Sur nitol versus hypertonic saline on intraoperative brain relaxation and electrolyte
gery): Developed in Collaboration With the American Society of Echocardiog balance. Anesthesiology. 2007;107(5):697–704.
raphy, American Society of Nuclear Cardiology, Heart Rhythm Society, Society 125. Rizoli SB, Rhind SG, Shek PN, et al. The immunomodulatory effects of hyper
of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and tonic saline resuscitation in patients sustaining traumatic hemorrhagic shock: A
Interventions, Society for Vascular Medicine and Biology, and Society for Vascu randomized, controlled, double-blinded trial. Ann Surg. 2006;243(1):47–57.
lar Surgery. Circulation. 2007 23;116(17):1971–1996. 126. Pascual JL, Khwaja KA, Chaudhury P, et al. Hypertonic saline and the microcir
99. Devereaux PJ, Yang H, Guyatt GH, et al. Rationale, design, and organization of culation. J Trauma. 2003;54(5 suppl):S133–S140.
the PeriOperative ISchemic Evaluation (POISE) trial: A randomized controlled 127. Corso CO, Okamoto S, Leiderer R, et al. Resuscitation with hypertonic saline
trial of metoprolol versus placebo in patients undergoing noncardiac surgery. Am dextran reduces endothelial cell swelling and improves hepatic microvascular
Heart J. 2006;152(2):223–230. perfusion and function after hemorrhagic shock. J Surg Res. 1998;80(2):210–220.
100. Juul AB, Wetterslev J, Gluud C, et al. Effect of perioperative beta blockade in 128. Manninen PH, Lam AM, Gelb AW, et al. The effect of high-dose mannitol on
patients with diabetes undergoing major non-cardiac surgery: Randomised pla serum and urine electrolytes and osmolality in neurosurgical patients. Can J
cebo controlled, blinded multicentre trial. BMJ. 2006;332(7556):1482. Anaesth. 1987;34(5):442–446.
101. Chestnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury 129. Muizelaar JP, Wei EP, Kontos HA, et al. Mannitol causes compensatory cerebral
in determining outcome from severe head injury. J Trauma. 1993;34(2):216–222. vasoconstriction and vasodilation in response to blood viscosity changes. J Neu-
102. Fujii Y, Takeuchi S, Sasaki O, et al. Ultra-early rebleeding in spontaneous sub rosurg. 1983;59(5):822–828.
arachnoid hemorrhage. J Neurosurg. 1996;84(1):35–42. 130. Burke AM, Quest DO, Chien S, et al. The effects of mannitol on blood viscosity.
103. Kolenda H, Gremmelt A, Rading S, et al. Ketamine for analgosedative therapy J Neurosurg. 1981;55(4):550–553.
in intensive care treatment of head-injured patients. Acta Neurochir (Wien). 131. Rosner MJ, Coley I. Cerebral perfusion pressure: A hemodynamic mechanism of
1996;138(10):1193–1199. mannitol and the postmannitol hemogram. Neurosurgery. 1987;21(2):147–156.
104. Bourgoin A, Albanese J, Wereszczynski N, et al. Safety of sedation with ketamine 132. Mendelow AD, Teasdale GM, Russell T, et al. Effect of mannitol on cerebral
in severe head injury patients: Comparison with sufentanil. Crit Care Med. blood flow and cerebral perfusion pressure in human head injury. J Neurosurg.
2003;31(3):711–717. 1985;63(1):43–48.
LWBK1137-C36_p996-1029.indd 1026 11/01/13 7:53 PM

133. Kirkpatrick PJ, Smielewski P, Piechnik S, et al. Early effects of mannitol in 163. Kriner EJ, Shafazand S, Colice GL. The endotracheal tube cuff-leak test as a pre
patients with head injuries assessed using bedside multimodality monitoring. dictor for postextubation stridor. Respir Care. 2005;50(12):1632–1638.
Neurosurgery. 1996;39(4):714–720; discussion 20–21. 164. Kwon B, Yoo JU, Furey CG, et al. Risk factors for delayed extubation after single-
134. Torre-Healy A, Marko NF, Weil RJ. Hyperosmolar therapy for intracranial stage, multi-level anterior cervical decompression and posterior fusion. J Spinal
hypertension. Neurocrit Care. 2012;17(1):117–1130. Disord Tech. 2006;19(6):389–393.
135. Warner MA, O’Keeffe T, Bhavsar P, et al. Transfusions and long-term functional 165. Emery SE, Akhavan S, Miller P, et al. Steroids and risk factors for airway com
outcomes in traumatic brain injury. J Neurosurg. 2010;113(3):539–546. promise in multilevel cervical corpectomy patients: A prospective, randomized,
136. Hebert PC, Wells G, Blajchman MA, et al. A multicenter, randomized, controlled double-blind study. Spine (Phila Pa 1976). 2009;34(3):229–232.
clinical trial of transfusion requirements in critical care. Transfusion Require 166. Dunbar PJ, Visco E, Lam AM. Craniotomy procedures are associated with less
ments in Critical Care Investigators, Canadian Critical Care Trials Group. N Engl analgesic requirements than other surgical procedures. Anesth Analg. [Compara
J Med. [Clinical Trial]. 1999;340(6):409–417. tive Study]. 1999;88(2):335–340.
137. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment 167. Venkatesan T, Korula G. A comparative study between the effects of 4% endo
of severe sepsis and septic shock. N Engl J Med. 2001;345(19):1368–1377. tracheal tube cuff lignocaine and 1.5 mg/kg intravenous lignocaine on coughing
138. Zygun DA, Nortje J, Hutchinson PJ, et al. The effect of red blood cell transfusion and hemodynamics during extubation in neurosurgical patients: A randomized
on cerebral oxygenation and metabolism after severe traumatic brain injury. Crit controlled double-blind trial. J Neurosurg Anesthesiol. 2006;18(4):230–234.
Care Med. 2009;37(3):1074–1078. 168. Butler BD, Hills BA. Transpulmonary passage of venous air emboli. J Appl
139. Smith MJ, Stiefel MF, Magge S, et al. Packed red blood cell transfusion increases Physiol. 1985;59:543.
local cerebral oxygenation. Crit Care Med. 2005;33(5):1104–1108. 169. Vik A, Brubakk AO, Hennessey TR, et al. Venous air embolism in swine: Transport
140. Carlson AP, Schermer CR, Lu SW. Retrospective evaluation of anemia and trans of gas bubbles through the pulmonary circulation. J Appl Physiol. 1990;69:237.
fusion in traumatic brain injury. J Trauma. 2006;61(3):567–571. 170. Yahagi N, Furuya H. The effects of halothane and pentobarbital on the threshold
141. Wass CT, Long TR, Faust RJ, et al. Changes in red blood cell transfusion practice of transpulmonary passage of venous air emboli in dogs. Anesthesiology. 1987;
during the past two decades: A retrospective analysis, with the Mayo database, 67:905.
of adult patients undergoing major spine surgery. Transfusion. 2007;47(6):1022– 171. Glasker S, Pechstein U, Vongionkas VI, et al. Monitoring motor function during
1027. resection of tumours in the lower brain stem and fourth ventricle. Childs Nerv
142. Myburgh J, Cooper DJ, Finfer S, et al. Saline or albumin for fluid resuscitation in Syst. 2006;22:1288.
patients with traumatic brain injury. N Engl J Med. 2007;357(9):874–884. 172. Neuloh G, Pechstein U, Schramm J. Motor tract monitoring during insular
143. Holcomb JB, Wade CE, Michalek JE, et al. Increased plasma and platelet to red glioma surgery. J Neurosurg. 2007;106:582.
blood cell ratios improves outcome in 466 massively transfused civilian trauma 173. Kaal EC, Vecht CJ. The management of brain edema in brain tumors. Curr Opin
patients. Ann Surg. [Multicenter Study]. 2008;248(3):447–458. Oncol. 2004;16:593.
144. Karlsson M, Ternstrom L, Hyllner M, et al. Prophylactic fibrinogen infusion 174. Beneficial effect of carotid endarterectomy in symptomatic patients with high-
reduces bleeding after coronary artery bypass surgery. A prospective randomised grade carotid stenosis. North American Symptomatic Carotid Endarterectomy
pilot study. Thromb Haemost. 2009;102(1):137–144. Trial Collaborators. N Engl J Med. 1991;325:445.
145. Shakur H, Roberts I, Bautista R, et al. Effects of tranexamic acid on death, vas 175. Chaturvedi S, Bruno A, Feasby T, et al. Carotid endarterectomy—an evidence-
cular occlusive events, and blood transfusion in trauma patients with signifi based review: Report of the Therapeutics and Technology Assessment Subcom
cant haemorrhage (CRASH-2): A randomised, placebo-controlled trial. Lancet. mittee of the American Academy of Neurology. Neurology. 2005;65:794.
2010;376(9734):23–32. 176. Endarterectomy for asymptomatic carotid artery stenosis. Executive Committee
146. Sena MJ, Rivers RM, Muizelaar JP, et al. Transfusion practices for acute trau for the Asymptomatic Carotid Atherosclerosis Study. JAMA. 1995;273:1421.
matic brain injury: A survey of physicians at US trauma centers. Intensive Care 177. Halliday A, Mansfield A, Marro J, et al. Prevention of disabling and fatal strokes
Med. 2009;35(3):480–488. by successful carotid endarterectomy in patients without recent neurological
147. Brasel KJ, Vercruysse G, Spinella PC, et al. The association of blood component symptoms: Randomised controlled trial. Lancet. 2004;363:1491.
use ratios with the survival of massively transfused trauma patients with and 178. Ederle J, Brown MM. The evidence for medicine versus surgery for carotid steno
without severe brain injury. J Trauma. 2011;71(2 suppl 3):S343–S352. sis. Eur J Radiol. 2006;60:3.
148. Rhodes KE, Raivich G, Fawcett JW. The injury response of oligodendrocyte pre 179. de Sousa AA, Filho MA, Faglioni W Jr, et al. Superficial vs combined cervical
cursor cells is induced by platelets, macrophages and inflammation-associated plexus block for carotid endarterectomy: A prospective, randomized study. Surg

cytokines. Neuroscience. 2006;140(1):87–100. Neurol. 2005;63(suppl 1):S22.
149. Liu-DeRyke X, Collingridge DS, Orme J, et al. Clinical impact of early hyper 180. Pandit JJ, Bree S, Dillon P, et al. A comparison of superficial versus combined
glycemia during acute phase of traumatic brain injury. Neurocrit Care. (superficial and deep) cervical plexus block for carotid endarterectomy: A pro
Subspecialties
2009;11(2):151–157. spective, randomized study. Anesth Analg. 2000;91:781.
150. Jeremitsky E, Omert LA, Dunham CM, et al. The impact of hyperglycemia on 181. GALA Trial Collaborative Group, Lewis SC, Warlow CP, et al. General anaes
patients with severe brain injury. J Trauma. 2005;58(1):47–50. thesia versus local anaesthesia for carotid surgery (GALA): A multicentre, ran
151. Sharma D, Jelacic J, Chennuri R, et al. Incidence and risk factors for periopera domised controlled trial. Lancet. 2008;372(9656):2132–2142.
tive hyperglycemia in children with traumatic brain injury. Anesth Analg. 2009; 182. Moritz S, Kasprzak P, Arlt M, et al. Accuracy of cerebral monitoring in detecting
108(1):81–89. cerebral ischemia during carotid endarterectomy: A comparison of transcranial
152. Mitchell I, Knight E, Gissane J, et al. A phase II randomised controlled trial of Doppler sonography, near-infrared spectroscopy, stump pressure, and somato
intensive insulin therapy in general intensive care patients. Crit Care Resusc. 2006; sensory evoked potentials. Anesthesiology. 2007;107:563.
8(4):289–293. 183. SPACE Collaborative Group, Ringleb PA, Allenberg J, et al. 30 day results from
153. Thomas G, Rojas MC, Epstein SK, et al. Insulin therapy and acute kidney injury the SPACE trial of stent-protected angioplasty versus carotid endarterectomy in
in critically ill patients a systematic review. Nephrol Dial Transplant. 2007; symptomatic patients: A randomised non-inferiority trial. Lancet. 2006;368:1239.
22(10):2849–2855. 184. Mas JL, Chatellier G, Beyssen B, et al. Endarterectomy versus stenting in patients
154. Finfer S, Chittock DR, Su SY, et al. Intensive versus conventional glucose control with symptomatic severe carotid stenosis. N Engl J Med. 2006;355:1660.
in critically ill patients. N Engl J Med. 2009;360(13):1283–1297. 185. Yadav JS, Wholey MH, Kuntz RT, et al. Protected carotid-artery stenting versus
155. Oddo M, Schmidt JM, Carrera E, et al. Impact of tight glycemic control on cere endarterectomy in high-risk patients. N Engl J Med. 2004;351:1493.
bral glucose metabolism after severe brain injury: A microdialysis study. Crit Care 186. McClelland S 3rd. Multimodality management of carotid artery stenosis: Review
Med. 2008;36(12):3233–3238. ing the class-I evidence. J Natl Med Assoc. 2007;99:1235.
156. Bagshaw SM, Egi M, George C, et al. Early blood glucose control and mortality in 187. Brott TG, Hobson RW 2nd, Howard G, et al. Stenting versus endarterectomy for
critically ill patients in Australia. Crit Care Med. 2009;37(2):463–470. treatment of carotid-artery stenosis. N Engl J Med. 2010;363(1):11–23.
157. Krinsley JS. Glycemic variability: A strong independent predictor of mortality in 188. Zanettini R, Antonini A, Gatto G, et al. Valvular heart disease and the use of
critically ill patients. Crit Care Med. 2008;36(11):3008–3013. dopamine agonists for Parkinson’s disease. N Engl J Med. 2007;356(1):39–46.
158. Ali NA, O’Brien JM Jr, Dungan K, et al. Glucose variability and mortality in 189. Nicholson G, Pereira AC, Hall GM. Parkinson’s disease and anaesthesia. Br J
patients with sepsis. Crit Care Med. 2008;36(8):2316–2321. Anaesth. 2002;89(6):904–916.
159. Hirshberg E, Larsen G, Van Duker H. Alterations in glucose homeostasis in the 190. Burton DA, Nicholson G, Hall GM. Anaesthesia in elderly patients with neurode
pediatric intensive care unit: Hyperglycemia and glucose variability are associ generative disorders: Special considerations. Drugs Aging. 2004;21(4):229–242.
ated with increased mortality and morbidity. Pediatr Crit Care Med. 2008;9(4): 191. Krauss JK, Akeyson EW, Giam P, et al. Propofol-induced dyskinesias in Parkin
361–366. son’s disease. Anesth Analg. 1996;83(2):420–422.
160. Dossett LA, Cao H, Mowery NT, et al. Blood glucose variability is associated 192. Erickson KM, Cole DJ. Anesthetic considerations for awake craniotomy for epi
with mortality in the surgical intensive care unit. Am Surg. 2008;74(8):679–685; lepsy. Anesthesiol Clin. 2007;25(3):535–555, ix.
discussion 85. 193. Skucas AP, Artru AA. Anesthetic complications of awake craniotomies for epi
161. Pecha T, Sharma D, Hoffman NG, et al. Hyperglycemia during craniotomy for lepsy surgery. Anesth Analg. 2006;102(3):882–887.
adult traumatic brain injury. Anesth Analg. 2011;113(2):336–342. 194. Manninen PH, Balki M, Lukitto K, et al. Patient satisfaction with awake crani
162. De Backer D. The cuff-leak test: What are we measuring? Crit Care. 2005;9(1): otomy for tumor surgery: A comparison of remifentanil and fentanyl in conjunc
31–33. tion with propofol. Anesth Analg. 2006;102(1):237–242.
LWBK1137-C36_p996-1029.indd 1027 11/01/13 7:53 PM

195. Khatib R, Ebrahim Z, Rezai A, et al. Perioperative events during deep brain stim 225. Bulger EM, May S, Brasel KJ, et al. Out-of-hospital hypertonic resuscitation
ulation: The experience at cleveland clinic. J Neurosurg Anesthesiol. 2008;20(1): following severe traumatic brain injury: A randomized controlled trial. JAMA.
36–40. 2010;304(13):1455–1464.
196. Lotto M, Boulis NM. Intrathecal opioids for control of chronic low back pain 226. Contant CF, Valadka AB, Gopinath SP, et al. Adult respiratory distress syndrome:
during deep brain stimulation procedures. Anesth Analg. 2007;105(5):1410– A complication of induced hypertension after severe head injury. J Neurosurg.
1412. 2001;95(4):560–568.
197. Deiner S, Hagen J. Parkinson’s disease and deep brain stimulator placement. 227. Steiner LA, Johnston AJ, Czosnyka M, et al. Direct comparison of cerebrovascular
Anesthesiol Clin. 2009;27(3):391–415. effects of norepinephrine and dopamine in head-injured patients. Crit Care Med.
198. Souter MJ, Rozet I, Ojemann JG, et al. Dexmedetomidine sedation during awake 2004;32(4):1049–1054.
craniotomy for seizure resection: Effects on electrocorticography. J Neurosurg 228.
Anesthesiol. 2007;19(1):38–44. 229. Chen JW, Gombart ZJ, Rogers S, et al. Pupillary reactivity as an early indicator of
199. Bulger EM, Copass MK, Sabath DR, et al. The use of neuromuscular blocking increased intracranial pressure: The introduction of the neurological pupil index.
agents to facilitate prehospital intubation does not impair outcome after trau Surg Neurol Int. 2011;2:82.
matic brain injury. J Trauma. 2005;58(4):718–723; discussion 23–24. 230. Sheinberg M, Kanter MJ, Robertson CS, et al. Continuous monitoring of jugu
200. Winchell RJ, Hoyt DB. Endotracheal intubation in the field improves survival in lar venous oxygen saturation in head-injured patients. J Neurosurg. 1992;76(2):
patients with severe head injury. Trauma Research and Education Foundation of 212–217.
San Diego. Arch Surg. 1997;132(6):592–597. 231. Wang GJ, Deng HY, Maier CM, et al. Mild hypothermia reduces ICAM-1 expres
201. Davis DP, Hoyt DB, Ochs M, et al. The effect of paramedic rapid sequence intu sion, neutrophil infiltration and microglia/monocyte accumulation following
bation on outcome in patients with severe traumatic brain injury. J Trauma. experimental stroke. Neuroscience. 2002;114(4):1081–1090.
2003;54(3):444–453. 232. Jiang JY, Xu W, Yang PF, et al. Marked protection by selective cerebral pro
202. Murray JA, Demetriades D, Berne TV, et al. Prehospital intubation in patients found hypothermia after complete cerebral ischemia in primates. J Neurotrauma.
with severe head injury. J Trauma. 2000;49(6):1065–1070. 2006;23(12):1847–1856.
203. Davis DP, Peay J, Sise MJ, et al. The impact of prehospital endotracheal intuba 233. Ehrlich MP, McCullough JN, Zhang N, et al. Effect of hypothermia on cerebral
tion on outcome in moderate to severe traumatic brain injury. J Trauma. 2005; blood flow and metabolism in the pig. Ann Thorac Surg. 2002;73(1):191–197.
58(5):933–939. 234. Maier CM, Sun GH, Cheng D, et al. Effects of mild hypothermia on superoxide
204. Davis DP. Early ventilation in traumatic brain injury. Resuscitation. [Review]. anion production, superoxide dismutase expression, and activity following tran
2008;76(3):333–340. sient focal cerebral ischemia. Neurobiol Dis. 2002;11(1):28–42.
205. Bochicchio GV, Ilahi O, Joshi M, et al. Endotracheal intubation in the field does 235. Sydenham E, Roberts I, Alderson P. Hypothermia for traumatic head injury.
not improve outcome in trauma patients who present without an acutely lethal Cochrane Database Syst Rev. 2009;(2):CD001048.
traumatic brain injury. J Trauma. 2003;54(2):307–311. 236. Clifton GL, Valadka A, Zygun D, et al. Very early hypothermia induction in
206. Michael DB, Guyot DR, Darmody WR. Coincidence of head and cervical spine patients with severe brain injury (the National Acute Brain Injury Study: Hypo
injury. J Neurotrauma. 1989;6(3):177–189. thermia II): A randomised trial. Lancet Neurol. 2011;10(2):131–139.
207. Holly LT, Kelly DF, Counelis GJ, et al. Cervical spine trauma associated with 237. Hutchison JS, Ward RE, Lacroix J, et al. Hypothermia therapy after traumatic
moderate and severe head injury: Incidence, risk factors, and injury characteris brain injury in children. N Engl J Med. 2008;358(23):2447–2456.
tics. J Neurosurg. 2002;96(3 suppl):285–291. 238. Polderman KH. Application of therapeutic hypothermia in the intensive care
208. Lennarson PJ, Smith D, Todd MM, et al. Segmental cervical spine motion during unit. Opportunities and pitfalls of a promising treatment modality–Part 2: Prac
orotracheal intubation of the intact and injured spine with and without external tical aspects and side effects. Intensive Care Med. 2004;30(5):757–769.
stabilization. J Neurosurg. 2000;92(2 suppl):201–206. 239. http://www.anzicrc.monash.org/polar-rct.html
209. Hastings RH, Wood PR. Head extension and laryngeal view during laryngoscopy 240. http://www.eurotherm3235trial.eu/home/index.phtml
with cervical spine stabilization maneuvers. Anesthesiology. 1994;80(4):825–831. 241. Eisenberg HM, Frankowski RF, Contant CF, et al. High-dose barbiturate control
210. Sultan P. Is cricoid pressure needed during rapid sequence induction? Br J Hosp of elevated intracranial pressure in patients with severe head injury. J Neurosurg.
Med (Lond). 2008;69(3):177. 1988;69:15–23.
211. Gobindram A, Clarke S. Cricoid pressure: Should we lay off the pressure? Anaes- 242. Cremer OL, Moons KG, Bouman EA, et al. Long-term propofol infusion and
thesia. 2008;63(11):1258–1259. cardiac failure in adult head-injured patients. Lancet. 2001;357(9250):117–118.
212. Rice MJ, Mancuso AA, Gibbs C, et al. Cricoid pressure results in compression of 243. Otterspoor LC, Kalkman CJ, Cremer OL. Update on the propofol infusion syn
the postcricoid hypopharynx: The esophageal position is irrelevant. Anesth Analg. drome in ICU management of patients with head injury. Curr Opin Anaesthesiol.
2009;109(5):1546–1552. 2008;21(5):544–551. Review.
213. Rice MJ, Mancuso AA, Morey TE, et al. The anatomical correction of cricoid 244. Hutchinson PJ, Kirkpatrick PJ. Decompressive craniectomy in head injury. Curr
pressure. Minerva Anestesiol. 2010;76(4):304. Opin Crit Care. [Review]. 2004;10(2):101–104.
214. Donaldson WF 3rd, Towers JD, Doctor A, et al. A methodology to evaluate 245. Sahuquillo J, Arikan F. Decompressive craniectomy for the treatment of refrac
motion of the unstable spine during intubation techniques. Spine (Phila Pa 1976). tory high intracranial pressure in traumatic brain injury. Cochrane Database Syst
1993;18(14):2020–2023. Rev. [Review]. 2006;(1):CD003983.
215. Butler J, Sen A. Best evidence topic report. Cricoid pressure in emergency rapid 246. Jaeger M, Soehle M, Meixensberger J. Effects of decompressive craniectomy on
sequence induction. Emerg Med J. 2005;22(11):815–816. brain tissue oxygen in patients with intracranial hypertension. J Neurol Neurosurg
216. Unni VK, Johnston RA, Young HS, et al. Prevention of intracranial hypertension Psychiatry. [Review]. 2003;74(4):513–515.
during laryngoscopy and endotracheal intubation. Use of a second dose of thio 247. Stiefel MF, Heuer GG, Smith MJ, et al. Cerebral oxygenation following decom
pentone. Br J Anaesth. 1984;56(11):1219–1223. pressive hemicraniectomy for the treatment of refractory intracranial hyperten
217. Albrecht RF, Miletich DJ, Rosenberg R, et al. Cerebral blood flow and metabolic sion. J Neurosurg. 2004;101(2):241–247.
changes from induction to onset of anesthesia with halothane or pentobarbital. 248. Aarabi B, Hesdorffer DC, Ahn ES, et al. Outcome following decompressive
Anesthesiology. 1977;47(3):252–256. craniectomy for malignant swelling due to severe head injury. J Neurosurg. 2006;
218. White PF, Schlobohm RM, Pitts LH, et al. A randomized study of drugs for pre 104(4):469–479.
venting increases in intracranial pressure during endotracheal suctioning. Anes- 249. Cooper DJ, Rosenfeld JV, Murray L, et al. Decompressive craniectomy in diffuse
thesiology. 1982;57(3):242–244. traumatic brain injury. N Engl J Med. 2011;364(16):1493–1502.
219. Kovarik WD, Mayberg TS, Lam AM, et al. Succinylcholine does not change intra 250. Kawaguchi M, Sakamoto T, Ohnishi H, et al. Preoperative predictors of reduc
cranial pressure, cerebral blood flow velocity, or the electroencephalogram in tion in arterial blood pressure following dural opening during surgical evacuation
patients with neurologic injury. Anesth Analg. 1994;78(3):469–473. of acute subdural hematoma. J Neurosurg Anesthesiol. 1996;8(2):117–122.
220. Brown MM, Parr MJ, Manara AR. The effect of suxamethonium on intracranial 251. Pelligrino DA, Miletich DJ, Hoffman WE, et al. Nitrous oxide markedly increases
pressure and cerebral perfusion pressure in patients with severe head injuries fol cerebral cortical metabolic rate and blood flow in the goat. Anesthesiology. 1984;
lowing blunt trauma. Eur J Anaesthesiol. 1996;13(5):474–477. 60(5):405–412.
221. Bratton SL, Chestnut RM, Ghajar J, et al. Guidelines for the management of 252. Matta BF, Lam AM. Nitrous oxide increases cerebral blood flow velocity dur
severe traumatic brain injury. IX. Cerebral perfusion thresholds. J Neurotrauma. ing pharmacologically induced EEG silence in humans. J Neurosurg Anesthesiol.
[Practice Guideline]. 2007;24(suppl 1):S59–S64. 1995;7(2):89–93.
222. Sekhon MS, Dhingra VK, Sekhon IS, et al. The safety of synthetic colloid in 253. Moss E, McDowall DG. I.c.p. increases with 50% nitrous oxide in oxygen in severe
critically ill patients with severe traumatic brain injuries. J Crit Care. 2011;26(4): head injuries during controlled ventilation. Br J Anaesth. 1979;51(8):757–761.
357–362. 254. Hadani M, Bruk B, Ram Z, et al. Application of transcranial Doppler ultrasonog
223. Huang SJ, Chen YS, Hong WC, et al. Clinical experience of hydroxyethyl starch raphy for the diagnosis of brain death. Intensive Care Med. 1999;25(8):822–828.
(10% HES 200/0.5) in cerebral perfusion pressure protocol for severe head injury. 255. Grotz MR, Giannoudis PV, Pape HC, et al. Traumatic brain injury and stabilisa
Surg Neurol. 2006;66(suppl 2):S26–S31. tion of long bone fractures: An update. Injury. [Review]. 2004;35(11):1077–1086.
224. Neff TA, Doelberg M, Jungheinrich C, et al. Repetitive large-dose infusion of 256. Pietropaoli JA, Rogers FB, Shackford SR, et al. The deleterious effects of intraop
the novel hydroxyethyl starch 130/0.4 in patients with severe head injury. Anesth erative hypotension on outcome in patients with severe head injuries. J Trauma.
Analg. 2003;96(5):1453–1459. 1992;33(3):403–407.
LWBK1137-C36_p996-1029.indd 1028 11/01/13 7:53 PM

257. Vallier HA, Cureton BA, Ekstein C, et al. Early definitive stabilization of unsta 269. Kumar A, Anel R, Bunnell E, et al. Pulmonary artery occlusion pressure and
ble pelvis and acetabulum fractures reduces morbidity. J Trauma. 2010;69(3): central venous pressure fail to predict ventricular filling volume, cardiac perfor
677–684. mance, or the response to volume infusion in normal subjects. Crit Care Med.
258. Morshed S, Miclau T 3rd, Bembom O, et al. Delayed internal fixation of femoral 2004;32(3):691–699.
shaft fracture reduces mortality among patients with multisystem trauma. J Bone 270. Friese RS, Shafi S, Gentilello LM. Pulmonary artery catheter use is associated with
Joint Surg Am. 2009;91(1):3–13. reduced mortality in severely injured patients: A National Trauma Data Bank
259. Rothman SM, Olney JW. Glutamate and the pathophysiology of hypoxic– analysis of 53,312 patients. Crit Care Med. 2006;34(6):1597–1601.
ischemic brain damage. Ann Neurol. 1986;19(2):105–111. 271. Montenij LJ, de Waal EE, Buhre WF. Arterial waveform analysis in anesthesia and
260. Biffl WL, Egglin T, Benedetto B, et al. Sixteen-slice computed tomographic angi critical care. Curr Opin Anaesthesiol. 2011;24(6):651–656.
ography is a reliable noninvasive screening test for clinically significant blunt 272. Malhotra NR, Shaffrey CI. Intraoperative electrophysiological monitoring in
cerebrovascular injuries. J Trauma. 2006;60(4):745–751; discussion 51–52. spine surgery. Spine (Phila Pa 1976). 2010;35(25):2167–2179.
261. Hackl W, Hausberger K, Sailer R, et al. Prevalence of cervical spine injuries in 273. Ozcan MS, Praetel C, Bhatti MT, et al. The effect of body inclination during
patients with facial trauma. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. prone positioning on intraocular pressure in awake volunteers: A comparison of
2001;92(4):370–376. two operating tables. Anesth Analg. 2004;99(4):1152–1158.
262. McKevitt EC, Kirkpatrick AW, Vertesi L, et al. Identifying patients at risk for intra 274. Griepp RB, Griepp EB. Spinal cord perfusion and protection during descending
cranial and extracranial blunt carotid injuries. Am J Surg. 2002;183(5):566–570. thoracic and thoracoabdominal aortic surgery: The collateral network concept.
263. Rabinovici R, Ovadia P, Mathiak G, et al. Abdominal injuries associated with Ann Thorac Surg. [Review]. 2007;83(2):S865–S869.
lumbar spine fractures in blunt trauma. Injury. 1999;30(7):471–474. 275. Dietrich WD 3rd. Therapeutic hypothermia for spinal cord injury. Crit Care Med.
264. Bracken MB, Holford TR. Neurological and functional status 1 year after acute [Research Review]. 2009;37(7 suppl):S238–S242.
spinal cord injury: Estimates of functional recovery in National Acute Spinal 276. Levi AD, Casella G, Green BA, et al. Clinical outcomes using modest intravascu
Cord Injury Study II from results modeled in National Acute Spinal Cord Injury lar hypothermia after acute cervical spinal cord injury. Neurosurgery. [Research].
Study III. J Neurosurg. 2002;96(3 Suppl):259–266. 2010;66(4):670–677.
265. Hurlbert RJ. Methylprednisolone for acute spinal cord injury: An inappropriate 277. Crock HV, Yoshizawa H, Yamagishi M, et al. Commentary on the prevention
standard of care. J Neurosurg. 2000;93(1 Suppl):1–7. of paralysis after traumatic spinal cord injury in humans: The neglected factor–
266. Sayer FT, Kronvall E, Nilsson OG. Methylprednisolone treatment in acute spinal urgent restoration of spinal cord circulation. Eur Spine J. 2005;14(9):910–914.
cord injury: The myth challenged through a structured analysis of published lit 278. Marion D, Bullock MR. Current and future role of therapeutic hypothermia.
erature. Spine J. [Review]. 2006;6(3):335–343. J Neurotrauma. 2009;26(3):455–467.
267. Fehlings MG, Arvin B. The timing of surgery in patients with central spinal cord 279. Jia X, Kowalski RG, Sciubba DM, et al. Critical care of traumatic spinal cord
injury. J Neurosurg Spine. [Editorial]. 2009;10(1):1–2. injury. J Intensive Care Med. 2011.
268. Michard F. Changes in arterial pressure during mechanical ventilation. Anesthe- 280. Postoperative Visual Loss Study Group. Risk factors associated with ischemic
siology. [Review]. 2005;103(2):419–428. optic neuropathy after spinal fusion surgery. Anesthesiology. 2012;116(1):15–24.

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LWBK1137-FM_i-xxii.

indd 22 12/01/13 2:14 AM

LWBK1137-FM_i-xxii.indd 1 12/01/13 2:14 AM

Paul G. Barash, md Michael K. Cahalan, md

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© 2013 by LIPPINCOTT WILLIAMS & WILKINS, a WOLTERS KLUWER BUSINESS

Two Commerce Square

Library of Congress Cataloging-in-Publication Data

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Saint Adeogba, MD Honorio T. Benzon, MD

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Michael K. Cahalan, MD Marie Csete, MD, PhD

C. Richard Chapman, PhD Armagan Dagal, MD, FRCA

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Stephen F. Dierdorf, MD John H. Eichhorn, MD

Randal O. Dull, MD, PhD Ana Fernandez-Bustamante, MD, PhD

Thomas J. Ebert, MD, PhD Lynne R. Ferrari, MD

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Michael A. Fowler, MD, MBA Jay S. Grider, DO, PhD

Kevin Friede, BA Dhanesh K. Gupta, MD

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Simon C. Hillier, MB, ChB Girish P. Joshi, MBBS, MD, FFARCSI

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Peter G. Moore, MD, PhD Frank J. Overdyk, MSEE, MD

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Wanda M. Popescu, MD Richard W. Rosenquist, MD

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Benjamin M. Sherman, MD Mark Stafford-Smith, MD, CM, FRCPC

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Christer H. Svensén, MD, PhD, DEAA, MSc Mary E. Warner, MD

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SECTION I 14 Fluids, Electrolytes, and

4 Anesthetic Risk, Quality Improvement,

6 Genomic Basis of Perioperative Medicine 130 19 Opioids 501

SECTION III SECTION V

Anatomy and Physiology Preanesthetic Evaluation and

12 The Allergic Response 287 23 Rare Coexisting Diseases 612

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SECTION VI 4 0 Obstetrical Anesthesia 1144

25 Commonly Used Monitoring Techniques 699 41 Neonatal Anesthesia 1178

26 Echocardiography 723 4 2 Pediatric Anesthesia 1216

31 Office-Based Anesthesia 860 47 Anesthesia for Otolaryngologic Surgery 1356

SECTION VII 51 Transplant Anesthesia 1459

35 Peripheral Nerve Blockade 937 53 Emergency Preparedness for and Disaster

38 Anesthesia for Cardiac Surgery 1076

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55 Critical Care Medicine 1580 Appendix 1 Atlas of Electrocardiography 1701

56 Acute Pain Management 1611 Appendix 2 Pacemaker and Implantable

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36 Anesthesia for Neurosurgery

NEUROANATOMY Transfusion Therapy

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SECTION I 14 Fluids, Electrolytes, and

4 Anesthetic Risk, Quality Improvement,

35 Peripheral Nerve Blockade 937 53 Emergency Preparedness for and Disaster

4 Anesthesia for neurosurgery and spine surgery requires the stan

Table 36-1. Electroencephalogram Table 36-2. Indications for