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Library of Congress Cataloging-in-Publication Data

Bassett, Kathy B., author.

Local anesthesia for dental professionals I Kathy B. Bassett, RDH, BSDH, MEd, Professor/Clinical Coordinator,
Dental Hygiene Program, Pierce College, Lakewood, Washington, Arthur C. DiMarco, DMD, Director, RIDE Program
at Eastern Washington University, School of Dentistry, University of Washington, Seattle, Washington, Professor,
Department of Dental Hygiene, Eastern Washington University, Spokane, Washington, Doreen K. Naughton, RDH,
BSDH, Affiliate Instructor, Department of Oral Health Sciences, School of Dentistry, University of Washington.­
Second edition.
pages em
Includes bibliographical references and index.
ISBN 978-0-13-307771-1- ISBN 0-13-307771-3 1. Anesthesia in dentistry. 2. Local anesthesia.
I. DiMarco, Arthur C., author. II. Naughton, Doreen K., author. III. Title.
RK510.B367 2014
617.9'676-dc23
2014011549

10 9 8 7 6 5 4 3 2 1

PEARSON ISBN 10: 0-13-307771-3

ISBN 13: 978-0-13-307771-1
Bridging the Gap
More than 70 years ago, two young enthusiastic Swedish
chemists, Nils Lofgren and Bengt Lundqvist, created a
compound they designated "LL30." Their discovery, later
to be named lidocaine, and marketed as Xylocaine, was
the first of the amide local anesthetics. Within a few de­
cades, practitioners throughout the world found lidocaine,
and the subsequently developed amide anesthetics, to be
the most effective and safest local anesthetic agents for
dental practice. It is understandable why so many have
declared lidocaine to be "God's gift to dentistry." These
safe and highly effective local anesthetics have permitted
our profession to develop the advanced dental procedures
now routinely and safely provided to our patients. The
amide local anesthetics used today in dental practice ap­
proach the ideal for anesthetic agents, being non-irritating
to tissue, minimally allergenic or toxic, and completely
reversible.
An excellent anesthetic agent does not necessarily
translate to effective pain control. This chasm, between
pharmacology and pain management, has been identi­
fied by these authors and successfully bridged in this lat­
est edition of Local Anesthesia for Dental Professionals.
For Educators by Educators
Effective and comfortable pain control with local an­
esthesia has been practiced by dental hygienists in
Washington State since 1971. It has become a matter of
pride and principle for hygienists to become not only pro­
ficient but highly skilled in providing this valuable clinical
procedure, so it has been with great anticipation that we
looked forward to the publication of the second edition of
Local Anesthesia for Dental Professionals.
It is the first textbook that I have thoroughly enjoyed
reading, and we have used it from its first publication. It
was obvious from the beginning that this textbook was
written by educators with an understanding of how to
teach and sequence concepts in ways that create maximum
learning. The diagrams, photos, and explanations in each
chapter make for easy and interesting reading for students,
instructors, and practicing clinicians. Our faculty paid out
of pocket to have their own copies-a first in my experi­
ence as an educator and director. In fact, it is the one text­
book that graduates have refused to sell back at the end of
their education program.
As experienced and passionate educators, they recog­
nize that the success of local anesthesia requires that oral
healthcare providers be knowledgeable, prepared, caring,
and skilled. Through this text, readers are provided with
comprehensive materials, excellent graphics, and complete
descriptions of common and advanced techniques. Patient
health issues are clearly addressed, and the need for care­
ful attention to patient fears and phobias is provided. The
presentation is up to date and comprehensive, and can eas­
ily serve as one's primary source for applying anesthesia
and pain control in dentistry.
Future research may develop needleless delivery sys­
tems and effective non-pharmacologic methods for pain
control. Until then, pain control is in the hands of practi­
tioners and relies on their unsurpassed skills, as presented
in this comprehensive text. The goal of these educators
and the goal of the profession are identical: the elimina­
tion of pain and discomfort when receiving dental care.
Paul A. Moore DMD, PhD, MPH
Professor, Pharmacology and Anesthesiology
Department of Dental Anesthesiology
University of Pittsburgh, School of Dental Medicine
Pittsburgh, PA
This text has set a new standard for not only North
American dental professionals, but also abroad. Within its
first year, it was chosen from a number of texts for publica­
tion in China, which speaks volumes for its value.
Now in its second edition, the up-to-date information
on pharmacology, dosages, and delivery systems, such as
computer-controlled local anesthesia delivery (CCLAD)
devices, helps guide successful implementation of this tech­
nology. Students and clinicians alike appreciate the review
of head and neck anatomy included in the appendix. In ad­
dition, the inclusion of a chapter on nitrous oxide-oxygen
sedation was brilliant.
This textbook is a must-have for all dental profession­
als when studying this important skill.
Lynn Stedman, RDH, BS, MEd, MA
Dental Hygiene Program Director
Associate Professor, Dental Hygiene
Columbia Basin College
Pasco, WA
v
vi FOREWORD
Expanding Your Local
Anesthesia Tool Kit
After 25 years of practice, I got tired of not knowing how
to give a Gow-Gates block or an AMSA injection. I lec­
ture at numerous dental schools only to find that very few
teach their students these injections. When I found out that
these authors have been teaching these injections to their
dental hygiene students for years, I felt cheated! I ordered
Local Anesthesia for Dental Professionals and thanks to
the excellent clinical photographs and precise descriptions;
within 3 weeks of purchasing the book, I was successfully
giving both of these injections! They have been a great
addition to my anesthesia tool kit, as has this wonderful
textbook! I recommend this text to practicing clinicians
seeking to update their skills and as a chairside resource
for patient assessment and drug selection, dosing recom­
mendations, and injection troubleshooting.
Michael C. DiTolla, DDS, FAGD
Director of Clinical Education & Research
Glidewell Laboratories
Editor-in-Chief, Clinical Editor
Chairside Magazine
Comfortable and effective pain control is expected in den­
tistry. To meet this expectation, dental professionals who
administer local anesthesia and nitrous oxide sedation must
be able to think critically and integrate concepts and theo­
ries from multiple perspectives. Regardless of the nature of
individual practice acts, no clinician is exempt from under­
standing and performing allowed techniques to the highest
standards. In other words, patients should reasonably expect
that all credentialed dental professionals are equally knowl­
edgeable about the techniques and drugs they administer.
This second edition represents a broad-based, col­
laborative effort of a well-respected, diverse group of
dental hygiene and dental experts. Local Anesthesia for
Dental Professionals continues to focus on a high level of
knowledge and technical skill for students and clinicians,
enabling the safe, comfortable administration of local an­
esthetic injections and nitrous oxide sedation. Updates in
pharmacological agents and technological advances and
modifications for medical compromise are included that
emphasize the importance of evidence-based practice
highlighting efficiency and safety.
Together with ancillary materials and a companion
DVD, Local Anesthesia for Dental Professionals pres­
ents concepts and techniques with students, instructors,
and practicing clinicians in mind. Ancillary materials in­
clude case studies, in-depth references, clinically applica­
ble appendices, an anatomy review, editable Power Point
templates, workbook exercises, a library of text figures,
video clips, skill evaluation forms, word games, and figure
identifications.
vii
We wish to recognize the many exceptional educators and clinicians who contributed to this second edition of Local
Anesthesia for Dental Professionals. We are incredibly grateful for the vision and expertise of this diverse and talented
group of professionals who not only share our enthusiasm for pain control but also understand the profound significance
of clarity and accuracy of content. In addition to the many contributors and reviewers who worked tirelessly with us to as­
sure accuracy and readability, we wish to thank the following individuals and companies that so generously shared with us
their time, talents, expertise, and unique resources, all of which have allowed us to enhance this work significantly before
bringing it to press.

Paul Moore, DDS Elizabeth Pratt Ron Oyama

Vance Bingham, DDS Jordan Mikel, RDH Karen DiMarco

Michael DiTola, DDS Sheila Norton, RDH Jack Naughton

Blake Davis, DDS Laura Schaffner, RDH Brian Loke

Keavin Mcintosh, DMD Laura Stoddard, RDH Jon Roberton

Stanley Tang, DDS Megan Harkness, RDH Lee Clement

Aaron Shepard, RDH

Samantha Shira, RDH

Lynn Stedman, RDH

Pierce College Dental Hygiene Students

Eastern Washington University Dental Hygiene Students

Aseptico, Inc., CAO Group, Cetylite, Inc., DentalVibe, Dentsply Pharmaceuticals,

Gebauer Company, Injex, LED Dental Inc ( Velscope) , Milestone Scientific, MMJ
Labs, Onpharma, Practicon, St. Renatus, LLC, Septodont USA
We appreciate the considerable contributions of Sean Boynes, DDS and
Royann Royer, RDH to the 2nd edition of this text, especially the addition
of the Nitrous Oxide-Oxygen chapter.
We extend a special thanks to Patrick McKeown, Dysfuntional Breathing
Practitioner, Asthma Care Ireland, Republic of Ireland for his contributions to
our understanding of breathing and anxiety.

We thank our publisher, Pearson Education, for their invaluable

assistance and support. Special thanks to Nikki, Patty and Saraswathi for
all your help on the "home stretch':

We acknowledge the lifelong vision and commitment to safety and comfort in

oral healthcare of Dr. Stanley Malamed, DDS, and dedicate this edition to the
memory of a truly brilliant modern pioneer, Dr. John Yagiela, DDS, PhD.

viii
Section 1-Pain Control Concepts Dental Hygiene Program
Johnson County Community College
Chapter 2-Fundamentals of Pain Management Overland Park, Kansas

Ann Eshenaur Spolarich, RDH, PhD Chapter 17-Local Anesthesia Complications

Clinical Associate Professor and Management
USC School of Dentistry
Los Angeles, California Sean G. Boynes, DMD, MS, DAs
Course Director of Clinical Medicine and Pharmacology Director of Dental Medicine
Arizona School of Dentistry and Oral Health Public Health Dentistry
Mesa, Arizona CareSouth Carolina
Clinical Instructor, Dean's Faculty Society Hill, South Carolina
University of Maryland Dental School Chief Consultant/Owner
Baltimore, Maryland Dentist Anesthesiologist
Dental Medicine Consulting
Jackie Foskett, RDH, BA, CHT Florence, South Carolina
General and Periodontal Practice ( Retired )
Certified Clinical Hypnotherapist
Holistic Counselor and Educator
Section V-Special Considerations
Founder/Owner of Healing Hypnotherapy for Local Anesthesia
Newcastle, Washington
Chapter 18-lnsights for Fearful Patients

Section Ill-Injection Fundamentals Marilynn Rothen, RDH, MS

Clinical Assistant Professor
Chapter 9-Local Anesthetic Delivery Devices Associate Director Dental Hygiene Master of Science in Oral
Biology Program
Mark N. Hochman, DDS
Department of Oral Health Sciences
Private Practice Limited to Periodontics and Orthodontics
Manager, Regional Clinical Dental Research Center and Dental
Specialized Dentistry of New York
Fears Research Clinic
New York City, New York
School of Dentistry
Clinical Associate Professor
University of Washington
New York University, College of Dentistry
Seattle, Washington
New York City, New York
Clinical Director and Consultant Agnes Spadafora, RDH, BS
Milestone Scientific, Inc. Department of Dental Public Health Sciences and Dental Fears
Livingston, New Jersey Research Clinic ( Retired )
School of Dentistry

Chapter 1D-Patient Assessment for Local Anesthesia University of Washington

Seattle, Washington
Sean G. Boynes, DMD, MS, DAs
Director of Dental Medicine Chapter 19-lnsights from Pediatric Dentistry
Public Health Dentistry
CareSouth Carolina Gregory L. Psaltis, DDS
Society Hill, South Carolina Specialist in Pediatric Dentistry

Chief Consultant/Owner Olympia, Washington

Dentist Anesthesiologist
Sean G. Boynes, DMD, MS, DAs
Dental Medicine Consulting
Director of Dental Medicine
Florence, South Carolina
Public Health Dentistry
CareSouth Carolina
Chapter 11-Fundamentals for Administration Society Hill, South Carolina
of Local Anesthetic Agents Chief Consultant/Owner
Dentist Anesthesiologist
Kimberly Stabbe, RDH, MS Dental Medicine Consulting
Professor of Dental Hygiene Florence, South Carolina

ix
X CONTRIBUTORS
Chapter 20-lnsights from Specialties:
Oral Surgery-Melanie Lang, DDS,
Specialist in Oral Surgery
Spokane,Washington
Periodontics- William C. Lubken, DMD
Specialist in Periodontics
Gig Harbor,Washington
Periodontics-Mark N. Hochman, DDS
Private Practice Limited to Periodontics and Orthodontics
Specialized Dentistry of New York
New York City,New York
Clinical Associate Professor
New York University,College of Dentistry
New York City,New York
Clinical Director and Consultant
Milestone Scientific,Inc.
Livingston,New Jersey
Endodontics-Albert (Ace) Goerig, DDS,
Specialist in Endodontics
Olympia,Washington
Section VI-Nitrous Oxide-Oxygen
Sedation
Chapter 21-Fundamentals for the Administration
of Nitrous Oxide-Oxygen Sedation
Sean G. Boynes, DMD, MS, DAs
Director of Dental Medicine
Public Health Dentistry
Reviewers
Sheryl Armstrong,RDH,BSDH,MEd©
Mohave Community College
Colorado City,Arizona
Sandra Beebe,RDH,PhD
Southern Illinois University
Carbondale,Illinois
Roderic Caron,DMD
New Hampshire Technical Institute
Concord,New Hampshire
Kathleen Di\mbrisi,RDH,MS,PhD
The Community College of Baltimore County
Baltimore, Maryland
Terry Dean,DMD
Western Kentucky University
Bowling Green,Kentucky
David Lund,DDS
Truckee Meadows Community College
Reno,Nevada
CareSouth Carolina
Society Hill,South Carolina
MD Chief Consultant/Owner
Dentist Anesthesiologist
Dental Medicine Consulting
Florence,South Carolina
Royann Royer, RDH, MPH
Educator,Consultant,Clinical Hygienist
Public Health Dentistry
Southcentral Foundation
Anchorage,Alaska
Advisory Member,Retired Faculty
University of Alaska Anchorage
Anchorage,Alaska
Fred Quarnstrom, DDS, FADSA, FAGD, FICD, CDC
Dental Anesthesiologist
Private Practice
Beacon Hill Dental Associates
Seattle,Washington
MS
Affiliate Assistant Professor
Department of Oral Health Sciences
Dental Public Health Sciences
School of Dentistry
University of Washington
Seattle,Washington
Elaine Madden,AS,BS,MEd
Cape Cod Community College
West Barnstable,Massachusetts
Julius N. Manz,DDS
San Juan College
Farmington,New Mexico
Linda Munro,RDH
Portland Community College
Portland, Oregon
Debra Sidd,RDH,RF,MEd
Normandale Community College
Bloomington,Minnesota
Marsha Voelker,CDA,RDH,MS
University of Missouri-Kansas City
Kansas City,Missouri
Paula Watson,MS,RDH,RDH,AP
University of the Pacific
Stockton,California
Kathy Bassett, BSDH, RDH, MEd, is professor and clini­
cal coordinator in the Department of Dental Hygiene at
Pierce College, Lakewood, Washington. She has more than
35 years of clinical experience in both local anesthesia and
restorative expanded functions and currently serves as
course lead for the Local Anesthesia curriculum at Pierce
College. Along with student researchers, she is investigat­
ing the effectiveness of using CCLAD technology as pri­
mary devices when teaching local anesthesia techniques.
Ms. Bassett actively teaches dental hygiene pre-licensure
courses in local anesthesia and restorative expanded func­
tions for the Pacific Northwest Dental Hygiene Institute, also
at Pierce College. In addition, she is an affiliate professor in
the Departments of Oral Health Sciences and Periodontics
at the University of Washington, School of Dentistry.
Arthur DiMarco, DMD, is director of the RIDE program
and affiliate faculty of restorative dentistry at the University
of Washington, School of Dentistry at Eastern Washington
University (EWU), Spokane, Washington, where he is also
professor in the Department of Dental Hygiene. A veteran
of nearly 30 years of clinical practice and more than 20 years
of dental hygiene and dental education, he is course direc­
tor for the Pain Control curriculum for both dental hygiene
and dental students in Spokane. His most recent research
involved the method of application of a fast-acting topical
anesthetic before administering AMSA injections.
Doreen Naughton, RDH, BSDH, has more than 30 years
of clinical experience, including sole proprietorship of
Dental Hygiene Health Services for the past 25 years.
She is an affiliate instructor in the Departments of Oral
Health Sciences and Periodontics at the University of
Washington, School of Dentistry. Additionally, she served
6 years as administrator and instructor of dental hygiene
pre-licensure courses, including local anesthesia and restor­
ative functions, for the University of Washington's Continuing
Dental Education program.
Ms. Bassett, Dr. DiMarco, and Ms. Naughton have pre­
sented hundreds of local, regional, state, national, and in­
ternational continuing education programs on topics that
include didactic and clinical courses in local anesthesia
for dental healthcare educators, professionals, and corpo­
rate clinical educators. In addition, Ms. Bassett and Dr.
DiMarco have collaborated on numerous publications on
the topic of local anesthesia. Between them, they have re­
ceived numerous honors and awards in recognition of out­
standing contributions and dedication to dental hygiene
and dental education, characterizing excellence in teach­
ing, mentoring, and devotion to student achievement. Ms.
Naughton has received significant state and national rec­
ognition for her outstanding contributions to the profes­
sion of dental hygiene.
xi
 Techniques for Successful Local Anesthesia:
For Dental Professionals DVD

Techniques for

SUCCESSFUL
LOCAL
ANESTHESIA
for Dental Professionals

Royann Royer
Carlene Paarmann

Royann Royer & Carlene Paarmann

ISBN-1 0: 0132725398 • ISBN-13: 9780132725392

Techniques for Successful Local Anesthesia was developed
in conj unction with the authors of this textbook as a
companion to the text and is calibrated to the recommen­
dations and guidelines specified throughout.
This DVD provides clear, easy-to-follow visual learning
components divided into several units:
The first unit discusses Basic Injection Techniques
that should be utilized when administering any type of
local anesthesia injection. It is further divided into
Maxillary and Palatal Injections (Unit 2) and Man­
dibular Injections (Unit 3). The video then provides
demonstrations of Adjunct Injections and Techniques
(Unit 4), which include a periodontal ligament in­
j ection and a video on Adjunct Techniques and
Equipment. Unit 5, Supplemental Videos, contains
additional video clips provided by the authors of
Local Anesthesia for Dental Professionals. A Resource
Unit (Unit 6) contains a presentation on injection tech­
niques for pediatric patients as well as two "Summary
Charts" to print and use as a reference in the operatory.
The DVD will assist the reader of this text by demon-
strating the techniques presented by the authors and will
enhance the learning process of providing successful and
comfortable injections to your patients.

Sold separately at www.pearsonhighered.com

xii
Chapter 1 Perspectives on Local Anesthesia for Dental Professionals

Chapter 2 Fundamentals of Pain Management

Chapter 3 The Neuroanatomy and Neurophysiology of Pain Control

··························································· CD ························································· ·

Pe rspectives on Loca l An esth esi a

for Denta l Profession a l s

OBJECTIVES KEY TERMS

• Defi n e a n d d i scuss the key terms i n t h i s cha pter. d e nta l l oca l a n esthesia
p rovi d e rs 3
• Id e n tify a vari ety of denta l l oca l a n esthesia providers in North
fu n d a m entals of p a i n
A m erica . m a n a g e m ent 3
• D i scuss the respo n si b i l ities of loca l a n esthesia providers. tro u b l eshooti n g 3
 CHAPTER 1 PERSPECTIVES ON LOCAL ANESTHESIA FOR DENTAL PROFESSIONALS
• 3

Introd u ction
A recent Gallup p o l l focusing on honesty a n d ethical
standards placed dentists at the number 5 spot out of 22
professional occupations, ahead of police officers, chiro­
practors, and members of the clergy (Gallup, 2012). High
levels of confidence are likely similar for dental hygienists,
as well.
As trustworthy as patients may find dental profes­
sionals, it only takes a little pain for patients to begin to
lose confidence, a circumstance that is wholly avoidable.
This text is designed to leverage knowledge and skills in
order to optimize patient confidence. It represents a col­
laboration of experts in the field of dental local anesthesia
and nitrous oxide-oxygen sedation to focus clinicians on
the relevance of technique factors, on appropriate integra­
F I G U R E 1 -1 Mastery of Techniques. Mastering a wide variety
tion into clinical decision making, and on troubleshooting
of techniques is critical to safe and effective pain control.
strategies (assessment of inadequacies and their resolu­
tions). These are critical skills every dental professional
can and should have. Confidence in pain control strategies, responding to patient factors, integrating evidence-based
ready troubleshooting skills, and familiarity with pain con­ knowledge, and understanding relevant drugs, their effects,
trol alternatives are within the grasp of every clinician. indications, and contraindications. Fundamentals also
include developing clinical decision-making skills and
Local Anesthesia Scope of Practice mastering a wide variety of techniques and appropriate
modifications (see Figure 1-1 •) .
Local anesthetics have been available in dentistry since
Factors critical for safe and effective local anesthesia
1884. D entists have been able to deliver local anesthetic
are well within the grasp of any individual who adminis­
drugs in cartridge form since 1921. Dental hygienists were
ters local anesthetic drugs regardless of their ultimate
first licensed to deliver local anesthetics in the state of
degree or educational pathway.
Washington, in 1971.
The roles of non-dentist clinicians have expanded in
recent years. Today, in most states and provinces, dental
local anesthesia providers, including dental hygienists (and
-�.h. ()J>.t.e. r.. 9. LJ.E! �� i_() .':1 � ........................................... .
in some states and provinces, mid-level and/or expanded These questions are provided to generate discussion.
function providers) are allowed to administer local anes­
1. Identify a variety of local anesthesia providers in
thesia for effective pain control of the oral cavity.
North America.
Specific requirements for dental hygienists and mid­
level providers vary regarding the type, degree, or extent 2. Identify and discuss the importance of the
of inj ections, as well as the required extent of supervision, fundamentals of pain management.
education, and examination. Clinicians must be knowl­
3. Identify and discuss the responsibilities of local
edgeable regarding the specifics of the practice acts gov­
anesthesia providers.
erning their particular practice locations (Bassett, Boynes,
& DiMarco, 20 1 1 ) .
Refe re n ces
Philosophy o f Responsibility
Bassett, K. B. , Boynes, S . G. , & DiMarco, A . C. (201 1 ) .
Providing safe, effective, and appropriate pain control Understand the rules. Dimensions of Dental Hygiene, 9(7),
is a responsibility of all dental local anesthesia provid­ 38, 40-41.
ers. This requires knowledge of and competency with Gallup. ( 201 2, December 3) . Congress retains low honesty
the fundamentals of pain management, which include rating. Retrieved July 31 , 201 3, from http://www.gallup.com/
conducting comprehensive assessment, recognizing and poll/1 59035/congress-retains-low-honesty-rating.aspx

Visit www.pearsonhighered.com/healthprofessionsresources to access the student resources that accompany

this book. Simply select Dental Hygiene from the choice of disciplines. Find this book and you will find the
complimentary study tools created for this specific title.
··························································· ® ··························································

Fu nda m enta l s of
P.a i m IMia m agemilemrt!

OBJECTIVES KEY TERMS

• Defi n e a n d d i scuss the key terms i n this cha pte r. a cute p a i n 6

c h ro n i c p a i n 6
• D iscuss the va l u e of p a i n as a p rotective response.
cogn itive d istra ction 1 0
• D iscuss fa ctors that ca n contri bute to a n i n d iv i d u a l's response d e b riefi n g 9
to a pai nfu l experi e n ce . fig h t or fli g h t 8
• D iscuss t h e t h ree g e n e ra l types o f p a i n . n e u ropathic p a i n 7
nociceptive p a i n 6
• D iffe renti ate betwee n acute a n d c h ro n i c pa i n . nocicepto rs 6
• Explain the d ifferences between pain perception a n d nociception. pain 5
• D iscuss the physio l o g i ca l reactions of the sym pathetic n e rvou s p a i n d isord e rs 8
p a i n t h res h o l d 5
system re l ated t o pa i n .
p a i n to l e ra n ce 5
• D i scuss a n xiety a n d fea r as they re l ate t o su ccessfu l a n esthesia . p o l ym o d a l 6
• Give exa m p l e s of strate g i es that ca n h e l p patie nts cope with PREP 9
fea r and a nxi ety. p rotective res ponse 5
• D i scuss the i n fl u e n ce of p revi o u s p a i n expe rien ces on the psyc h o g e n i c fa ctors 8
re l axati o n response 1 0
a b i l ity to a d m i n ister loca l a n esthetic i n jecti o n s.
sensory m o d a l ity 6
somatic p a i n 6
sym pathetic n e rvous
system 8
viscera l p a i n 6
visua l izati o n 1 0

4

Introd u ction
Pain control i n dentistry requires the study o f local anesthesia
and an understanding of the science of pain. This chapter will
provide an introduction to the fundamentals of pain. It will
focus on pain as having both physiological and psychological
aspects. Categories of pain and factors that have an effect on
the ability to tolerate pain will also be discussed.
Pain Pe rspectives
Pain Experience
Pain is unique and is reported subj ectively. Even within an
individual's unique experience, the perception of pain on a
given day at a given time is not necessarily identical to a pre­
vious or future perception of pain in response to an identical
stimulus. Pain perception (and reactions to the perceptions
of pain) cannot be described as necessarily proportional to
the intensity of physical injury or to the degree of harm.
An individual's pain experience is influenced by a
number of variables. For example, gender provides both
genetic and hormonal influences. Gender also may add
many complex components, including socially constructed
roles and relationships, personality traits, attitudes, behav­
iors, values, and degrees of power and influence. Other
variables, such as age, physical health, mental health, emo­
tional status, expectations, previous experiences, learned
responses, and ethnic and cultural norms, also impact the
experience of pain and individual reactions to it.
The definition of pain provided by the International
Association for the Study of Pain (IASP) describes it as a
negative experience (see Box 2 1 •) (Merskey & Bogduk,
1994). While the experience of pain is accurately described
in negative terms, rapid s e quences of perception and
response that make up the experience also serve a protec­
tive function, a decidedly positive benefit.
Avoidance of pain is a strong, innate trait. In dentistry,
painful experiences can lead to a strategy of avoiding pain
and, therefore, treatment. Pain can lead to anxiety and fear,
which may result in heightened perceptions of pain, which
in turn may cause further avoidance of dental care. The abil­
ity to identify factors that can contribute to painful expe­
riences and proactive strategies to avoid unnecessary pain
can ensure patient comfort during treatment (Howard,
2007; Pappagallo & Chapman, 2005; Spitzer, 2004) .
The I nternatio n a l Association for the Study of Pa i n defines
pain as "an u n p l easant sensory and emoti o n a l experience
associated with actual or potentia l tissue damage, or described
i n terms of such damage" (Merskey & Bogduk, 1 994).
"Defini t i o n on Pain". Copyright© 2014 by Internationa
Association for the Study of Pain. Used by Permission of lnterna-l
Source:
tiona I Associati o n for the Study of Pain.
• •
• used interchangeably despite distinct differences. Patients
: . . . . . . . . . . . . . . . . .
CHAPTER 2 FUNDAMENTALS OF PAIN MANAGEMENT
• 5
Protective Respo n se
As a physiological reaction to the environment, pain is a
protective response, protecting the body from harm. This
protection is rapid, reflexive, and subconscious.
An example of a protective response to pain is known
as a withdrawal reflex. This reflex prevents damage by
removing tissues from harm when harm is sensed or is
imminent. When a hot stove is touched, for example, hands
are quickly withdrawn from the stimulus (heat) . Without
protective reflexes, the ability to maintain a healthy body
would be seriously compromised. This is the case when an
individual with a spinal cord inj ury is not able to feel sen­
sations or initiate movement below the level of injury. The
normal protective neuronal activity and subsequent mus­
cular reaction are absent, and there is a constant need for
monitoring and repositioning in order to avoid pressure
sore injuries or injuries caused by thermal stimuli.
The protective response is also linked to behavior.
If an individual has been stung by a wasp in the past, the
mere sight of a wasp might cause the individual to react
in order to avoid a sting. This withdrawal is governed by
memory (Howard, 2007).
Pain T hresho l d ve rs u s Pain Tole ra n ce
The terms pain threshold and pain tolerance are not syn­
onymous. Pain threshold may be defined as the point
at which a stimulus first produces a sensation of p ain
( Taber's Cyclopedic Medical Dictionary [Taber's], 1997 ) .
Pain thresholds a r e innate a n d a r e highly reproducible
in individuals. They do not usually change appreciably
-
over time. An individual's p ain threshold is a function
of their physiological reaction to painful stimuli. For
example, in dentistry a pulp tester is used to determine
viability of teeth. Patients will respond when estab­
lished levels of stimulation are perceived. This identifies
threshold of pain.
Pain tolerance may be defined as an individual's reac­
tion to painful stimuli. It indicates the amount of pain an
individual is willing or able to endure. Tolerance can vary
from day to day and from appointment to appointment,
and may be influenced by current events and stresses. It
can also be altered by environment, experience, and social
attitudes. Research has shown that gender and genetics
also play key roles in understanding individual variations
in pain perception and stimulus processing ( D i onne,
Phero, & Becker, 2002) .
Common pain stimuli produce highly variable reactions
from individual to individual. When using pulp testers, for
example, pain is elicited at reproducible levels, but individu­
als may react to the electric current in markedly different
ways. Both emotional and psychological factors influence
their reactions. These factors are modified by the signifi­
cance individuals place on their present circumstances.
The terms pain tolerance and pain threshold are often
. . . . . . . . . . . . . . . . . . . . . . • may state that they have very low pain thresholds while
6 SECTION I PAIN CONTROL CONCEPTS
•
they are actually relating that they are not able to tolerate
a lot of pain.
Pre-appointment medications such as anti-anxiety and
anti-inflammatory agents, and local anesthesia adminis­
tered during appointments, are used to modify a patient's
tolerance to treatment. It is also important to recognize
that an individual who suffers from long-term pain may
have altered responses and an intolerance to pain of any
nature. Pre-treatment assessment in this area can improve
clinical experiences (American Psychiatric Association,
2000; Pappagallo & Chapman, 2005 ) .
Pain D u rati o n
Pain may b e categorized i n a variety o f ways. A common
classification categorizes pain according to its duration,
acute or chronic. Acute pain may last from a few seconds
to no more than 6 months depending on causative factors.
It is generally caused by tissue damage from injury or dis­
ease. Individuals suffering from acute pain expect to get
better and adopt behaviors that either remove or ease the
cause or causes of pain. For example, a patient experienc­
ing postoperative dental pain may rely on pain relievers
or ice packs to stop the pain. Pain is often a strong motiva­
tor for seeking treatment, regardless of a patient's level of
dental anxiety and fear.
Chronic pain may be defined as pain that persists for
more than 6 months with or without an identifiable cause.
The longer acute pain continues, the more likely it is to
become chronic. Occasionally, patients who suffer from
chronic pain tend to lose hope of getting better, providing
an unfortunate pathway to depression.
Individuals suffering from chronic pain may be re­
ferred to specialized clinics with experience in managing
long-term patterns of pain. Pain clinics provide a wide
variety of services, including evaluation, education, and
treatment (physical therapy, massage, and acupuncture) .
They also teach coping skills that can influence reactions
to pain and modify behavior through appropriate use of
medications and techniques such as biofeedback (Howard,
2007).
Pain a n d Noci ceptio n
Sensory receptors detect a variety of stimuli that are then
relayed to the central nervous system (CNS) for interpreta­
tion. Specific receptors are associated with each type of sen­
sory input. For example, there are specific taste receptors on
the tongue that detect sweet, sour, bitter, and salt. In the eye
there are two types of photoreceptors: cones and rods.
The ability of a stimulus to be detected by a specific
receptor is known as a sensory modality. Sensory modali­
ties include hearing, sight, touch, taste, and sound. Changes
in temperature are detected by thermoreceptors. Changes
in pressure are detected by mechanoreceptors. Altera­
tions in body chemicals are detected by chemoreceptors
(Howard, 2007; Pappagallo & Chapman, 2005).
S e n s o r y receptors that d e t e ct inj ury are c a l l e d
nociceptors ( s e e Figure 2 - 1 •) . Unlike o t h e r sensory
receptors, nociceptors are activated by inj ury and relay
sensory input whether or not individuals are aware that
inj ury has occurred. This process is influenced by an indi­
vidual's age, general health, and genetics (Nani, Mellow,
& Getz, 1999).
Nociceptors differ in another important way from
other sensory receptors in that they are polymodal, re ­
sponding to all types of stimuli. In addition to activat­
ing receptors specific for them, thermal, mechanical, and
chemical stimuli can all activate nociceptors, which relay
pain information to the CNS. Despite obvious differences
between these stimuli, all can be perceived by nociceptors
as painful.
Nociceptors also differ from other sensory recep­
tors in that nociceptors never adapt to stimulation. In the
presence of constant stimulation, nociceptors will always
respond to stimulation. This is a key aspect of the protec­
tive response to pain. Sensory warnings are constantly pro­
vided when injury is pending or occurring.
As previously noted, experience or perception of pain
does not lend itself well to obj ective measurement. While
this is an accurate statement, pain intensity rating scales
nevertheless can be useful for both patients and clinicians.
They provide patients with a means of communicating
the degree of pain experienced, and they provide clini­
cians with an opportunity to respond appropriately. An
example of a subj ective pain intensity measurement tool
is the Wong-Baker FACES Pain Rating Scale. This simple
numeric scale (with associated facial expressions) uses "0"
to represent no pain (very happy face) and "5" to repre­
sent severe pain (crying face) (see Figure 2-2 •) . Other
scales use similar graduated numbers to report the degree
of pain experienced.
Pain Classification by Etiology
Pain may b e categorized according t o its etiology (American
Psychiatric Association, 2000; Howard, 2007), as follows:
1. nociceptive pain
2. neuropathic pain
3. pain disorders associated with psychogenic factors
In addition, in response to nociceptive input, fear and
other physical conditions can alter the ability to receive,
transmit, interpret, and respond to pain.
Nociceptive Pain
Nociceptive pain is caused by inj ury or disease in body
tissues. This pain may be constant or intermittent and
often escalates with movement. Nociceptive pain can
be further subdivided into somatic and visceral pain.
Somatic nociceptive pain o ccurs on superficial struc­
tures such as skin and muscles and is caused by trau­
matic inj uries. The resulting pain may be sharp, aching,
 CHAPTER 2 FUNDAMENTALS OF PAIN MANAGEMENT
• 7

Pain
perception point -- --i�---'----.:<T'---;;..__... 1

@ Dorsal horn; location of

Substantia gelatinosa
(pain signal modified)

Spinal ganglia

A-delta fibers
(last transmission of
sharp, localized pain)

F I G U R E 2-1 Nociceptors. Nociceptors are sensory receptors that detect when a body tissue has been injured.
Source: BALL, JANE W.; BINDLER, RUTH C., PEDIATRIC NURSING: CARING F OR CHILDREN, ESSENTIALS VERSION,
4th, © 2008. Printed and Electronically reproduced by permission of Pearson Education, Inc. Upper Saddle River, New Jersey.

or throbbing. Visceral nociceptive pain occurs in internal Neuropathic Pain

body cavities and is caused by compression, expansion, Neuropathic pain is caused by nerve injury or dysfunction
stretching, and infiltration. It usually produces squeez­ of the sensory nerves in the central or peripheral nervous
ing or gnawing sensations (Howard, 2007; Pappagallo & systems (Howard, 2007 ; Pappagallo & Chapman, 2005 ) .
Chapman, 2005 ) . There are numerous types o f neuropathic pain, most of
8 SECTION I PAIN CONTROL CONCEPTS
•
0 2
No Hurt Hurts Hurts
Little Bit Little More
F I G U R E 2-2 Wong-Baker FA CES Pain Rating Scale. Instructions: Point to each face
using the words to describe the pain intensity. Ask the child to choose face that best
describes own pain and record the appropriate number.
Source: Copyright 1983,Wong-Baker FACES® Foundation, www.WongBakerFACES.org. Used
with permission . Originally published in Whaley & Wongs Nursing Care of Infants and Children.
© Elsevier Inc.
which are complex and frequently chronic in nature. They
may have inflammatory, noninflammatory, and/or immune
system components. Pain may be generated in the CNS
such as phantom pain from a missing limb or tooth, or it
may occur because of what is referred to as peripherally
generated polyneuropathy, as seen in diabetes. Mononeu­
ropathy is usually associated with a single nerve injury or
compression, which is seen in trigeminal neuralgia, carpal
tunnel syndrome, and post-herpetic neuralgia.
Pain Disorders Associated with Psychogenic Factors
Pain disorders associated with psychogenic factors are re­
lated to mental or emotional issues that affect the experi­
ence of pain. They are diagnosed only after other causes
of pain have been eliminated . They are also diagnosed
far less frequently than nociceptive and neuropathic pain.
Although not attributable to specific inj uries or pathol­
ogy, the experience of pain is real and can occur at any age,
manifesting as head, stomach, chest, or muscle discomfort,
or it may occur in any other location or combination of
locations. Individuals with depressive or anxiety disorders
may experience complications with any type of pain. These
individuals may report pain beyond typical intensities and
durations. In some instances, previously diagnosed physi­
cal pain from known pathogenic origins can be increased
or prolonged by psychogenic factors.
Pain is multidimensional and often requires more than
one treatment modality. These may include psychotherapy,
biofeedback, hypnosis, and antidepressant and nonnarcotic
analgesic medications. Patients with pain disorders may re­
spond differently to dental pain (American Psychiatric Asso­
ciation, 2000; Howard, 2007; Pappagallo & Chapman, 2005).
Sympathetic Ne rvo u s System a n d Pa i n
In response to pain, the CNS simultaneously directs acti­
vation of the sympathetic nervous system. The sympathetic
nervous system stimulates the adrenal medulla, resulting in
release of norepinephrine and epinephrine (see Chapter 6,
"Vasoconstrictors in Dentistry"). These neurotransmitters
mediate so-called "fight or flight" mechanisms, resulting
in a host of potential reactions, including increased heart
3 4 5
Hurts Hurts Hurts
Even More Whole Lot Worst
rate and blood pressure ; dilation of the pupils and the
bronchial and skeletal muscle vasculature ; and constric­
tion of mesenteric vessels. B oth anticipation of pain and
the perception of pain stimulate this response.
If these reactions occur, they can be exacerbated by
the psychological state of a patient during a dental appoint­
ment. Fearful patients often demonstrate similar sympa­
thetic nervous system reactions before, during, and after
injections. While physical manifestations are similar and are
typically of short duration, all adverse reactions to dental
anesthesia require prompt and appropriate management,
regardless of their etiology (Dionne, Phero, & Becker, 2002;
Howard, 2007; Pappagallo & Chapman, 2005).
Pain Ma n a g ement Impli cat i o n s
fo r Dentistry
The maj ority of patients willingly schedule and attend
their dental appointments. Previous dental experiences
have been generally positive. Some avoid dental treat­
ment, primarily because of fears surrounding the admin­
istration of local anesthesia. Their experiences have been
negative, and they are convinced there is little reason to
expect better. In other words, fears override the need for
dental treatment. In order to develop positive treatment
interactions, it is important for clinicians to understand
the etiology of the fear and pain experience. B oth physi­
ological and psychological factors contribute to difficulties
related to treatment.
It has been reported that the main reason individuals
avoid dental appointments is fear (Naini, Mellow, & Getz,
1999) . About 40 % of patients report some level of anxiety
related to dental treatment, and roughly 5 % avoid den­
tistry because of fear of inj ections. Patients experience fear
on a continuum ranging from mild anxiety to phobia.
Fear can be a barrier to obtaining adequate anesthe­
sia. Fearful patients are typically no less concerned than
others about their need for dental treatment but fear can
prevent them from experiencing successful treatment.
Some patients are fearful only of inj e ctions and report
their anxiety and fear subsides following the inj ection. As­
sessing and addressing fear before inj ections can improve
 CHAPTER 2 FUNDAMENTALS OF PAIN MANAGEMENT
• 9

the results of anesthesia. Clinicians need to be aware of

strategies associated with treating anxious and fearful
patients (Dionne, Phero, & Becker, 2002; Fiset, Milgram,
& Weinstein, 1985 ; Milgram, Weinstein, & Heaton, 2009).
To h e l p patie nts cope with a n x i ety a n d fear:

1. Prepare by uti l iz i n g re l axati o n tech n i q u es s u c h as

Patient Ma n a g ement Pe rspectives focused b reath i n g , d i stract i o n s u c h as music o r visu a l ­
Everyone working in dental settings can offer support to anx­ izat i o n , a n d m u s c l e re l axat i o n .
ious or fearful patients. Dental personnel can identify fearful 2. Rehearse proce d u res a l l o w i n g patie nts to p ractice
patients at the time of initial contact whether by telephone co ntro l and s e l f-ca l m i n g tech n i q u e s .
or in person. As with nondental-related fears, it may not be 3. Empower patie nts w i t h strate g i es that g ive t h e m con­
easy for fearful patients to acknowledge their dental fears or tro l d u r i n g p roce d u res s u c h as ra i s i n g a hand to ask
the degree of their fears. Deliberate behavior by clinicians t h e c l i n i c i a n to sto p .
can be helpful in developing successful patient experiences 4. Praise patie nts fo r u s i n g s pecific cop i n g tech n i q ues
• •

and can create an environment that encourages discussions t ta � ul h

of fear. For example, using controlled, calm speech and posi­
tive demeanor conveys comfort and instills confidence. Signs
of impatience or disapproval should be avoided.
A standard protocol for all patients including those
with specific fears, will incorporate the following:
1. Ask about previous dental experiences and be attentive
to responses
2. Assure that difficulties during past experiences can be
managed and overcome
3. Involve patients when identifying strategies to help
manage anxiety and fear
Some strategies to help patients cope with anxiety and
fear include a sequence of steps the authors refer to as
PREP (Prepare, Rehearse, Empower, and Praise). Apply­
ing a PREP strategy can build trust and provide reassur­
ance. These steps can be found in Box 2-2 •, and when used
along with a process known as debriefing can further build
trust and reassurance. Clinicians may find the use of these
stress-reducing techniques helpful for themselves as well.
The debriefing process can be useful when managing
fearful patients. This process allows for discussion periods
at the end of appointments to give patients opportunities
to relate which aspects of treatment went well and which
aspects did not go well. Discussions of treatment to be ac­
complished at future appointments can be quite helpful,
: • • • • � � :� � � : : :� : ��.. . . . . . . . . .
. . . . . . . . . . . . .
particularly if they rely heavily on patient input when
determining how ambitious the next appointment should
be. Plans for modifying aspects that were identified as
not going well can be discussed and then applied to sub­
sequent appointments. By proceeding in this manner, the
patient not only agrees to go to the next step but also has
an active role in determining the content of the step.
It is important that adequate time is scheduled for the
debriefing process. Rushing through discussions does little
to reassure patients that recommendations will be heeded.
Power of Suggestion and Vocabulary
Positive communication and establishing trust are impor­
tant with all patients but especially important for those
who are anxious or fearful. Trust provides a foundation for
relieving anxiety and fear. The power of suggestion is well
documented in the literature. Both pediatric and adult pa­
tients can attach broad interpretations to the terminology
that is used during dental inj ections. Careful selection of
words can reduce negative imagery that may be associated
with words such as "poke," "pinch," " sting," "burn," and
"hurt" (Milgram, Weinstein, & Heaton, 2009). Additional
strategies to enhance positive communication are sug­
gested in Table 2-1 •·

Table 2-1 Strategies to Enhance Positive Communication

• Display a genuinely warm and caring attitude

• Review treatment plan addressing fears, including of the unexpected and of loss of control

• Obtain permission to begin, addressing fear of loss of control if necessary

• (
Establish patient control strategy time-out signal such as raising hand to stop )
• (
Direct the focus on positive outcomes "You may feel a bit of pressure." )
• (
Acknowledge and compliment success "You did great with the anesthesia today!" )
• (
Create positive expectations "That went well today and I expect your next appointment will too." )
10 SECTION I PAIN CONTROL CONCEPTS
•
COG N ITIVE DI STRA CTION The practice of distraction that
actively shifts a patient's focus away from a stressful situ­
ation to a less stressful point of focus is considered cog­
nitive distraction. Distraction is thought to be one of the
easiest and most familiar coping strategies employed by
dental professionals (Milgrom, 2009). Distraction is more
useful for short-duration procedures on patients with mild
to moderate anxiety; however, it may be less effective dur­
ing the administration of local anesthetics compared with
other procedures. Table 2-2 • suggests a variety of distrac­
tion techniques that can be useful for dental patients.
VISUA LIZATION Visualization (also referred to as guided
visualization and guided imagery) is a cognitive strategy
to help patients reduce stress and can be especially ben­
eficial in dentistry to manage fears, particularly fear of
needles. Patients who are mentally and physically relaxed
usually experience less discomfort compared with those
who are tense (Milgrom, Weinstein, & Heaton, 2009 ) .
Visualization often accompanies physical relaxation, a
behavioral strategy.
Tension can reduce the supply of air reaching the lungs.
Reduced oxygenation contributes not only to anxiety and
stress but also to fatigue and depression, increasing the
perception of stress (Milgrom, Weinstein, & Heaton, 2009) .
What is known as focused breathing can increase oxygen­
ation and help patients relax their muscles; at the same time
it can help provide an overall sense of relaxation. Visualiza­
tion can enhance this relaxation by distracting patients from
sources of stress and can provide the relaxation needed to
cope with physical discomforts or their expectation.
Relaxation Response
The relaxation response is a restful state that modifies
physical and emotional responses to stress (Benson, 2000) .
Parasympathetic pathways that allow recovery from stress
(fight and flight) are activated by this response that low­
ers heart and respiratory rates, blood pressure, and mus­
cle tension. Physiological relaxation when incorporating
Table 2-2 Suggested Distraction Techniques*
• Light, casual conversation or guided relaxation
• Gate control strategies and devices
• pressure applied with cotton swab to palatal tissues
• gentle lip shaking during needle insertion
• the use of vibration devices
• Audio devices with headphones for music, audio books (selected by patient)
• Television, video devices, and audiovisual glasses (not for highly anxious)* *
*Adapted from: DiMarco, A. C., Bassett, K.B., Foskett, J.M. (2012). Mind over Matter. Dimensions of Dental Hygiene. Santa Ana,
CA: Belmont Publications.
**Frere, C.L., Crout, R., Yorty, J., McNeil, D.W. (2001). Effects of audiovisual distraction during dental prophylaxis. Journal of the American Dental
Association, 132(7): 1031-1038.
guided visualization techniques enhances patient coping
skills (Milgrom, Weinstein, & Heaton, 2009) .
When patients are well informed, better management
of stress is possible. Explaining the benefits of relaxation to
patients ahead of time is an important component of success­
ful relaxation response strategies. Securing permission and
consent before guiding patients through a relaxation process
is necessary. (See Table 2-3 •: Suggestions for Preparing
Patients for Guided Relaxation and Guided Visualization.)
Guided visualization usually starts with guided physi­
cal relaxation or focusing patients on what has been re­
ferred to as their "inner world" (Naparstek, 1994) . The
concept of an "inner world" of thoughts relates directly to
feelings and can be focused toward positive outcomes. It
can distract from specific circumstances such as glancing
at a needle by guiding attention away from the needle to a
pleasant daydream or vacation that has been pre-selected,
for example (Milgrom, Weinstein, & Heaton, 2009) .
In this technique, clinicians guide patients to focus on
scenarios of choice (Milgrom, Weinstein, & Heaton, 2009;
Naparstek, 1994; Rossman, 2000) . Clinicians support guided
visualizations by verbally cueing patients with details of
images such as colors, sounds, and textures (Milgrom,
Weinstein, & Heaton, 2009) . This helps engage imagina­
tions while allowing patients a pleasant inner experience,
away from any currently stressful experience. Speaking
in a slow, soft voice can enhance pleasurable experiences
(Milgrom, Weinstein, & Heaton, 2009; Naparstek, 1994;
Rossman, 2000) . Clinicians can preface relaxation exercises
by informing patients that they are going to do something
different today to help them feel more at ease. It is impor­
tant to seek permission before proceeding by asking if it is
okay to proceed. Suggestions for guided visualization are
provided in Table 2-3 and a guided relaxation and visual­
ization sample script can be found in Appendix 2-1 •.
Hypnosis
Many are intrigued by hypnosis, particularly how it works
and its applications. Growing evidence suggests a strong
 CHAPTER 2 FUNDAMENTALS OF PAIN MANAGEMENT
• 11

Table 2-3 Suggestions for Preparing Patients for Guided Visualization

and Relaxation

• Demonstrate confidence in a positive outcome

Speak and act with confidence even if you feel awkward or new at using these tools
(patients look to you as a professional for guidance)

• Ask the patient to focus on breathing "(Name), I'd like to invite you to focus your
attention on your breathing."

• Explain that slow breathing allows more oxygen to get into lungs

• Explain that oxygen allows the muscles to relax better, releasing tension

• Explain that it is easier for the whole body to relax when muscles are relaxed, heart rate
slows, breathing slows, mind and body calm

• Use your voice as a tool by speaking slowly and softly maintaining patience and calmness

link between hypnosis and the physiology of pain for effec­
tive management of pain and anxiety (Beck, 20 12). When
in a state of hypnosis, patients usually feel calm and relaxed
and are able to concentrate intensely on a specific thought,
memory, feeling, or sensation while blocking out distractions.
In this state, individuals are more open to suggestion and
become more aware of their inner worlds. Thoughts and im­
ages from this inner world can be used to create a sense of
comfort and pleasure and help reduce fears and anxiety.
Brain imaging studies have demonstrated that while
parts of the brain are registering painful sensations the
anterior cingulate cortex (responsible for attention) is less
engaged in painful sensations. This type of research may
have significant implications for dental local anesthesia.
Although the formal practice of hypnosis requires spe­
cialized training and certification, untrained clinicians can
nevertheless use suggestive words to help promote posi­
tive experiences. Equally important is avoiding words that
may focus attention on anticipation of pain, as previously
discussed (Milgrom, Weinstein, & Heaton, 2009).
An alternative to pharmacological approaches, patients
with unmanageable levels of anxiety can also be referred
to qualified hypnotherapists who can help them overcome
their fears. A more in-depth discussion of dental fears can
be found in Chapter 18, "Insights for Fearful Patients." The
benefits of hypnosis for both patients and clinicians before
and during local anesthetic administration may include en­
hancing pain management while reducing anxiety, stress,
and salivation. Hypnosis can also help reduce stimulation
of the gag reflex. In addition to hypnotherapy sessions, self­
warrant. Pharmacological solutions are especially help­
ful for anxious patients who avoid dental treatment and
present only for emergent care. In these situations, phar­
macological agents may be incorporated into treatment.
For some patients, medical consultation may be necessary.
These individuals often must resort to emergent care be­
cause of their intense fear and avoidance of routine dental
care, and pharmacological agents can be incorporated into
treatment when indicated.
Considerations for Clinicians
The phenomena of anxiety and pain related to dental in­
j ections are not limited to patient experience. Clinicians
should also consider their own personal experiences with
pain. Learning to give inj ections can be unsettling for clini­
cians, especially those who are fearful of receiving injections.
Previous experiences and perceptions can interfere with the
learning process and limit confidence building. On the other
hand, a painful past experience can also provide a positive
motivation to provide comfortable injection experiences for
others. If necessary, psychological therapy may be helpful in
recognizing personal inhibitions that may delay learning and
can undermine clinical success in the delivery of injections.
In some cases, it may be appropriate to recommend in­
tervention with a professional psychologist. More in-depth
strategies for management of patient fear and phobia are
discussed in Chapter 18.
� �� P.tE! r. q �.E! ���.�.�� ...........................................
. . . . . . .

hypnosis is also typically taught for patients to use at future
dental appointments.
Pharmacological Intervention
For some patients, pharmacological intervention may be
helpful and necess ary. Nitrous oxide-oxygen sedation,
oral conscious sedation, intravenous sedation, and general
anesthesia should be discussed with patients as situations
1 . Which statement best describes pain as a protective
response?
a. Pain is a physiological, conscious reaction.
b. Pain is a psychological re action based on blood
flow to the injured site.
c. Pain is a rapid, reflexive, subconscious reaction.
d. Pain is a slow, deliberate reaction to avoid further
tissue injury.
12 SECTION I PAIN CONTROL CONCEPTS
•
2. Which of these groups of variables does not affect the
experience of pain?
a. Sex, genetics, mental health
b. Personality, age, hormones
c. Attitudes, learned responses
d. Body weight, height
3. Which one of the following statements regarding no­
ciception is true?
a. Nociception is polymodal.
b. No ciceptive receptors can distinguish between
chemical and thermal stimuli.
c. Nociception is a physiological and psychological
process.
d. Nociceptive pain is identical in somatic and visceral
structures.
4. Which one of the following is an example of neuro­
pathic pain?
a. Fractured bone
b. Psychological disorder
c. Postsurgery pain
d. Trigeminal neuralgia
5. Which one of the following will help patients cope
with anxiety and fear?
a. Avoid discussions about anxiety and fear.
b. Only the dentist should ask about anxiety and fear
to avoid patient embarrassment.
c. Assure the patient that difficulties during past den­
tal visits could not have been avoided.
d. Prepare, rehearse, empower, and praise patients to
reduce anxiety and fear.
6. In the process of debriefing, which one of the follow­
ing is not useful when managing fearful patients?
a. Patient and clinician discussion period at the end of
each appointment.
b. Patient gives input on the duration and plan for the
next appointment.
c. Future appoints are modified based on the insights
from the patient/clinician discussion.
d. Clinicians select strategies for the patient for his or
her next appointment.
Visit www.pearsonhighered.com/healthprofessionsresources to access the student resources that accompany
this book. Simply select Dental Hygiene from the choice of disciplines. Find this book and you will find the
complimentary study tools created for this specific title.
Refe re n ces
American Psychiatric Association. (2000). Diagnostic and
statistical manual of mental disorders (4th ed.). Washington,
DC: Author.
Beck, M. (2012). Medical hypnosis: You are getting very healthy.
Health Journal. The Wall Street Journal, http://online.wsj.com/
news/articles/SB10001424052702303815404577333751488988824?
mg=reno64-wsj&url=http%3A%2F%2Fonline.wsj.com%
2Farticle%2FSB10001424052702303815404577333751488988824.
html, accessed May 17,2014.
Benson, H. (2000). The relaxation response. New York: Harper­
Torch; 1st Avon Books Printing.
Dionne, R., Phero, J., & Becker, D. (2002). Management ofpain
and anxiety in the dental office (Chapters 1, 5). Philadelphia,
PA: Saunders.
Fiset, L., Milgrom, P., & Weinstein, P. (1985). Psychophysiological
responses to dental injections. Journal of the American Dental
Association, III, 578-583.
Foskett, J. M. (2007). Calming dental anxiety relaxation script.
Calming Dental Anxiety Seminars. Author.
Frere, C. L., Crout, R., Yorty, J., & McNeil, D. (2001). Effects of
audiovisual distraction during dental prophylaxis. Journal of
American Dental Association, 132, 1031-1038.
Howard, M. (2007). Chronic pain. Institute for Natural Resources
Educational Program. Seattle.
Merskey, H., & Bogduk, N. (1994). Classification of Chronic Pain
(2nd ed). IASP Task Force on Taxonomy. IASP Press, Seattle.
www.iasp-pain.org, accessed January 20, 2014.
Milgrom, P., Weinstein, P., & Heaton, L. (2009). Treating fearful
dental patients: A patient management handbook (3rd ed.).
Seattle: Dental Behavioral Resources.
Naini, F. B., Mellow, A. C., & Getz, T. (1999). Treatment of dental
fears: Pharmacology or psychology? Dental Update, 26, 270-276.
Naparstek, B. (1994). Staying well with guided imagery. Wellness
central. New York: Hachette Book Group.
Pappagallo, M., & Chapman, C. R. (2005). The neurological basis
ofpain (Chapters 1, 11). New York: McGraw-Hill.
Rossman, M. (2000). Guided imagery for self-healing. Novato,
CA: H.J. Kramer & New World Library.
Spitzer, D. (2004). Gender and sex-based analysis in health re­
search: A guide for CIHR peer review committee, final report.
Canadian Institutes of Health Research, Ottawa, Ontario,
Canada.
Taber's cyclopedic medical dictionary. (1997). Philadelphia, PA:
F.A. Davis.
Guided Relaxation and Visualization Sample Script
The following script can be used to facilitate a guided re­
laxation or visualization session. B est practices suggest
that this activity be prefaced with a statement explaining
to the patient that this may be a new experience to help
him or her relax. B efore beginning the activity, ask the pa­
tient's permission to proceed (such as "Is this ok? ").
Once permission is granted, guide the patient as follow:
I'd like to invite you, (NAME), to simply bring your
attention to your breathing.
When you bring your attention to your breath, you
begin to naturally bring in more oxygen, which then cir­
culates through your body to your muscles. Your mus­
cles will begin to relax, release and let go. That's a good
thing because as your muscles begin to soften and let
go, you feel more relaxed, and when you feel relaxed,
everything else shifts to help you relax more deeply . . .
even if just a little bit. So, simply by breathing a little
deeper, down into your belly, now . . . you may notice
how your belly expands when you inhale . . . and then
notice how as you exhale, it seems as if your naval is
falling toward your back . . . that's all you have to do
right now . . . simply notice your breathing . . . notice the
rise and fall of your abdomen. That's it . . . good . . . (as
you watch his or her abdomen rise and fall) .
If the patient hasn't already closed his or her eyes,
guide him or her by saying:
If you are comfortable, and when you are ready, you
may simply close your eyes, allowing you to focus even
more on your breathing. You may even notice how
comfortable it feels now to simply let go . . . sink into
the chair, allowing the chair to fully support you. As
the dental chair supports you now, you can continue
to keep your focus on your breathing . . . noticing how
natural and easy it is now . . . each breath allowing
you to relax into your body . . . each and every exhale
allows any tension, any worries, any concerns . . . to
simply be released.
Now, you may imagine a be autiful place in nature,
someplace you've been to (you may ask about a favor­
ite vacation spot before you begin) . . . or simply create
a place now in your own mind. As your body further
relaxes, your imagination becomes fluid . . . allowing
you to create a place in your mind.
This is a place where you feel very safe, secure and
strong . . . a place where you can be alone and yet
never feel lonely . . . a place where you feel very
calm a n d p e a c e fu l . S i m p l y imag in e b e i n g t h e r e
now . . . n o t i c e the c o l o r s h e r e , n o t i c e a n y sounds
you might hear in this b e autiful place, and notice
how the air fe els on your skin . . . you may notice
aromas o r smells . . . e s p e cially notice now, how
calm and peaceful you feel being here, in this beau­
tiful place.
Simply allow yourself to be there . . . completely . . .
I'm going to be quiet now . . . as you keep your focus
on this beautiful place . . . where you feel so calm . . . so
relaxed . . . so peaceful . . .
If the patient has told you beforehand about their
scene, you may keep talking and describing all the aspects
he or she has told you, or simply repeat:
" . . . feeling calm, feeling peaceful, feeling relaxed."
When you're ready to complete, begin again with sug­
gestions that "anchor" his or her pleasant relaxed experi­
ence to the dental chair, the dental office, and the dental
procedures.
So, (NAME), we're almost finished for today . . . you
can simply keep your focus on your bre athing for
now . . . in a few moments, I ' m going to simply ask
you to come back into alertness . . . but for now, sim-
ply focus on your breathing . . . as you remember this
pleasant experience today . . . remembering now that
it was different, better, easier than ever before . . .
remembering now, every time you think about our
dental office, you'll be reminded of this relaxing
experience . . . every time you are driving on your
way to our office, you'll again be reminded of this
pleasant experience . . . and even when you put your
hand on the doorknob, you'll be reminded of your
pleasant experience today.
And when you see any of the staff, you immediately
think about and also feel this very pleasant experi­
ence . . . it feels good now . . . when you sit in the dental
chair, so supporting, so relaxing, so pleasant . . . as you
imagine your beautiful place. So now, every time you
even make a dental appointment, you remember and
13
14 SECTION I PAIN CONTROL CONCEPTS
•
feel this pleasant experience . . . you remember it's eas­
ier now . . . every time you sit or lie back in this chair, it
reminds you to relax, release and let go . . . you remem-
ber it is safe to relax, release and let go . . . and you do.
Now I am going to ask you to simply began to wiggle
your toes, wiggle your fingers - stretch - and when
you are ready, open up your eyes gently . . . GREAT ! ! !
Anchor in the relaxation by commenting o n how
" soft " and relaxed their face looks. Acknowledge him
or her for experiencing something different, and again
remind the patient:
"Now, every time you sit or lie down in the dental
chair, you are reminded to relax and let go, and your
beautiful place will be here for you."
Acknowledge him or her for trusting you:
"Wow . . . great" That's awesome job ! , "Thank you for
trusting me" (a gentle exclamation to acknowledge
the patient's coping, trust, and success)
Source: " Guided Relaxation And Visualization Sample Scrip t" from
Calming Den tal Anxie ty relaxa tion script . Calming Dental Anxie ty
Seminars. Copyright © by Jackie Foskett. Used by permission of Jackie
Foskett.
What Is a Deep B reath ?
U nve i l i n g the Myth
A common approach to stress reduction and relaxation
is to take a deep breath. This often results in a big breath
of air being drawn into the lungs, often through an open
mouth, by activating the muscles of the upper chest. Such
bre athing is both big and shallow, but not deep, and is
counterproductive to activating relaxation and to deliver
more oxygen throughout the body.
Taking a deep breath means to draw air down into the
full depth of the lungs using the diaphragm. During rest, ba­
bies naturally take deep, silent breaths. With each inhalation
and exhalation the tummy gently expands and contracts.
Conversely, many adults habitually take noticeable
breaths during rest through the mouth, by activating the
upper chest, typically characteristic of dysfunctional
breathing. Upper chest breathing evokes a greater stress
response, whereas nasal breathing helps ensures regular,
calm, steady breathing using the diaphragm. In addition,
breathing greater volumes of air than needed for metabolic
requirements results in a variety of negative biochemical
influences, including respiratory alkalosis, constriction by
smooth muscle, reduced oxygenation of tissues and organs
including the brain, and heightened p ain p e rception
(Chaitow, 2004), none of which induce relaxation.
To help deal with stress, instructions to take a deep
breath are actually correct, but a true deep breath is dia­
phragmatic, gentle, and quiet-the exact opposite of the
big breaths usually taken in an attempt to calm down.
Other effects of deep breathing include increased sa­
liva production, which is an indicator of activation of the
parasympathetic nervous system.
Furthermore, soft and gentle breathing through the
nose helps ensure that nitric oxide (NO) is carried from
the nasal cavity into the lungs and the blood (Lundbergm
2008) . Nitric oxide plays an important role in vasoregula­
tion (the opening and closing of blood vessels), homeostasis,
and neurotransmission (Chang, 20012; Rabelink, 1998). All
of these functions are directly influenced by breathing and
evoke the relaxation response and improve delivery of oxy­
gen to all organs and systems, including the brain. The ben­
efits of a better oxygenated brain include reduced brain cell
excitability and anxiety (Rabelink et a!., 1999).
It is no coincidence therefore that those individuals
who breathe through an open mouth experience greater
fatigue, stress, and anxiety, and reduced concentration
in comparison to their nasal bre athing counterp arts
(McKeown, 20 14) .
Refe re n ces
Chaitow, L . (2004). Breathing pattern disorders (BPD), motor
control, and low back pain. Journal of Osteopathic Medicine,
7(1) 34 -41.
McKeown P. (2014). Anxiety free: Stop worrying and quieten
your mind- Featuring the Buteyko Breathing Method and
mindfulness. Ireland: OxyAt Books.
Lundberg J.O. (2008, November). Nitric oxide and the paranasal
sinuses. Anat Rec (Hoboken), 291(11): 1479 -84.
Chang, H.R. (Editors) (2012). Nitric Oxide, the Mighty Molecule:
Its Benefits for Your Health and Well-Being. 1st ed. Mind
Society.
Rabelink, A.J. (1998, December 26). Nobel prize in Medicine
and Physiology 1998 for the discovery of the role of nitric
oxide as a signalling molecule, Nederlands tijdschrift voor
geneeskunde, 142(52): 2828-30.
Huttunen J., Tolvanen H., Heinonen E., Voipio J., Wikstrom H.,
Ilmoniemi R.J., Hari R., Kaila K., Effects of voluntary
hyperventilation on cortical sensory responses. (1999).
Electroencephalographic and magnetoencephalographic
studies, Exp Brain Res, 125(3): 248-254.
OBJECTIVES KEY TERMS

• Defi n e a n d d i scuss the key terms in this cha pter. absol ute refra cto ry state 24
action pote ntials 2 1
• Exp l a i n the n orm a l mech a n isms of n erve i m p u lse g e n eration
axo l e m m a 1 8
and co n d u cti o n . axo ns 1 6
• Defi n e t h e eve nts i n su ccessfu l n erve i m pu lse g e n erati o n , axo p l a s m 2 1
i n c l u d i n g t h e resting state, slow depolarization, firing ce l l bodies 1 6
th reshold, rapid depolarization, a n d recovery. conce ntrati o n g ra d i e n t 25

•
co re b u n d les 20
Exp l a i n the s i g n ifica n ce of Schwa n n ce l l sheaths a n d nodes of
d e n d ritic zo n e 1 6
Ranvier on the a b i l ity of l oca l a n esthetic ag ents to b l ock n erve
d e ntal n e u ra l p l exus 20
i m p u lses. d e p o l a rized 26
• Descri be the s i g n ifica n ce of the a n ato m i ca l d iffere n ces d u ra b l e b l ocka d e 27
between sen sory and m otor n e uro n s . e l ectrica l pote nti a l 2 1
•
endoneurium 19
D i scuss the differe nt types o f n erve fi bers re l ated to p a i n
e p i n e u r a l sh eath 1 9
percepti o n .
e p i n e u ri u m 1 9
• I d e n tify t h e n erve fi bers that n orm a l ly tra n s m it p a i n sensati o n s extrace l l u l a r 2 1
from denta l a n d peri odo nta l structures. fascicu l i 1 9
• Differe ntiate a n ato m i ca l ly and fu n ctio n a l l y between fi ri n g t h res h o l d 23
mye l i n ated a n d u n m ye l i n ated n erves. ganglia 16
hyd ro p h i l i c 1 6
hat is meant b anatomic barriers to the diffusion i m p u l se exti n ction 27
l tltons a n d those that present the greatest i m p u lses 1 6
1ffusion . i ntrace l l u l a r 2 1
• Descri be the l ocati o n of the i o n channels 21
p l exus. lipophilic 16
local a n esth esia 28
m a ntle b u n d les 20
m otor n e rves 28
16

15
16 SECTION I PAIN CONTROL CONCEPTS
•
KEY TERMS (contin ued)
n e rve fi b e rs 1 8
n e u ro l e m m as 1 6
n e u ro n s 7 6
n o d es o f Ranvier 7 8
n o n mye l i nated ( u n m ye l i n ated) 1 8
p e ri l e m m a 1 9
p e ri n e u r i u m 7 9
p o l a rized 26
propagation 2 1
ra p i d d e p o l a rization 23
refra cto ry state 24
re l ative refractory state 25
Introd u ction
Before administering local anesthetic drugs it i s important to
review the anatomy and physiology of nerves and the normal
mechanisms for the generation and conduction of pain sig­
nals to the central nervous system. This chapter will discuss
these topics as a foundation for understanding the inhibiting
effect of local anesthetic drugs on these processes.
The mechanisms for the normal generation and con­
duction of pain signals to the central nervous system
(CNS) will be discussed in this chapter as a foundation for
understanding the effects of local anesthetic drugs upon
them. In addition, it is important to understand the anat­
omy and physiology of nerves before administering local
anesthetics (Daniel, Harfst, & Wilder, 2008).
Ne u roa n atomy
U n d e rstanding the m e chanisms involved in periph­
eral nerve anesthesia requires a sound knowledge of
anatomy (Jastak, Yagiela, & Donaldson, 1995; Seeley, Tate,
& Stephens, 2008) . It has been suggested that the most
important aspect of delivering profound and reliable local
anesthesia comes from a solid understanding of neuro­
anatomy (Blanton & Jeske, 2003).
Nerve Cell Anatomy
Nerve cells, called neurons, are the basic units of nerves.
All neurons have four structural areas, their dendritic
zones, axons, cell bodies, and terminal arborizations (see
Figure 3-1 •) . Although similar in some respects, sensory
and motor neurons differ in both structure and function.
A primary distinction is that sensory neurons carry in­
coming signals, referred to as impulses, from the body to the
CNS for processing, whereas motor neurons carry impulses
away from the CNS to effector cells, tissues, and organs.
Nerve impulses are initiated in dendritic zones of
sensory neurons in response to stimulation of tissue. The
terminal zones of nerve axons, known as j unctions, or
re p o l a rizati o n 26
rest i n g state 2 1
sa ltatory co n d u ction 1 9
Schwa n n ce l l sheath 1 8
Schwa n n ce l l s 1 7
sensory n e rves 2 1
sensory n e u ro n s 7 6
slow d e p o l a rization 23
sod i u m i o n p u m ps 25
specific p rote i n receptor sites 22
syn a pses 7 6
term i n a l a rbo rizati o n s 1 6
synapses, contain numerous organelles. These organelles,
when stimulated by impulses, release neurotransmitters
that convey information to excitable tissues, including
other neurons. In the terminal arborization zones of
sensory neurons, impulses or signals are transmitted to
processing nuclei called ganglia.
Nerve Axons, Cell Bodies, and Membranes
Following their initiation, impulses travel along axons, the
processes or fibers of individual nerve cells that transmit
signals to the central nervous system. Neuronal processes
may span considerable lengths. In the case of the sensory
nerves that innervate oral tissues, cell bodies are located
within trigeminal ganglia.
Regardless of the type of neuron, sensory or motor,
the cell body provides metabolic support. In motor neu­
rons, the cell body is closely associated with the axon and
conducts nerve impulses. In sensory neurons, cell bod­
ies are farther away from axons and do not participate in
impulse transmission (see Figure 3-1 ) .
Nerve membranes, called neurolemmas, a r e bilay­
ered phospholipid membranes. The function of a bilayered
membrane is to act as a barrier. Lipid membranes are
comp o s e d of p h o s p h o li p i d s having b o t h lip o p hilic
("fat-loving") and hydrophilic ("water-loving") ends. The
membranes are held together by the attraction of the
lipophilic ends at their centers.
The hydrophilic ends face outward along a membrane
and the lipophilic ends face inward to create a fatty core at
the center (see Figure 3-2 •) . This fatty core allows small li­
pophilic molecules, such as local anesthetic molecules called
neutral bases, to pass through freely, whereas water soluble
substances, such as sodium ions, are able to pass through
the membrane only by means of designated channels
(Disalvo & Simon, 1995). Other hydrophilic local anesthetic
molecules, known as cations, are unable to pass through
either the membranes or their channels. These lipophilic
and hydrophilic local anesthetic molecules will be explained
in more detail in Chapter 4, "Pharmacology Basics."
 CHAPTER 3 NEUROANATOMY AND NEUROPHYSIOLOGY OF PAIN CONTROL
• 17

Ill
Ill
0
()
:s
:::IE

Axon
Sensory N e rves

N e rve
Endings

= Neu rotransmitters

Axo n

M otor N e rves

FIGURE 3-1 Anatomy of Sensory and Motor Neurons.

Nerve Myelination
Nerves are classified as myelinated or nonmyelinated
according to the extent of the surrounding connective tis­
sue (see Box 3-1 •) . Schwann cells, which produce myelin,
are specialized connective tissue cells that surround and
protect peripheral nerves (cells that perform this function
in the central nervous system are known as oligodendro­
cytes) . By producing myelin and forming extensive myelin
sheaths around axons, Schwann cells insulate and protect

M ye l i n is a p rotective cove ri n g fo r n e rves. It is a p p roxi­

mately 80% l i p i d , 20% p rote i n , and a very m i n o r p e rce nt-
• age carbo hyd rate in n a t u re ( B e n n ett, 1 978). M ye l i n is
res p o n s i b l e fo r what is known as the "wh ite" m atte r of t h e :
b ra i n a n d h a s a p r i m a ry fu n cti o n of p rovi d i n g e l ectrica l
i n s u l at i o n to n e rves to p rotect t h e i nteg rity of i m p u l s e
tra n s m iss i o n , m u ch as t h e i n s u l at i o n a ro u n d e l ectri c a l w i res
•

FIGURE 3-2 Anatomy of Neurolemma. Hydrophilic p rotects a g a i nst cross-ci rcu iti n g .
and Lipophilic Components of Nerve Membranes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . •
18 SECTION I PAIN CONTROL CONCEPTS
•

nerve membranes from their surrounding environments.

Axons and their associated Schwann cells are collectively
referred to as nerve fibers (Pogrel et al., 2003).
In addition to providing insulation, S chwann cells
isolate neurons from changes in their environment, minimiz­
ing exposure to injury and, in the event of injury, facilitating
healing. Although these protective features are important to
proper nerve function and health, they are also responsible
for significant obstacles to the diffusion of local anesthetic
solutions. These solutions cannot diffuse through myelin­
ated nerves except in the areas where they come into direct
contact with nerve membranes at the nodes of Ranvier.
Nonmyelinated neurons, also known as unmyelinated
neurons, have Schwann cell sheaths but groups of unmy­
elinated neurons share the same sheaths. Myelinated neu­
rons are enclosed by multiple spiral layers of Schwann cells.
These spiral layers wrap around myelinated neurons as
many as 300 times creating what is known as a Schwann
cell sheath providing some of the most efficient cellular
protection in the body (Jastak, Yagiela, & Donaldson,
The signs and symptoms of certain diseases such as mul t iple
scl e rosi s (M S) are thought to be the resul t of an unexplained
demyelination of oligodendrocytes that occurs in certain
locations in the central nervous system. Without their myelin
protection, these nerves cannot function or heal properl y,
• typically transmitting impul s es at greatl y reduced speeds •
: .(��� ��:c� .�a.n��/•o•f �:a•g•n ��i� ��� ��e:��y: �0.1 �): • • • • .
Tetzlaff, 2000). Nonmyelinated nerves are less isolated
from extracellular environments. They are more vulnerable
to injury and less able to heal if injured (see Box 3-2 •) .
I n myelinated nerves, there are minute gaps consist­
ing of unprotected nerve membranes between adj acent
Schwann cells called nodes of Ranvier (see Figure 3-3 •) .
The outer membrane o f a neuron underlying its sheath is
1995; referred to as its axolemma or neurolemma.

Peri neurium
( i n n e r layer of perineu r i u m )

l l Myelin Sheath
(wraps)
Schwahn Cells

F I G U R E 3-3 Anatomy of Myelinated Axons.

 CHAPTER 3 NEUROANATOMY AND NEUROPHYSIOLOGY OF PAIN CONTROL
Saltatory Conduction
Nerve impulses in nonmyelinated nerves, which have very
thin myelin sheaths that cover groups of fibers, have been
described as "creeping" along their membranes. While by
no means a slow process, this requires activity over the en­
tire length of the membrane of the axon from the point of
stimulation to the point of registration in the central ner­
vous system. The incremental passage of impulses can be
visualized as multiple rows of falling dominos, each trans­
ferring its energy to the next to propagate the impulse (see
Figure 3-4 •) .
S altatory conduction refers to t h e process whereby
impulses are more rapidly conducted along myelinated
nerves (Jastak, Yagiela, & Donaldson, 1995; Narhi et al.,
1994; Seeley, Tate, & Stephens, 2008). In saltatory conduc­
tion, impulses have been characterized as "jumping" over
S chwann cells from one node of Ranvier to another, at
times having enough energy to j ump over several nodes
at once. Although skipping nodes has been demonstrated,
particularly in larger, more heavily myelinated nerves, the
impulses do not accomplish this by actually "jumping" over
Schwann cells. Instead, they have enough energy to travel
through one or more internode region (the portion of an
axon covered by a Schwann cell) before another impulse is
generated. It is impossible for an area of myelinated nerve
that is covered by a Schwann cell to respond to changes in
its environment because it lacks exposure to extracellular
fluids and sodium ion exchange is prevented. With increas­
ing degrees of myelination there is often enough energy
to bypass the next node and travel directly to a subse­
quent node (up to 8-10 mm) increasing conduction speeds
(Malamed, 20 1 3 ) . In general, larger, more heavily myelin­
ated nerves transmit impulses more rapidly than smaller,
nonmyelinated nerves (see Figure 3-4).
Nodes of Ranv i e r
O mm 2 mm 4 mm
F I G U R E 3- 4 Impulse Conduction and Nodes of Ranvier. A - Nonmyelinated nerve;
B - Myelinated nerve.
• 19
Nerve Fiber Types
Nerve fib ers are typ e d as A, B, or C, with numerous
subcategories falling within these classifications ( s e e
Table 3 - 1 •) . By far the most numerous fiber type of the
peripheral nervous system is the C fiber. C fibers, which
are nonmyelinated, conduct more slowly, providing the
sensation of dull and aching pain. Some A fibers, known
as A delta fibers (A8), are lightly myelinated and bear
primary responsibility for the experience of sharp pain.
Note the difference in Table 3-1 between the conduction
speeds of the A8 fibers, which convey sharp, stabbing pain
information rapidly, versus the C fibers, which convey dull,
aching information slowly. Both A and C fibers have been
found in dental pulps with a greater distribution of C fi­
bers than A (Narhi et al., 1994; Pashley, 1990; Seeley, Tate,
& Stephens, 2008).
Peripheral Nerve Anatomy
Peripheral nerves are made up of many axons that are
bundled, protected, and provided with metabolic sup­
port by layers of connective tissue. The anatomy from the
deep to the superficial aspect of a peripheral nerve starts
with individual nerve fibers separated from one another
by an endoneurium, a structure that insulates the electri­
cal activity of individual nerve fibers (see Figure 3-5 •) .
The perineurium bundles these fibers into what are known
as fasciculi. The inner layer of the perineurium is referred
to as its perilemma. A very loose connective tissue layer,
the epineurium, surrounds all of the fasciculi, their associ­
ated supporting connective tissue, including blood vessels
and lymphatics, and the perineuria. The epineurium has its
own sheath on its superficial circumference that surrounds
the entire nerve called the epineural sheath. Of these lay­
ers, the two most significant barriers to the diffusion of
Reg ion
S mm B mm 1 0 mm
20 SECTION I PAIN CONTROL CONCEPTS
•

Table 3-1 Nerve Fiber Types

Cond uction Velocity

Fiber Type Function Diameter (mu) (meters/second m/s) =

Aa Proprioception, body movements 12-20 100

A � Touch, pressure 5-12 30-70

Ay Motor to stretch receptors 3-6 15-30

Ao Pain, especially cold, touch 2-5 12-30

B Preganglionic autonomic <3 3-15

c Thermal pain, tension, pressure, 0.4-1.2 0. 5-2

displacement receptors

c Postganglionic autonomic 0. 3-1. 3 0. 7-2. 3

anesthetic solutions and the development of anesthesia
are ( in order ) the perilemma and the perineurium ( see
Box 3-3 •) . The larger the nerve, the greater the signifi­
cance of these barriers ( Jastak, Yagiela, & D onaldson,
1995 ; Noback & Demarest, 1981 ) .
The outer region o f a nerve i s referred t o a s its mantle
and the central region is its core. Fasciculi located in the
mantle region are called mantle bundles. The fasciculi in
the central region are referred to as core bundles. The ar­
rangement of bundles into outer ( mantle ) and inner ( core )
segments in larger nerves has an impact on the order in
which anesthesia develops when exposed to local anes­
thetic drugs ( see Figure 3-6 •) . The significance of core
and mantle bundles on local anesthesia will be discussed
later in this chapter.
Dental Neural Plexus
A dental neural plexus is an interwoven, interconnect­
ing network of nerves supplying the teeth and their sup­
porting structures ( B ennett, 1978) ( see Figure 3-7 • ) . The
superior ( maxillary ) dental plexus derives from terminal
branches of the second division of the trigeminal nerve
and includes dental, interdental, and interradicular divi­
sions. The inferior ( mandibular ) dental plexus derives
from terminal branches of the third division of the trigem­
inal nerve. These extensive networks of nerves innervate
the maxillary and mandibular teeth and their supporting
structures.

Of all the structures through which local anesthetic drugs

must diffuse to provide anesthesia, the perilemma presents
the greatest obstacle to di ffusion (Jastak, Yagiela, &
Donaldson, 1 995) . Schwann cells are not among structures
that slow the diffusion of drugs in myelinated nerves.
erineurium
Rather than decrease the rate of a l o cal anesthetic drug's
diffusion through a nerve membrane, they simply do not
allow it. Schwann cells protect axons from exposure to
Schwa n n C e l l s
� extracellular substances, including local anesthetic drugs.
These drugs are effective onl y at the nodes of Ranvier,
y
Axon , where they are able to make direct contact with exposed ,
ra ·
F I G U R E 3-5 Anatomy of a Neuron. : . �� � � . � � � • • • • • • • • • • • •. • • • • • • • • • • • • • • • • • •
 CHAPTER 3 NEUROANATOMY AND NEUROPHYSIOLOGY OF PAIN CONTROL
Schwann Cells -[;
y
Axon
F I G U R E 3-6 Mantle and Core Bundles.
FIGURE 3-7 Dental Neural Plexus.
Ne u rophys i ology
Nerve impulses are electrical i n nature and depend entirely
upon changes in ionic activity along nerve membranes
for their generation and conduction. Specific thresholds
must be achieved before transmission of impulses to the
CNS occurs. In sensory nerves, energy from an impulse is
duplicated and transferred to succeeding impulses along
the axon in the direction of the CNS. These successive
impulses are identical in size and nature to the original
impulses ( also known as action potentials) . Impulses do
not lose any of their strength in the transfer of energy from
one section of membrane to the next; in fact, it has been
demonstrated that the current flow at successive areas of
nerve membranes actually exceeds that which is necessary
• 21
M antle
Bundles
Core
Bundles
to fire nerve impulses ( Malamed, 20 13). The process of se­
quential impulse generation to the processing areas in the
CNS ( ganglia and relevant centers in the brain ) is referred
to as propagation.
When a nerve is receiving little to no stimulation its
membrane is said to be in a resting state. In reality, nerves
respond to some degree of stimulation almost constantly
and seldom, if ever, rest even when providing little more
than sensory feedback ( Jastak, Yagiela, & D onaldson,
1995). This is accomplished by ion exchange through nerve
membranes via designated p athways or ion channels
through which ions selectively pass on a continuous basis
(Tetzlaff, 2000).
The inner environment of a nerve is known as its
intracellular environment or axoplasm, whereas the
outer environment is designated the extracellular envi­
ronment ( see Figure 3-8 •) . The axoplasm of a nerve at
rest is maintained in an electrically negative state rela­
tive to the more positively charged extracellular envi­
ronment. It has been determined that the resting state of
the axoplasm averages -70 m V ( millivolts ) . This resting
state electrical potential represents the difference in the
electrical charge across the membrane. An imbalance of
electrolytes on either side of the membrane, primarily
sodium ( Na+ ) and potassium ( K+ ) ions, is responsible for
this difference.
G e n e ration a n d Co n d u ction
of Ne rve Impulses
The generation and conduction of nerve impulses oc­
cur over a series of phases or " states." In the resting
state, gates in the Na+ ion channels remain closed. This
22 SECTION I PAIN CONTROL CONCEPTS
•
Extrac e l l u lar Envi ro n m e nt
..
FIGURE 3-8 Intracellular and Extracellular Environment of Nerve. In response to
stimulation, Ca+2 ions are released. Na+ ion channels open, allowing Na+ influx into the
axoplasm.
prevents significant influx of Na+ ions, either via sodium
ion pumps or along their concentration gradient or electri­
cal attraction.
In response to stimulation, Ca+2 ions release and open
the channels to Na+ ion influx into the axoplasm, slowly at
first. Once there are sufficient Na+ ions in the axoplasm to
reduce the electrical potential by approximately 15-20 mV,
the firing threshold for impulse generation is reached and
Na+ ions flood the axoplasm. In sensory nerves, successive
impulses propagate to processing centers in the CNS.
Upon successful impulse prop agation to an adj a­
cent site, the previous site is unresponsive and unable
to generate an impulse. This pattern continues along the
length of the membrane, which forces all subsequent im­
pulses to be generated in one direction only. While the
impulses that are propagated toward the CNS eventually
prompt efferent responses, impulses are also generated
from sites of stimulation in a direction away from the
CNS. Unlike the impulses propagated in the direction of
the CNS, these impulses extinguish once they arrive at
peripheral destinations that have no ability to respond.
B ecause the unresponsive period lasts only about one
millis econd, the membrane in the area may be stimu­
lated again quickly.
These stages are discussed in more detail in the next
section and are presented as a group in Appendix 3-1.
Resting State
The electrical potential of nerve axoplasm in the resting
state is approximately -70 mV, although the range can ex­
tend from -40 to -95 mV for some cells (Jastak, Yagiela,
& Donaldson, 1995 ) . This potential is maintained relative
to the extracellular environment primarily by Na+ and K+
Axoplasm
(intracellular environment)
ions, which can enter the axoplasm only through selec­
tive channels in the nerve membrane called ion channels
(see Figure 3-9 •) . Chloride ions participate in a more
minor way by concentrating in the extracellular fluid with
the sodium ions, helping maintain the resting membrane
potential.
Ion channels are closed or gated by Ca+2 ions bind­
ing to specific protein receptor sites within the channels
in the resting state (see Box 3-4 •) . There are numerous
electrolytes in both intra- and extracellular environments
of nerve membranes. An imbalance is the result of differ­
ences in the concentrations of these electrolytes, primar­
ily Na+ and K+ ions on either side of the membrane. Na+
ions are small enough to pass freely through ion chan­
nels. B ecause of their high affinity for water, however, the
maj ority hydrate and are too large to pass through the
channels. Even though somewhat larger than Na+ ions,
K+ ions have a lower affinity for water and the maj ority
easily pass through the channels unhydrated. The nega­
tive electrical charge of the axoplasm, however, prevents
potassium ions from leaving the axoplasm in significant
numbers despite their smaller size and the substantially
larger numbers of K+ ions in the axoplasm. The net result
is an excess of extracellular Na+ and an excess of intra­
cellular K+. Along with the contribution of Cl-, this ionic
imbalance maintains the resting electrical potential of
nerves.
It is the imbalance between K+ and Na+ ions on either
side of a membrane that largely accounts for the uninter­
rupted maintenance of the resting potential. This is aided
by protein pumps in the membrane, which actively pump
ions both in and out of the axoplasm against resistance.
If undisturbed, the resting state ionic imbalance will con­
tinue indefinitely.
 CHAPTER 3 NEUROANATOMY AND NEUROPHYSIOLOGY OF PAIN CONTROL
Resti n g Potenti a l - - 70 mV
FIGURE 3-9 Nerve Membrane Ion Exchange - Resting Potential ( Resting State ) . In a resting state, the electrical
potential of nerve axoplasm is approximately -70 mV. This potential is maintained primarily by K+ and Na+ ions.
The mechanism of the speci f i c binding of protein si t es is
based on the knowledge of vol t age-gated sodium chan­
nel s , of which nine di fferent types have been identi fied.
Higher densities of sodium ion channels are found in
the nodes of Ranvier. Not all types of sodium channels
are equal. Some are more susceptible than others to the
actions of local anesthetics. These differences may explain
some failures of local anesthesia. For example, in the
presence of inflammation, the development of al t ered
channels may be responsible for failures.
Sodium channels consist of three subuni t s. Onl y one
of these subunits allows the exchange of sodium ions.
Within a subuni t there are four zones containing six protein
segments. When the nerve is at rest, the channel is blocked
by one of these proteins.
Once the threshold is reached, rapid depolari z ation
begins and sodium ions fl o od the channel. During this
phase, these protein segments twist into the body of the
pore by an action known as a "sliding heli x ."
After depolari z ation, when the refractory phase begins,
a protein loop extends into the channel and continues to
block sodium ion entry. Local anesthetics further block the
entry of sodium ions by maintaining the position of the pro­
tein loop in the channel during the refractory phase.
Understanding this mechanism and identifying the
nature of the binding si t es may lead to the development of
drugs that target cri t ical sodium channel pathways as well
as drugs that are able to function better in the presence of
inflammation. I t may al s o reduce the unwanted effects of
the current local anesthetic drugs.
• 23
+ Charged
Extracellular
Slow Depolarization and Firing Thresholds
Once a nerve is stimulated, the ion channels respond by
opening their gates (Jastak, Yagiela, & Donaldson, 1995).
This is accomplished by the release of calcium (Ca+2) ions
from receptor sites on the gates (Malamed, 20 1 3 ) . Ca+2
ions may be thought of as the gatekeepers of the rest­
ing state. Once the gates are open, the channels are now
wide enough for the p ositively charged and hydrated
Na+ ions to enter the negatively charged axoplasm. Slow
depolarization occurs until the axoplasm has depolarized
approximately 15 to 20 mV, from -70 to somewhere be­
tween -55 and -50 m V, which is the threshold for impulse
generation. This is known as the nerve's firing threshold
(see Figures 3-10 • and 3-1 1 •) .
A s long a s this threshold i s not achieved, the nerve is
said to be slowly depolarizing and no impulses will be gen­
erated. If stimulation proves insufficient to depolarize a
membrane, no impulse will be generated (see Figure 3-12 •) .
A n example o f "failure o f impulse generation" occurs
when someone tries to tickle an individual's ear with a
feather. If the action is insufficient to gain the individual's
attention, the nerve is not receiving a strong enough stimula­
tion to raise the threshold to conduct an impulse to the CNS.
In this case, this is insufficient Na+ ion influx to depolarize the
membrane 15-20 mV to its firing threshold (see Figure 3-12).
Rapid Depolarization
Once the firing threshold has been achieved, the nerve
quickly depolarizes at the site of stimulation because of the
flood of positively charged Na+ ions into its axoplasm in a
process known as rapid depolarization (see Figures 3-1 1
and 3-13 • ) . The impulse propagates along the entire
length of the nerve, the ganglia, the nerve synapses, and
24 SECTION I PAIN CONTROL CONCEPTS
•

D e p o l a rizat i o n -50 to -60 m V

(Slow Phase)
..
.. ..
+ Charged
..
Extrace l l u l a r

F I G U R E 3-1 0 Nerve Membrane Ion Exchange - Depolarization (Slow Phase). Once a nerve i s stimulated,
ion channel gates open in response to calcium (Ca+2) ion release. Slow depolarization occurs until the axo­
plasm has depolarized, approximately 15 to 20 mV, to -50 to -55 mV (firing threshold).

successive nerves along the pathway to the CNS. This is
not an isolated process. It occurs simultaneously on many
adj acent sites on the membrane. Sensory impulses travel
only toward the CNS, because once the impulse or ac­
tion potential has transferred to an adj acent site on the
membrane, the previous site is temporarily unresponsive.
The inability to successfully restimulate a section of mem­
brane after impulse generation and conduction is known
as a refractory stat e . Initially, the membrane is in an
absolute refractory state and the previously fired section
of membrane cannot be restimulated no matter how great
the stimulus (Malamed, 20 13).

S u ccesfu l N e rve I m p u l s e G e n e ratio n

A ,\ A � -� .� -� A

dmsec v
2Vmaac v
�maec �msec imaac 10� sec
CIJ
-
8 c
0
.�
�
+40 mV
1\
Cii
:;:; O mV
c:
-
Q)
0
a.
Q)
c:
...
ell
..c
E
Q)
:::2: -70 mV
A
•

--V
l/ \ \
I
I
I
-55 to -50 mV = F i ri n g Th reshold

...

A - S l ow Depola rizat i o n , B - R a p i d Depola rizatio n , C - Repola rizati o n

F I G U R E 3-1 1 Impulse Generation Firing T hreshold. T he firing threshold i s reached once the axoplasm has
depolarized to -50 to -55 mV.
 CHAPTER 3 NEUROANATOMY AND NEUROPHYSIOLOGY OF PAIN CONTROL
• 25

F a i l u re to Ach i eve F i ri ng Th res h o l d

A � .� .� .� .� .� A

dmsec v 2vmsac v rmsec �msec i'msac 10� sec

en
-
0 +40 mV
�
�
(ii
.. 0 mV
c:
Q)
-
0
c.
Q)
c:
�
ca
.c -55 to -50 mV = F i ri n g Th res h o l d
E
Q)
:::E -70 mV
_...
/ "'-
.....____

Impulse Generation F ailure. When Na+ ion influx is insufficient to depolarize the membrane
F I G U R E 3-1 2
15 to 20 mV, no impulse is generated.

At this p oint, the nerve axoplasm has attaine d a
potential of +40 mV (Hodgkin & Huxley, 1954; Jastak,
Yagiela, & D onaldson, 1995 ) . After impulse generation
and conduction, additional Na+ ion influx is prevented.
Instead, Na+ ions are actively transported out by sodium
ion pumps, which enhance the outward movement of Na+
ions now in greater excess in the axoplasm along their
concentration gradient. This is also facilitated by the vigor­
ous extracellular movement of Na+ ions due to repulsive
forces of the now positively charged axoplasm . As ions
continue to move out, the axoplasm eventually returns to
its resting state of -70 m V.
D uring this return to the resting state but before
its complete r e e s tablishment, stimulation m ay once
again prove to b e s u c c e s sfu l . With the resting state
only partially attained, a larger stimulus is required to
achieve a successful firing. This is known as the relative
refractory state.

D e p o l a rizat i o n - +40 mV
(Rapid Phase)
- Charged
Extrace l l u l a r

FIGURE 3-1 3 Nerve Membrane Ion Exchange - Depolarization ( Rapid Phase ) . Once enough Na+ ions have
flooded the axoplasm, the firing threshold is achieved and the nerve quickly depolarizes, generating an impulse.
26 SECTION I PAIN CONTROL CONCEPTS
•

Repolarization
Once a nerve has attained a potential of approximately
+40 mV, the process begins to reverse. The reversal of ion
concentrations in this recovery phase is called repolariza­
tion. The axoplasm has an excess of positive charge and
an excess concentration of Na+ ions. As previously stated, The potential across a nerve membrane is identified as
pola rized whenever i t is not 0 mV. For example, the normal
•

Na+ ions exit the nerve by passive diffusion through the

ion channels along their concentration gradient, by repul­
sion due to the positive electrical charge of the axoplasm,
and through active transport of the Na+ ion pumps. As the
passive forces of Na+ ion movement out of the axoplasm
weaken, further movement is assisted by the ion pumps
which continue to remove Na+ and K+ ions until a poten­
tial of -70 mV is reestablished. Na+ ion movement is then
physiol o gical resting state of a nerve averaging about -70 mV
is polarized and a stimulated state of +40 mV is also, by
•
strict definit ion, polari z ed. A nerve is said to be d e p o l a r­
ized when the potential across the membrane is 0 mV.
Thi s is the case regardless of whether it is becom-
ing less posi t i v e or less negative. Stri c tl y speaking for a
nerve, any change toward 0 mV is a depolarization and any
: change away from 0 mV is a polarization . •

limited to resting state levels by the rebinding of Ca+2 ions : . . . . . . . . . . . . . . . . . •

. . . . . . . . . . . . . . . . . . . . . .

to receptor sites. This closes the ion channels and assures

that Na+ will not continue to depolarize the axoplasm (see
Figure 3-14 •).
For purposes of this discussion the terms depolariza­
tion and repolarization are used to define processes; de­
polarization referring to a potential change across the
membrane from -70 mV to +40 mV and repolarization refer­
ring to a return to a resting state from +40 mV to -70 mY.
Box 3-5 • provides a discussion of the strict definitions of
these terms.
Return to Resting State
With the reattainment of a potential between -60 m V to
-90 mV, the nerve membrane has now fully recovered and is
ready to repeat the process in response to another sufficient
stimulation. As described, this process may seem long and
tedious. In reality, however, it requires only one millisecond
for a nerve membrane to react and recover after a success­
ful impulse-generating stimulation (Malamed, 20 13).
Act i o n s of Local Anestheti cs
o n Ne rve Impulses
Two important factors to consider when discussing the im­
pact of local anesthetics on nerve impulses are the inter­
ruptions of those impulses (impulse extinction) and the
diminishing effects of the drugs on the nerve bundles (core
and mantle bundles).

Re pol a rizatio n = -60 to -90 mV

(Return to resting state) ..
.. + Charged
Extrace l l u l a r

Exit assited by Sodium Pump

F I G U R E 3-1 4 Nerve Membrane Ion Exchange - Repolarization ( Return t o Resting State ) . The reversal of
ion concentrations in the recovery phase is called repolarization. Once a nerve has attained a potential of
approximately + 40 mV, Na+ ions exit the nerve by passive diffusion through ion channels and through active
transport of Na+ ion pumps. Repolarization is complete when the potential is -60 mV to -90 mV.
 CHAPTER 3 NEUROANATOMY AND NEUROPHYSIOLOGY OF PAIN CONTROL
• 27

Impulse Extinction The Significance o f Core and Mantle Bundles on

When discussing nerve impulses and local anesthesia,
the likelihood that impulse propagation may be inter­
rupted at a particular are a of a nerve by local anesthe­
sia is known as nontransmission, or impulse extinction
( Tetzlaff, 2000) . This is somewhat analogous to crimping
a hose to stop the flow of water ( extinction ) ; uncrimp­
ing the hose will reestablish the flow ( propagation ) . Lo­
cal anesthesia is a deliberate method to achieve impulse
extinction. When discussing impulse extinction due to lo­
cal anesthetics, it is directly related to the volume of local
anesthetic delivered, the concentration of the drug, and
the length of nerve that has been exposed to the drug
(Tetzlaff, 2000) .
Upon administration of local anesthetic drugs, Na+
ion influx through the nerve membrane is blocked and
sodium-dependent depolarization is prevented. B oth the
generation and conduction of nerve impulses can be inhib­
ited by local anesthetic drugs. Decreased responsiveness to
stimuli and the failure to transmit an impulse toward the
CNS are direct consequences of impulse extinction due to
local anesthetic drugs.
Impulse extinction is also related to the presence or
absence of myelin ( Tetzlaff, 2000). As previously noted,
in myelinated nerves, local anesthetic drugs are effective
only at the nodes of Ranvier and multiple nodes must be
exposed to the drugs to block impulses. It is considered
that a minimum of 8-10 mm of the nerve membrane
must be flooded by an anesthetic solution to achieve an­
esthesia particularly in larger more heavily myelinated
nerves ( Malamed, 20 1 3 ) . Greater volumes of solution
are required to accomplish impulse extinction (durable
blockade) in the presence of these nerves, an example of
which is the inferior alveolar nerve.
Local Anesthesia
Nerve fib ers h o u s e d in mantle ( outer ) bundles tend
to innervate structures in close proximity to them ( see
Figure 3-15 •) . Fib ers housed in core ( inner ) bundles
tend to innervate structures at some distance away from
them. For example, in the case of the inferior alveolar
nerve at a location near the entrance to the mandibular
canal, fibers from the mantle layer tend to innervate the
molar region whereas fibers from the core layer tend to
innervate the anterior mandible including the chin and
lips. Molar regions anesthetize e arlier and more eas­
ily in this example, whereas the lips, chin, and anterior
dentition and supporting structures anesthetize later and
with more difficulty. This is because anesthetic solution
reaches the core only after the solution has penetrated
through the mantle layer. It takes longer to reach the
core and the solution does so in a diluted form primar­
ily because of the binding of drug molecules to receptor
sites in the mantle bundles. Once at the core, there are
fewer molecules remaining to bind to sites in the core
( Malamed, 20 1 3 ) .
A lack o f labial and mental soft tissue signs and symp­
toms of anesthesia after administration of what is known
as an inferior alveolar nerve block indicates that the core
bundles have not yet been adequately anesthetized. While
the absence of signs and symptoms of anesthesia is a good
indication that profound anesthesia has not been achieved,
the presence of these signs and symptoms is not necessarily a
guarantee of profound anesthesia. The lack of profound anes­
thesia may be due to incomplete penetration of the local an­
esthetic drug to the deepest core bundles (pulpal fibers tend
to be more centrally located ) and to accessory innervation
(see Chapter 16, "Troubleshooting Inadequate Anesthesia" ) .

m Mantle Bundles
.... Core Bundles

CNS Periphery

Proximal D i stal

F I G U R E 3-1 5 Distribution of Core and Mantle Bundles. Mantle

bundle fibers in a particular location tend to innervate structures
in close proximity. Core bundle fibers in that same location tend to
innervate structures peripheral to the location. In the example of
the inferior alveolar nerve, posterior teeth are innervated by mantle
fibers. T his results in molars being anesthetized earlier and more
easily than anteriors.
28 SECTION I PAIN CONTROL CONCEPTS
•
Introd u ctio n to Local An esthesia
Local anesthesia may b e defined a s a temporary loss o f sen­
sation in a specific, usually small area of the body (Malamed,
2 0 1 3 ) . A primary distinction between local and general
anesthesia is that when local anesthesia alone is in effect,
patients remain conscious (Daniel, Harfst, & Wilder, 2008).
This distinction is important when procedures are to be
performed while a patient is under the influence of sedation
or general anesthesia, because in the absence of specific
procedures to anesthetize local tissues no local anesthesia
exists. For example, a third molar extraction under general
anesthesia is typically performed after the administration of
local anesthesia. It is important to add that, in the majority
of dental procedures, sedation and general anesthesia are
seldom necessary to achieve good pain control.
Local anesthesia can be induced by various methods.
The applications of pressure, cold, electrical stimulation,
and trauma have the potential to cause temporary losses
of sensation. Although not commonly thought of as local
anesthetics, some of these alternatives to inj ectable drugs
are frequently utilized in medicine. In dentistry, combina­
tions of commercial preparations of topical and inj ectable
local anesthetic drugs are more commonly used when dis­
comfort is anticipated. This is accomplished by anesthetiz­
ing specific teeth and tissues without anesthetizing all of
the teeth and all of the tissues. It is important to note that
even when all of the teeth and their surrounding tissues
are anesthetized, the anesthesia is still described as local.
Local Anesthetic Drugs and How They Work
Local anesthetic drugs all work similarly. Local anesthetic
molecules have a greater affinity for protein receptor sites
within the nerve membrane compared with Ca+2 ions and
subsequently displace them. Different local anesthetic drugs
have varying affinities for these receptor sites, which account
for clinically significant differences in drug action. One drug,
for example, bupivacaine, aggressively bonds to the recep­
tor sites resulting in the longest duration of action of all local
anesthetic drugs in current use in dentistry today (Danielsson
et al., 1986; Fawcett et al., 2002; Moore & Dunsky, 1983).
Local anesthetic drugs are effective on both sensory and
motor nerves. They typically anesthetize smaller nerves be­
fore larger nerves and sensory nerves before motor nerves
(Jastak, Yagiela, & Donaldson, 1995). While the desired ef­
fects of these drugs are localized, their inevitable systemic
absorption exposes other tissues to their potentially toxic
actions, including the central nervous system (CNS), the car­
diovascular system (CVS), and skeletal muscle (Easson &
Carlson, 1980; Dudkiewicz, Schwartz, & Laliberte, 1987). All
of the currently available injectable dental local anesthetics
interrupt the transmission of nerve impulses. The five local
anesthetic drugs packaged for inj ection in dentistry today
include articaine, bupivacaine, lidocaine, mepivacaine, and
prilocaine (see Chapter 5, "Dental Local Anesthetic Drugs").
Chapte r Q u esti o n s
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1 . Which of the following statements most accurately
describe(s) the major differences between sensory
and motor neurons?
1 . Sensory neurons are afferent and conduct impulses
toward the CNS.
2. Motor neurons are efferent and conduct impulses
to effector tissues and organs.
3. Sensory neuronal cell bodies do not participate
in impulse conduction and they are located away
from the axon.
4. Motor neuronal cell bodies participate in impulse
conduction and are located along the length of the
neuron at their terminal arborizations.
a. 3 only
b. 1 and 2
c. 1, 3, and 4
d. All of the above
2. Which of the following sequences best describes the
events in a successful impulse generation?
a. Stimulation, slow depolarization, firing threshold,
rapid depolarization, recovery
b. Stimulation, firing threshold, rapid depolarization,
slow repolarization, resting state
c. Resting state, stimulation, slow depolarization,
rapid depolarization, firing threshold
d. Resting state, stimulation, slow depolarization,
rapid depolarization, slow depolarization
3. How are Schwann cells and nodes of Ranvier related?
a. Schwann cells are nodes of Ranvier.
b. At the nodes of Ranvier, S chwann cells are one
layer thick.
c. Gaps between Schwann cells are called nodes of
Ranvier.
d. They are not related.
4. Which fiber types are responsible for providing sen­
sory information from dental and periodontal tissues?
a. C and B fibers
b. B and A delta fibers
c. Gamma and C fibers
d. A delta and C fibers
5. Which of the fibers in question #4 are myelinated?
a. Both A delta and C fibers
b. Both B fibers and C fibers
c. A fibers
d. None of the above
6. What are three divisions of the dental plexus?
a. Interdental, interradicular, and periodontal
b. Inner dental, interradicular, and dental
c. Interdental, interradicular, and dental
d. Inner dental, interradicular, and periodontal
 CHAPTER 3 NEUROANATOMY AND NEUROPHYSIOLOGY OF PAIN CONTROL
• 29

Refe re n ces Hodgkin, A. L., & Huxley, A. F. ( 1954 .

) A quantitative descrip­
tion of membrane current and its application to conduction
Basson, M. D. , & Carlson, B . M. (1980 . ) Myotoxicity o f single and and excitation in nerve. Journal of Physiology (London), l/ 7,
500-544.
repeated injections of mepivacaine in the rat. Anesthesia &
Analgesia, 59, 275-282. Jastak, J. T., Yagiela, J. A., & Donaldson, D. (1995 .
) Local
Beers, M. H., & Berkow, R. ( 1999 .
) [The] Merck manual of anesthesia of the oral cavity. Philadelphia, PA: Saunders.
Malamed, S. F. (2013 . ) Handbook of local anesthesia (6th ed.).
diagnosis and therapy (17th ed. , pp. 1474-1477 . ) Hoboken, NJ:
St. Louis: Elsevier Mosby.
John Wiley & Sons.
Bennett, C. R. ( 1978 .) Manheim's local anesthesia and pain 1983 .
Moore, P. A . , & Dunsky, J. L. ( ) Bupivacaine anesthesi a ­
control in dental practice (6th ed.). St. Louis: Mosby. A clinical trial for endodontic therapy. Oral Surgery, 55,
Blanton, P. L., & Jeske, A. H. (2003, June). The key to profound 176-179.
local anesthesia, neuroanatomy. Journal of the American Narhi, M., Yamamoto, H . , Ngassapa, D., & Hirvonen, T. ( 1994 ) .
Dental Association [JADA], 753-760. The neurophysiological basis and the role of inflammatory
2008 .
Daniel, S. J., Harfst, S. A., & Wilder, R . S. ( ) Mosby's dental reactions in dentine hypersensitivity. Archives of Oral Biology,
39(Supplement), 23S.
hygiene: Concepts, cases, and competencies (2nd ed.). St. Louis:
Mosby. 1981 .
No back, C. R . , & Demarest, R. J. ( ) The human nervous
Danielsson, K., Evers, H . , Holmlund, A., Kjellman, 0., system: Basic principles of neurobiology (3rd ed.). New York:
Nordenram, A., & Persson, N. E. ( 1986 . ) Long-acting local McGraw-Hill.
Pashley, D. H. (1990 . ) Mechanisms of dentin sensitivity. Dental
anaesthetics in oral surgery. International Journal of Oral and
Maxillofacial Surgery, 15, 119-126. Clinics ofNorth America, 34, 449.
Disalvo, E. A., & Simon, S. A. (1995 . ) Permeability and stability Pogrel, M. A., Schmidt, B. L., Sambajon, V. , & Jordan, R . C. K.
( 2003 .
) Lingual nerve damage due to inferior alveolar nerve
of lipid hi/ayers. Boca Raton, F L: CRC Press.
Dudkiewicz, A., Schwartz, S. , & Laliberte, R. ( 1987 . ) blocks. A possible explanation. Journal of the American Dental
Association (JADA), 134(2), 195-199.
Effectiveness of mandibular infiltration in children using the
local anesthetic Ultracaine (articaine hydrochloride). Journal 2008 .
Seeley, R . R., Tate, P. , & Stephens, T. D. ( ) Anatomy &
of the Canadian Dental Association, 53, 29-31. physiology (8th ed.). Boston: McGraw-Hill.
2000 .
Tetzlaff, J. E. ( 3-8 .
) Pharmacology of local anesthetics (pp. )
Fawcett, J. P., Kennedy, J. M., Kumar, A., & Ledger, R. ( 2002 . )
Woburn, M A: Butterworth-Heinemann.
Comparative efficacy and pharmaco-kinetics of racemic
bupivacaine and s-bupivacaine in third molar surgery. Journal
of Pharmacy and Pharmaceutical Sciences, ( ) 5 2 , 199-204.

Vi sit www.p earsonhighered.com/he �lthprofessionsresources to access the student resources that accompany
.
. b�ok. S1mply
th1s select Dental Hyg1ene from the choice of disciplines. Find this book and you will find the
comphmentary study tools created for this specific title.
 Events in a Successful N erve Impulse G eneration

Resting Potential = -70 mV

+ Charged
Extracellular

Resting
State

Depolarization = -50 to -60 mV

(Stow Phase)

+ Charged
Extracellular

"t)
c:
0
(.)
Depola rization = +40 mV (I)
(Rapid Phase) .�
::::::
E

Repolarization = -60 to -90 mV

(Return t o resting state)

+ Charged
Extracellular

30
Chapter 4 Pharmacology Basics

Chapter 5 Dental Local Anesthetic Drugs

Chapter 6 Vasoconstrictors in Dentistry

Chapter 7 Dose Calculations for Local Anesthetic Solutions

Chapter 8 Topical Anesthetics

··························································· @ ··························································

P h a rm a co l ogy Basics

OBJECTIVES KEY TERMS

• Defi n e a n d d i scuss the key terms in this cha pte r. a bsorption 3 7

a m ides 3 5
• An a l yze, eva l u ate, a n d be p repared to d iscuss the
b i otra nsformation 3 3
p h a rm a co l og i c p roperties of l oca l a n esthetic d ru g s and b i p h as i c 4 0
vasoco n strictors. cati o n 3 7
• Eva l u ate the d iffe re n ces betwee n the specific rece pto r c h o l i n este rase 4 1
theory a n d the m e m bra n e expa n s i o n theory a n d exp l a i n why coca i n e 33
neither theory acco u n ts fo r local a n esth etic effects on n e rve d issociation consta nt 39
m e m b ra n e s . d istri bution 3 7
e l i m i n ation 3 7
• Exp l a i n why t i s s u e i nfl a m m ation affects the su ccess of l o ca l e l i m i n ation h a lf-l ife 42
a n esth esia. e p i n e p h ri n e 33
• Eva l u ate the re lati onsh i ps between p H a n d p Ka a n d d iscuss este rs 35
the c l i n ica l re l eva n ce of both . H e n d e rs o n - H asse l ba l ch

•
e q u ation 3 9
D iscuss the p h a rmacodyn a m i cs a n d p h a r m a cokinetics of loca l
intermed iate chains 3 5
a n esth etic d ru g s .
m e m brane exp a n s i o n
• Eva l u ate the s i g n s a n d sym pto ms of a n d d iscuss the effects theory 3 7
of l o ca l a n esthetics on the centra l n e rvous system (C N S) . m eta b o l i s m 3 7
n e utra l b a s e 3 7
n ovoca i n e 3 3
p450 isoenzyme system 4 1
p h a rm a codyn a m i cs 36
p h a rmacokinetics 36
p Ka 39
p roca i n e 33
specific p rote i n recepto r
theory 3 7
vasoconstricto rs 3 4

32
 CHAPTER 4 PHARMACOLOGY BASICS
• 33

Introd u ction drugs (Holroyd, Wynn, & Requa-Clark, 1988; Wilwerding,

200 1 ) .
Local anesthetics are t h e most common drugs u s e d in I n 1 884, cocaine's potent local anesthetic effects o n
dental practice (Ayoub & Coleman, 1992). These agents are the eye and its benefit i n eye surgery were identified. That
used to control pain during oral procedures. When vasocon­ same year, local anesthetics were introduced in dentistry.
strictors are added, drug actions are enhanced, local bleed­ Of parallel interest, in 1885, the original formula for Coca­
ing is controlled, and safety is increased. The pharmacology Cola (which contained cocaine) was developed (Jastak &
of local anesthetic solutions in dentistry includes the phar­ Yagiela, 1981).
macology of local anesthetic drugs and the vasoconstrictors S everal years later, in 1 90 1 , a Japanese rese archer,
used in combination with them. Understanding the mecha­ Jokichi Takamine, isolated epinephrine for pharmaceutical
nisms of action, biotransformation (metabolic pathways), use, which was followed by Heinrich Braun's observation
and toxic effects of each drug on local and systemic tissues that adding epinephrine to cocaine solutions decreased
is necessary for safe and effective administration. its systemic absorption (reducing toxicity) while increas­
It is also important to understand that pharmacology ing its anesthetic duration. Braun described this effect as
is far from a static discipline. Clinicians are encouraged to a "chemical tourniquet," which allowed lower doses of co­
follow developments in this area as new drugs, new drug caine to be administered while achieving similar or better
combinations, and new delivery technologies are intro­ therapeutic effects (Jacobsohn, 1992). The euphoric and
duced to clinical practice. Upon mastering the principles in addictive properties of cocaine continued to trouble both
this chapter, clinicians should be well prepared to integrate researchers and clinicians, and the search for a nonaddic­
future developments into clinical practice. For historical tive alternative eventually led to the development of the
perspective on the evolution of dental local anesthetic local anesthetic drug procaine, in 1904.
drugs, see Box 4-1 •· Procaine was first synthesized in Germany and was
The current practice of local anesthesia owes its marketed in the United States in 1905 as novocaine. Lack­
existence to the pioneers of modem techniques and drugs, ing the addictive properties of cocaine, procaine repre­
including Niemann, Koller, Hall, Halsted, Freud, B raun, sented an important improvement in safety. D espite its
Einhorn, Takamine, Cook, Lofgren, and Lundquist. Their replacement in dentistry in the latter part of the twenti­
combined contributions span more than two centuries. eth century by more effective and less problematic drugs,
Cocaine was the precursor to modern dental anes­ procaine is recognized as the prototype of modern local
thetics. In 1860, cocaine extracts from the coca leaf were anesthetic agents. Procaine's almost universal acceptance
observed to cause a numbing effect on the tongue, leav­ in dental anesthesia is demonstrated by the observation
ing it ne arly without sens ation. The local therapeutic that many patients still refer to the local anesthetic they
effects of cocaine were explored for dental applications receive as novocaine, regardless of the actual drug admin­
at the same time that Sigmund Freud was studying its ef­ istered (see Figure 4-1 •) .
fects on the central nervous system (CNS) . His research
uncovered cocaine's toxic and highly addictive properties.
In papers to Dr. Carl Koller, Freud also reported "imme­
diate unpleasant side effects such as nausea, vomiting,
and collapse" (Jastak & Yagiela, 1981). These significant
adverse effects stimulated the search for more acceptable

Earl y civilizations experienced the effects of oral disease,

including pain. Evidence points to primi t i v e methods
having been used to alleviate dental pain. In the ancient
Middle East, for example, root canals were performed us­
ing malleable gol d and poul t ices made of fi g s to replace
diseased pulps. The Incas, Egyptians, and Chinese used a
variety of obtundents to control dental pain, including coca
leaves, henbane, mandrake, arsenic, and opium. Centuries
l a ter, nerve compression devices, exposure to cold, and
hypnosis were all used to control pain (Wil w erding, 200 1 ) . FIGURE 4- 1 Novocaine with NeoCobefrin
Al t hough some aspects of these remedies were success- Local Anesthetic Can, circa 1940s.
ful and a few are still used, most have been replaced with
: more effecti v e drugs and techniques.
•
Source: Used with permission. The Dr. Samuel
D. Harris National Museum of Dentistry,
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . • University of Maryland .
34 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•

In order to overcome procaine's somewhat unpre­
dictable anesthetic effects and a disturbing incidence of
allergic responses, lidocaine was developed and approved
for use in the United States in 1 948, followed by mepi­
vacaine (1960), prilocaine (1965), bupivacaine (1983), and
articaine (2000).
Local Anesthesia
The obj ective in using local anesthetic drugs during treat­
ment is to produce anesthesia for a specific area and, in
some instances, to reduce localized bleeding. The primary
benefit of local anesthesia is that pain sensations can
be suppressed without significant central nervous sys­
tem (CNS) depression (D aniel, Harfst, & Wilder, 2008;
Hardman et al., 1996). As mentioned in Chapter 3, this al­
lows the maj ority of dental procedures to be performed
under local anesthesia without exposing patients to the
risks of general anesthesia.
Regardless of the particular type of healthcare proce­
dure, loss of sensation due to local anesthesia is produced
by preventing the generation and conduction of nerve im­
pulses. The purpose of these impulses is to alert the CNS
to localized stimulation or tissue injury. Although there are
many techniques to produce local anesthesia, the majority
are used in medicine and some are non-pharmacological.
This discussion will be confined to local anesthetic drugs
used specifically for dentistry.
A sound understanding of local anesthetic drug ef­
fects and specific techniques is the foundation for safe and
successful administration. Considerations of the impact
of compromised physiologic function, the potential for
adverse reactions, and an awareness of drugs and supple ­
ments the patient may be using, whether prescribed or not,
Five local anesthetic drugs are packaged for inj ec­
tion in dentistry today. Although this number may seem
small, it has proven to be adequate for most applications.
In addition to these drugs, others that are not available in
dental cartridges will be discussed due to rare occasions
where patients may be allergic to all five. In addition to the
inj ectable drugs, topical anesthetics provide an important
adjunct in pain management.
Routes of Delive ry
There are two primary routes of delivery for dental local
anesthetic drugs, topical and submucosal inj ection. Topi­
cal application of local anesthetic drugs is more effective
on mucosa than on skin because of the ease of penetration
through thin mucosal barriers in order to reach underlying
nerves. Submucosal (and subcutaneous) injections produce
more profound anesthesia than topical routes of adminis­
tration due to the direct placement of drugs in proximity to
nerves.
Des i ra ble Prope rties of Loca l
An esthetic D r u g s
A n ideal local anesthetic would have the following spe­
cific properti e s : a high level of biocompatibility with
no systemic effects; a rapid onset; no toxicity to tissue,
including nerve tissue; and a therapeutic duration and
potency without inducing hyp ersensitivity or uncon­
sciousness (Malamed, 20 1 3 ) . Further, it would be ster­
ilizable, readily biotransformed, and provide adequate
topical effects at low concentrations (Malamed, 20 1 3 )
(see B o x 4 2 •) .
-

are equally important. Legal and ethical principles man­

date that practitioners licensed to inj ect drugs into the
human body are responsible for these considerations and,
ultimately, their consequences.
D e n t a l l o c a l a n e s t h e t i c d r u g s u s e d t o d ay a r e
remarkably s afe (Malamed, 20 1 3 ) . F e w pharmaceuti­
cals, in fact, h ave such extensive s afety records; how­
e v e r, this d o e s not mean that clinicians can ignore Biocom patibility:
m anufacturer s ' r e c o m m e n d atio ns, n o r does it mean 1. Nonirri t able
that information provided by experts in the field may 2. Nontoxic to neural structures
be ignored. For example, disregard for maximum rec­ 3. Nonallergenic
o m m e n d e d d o s e s, e s p e cially w h e n c o n s i d e ring age, 4. Biotransformable and easily eliminated
body weight, and physiologic compromise has l e d to 5. Completel y reversible effects
serious and even fatal consequences in the past (Moore,
Safety and Efficacy (at therapeutic doses):
1999). Failure to take appropriate steps to avoid depos­
iting s olution into blood vessels has met with equally 1. Effecti v e in tissues and mucous membranes
regrettable c o n s e quences (Aldrete & Narang, 1975 ) . 2. Short onset of action and no residual effects
3. Reasonable duration of action
Vas o c o n s t r i c t o r s ( d r u g s t h a t c o n s t r i c t p e ri p h e r a l
4. Adequate potency
b l o o d v e s s e l s ) gre atly incre ase t h e overall s afety of
5. Sterilizable
local anesthetic drugs by slowing their entry into the
systemic circulation; however, to avoid adverse events
6. Patients remain conscious
their use must be carefully considered (Okada, Suzuki,
& Ishiyama, 1989).
 CHAPTER 4 PHARMACOLOGY BASICS
• 35

Table 4-1 Injectable Dental local Anesthetic Drugs

Generic Drug Drug's Trade Name* Suppliers

Articaine Zorcaine Cook-Waite (Kodak)

Septocaine Septodont
Articadent Dentsply

Bupivacaine Marcaine Cook-Waite (Kodak)

Vivacaine Septodont
Bupivacaine Hospira Worldwide

Lidocaine Lidocaine Cook-Waite (Kodak)

Xylocaine Dentsply
Lidocaine Henry Schein
Octocaine Novocol
Lignospan Septodont

Mepivacaine Carbocaine Cook-Waite (Kodak)

Polocaine Dentsply
Mepivacaine Henry Schein
Isocaine Novocol
Scandonest Septodont

Prilocaine Citanest Dentsply

Citanest Forte Dentsply

Procaine Not available in dental cartridges

Products and suppliers current as of 2014.

*All trade names are the property of their respective parent companies.

All five available dental local anesthetic agents in the
United States have reasonably low systemic toxicities with
adequate onsets and durations of action. All are readily
biotransformed and relatively nonallergenic. Only two are
acceptable as both topical and inj ectable agents in den­
tistry (lidocaine, prilocaine) and all are minimally irritat­
ing with the potential to damage nerve tissues (Pogrel &
Thamby, 2000). Table 4-1 • and Table 4-2 • list the drugs,
suppliers, and basic formulations.
P h a rmacology of Local An esthetic
Ag e n ts
Inj ectable local anesthetic drugs in dentistry are classified
as either amides or esters. Each has two separate and very
different chemical components linked by what are known
as intermediate chains. The distinction of these drugs as ei­
ther amide or ester is based on the chemical nature of their
intermediate chains. A relatively easy way to distinguish

Table 4-2 Available Dental local Anesthetic Drug Formulations 201 3

Drug Concentration Vasoconstrictor Mode of Del ivery

Articaine 4% 1:100,000 epinephrine Injectable

4% 1:200,000 epinephrine Injectable

Bupivacaine 0.5% 1:200,000 epinephrine Injectable

Lidocaine 2% 1:50,000 epinephrine Injectable

2% 1:100,000 epinephrine Injectable

Mepivacaine 3% None Injectable

2% 1:20,000 levonordefrin Injectable

Prilocaine 4% None Injectable, Topical

4% 1:200,000 epinephrine Injectable

For additional information on specific drugs, consult the manufacturers ' product inserts.
36 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•

between the two formulas is that the amide chain contains
a nitrogen atom whereas the ester chain does not. The
chemical formulas of these drugs and their components
are demonstrated in Figure 4-2 • highlighting the maj or
distinctions between them. An easy method of identifying
the drug classification by naming conventions is presented
in Box 4-3 •·
The amide and ester linkages between sep arated
chemical components serve two important functions
(see Figure 4-2 ) . The first is to provide proper sp acing
between the chemical components, an aromatic (lipo ­
philic) end a n d a secondary or tertiary amine (hydro­
philic) end, which allows the anesthetic to be effective
in the tissues (Jastak, Yagiela, & D onaldson, 1995 ) . The
lipophilic property allows the drug to pass through bio­
logic membranes of nerves and the hydrophilic property
allows the agent to disperse in extra- and intracellular
fluids. The second is to provide for maj o r p athways of
biotransformation.
Pha rmacodynami cs a n d
Pha rmaco k i n etics
The two activities of a drug are referred to as its phar­
maco dynamics and p harmacokinetics . Pharmacody­
namics refers t o t h e actions o f a drug o n t h e b o dy
(local anesthesia) discussed in this chapter and to a lesser

Drug I ntermediate
Hyrd rophilic Drug
Lipophilic
Name Chain
Portion Portion Class

P roca i n e Ester

Lidoca i n e Am i d e

B u p ivaca i n e

M e p i vaca i n e

Pri l oca i n e

CH
H

Artica i ne S
I3
NHCOCH2 -N�
C31 17

H3COOC

F I G U R E 4-2 Chemical Formulas of Amide and Ester Local Anesthetic Drugs.

 CHAPTER 4 PHARMACOLOGY BASICS
• 37

An easy method to identify the cl a ssi f i c ation of dental l o cal anesthetic drugs is to observe that the word amide, as well as all
names for these drugs, contain a letter "i" in the first and second syllable of the name. In contrast the word ester has no letter
"i," nor does the first syllable for any of the ester drugs. Esters and amides do share the common ending "-caine."
AM i DES ESTERS

L i do-caine Co-caine
Bup i va-caine Pro-caine
Mep i va-caine Benzo-caine
Pr i lo-caine Tetra-caine
Art i caine* Chloropro-caine
Metabolism: primarily i n the liver Metabolism: b y cholin esterase

: *Articaine is primaril y metabo l i z ed by cho l inesterase.

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . •
extent in Chapter 17, " Local Anesthesia Complications The Specific Protein Receptor Theory
and Management." Pharmacokinetics refers to the man­ The mechanism for the effect of local anesthetic drugs on
ner in which the body manages a drug, specifically the nerve membranes is best explained by the specific protein
m e chanisms of absorption, distribution, metabolism receptor theory. During normal nerve function calcium
(biotransformation), and elimination, discussed primarily ions are bound to receptor sites in ion channels and are
in this chapter. displaced when a membrane is stimulated. This allows
A major difference between local anesthetics and the sodium ion influx, impulse conduction, and stimulation of
maj ority of drugs is that systemic effects are undesirable the CNS.
with local anesthetics (Malamed, 20 13). The primary em­ As discussed in Chapter 3, sodium ion influx appears
phasis in this chapter therefore is the localized tissue ef­ to occur through selective channels with higher densities
fects of anesthesia. of these channels found in the nodes of Ranvier (Tetzlaff,
Although the intermediate linkages in local anesthetic 2000). The opening (and closing) of sodium ion channels
drugs provide an easy way to categorize them, it is the dis­ is referred to as gating and is controlled by changes in the
sociation of anesthetic molecules in solution that deter­ structural proteins of the nerve membrane adj acent to the
mines the effects of these drugs. Those commonly used in ion channels (Covino & Vasallo, 1976; Haydon & Kimura,
dentistry are prepared as acid salts. Once dissolved in ster­ 1981).
ile water, the drugs dissociate into two forms, a positively The action of local anesthetics on nerve membranes
charged molecule or cation and an uncharged or neutral is largely explained by the binding of local anesthetic
molecule the neutral base. In solution, the cation is more molecules to these structural proteins known as specific
stable. protein receptor sites in the ion channels. Only one mol­
Local anesthetic drug actions are dependent upon ecule can occupy a receptor at one time (see Box 4-4 ) .
the actions of both the neutral base and cation molecules. These receptors temporarily transform nerve membranes
D espite the greater stability of cations in solution, it is to nonexcitable states in which impulse propagation is
the behavior of both the neutral base and cation within a prevented. Sodium ions cannot pass through channels
nerve membrane that determines the potency, duration, blocked by anesthetic molecules. Receptor binding re­
and overall efficacy of local anesthetic drugs. Solutions in sults in closing of the channels, preventing the influx of
dental cartridges are designed to provide an optimal ini­ sodium and blocking the transmission of impulses. It is
tial balance of cation and neutral base molecules for stable estimated that approximately 90% of the actions of local
and effective local anesthetic action. anesthetic drugs are due to the binding of specific pro­
tein receptor sites by local anesthetic cations (Malamed,
Pharmacodynamics of Local Anesthetic Drugs 20 13).
The pharmacodynamics of local anesthetic drugs include
their actions on peripheral nerves, the CNS, CVS, and other The Membrane Expansion Theory
tissues. These actions interrupt the normal generation and A second theory, the membrane expansion theory, de­
conduction of nerve impulses and will be explained in the scribes a modification of the membrane structure in the
following section. presence of local anesthetic drugs that is not explained by
38 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•
Drug molecules bind to protein receptors to cause drug
effects (agonist effects). Onl y one mol e cule can occupy a
receptor at one time. Depending on the pH of the tissue,
drug molecules can exi s t in both the lipophilic or hydro­
philic form. Receptor-drug interactions occur as a result of
the lipophilic or hydrophilic nature of the drug molecule.
Re
: ( � � �k� : � . . � � ·. �0?�)
• •
. • • • • • • • • • • • •
the specific receptor theory (Lee, 1976; Malamed, 20 1 3 ) .
These membrane modifications have b e e n demonstrated
along affected nerve membranes, which may be caused by
diffusion of local anesthetic molecules to lipophilic regions
of the membranes. This alteration causes a narrowing of
the diameters of ion channels, further limiting their per­
meability to sodium ions (Seeman, 1972) . Although nei­
ther the specific receptor nor the membrane expansion
theory is able to explain the actions of local anesthetic
drugs entirely, both emphasize the actions of local anes­
thetic molecules on nerve membranes (Jastak, Yagiela, &
Donaldson, 1995). The dissociation of anesthetic molecules
to cations explains the maj ority of the actions of local an­
esthetic drugs in the specific receptor theory ( -90% ). The
actions of neutral base molecules in the membrane expan­
sion theory explain approximately 1 0 % of the anesthetic
effect (Malamed, 20 13).
The Ionic Basis o f Local Anesthesia
Local anesthetic molecules in their natural form are weak
bases, poorly soluble in water, and of little clinical value.
In cartridges solution is acidified with hydrochloric acid
to form stable salts of local anesthetic molecules. The salts
exist in two forms, a non-ionized molecule (neutral base)
and a positively charged ionic molecule (cation). For local
anesthetics to be stable in solution, they must be formu­
lated at a pH that favors water-soluble cations at the time
of inj ection, allowing dispersal of the anesthetic within
mucosal tissues ; however, this form will not penetrate
nerve membranes.
The process by which anesthesia is induced accord­
ing to the specific protein receptor theory may be ex­
plained as follows. Neutral base molecules are lipophilic
and pass through nerve membranes. Once beyond the
influence of the extracellular environment, neutral base
molecules combine with hydrogen ions to form cations,
which are hydrophilic. Only cations are able to bind to
receptor sites in the sodium ion channels of nerve mem­
branes in order to block nerve impulse generation and
transmission. Neutral base molecules are necessary to
provide adequate concentrations of cations in the sodium
channels. In order for anesthesia to develop, cations must
displace calcium ions.
In the formula RN + H+ � RNH+, RN represents
the neutral base, RNH+ represents the cation, and H+ is
the hydrogen ion. This equation describes the equilibrium
between neutral base molecules and cations in local an­
esthetic drug solutions (ADA/PDR, 2009; Bennett, 1974;
Jastak, Yagiela, & Donaldson, 1995).
As previously mentioned, cations (RNH+) repre­
sent the predominant molecules in local anesthetic drug
solutions because neutral base molecules (RN) are far less
stable.
• • • • • • • • • • • • •
After inj e ction into the tissues, the drug remains
briefly in a predominantly cationic (RNH+) form; however,
more neutral base molecules typically develop in response
to normal tissue pH. Once at the nerve membrane, hydro­
philic cations (RNH+) must convert to lipophilic neutral
bases (RN) in order to pass through. In the environment
of normal tissue pH, the equilibrium in the previous equa­
tion shifts to the left to favor an increase in neutral base
production outside the membrane:
RN + H+ � RNH+
This provides more neutral base molecules for mem­
brane penetration. As neutral base molecules (RN) pen­
etrate the membrane, fewer exist in the extracellular fluid.
This temporary extracellular depletion of neutral base
molecules fuels an equilibrium shift that favors neutral
base production.
In order to provide cations (RNH+) to bind to recep­
tor sites, neutral base molecules pass through the nerve
membrane. Once exposed to the axoplasmic environment,
the equilibrium shifts to the right, resulting in the forma­
tion of cations (RNH+):
RN + H + � RNH +
Hydrogen ions (H+) are available for this association
to RNH+ molecules in the axoplasm (pH - 7.4).
To summarize, neutral base molecules (RN) must
first penetrate nerve membranes before they convert
to cations (RNH+) in the axoplasm. Cations, and only
cations, are able to bind to receptor sites in sodium ion
channels. If adequate numbers of neutral base mole­
cules for any reason fail to penetrate the membrane and
convert to cations, profound local anesthesia will not
develop.
Inflammation and Local Anesthesia
When tissues are inflamed at sites of deposition of local
anesthetic drugs, the lowered pH inhibits the produc­
tion of neutral base molecules. This inhibition may result
in insufficient numbers of neutral base molecules (RN)
penetrating nerve membranes. Profound anesthesia may
become difficult to achieve or, if initially achieved, to sus­
tain (Keetley & Moles, 200 1 ; Quinn, 1998; Wong, 200 1 ) .
In addition t o t h e incre ase i n hydrogen ions, localized
edema and increased circulation may also contribute to
failure of profound anesthesia by removing drugs from
the delivery site.
 CHAPTER 4 PHARMACOLOGY BASICS
• 39

The Relevance of pKa and pH to Local Anesthetics Table 4-3 pKa of Injectable Local Anesthetic Drugs
Manufacturers manipulate the percentages of cations and in Dentistry
neutral bases in local anesthetic solutions by adjusting the
pH of the solution for optimal therapeutic benefit. The Drug Onset
inclusion of more cations than neutral base molecules in
Mepivacaine
solution has other specific benefits, including greater sta­
bility, increased solubility of the initially powdered local pKa = 7. 7 2-4 min.
anesthetic drugs in water, and ease of sterilization (Jastak,
Yagiela, & D onaldson, 1995). Increasing the pH in solu­ Lidocaine
tion will increase neutral base molecule concentrations,
whereas lowering the pH will favor cation concentrations. pKa = 7. 7 2-4 min.
These adjustments are calibrated for inj ection into normal
tissue pH. Prilocaine
The equilibrium concentrations of cationic and neu­
tral base molecules in solution are described by the pKa, pKa = 7. 7 2 min.
also known as the dissociation constant. When pKa pH, =

there is an equal distribution of cations (RN+) and neutral Articaine

base molecules (RN) in solution.
pKa 7. 8 1 -6 min.
The Henderson-Hasselbalch equation is an expression =

of pH as a function of the concentrations of weak acids

Bupivacaine
and bases in solution. It may also be thought of as a for­
mulaic definition of the dissociation constant, pKa. The pKa = 8.1 2-10 min.
Henderson-Hasselbalch provides manufacturers a means
of determining the percentage of cations and neutral base Procaine
molecules in solution at a specific pH. It is written:
pKa 9.1 6-10 min.
Log (Base/Acid) = pH - pKa =

Alternatively, it may be expressed in this manner: Source: http ://dailymed .nlm.nih .gov/dailymed/lookup.cfm ?setid=
C80C810A-60E0-49BD-139C-95AE C3A286F C.
pKa = pH - Log (Base/Acid)

CLI N I CAL APPLICATI O N OF pKa In local anesthesia, nar­

row pKa ranges of around 7.7-8.1 are common and include
all five of the inj ectable amides available in dentistry.
These values provide clinically useful onsets of anesthe­
sia. As a general rule, the higher the pKa, the longer the
onset of anesthesia. pKa values for the five amide dental
local anesthetic drugs and the ester, procaine, are listed in
Table 4-3 • · Procaine (pKa 9 . 1 ) has a relatively long
onset ( 6-10 minutes). Despite falling outside of this range
(7.7-8 . 1 ) , some agents used only as topical anesthetics in
dentistry are clinically effective, such as benzocaine (pKa
3.5) and tetracaine (pKa 8.4).
Vasoactivity of Local Anesthetic Drugs
Vasoactivity is an important property of dental local an­
esthetic drugs. All are peripheral vasodilators. This means
that vessels in areas of deposition will dilate when these
drugs are inj ected. This promotes entry of the anesthetic
into the circulation, leaving the local are a of inj ection.
Each drug expresses a different degree of vasodilation.
Articaine, bupivacaine, lidocaine, and procaine are potent
vasodilators and systemic uptake will be more rapid com­
pared with mepivacaine and prilocaine, which are weak
vasodilators.
Vasodilation is not a desirable characteristic of local
anesthetic drugs as it limits their duration and efficacy
while increasing their toxicity. Vasoconstrictor drugs are
added to local anesthetic solutions to oppose vasodilation
and block the rapid uptake of drugs into systemic circula­
tion. Some amides, such as prilocaine and mepivacaine, are
successfully used without vasoconstrictors because of their
weak vasodilative properties. Others, such as lidocaine, are
not particularly useful in dentistry without the addition
of vasoconstrictors because of their potent vasodilative
properties that lead to rapid uptake into the circulation.
Vasoconstrictors help retain drugs in areas into which they
have been inj ected. Local anesthetic drugs that remain in
deposition areas for longer periods are less available to
the systemic circulation, thereby reducing the risk of rapid
uptake, which can lead to rapid overdose.
CNS and CV S Actions of Local Anesthetic Drugs
It has been estimated that 5 % to 1 0 % of all reported ad­
verse reactions to anesthetic drugs occur because of the
administration of local anesthetic drugs (Atanassoff &
Hartmannsgruber, 2002). The CNS is p articularly sus­
ceptible to the effects of these drugs in the circulation.
Unbound (free) drug molecules are distributed to local
tissues or absorbed into the systemic circulation. It is im­
portant to note that molecules absorbed into the systemic
circulation are quickly distributed to highly sensitive cells
40 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•

of the CNS and CVS. All of the dental local anesthetic phase of excitation ( phase I ) may be explained as an early
drugs, with the exception of bupivacaine, affect the CNS depression of the normal inhibitory pathways of the CNS.
well before they impact the CVS and require significantly This early loss of inhibition may be absent in some cases
higher blood concentrations before they affect the CVS ( see Box 4-6 • ) . For further discussion on the impact of fear
( Levsky & Miller, 2005). and anxiety, see Chapter 18, "Insights for Fearful Patients."
Factors that can precipitate toxic overdose from local
anesthetic drugs include excessive doses, intravascular CVS E F F E CTS Similar to local anesthetic drug effects on
administration, rapid delivery, and/or slower than normal the CNS, at therapeutic blood levels there are usually
biotransformation or elimination. Other factors that may no clinically significant CVS effects ( Jastak, Yagiela, &
contribute to overdose include an individual's age, weight, D onaldson, 1995 ) . The CVS effects of local anesthetic
health status, and routes of administration ( Malamed, drugs at higher blood levels can be both h armful and
20 13). therapeutically beneficial. For example, toxic overdose
of both lidocaine and procaine can ultimately cause car­
CNS EFFECTS At therapeutic blood levels, local anesthetic diovascular collapse, while at the same time both have
drugs usually exert no clinically significant effects on the proven to b e quite us eful in treating cardiac arrhyth­
CNS (Jastak, Yagiela, & Donaldson, 1995; Malamed, 20 13). mias ( s e e Box 4-6) ( American Academy of Pediatric
At high blood levels, local anesthetic overdose manifests D entistry, 2005; Malamed, 20 1 3 ) .
as CNS depression. The symptoms of CNS depression Similar t o the CNS effects of local anesthetic drugs,
have been characterized as biphasic ( occurring in two typical CVS events are biphasic. Initially, heart rate and
phases ) and are consistent with a progression from early blood pressure may increase. As dosing continues, vaso­
signs of CNS excitation ( phase I ) to signs of CNS depres­ dilation occurs, leading to depression of the myocardium,
sion ( phase II ) that can lead to tonic-clonic convulsions, which may result in a fall in blood pressure. The contrac­
coma, and respiratory arrest ( ADA Council on Clinical tility of the myocardium may be so impaired that cardiac
Affairs, 2005). output is reduced. When combined with CNS seizure
An important consideration when identifying CNS activity, cardiac and respiratory arrest may result.
effects is that temporary signs of excitation which may be With the exception of bupivacaine, this is the usual
seen in local anesthetic overdose are also unfortunately course of local anesthetic overdose ( Prilocaine hydrochlo­
seen in non-overdose-related psychogenic reactions ( fear ride, 20 1 3 ) . B upivacaine is nearly equally toxic to both
and anxiety ) in dental settings. In order to distinguish the CNS and the CVS ( see B ox 4-7 • ) . It is more likely
between a fear reaction and a true overdose, a clinician to induce an overdose and once that overdose occurs, it
must be alert to the development of signs of CNS depres­ is typically more difficult to reverse compared with other
sion. If the excitation represents an early phase of overdose agents. For example, when comparing bupivacaine to lido­
and the excitation is replaced by signs and symptoms of caine, it has been demonstrated in animal studies that bu­
CNS depression, it is due to an overdose ( see Box 4-5 • ) . pivacaine is up to 16 times more cardiotoxic than lidocaine
This means that the excitatory pathways of the CNS are ( Levsky & Miller, 2005).
being depressed by the drug, leaving only signs and symp­ Fortunately, most overdoses are self-limiting. The
toms of CNS depression ( Malamed, 20 1 3 ) . The initial drugs are continuously biotransformed. Their effects on

(in alphabetical order) The presentation of symptoms of lidocaine and procaine

Apprehension, excitedness, talkati v eness overdose is the notable exception to the biphasic pro­
Bilateral numbness of tongue gression of local anesthetic overdose of the CNS. Often
Disorientation patients do not present with phase I signs and symptoms
Drowsiness more common with lidocaine of excitability; instead, they present with ini t ial signs and
Elevated BP, pul s e, breathing symptoms of phase I I depression only.
Headache Al t hough bupi v acaine has specific benefits for longer
Lightheadedness periods of anesthesia, i t is the most toxi c of the five local
Loss of consciousness anestheti c s. Both CNS and CVS toxi c i ty thresholds are
Muscl e twit ching/tremors in muscl e s of face, extremi t ies lower, and unlike other local anesthetic drugs, CNS and
Perioral numbness CVS susceptibili ty is nearl y equal. This characteristic, along
Shi v ering, chilled feeling of skin with bupivacaine's prolonged duration of action, limits its
Slurred speech choice as a primary drug for routine use in dentistry.
Visual /auditory disturbances
r f s ei k Source: Levsky & Mi ll er, 2005; Ma l amed, 201 3 .
• •

: .v:'� �. !� ��� �� ! �: �� � :�• • • • • • • • •• • • • • • • • • • •

I
 CHAPTER 4 PHARMACOLOGY BASICS
• 41

Effects on myocardium result in depression of:

Electrical excitability
Conduction rate
Force of contraction
Effects on smooth muscle resul t in vasodilation* of:
Peripheral vasculature
Effects on blood pressure resul t in:
Hypotension with increasing doses (more frequent with
procaine and lidocaine)
*Except wi t h cocaine, when used as a l o ca l anesthetic, which
produces vasoconstriction.
� •S.o �r.c: .J :s�a.k� �a :i� l.a •&• ��n� l�:o.n : :9��; .T:t�l��· ��0.0� • • • • Ji
the CNS and CVS, similar to those on the skin, mucosa,
periodontium, pulp, and other tissues are transient, and
disappearing rapidly once their concentrations fall below
FIGURE 4-3 Systemic Circulation, Absorption, and Distribu­
depressant levels. This explains why many mild overdoses
tion of Local Anesthetic Drugs. Local anesthetic drugs are ab­
may go unnoticed.
sorbed into the systemic circulation, and distributed throughout
Pharmacokinetics of Local Anesthetic Drugs the body. Highly perfused organs such as the lungs, brain, heart,
and kidneys will receive more systemically distributed drugs
B efore discussing the pharmacology of each specific drug,
than less perfused tissues. Muscle by mass receives the highest
pharmacokinetic properties common to all of the available
percentage of drug.
inj ectable dental local anesthetic drugs will be discussed.
This facilitates a better understanding of the similarities
and differences among them. Once metabolites reach the kidneys, they are eliminated
in the urine along with any unmetabolized fractions of a drug.
Absorption and Distribution
B I OTRAN S F O R M AT I O N O F A M I D E S B upivacaine, lido­
Once absorbed into the systemic circulation, drugs are dis­ caine, and mepivacaine are primarily biotransformed in
tributed throughout the body (see Figure 4-3 •) . Organs the liver by hepatic enzymes. This pathway is complex and
that are highly perfused with blood such as the lungs, involves a number of steps. Mepivacaine is less easily bio­
brain, heart, and kidneys receive more of systemically dis­ transformed compared with lidocaine, and bupivacaine is
tributed drugs than those with less perfusion (Pickett & more slowly biotransformed compared with either mepi­
Terezhalmy, 2009). Similarly, inj ection into highly vascular vacaine or lidocaine.
regions results in faster absorption and distribution away In addition to the liver, prilocaine is biotransformed in
from sites of deposition. In contrast, deposition into less the kidneys and lungs with very little excreted unchanged
vascular regions with slower vascular uptake prolongs the (Jastak, Yagiela, & D onaldson, 1995; Prilocaine hydro­
local actions of drugs. chloride, 20 13).
Articaine is an exception in its biotransformation
Biotransformation and Elimination
pathways. Product monographs state that only 5 % to
Biotransformation, or metabolism of local anesthetic drugs, 10% of articaine is metabolized via the liver's isoenzyme
reduces or eliminates their toxicity. This is accomplished system. It is a true amide, yet in intraoral administration
by biologically breaking the drug down into components the maj ority of its metabolism is nonhep atic, prim ar­
called metabolites. This process occurs primarily through ily via cholinesterase, similar to esters (Jastak, Yagiela, &
one of two pathways, either in the liver or in the blood. The Donaldson, 1995).
pathway of biotransformation in the liver is known as the
hepatic p450 isoenzyme system. This is a slower process B I OTRAN S F O R M ATION O F E S T E R S Benzocaine, procaine,
compared with metabolism in the blood by the enzyme, and tetracaine are esters. Similar to other esters, they are
cholinesterase (also referred to as plasma cholinesterase). biotransformed in the blood via cholinesterase. Procaine
This is the enzyme responsible for breaking down esters undergoes rapid metabolism by cholinesterase, while tetra­
and articaine. Manufactured primarily but not exclusively caine's metabolic pathway is similar, but slower, compared
in the liver, cholinesterase is widely distributed. with procaine and benzocaine.
42 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•

Box 4-8 Elimination Half-Life

Drug Reduction
M a xi m u m reco m m e n d e d dose (M R D) re p rese nts t h e maxi­
1 00% mum q u a ntity of d r u g that can b e safe l y a d m i n iste red in
1 st Y2 l ife .!. most situati o n s . These va l u es a re p rovi d e d by m a n ufact u r­
e rs p ro d u ct i nserts fo r each d r u g . P revi o u s conservative
2 n d Y2 l ife 50 50%
reco m m e n d at i o n s i n this text were based o n the l owest
3rd Y2 l ife 25 50% va l u es fro m seve ra l s o u rces w h e n co n s i d e ri n g M R D va l u es
4th Yz l ife 1 2.5 50% fo r the d r u g s . Cu rre nt FDA a p p roved M R D va l u es wi l l be
fu rt h e r d iscussed and a p p l i ed in C h a pter 7 , " Dose C a l c u l a -
5th Yz l ife 6.25 50% •

I An t
•

6th Yz l ife 3. 1 2 50% : � � �� ��� �� � �� � :� ��� �

t on
. .
r L
. · ·
i � ns "
. • • • • • • • • • • • • • • •
.!.
.
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

E L I M I NAT I O N HALF-LI F E (t1!2) The elimination half-life

of a drug may be defined as the rate at which it is removed
D uring biotransformation, ester local ane sthetics from the systemic circulation by the kidneys. Within the
break down to para-amino benzoic acid (PABA), a metab­ kidneys drug elimination occurs over time, as blood re­
olite that is the most likely source of their relatively high circulates through the organs (Pickett & Terezhalmy,
antigenic tendencies (Eggleston & Lush, 1996) . PABA has 2009) . Elimination half-life has also been expressed as
been an oral supplement for a number of conditions in the the time necessary to metabolize and excrete 5 0 % of a
past and can also be found in a few sunscreens because of drug (Malamed, 20 1 3 ; Pickett & Terezhalmy, 2009) (see
its ability to block UVB rays (WedMD, 20 1 3 ) . Its use in B ox 4-8 • ) . Lidocaine, for example, has a half-life of 1.6
both situations has declined in recent years. hours. This means it will take more than six half-lives to
B enzocaine and tetracaine are used in dentistry as clear this drug or more than 9 hours before only a trace
topical anesthetics. Inj ectable esters, such as procaine, remains. In dentistry, a variety of drugs with different
may be administered submucosally when there is docu­ half-lives are currently used. Understanding these differ­
mented allergy to amides (a rare occurrence) . Although ences can impact drug selection and treatment planning
e s t e r local anesthetic drugs are n o longer packaged (see Box 4-9 •) . B ased on pharmacological principles,
in dental cartridges, they are still occasionally used in elimination half-life values may become important when
inj ectable form in dentistry and somewhat more fre ­ calculating additional dosing after maximum recom­
quently in medicine. Ester topical anesthetics are com­ mended doses (MRD ) have been administered (see B ox
mon in dentistry. 4-1 0 •) . Shorter half-life drugs may be readministered
sooner with less risk of overdose.
A list of the elimination half-life for each of the five
local dental anesthetic drugs available in dental cartridges
is provided in Table 4-4 •·

C o n s i d e r t h e situati o n of a n u rs i n g m o t h e r. S e l e ct i n g a
d r u g that wi l l q u ickly c l e a r h e r system red u ces the l i ke l i ­ Table 4-4 Elimination Half- Life Value
h o o d o f t h e d r u g b e i n g passed t o t h e ch i l d wh i l e n u rs i n g .
If a rtica i n e is a d m i n istered fo r treatme nt, its h a lf- l i fe is t h e Drug Ha lf-Life (h rs)
s h o rtest o f a l l a m i d e s at a p p roxi m ately 45 m i n utes after
maximum d os i n g . It was d e m o n strated i n o n e study that Articaine* 0. 75*
a rtica i n e 's h a lf- l ife , after ora l a d m i n istrat i o n , was a p p roxi­
mately 1 6-20 m i n utes when n o m o re than 1 20 m i l l i g r a m s Prilocaine 1.6
(a p p roxi m ately % - 1 Yz cartridges) were a d m i n istered (Oe rtel
et a l . , 1 997).
Lidocaine 1.6
It s h o u l d b e n oted th at, desp ite d i stri b u t i o n i nto
b reast m i l k, t h e re is no d o cu m e ntati o n of adverse events
Mepivacaine 1.9
fo l l ow i n g l i d o ca i n e use in l a ctat i n g fe m a l es . This is l i ke l y
t r u e o f the oth e r l o ca l a n esthetics as wel l .
Bupivacaine 2. 7-3. 5
•
Source: ADA/PDR (2009) and Oertel et a l . (1 999) .
: . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
•
*Septocaine® Product insert.
Source: Malamed (2013), Oertel et a!. ( 1999) and Septodont (2013a).
 CHAPTER 4 PHARMACOLOGY BASICS
• 43

Chapte r Q uestio n s
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Refe re n ces
1 . Elimination half-life refers to which one of the ADA/PDR guide t o dental therapeutics ( 5th ed. ) . (2009).
following? Montvale, NJ: Thompson PDR Corporation.
a. The time it takes for a drug to be half-metabolized Aldrete, J. A., & Narang, R. (1975). Deaths due to local anesthe­
b. The time it takes for half of a drug to be out of the sia in dentistry. Anaesthesia, 30, 685-686.
American Academy of Pediatric Dentistry Council on Clinical
system
Affairs. (2005). Guideline on appropriate use of local
c. The time it takes for half of a drug to be out of the anesthesia for pediatric dental patients. Pediatric Dentistry, 27,
circulation 101 -106.
d. The time it takes for a drug to be out of half of the Atanassoff, P. G. , & Hartmannsgruber, M. W. B. (2002). Central
circulation nervous system side effects are Jess important after IV
regional anesthesia with ropivacaine 0.2% compared to
2. Ester local anesthetics are metabolized in which one lidocaine 0.5% in volunteers. Canadian Journal ofAnesthesia,
of the following pathways? 49, 169 -172.
a. In the liver Ayoub, S. T., & Coleman, A. E. (1992). A review of local anes­
b. In the blood thetics. General Dentistry, 40(4), 285-287,289-290.
c. In the kidneys Becker, D. E., & Reed, K. L. (2006). Essentials of local anesthetic
d. In the brain pharmacology. Anesthesia Progress, 53, 98-109.
Bennett, C. R. (1974). Manheim 's local anesthesia and pain
3. CNS toxicity occurs because of: control in dental practice ( 5th ed. ) . St. Louis: Mosby.
a. The expected response of neurons in the CNS to Covino, B. G., & Vasallo, H. G. (1976). Local anesthetics: Mecha­
the drug dose. nisms of action and clinical use. New York: Grune & Stratton.
b. Frank neural tissue damage due to the excessive Daniel, S. J., Harfst, S. A., & Wilder, R. S. (2008). Mosby's dental
dose. hygiene: Concepts, cases, and competencies ( 2nd ed. ) . St. Louis:
c. Compromised vascular supply in the CNS due to Mosby.
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vasoconstrictor doses.
injection and prilocaine hydrochloride and epinephrine injection,
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Eggleston, S.T. , & Lush, L.V.V. (1996). Understanding allergic
a. Compromised vascular supply.
reactions to local anesthetics. Annals of Pharmacotherapy, 30,
b. Frank tissue damage. 851 -857.
c. D ecreased myocardial contractility, vasodilation Hardman, J. G. , Limbird, L. E., Molinoff, P. B. , Ruddon, A. G. , &
and hypotension. Goodman, A. G. (1996). Goodman and Gilman's the
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tion, and hypertension. McGraw-Hill.
Haydon, D. A., & Kimura, J. E. (1981). Some effects of n-pentane
5. Which portion of the anesthetic molecule is on the sodium and potassium currents of the squid giant axon.
responsible for binding to the receptor site inside Journal of Physiology, 312, 57-70.
the nerve membrane, thereby preventing Holroyd, S. V. , Wynn, R. L., & Requa-Clark, B (1988). Clinical
depolarization? pharmacology in dental practice, ( 4th ed. ) St Louis: Mosby.
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Jastak, J. T., Yagiela, J. A., & Donaldson, D. (1995). Local
6. Which part of a local anesthetic molecule determines anesthesia of the oral cavity. Philadelphia, PA: Saunders.
the classification of the drug as an ester or amide? Keetley, A., & Moles, D. R . , Eastman Dental Institute for Oral
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success rate of inferior alveolar nerve block analgesia in gen­
b. Hydrophilic portion
eral dental practice. Primary Dental Care, 8(4), 139 -142.
c. Intermediate chain Lee, A. G. (1976). Model for action of local anesthetics. Nature,
d. Caine linkage 262, 545-548.
Levsky, M. E., & Miller, M. A. (2005). Cardiovascular collapse
7. Which of the following is not a systemic reaction to an
from low dose bupivacaine. Canadian Journal of Clinical
overdose of a local anesthetic agent? Pharmacology, 12(3), e240-e245.
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c. Vasodilation of peripheral blood vessels Moore, P. A. (1999, April ) . Adverse drug interactions in den­
d. Respiratory arrest tal practice: Interactions associated with local anesthetics,
44 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
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sedatives and anxiolytics series. Journal of the American Den­
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································ ·························· ® ··························································

Denta l Loca l An esth etic D ru g s

OBJECTIVES KEY TERMS

• Defi n e a n d d i scuss the key terms i n t h i s cha pter. a rtica i n e 55

b u p ivaca i n e 64
• D iscuss s i m i l a rities a n d d iffe re n ces betwee n denta l local
e p i n e p h ri n e 46
a n esthetic d ru g s . l evo n o rd efri n 59
• Exp l a i n how s i m i l a rities a n d d iffe re n ces between denta l l oca l l i d o ca i n e 46
a n esth etic d ru g s p ro m ote c l i n i ca l ly safe a n d su ccessfu l local maxi m u m reco m m e n d ed
a n esth esi a . dose ( M RD) 48
m e p ivaca i n e 58
• S e l ect a p p ro p riate l oca l a n esthetic a n d/o r vasoco n strictor
m eth e m o g l o b i n e m i a 50
d ru g s fo r vari o u s types of cl i n i ca l situati o n s .
p a resthesia 55
• D iscuss a n d d eterm i n e situati o n s i n w h i ch specific d ru g s a re prilocaine 6 7
i n d i cated or contra i n d icated . proca i n e 66
• D iscuss w h i ch loca l a n esthetic sol utions a re effective without
vasoco n stri ctors .
• Exp l a i n w h y l o ca l a n esthetic sol utions with out vasocon stri ctors
a re m o re effective in certa i n cl i n ica l situati o n s .
• Exp l a i n when a n d why s o l u t i o n s w i t h e p i n e p h ri n e a n d
l evo n o rd efri n a re i n d i cated or contra i n d i cated i n c l i n i ca l

45
46 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•
CAS E S T U DY
Elena Gagarin
E l e n a G a g a r i n , a 3 0 - y e a r- o l d m o t h e r of a n u rs i n g
i nfa nt, i s i n n e e d o f d e n ta l treat m e n t t o re l i eve p a i n
i n two o f h e r t e e t h . H e r m a i n c o n c e r n s a re to b e
r i d of t h e n a g g i n g p a i n s h e h a s exp e r i e n ce d fo r t h e
l a st s e v e r a l w e e ks a n d to m a k e s u re s h e d o e s n 't
p a s s o n a n y of t h e l o c a l a n e s t h e t i c d r u g s to h e r
i n fa n t .
Introd u ctio n
The inj ectable local anesthetic drugs intro duced in
Chapter 4, "Pharmacology Basics," share common charac­
teristics in their chemical structures and properties. These
characteristics help explain similarities in the manner in
which they may be used.
Local anesthetic drugs are selected by balancing pa­
tient factors with the requirements of treatment. In order
to administer the most appropriate agent, it is important to
recognize the differences among the drugs. For example, a
drug may provide safe and reliable anesthesia in a maj or­
ity of individuals, yet may wear off so quickly that it proves
to be of limited usefulness for others. In these situations
the use of a longer-acting drug may be beneficial.
This chapter will highlight similarities and differences
in injectable local anesthetic drugs for dentistry in an effort
to promote clinically safe and successful local anesthesia.
Maximum doses that appear in previous editions of this and
other texts differ significantly from the values used in the
FDA guidelines when calculating drug dosages for patients.
Although some clinicians may not know they exist, the
United States Food and Drug Administration (FDA) Center
for Drug Evaluation and Research, Office of Pharmaceutical
Science, Informatics and Computational Safety Analysis
created and consistently updates maximum recommended
doses (MRDs) for local anesthetic drugs. Two established
sets of recommendations for the use of the same drugs can be
confusing for clinicians. In order to minimize this confusion,
lower non-FDA-established values have been eliminated in
this text; however, although this is an important consideration,
not all published policy and recommendations have adopted
the higher FDA values. For example the American Academy
of Pediatric Dentistry still lists the lower values in its mono­
graph, "Guideline on Use of Local Anesthesia for Pediatric
Dental Patients" (American Academy of Pediatric Dentistry,
2005 ) . Similar to the AAPD, others may elect to observe
MRDs lower than the FDA standard to provide an extra layer
of safety without compromising treatment or comfort.
In all situations it is important to note that local anes­
thetic product inserts contain similarly worded advice recom­
mending that clinicians administer the lowest dosage needed
to provide effective anesthesia. A summary of the properties
of each drug discussed is provided in Appendix 5-1.
S h e is cu rre ntly n u rs i n g eve ry 3-4 h o u rs a n d h a s
m a d e n o p rovis i o n s fo r rese rves fo r t h e ba by, w h o is
n ot able to co n s u m e fo rm u l a .
Wh ich o f t h e d e nta l local a n esthetic d ru g s is a b l e
t o p rovi d e a d e q u ate p a i n re l ief a n d w i l l n ot be passed
o n to the baby in s i g n ificant q u a ntities 2-3 h o u rs after
her a p po i ntme nt?
Lidoca i n e
Background
Lidocaine was the first amide local anesthetic drug, de­
veloped by Lofgren in 1943. D espite the introduction of
other amides since that time, lidocaine remains the stan­
dard against which local anesthetic drugs are compared. It
has a long and impressive record of reliability, with a rapid
onset, rare reports of hypersensitivity, typical pulpal dura­
tions of 60 minutes or more, and soft tissue durations of up
to 5 hours (Moore, 1999; Noormalin et al., 2005). Lidocaine
has been described as a versatile drug because of its nearly
universal applicability in all areas of healthcare delivery
(Harn & Durham, 1990; Haugen & Brown, 2007; Jastak,
Yagiela, & D onaldson, 1 9 9 5 ; Moore, 1 9 9 9 ; Noormalin
et al., 2005 ) . D espite its universal appeal, it is particularly
well suited for dentistry. Combined with various dilutions
of vasoconstrictors, lidocaine has made profound and du­
rable pain control a routine expectation in clinical practice
(Carestream Health, Inc., 20 13; Malamed, 20 13).
Lidocaine has been noted to have anticonvulsant
properties and has been used to terminate seizures or de­
crease their durations. Similar to other local anesthetics
with anticonvulsant properties, lidocaine acts to prevent or
terminate seizures by depressing the excitability of corti­
cal neurons, thus raising seizure thresholds. Mepivacaine,
prilocaine, and cocaine have also demonstrated anticon­
vulsant properties and, similar to lidocaine, at blood levels
that are well below seizure thresholds (Malamed, 20 13).
Formulations for Use i n Dentistry
Lidocaine is provided in the following formulations:
2% lidocaine plain* (without vasoconstrictor)
(see Figure 5-1A •) (*Not available in dental car­
tridges in North America since August 20 1 1 )
2 % lidocaine with 1 : 100,000 epinephrine
(see Figure 5-lB •)
2 % lidocaine with 1 : 50,000 epinephrine
(see Figure 5-1 C •)
Drugs with vasoconstrictors are written in two common
conventions; for example, lidocaine with epinephrine
may be written as either 2% lidocaine with 1 : 1 0 0,0 0 0
 CHAPTER 5 DENTAL LOCAL ANESTHETIC DRUGS
• 47

�r ·-

_
_
--
_
_-
_
__""_.......
_ ._
_

,, __.

20 m��fmL

s��
.. ....

...... ..... ,_ ... .... _

2-(diethylamino)-N-(2,6-dimethylphenyl )acetamide

(A)

2-(diet h y lamino)-N-(2,6-dimethylphen y l )acetamide

(B)

...- ���'1?.::-.-=:::- . ��
. ....�
....- -· --

�\
�s
CHl NHCOOI2 --N
/C,H,

cf CH3
"'-c,H,

2-(diethy lamino)-N-(2,6-dimelhy lpheny l )acetamide

(C)

FIGURE 5-1 A - 2% Lidocaine Plain. B - 2% Lidocaine, 1:100,000 Epinephrine. C - 2% Lidocaine, 1:50,000 Epinephrine.
Source: Courtesy of Dentsply PharmaceuticaL
48 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•
epinephrine, or as 2 % lidocaine, 1 : 1 00,000 epinephrine
(epinephrine is a vasoconstrictor added to increase the
safety and duration of local anesthetic drugs). These con­
ventions are used interchangeably throughout this text.
Duration of Action
2 % lidocaine plain* (without vasoconstrictor) (*Not
available in dental car-tridges in North America since
August 20 1 1 )
Very short duration = 5-10 minutes pulpal; 60-120
minutes soft tissue
2% lidocaine with 1 : 100,000 epinephrine
Intermediate duration = 60 minutes pulpal; 180-300
minutes soft tissue
2% lidocaine with 1 :50,000 epinephrine
Intermediate duration = 60 minutes pulpal; 180-300
minutes soft tissue
Local anesthetic drugs are commonly classified as short,
intermediate, or long acting based on the duration of pulpal
and hard tissue anesthesia (ADA/PDR, 5th edition, 2009)
(see Table 5-1 •).A short pulpal duration in dentistry typically
lasts from approximately 20 to 40 minutes. Intermediate du­
rations last up to 70 minutes and long durations up to 8 hours
depending on the inj ection technique. Soft tissue durations
are usually much greater, even when no vasoconstrictors are
used (ADA/PDR, 5th edition, 2009; Malamed, 20 13).
The receptor binding strength of a local anesthetic
and its vaso activity are key considerations in its dura­
tion of action. Lidocaine without a vasoconstrictor has a
moderately strong binding strength to affected protein re­
ceptors; however, it is a vigorous vasodilator. B ecause of
its strong vasodilating effects, it provides only a very short
duration of action when used without a vasoconstrictor.
When inj ected with a vasoconstrictor, lidocaine pro­
vides profound and durable anesthesia, enough, in fact,
for most dental procedures (see Appendix 5-1 ) . Vaso­
constrictors, which prolong local anesthetic durations by
Table 5-1 Local Anesthetic Duration Comparisons
Drug Classification (Duration of Action)
Articaine Intermediate
Bupivacaine Long
Lidocaine Short (without vasoconstrictor)
Intermediate
Mepivacaine Short (without vasoconstrictor)
Intermediate
Prilocaine Short (without vasoconstrictor)
Intermediate
Procaine Short
constricting local vasculature, are discussed in Chapter 6,
"Vasoconstrictors in D entistry."
Similarity to Other Local Anesthetics
Lidocaine's formula has less similarity to the other amide
drugs discussed than to etidocaine, a long-acting amide
no longer packaged for dentistry and formerly marketed
as Duranest. Etidocaine is still available for use in other
healthcare settings.
A detailed discussion of lidocaine's properties fol­
lows, with a brief summary of properties, dosing recom­
mendations, and uses provided in Box 5-1 •· Appendix 5-2
provides a complete reference table for lidocaine and a
maximum dose reference is provided in Appendix 7-2.
M RD (Maximum Recommended Dose)
3.2 mg/lb (7.0 mg/kg); 500 mg absolute maximum (previously
2.0 mg/lb; 4.4 mg/kg; 300 mg absolute maximum)
The maximum recommended dose (MRD) of a local an­
esthetic drug represents the maximum quantity of drug that
can be safely administered during an appointment in most situ­
ations. The absolute MRD for lidocaine is 500 mg per appoint­
ment (Malamed 20 13; National Library of Medicine, 2013 ).
Formulations fo r Use in Dentistry: 2% with 1 : 1 00,000
e p i n e p h ri n e ; 2% with 1 : 50,000 e p i n e p h r i n e
• D u ration o f Action: I nterm e d i ate, 6 0 m i n utes p u l p a l ;
1 80-300 m i n utes soft tissue
M RD : 3 . 2 mg/lb (7 .0 m g/kg); 500 m g a b s o l ute m a xi m u m
(previ o u s l y 2 . 0 m g / l b ; 4 . 4 m g/kg; 300 m g a b s o l ute
m axi m u m)
Relative Potency: Twice p roca i n e ; s i m i l a r to m e p iva­
ca i n e and p r i l o c a i n e ; l ess than a rtica i n e ; m u ch l ess t h a n
b u p ivaca i n e
Relative Toxicity: Twice p roca i n e ; g reater t h a n p r i l oca i n e ;
s i m i l a r t o m e p ivaca i n e a n d a rtica i n e ; m u ch l e s s t h a n
b u p ivaca i n e
Meta b o l i s m : Liver
Excretio n : K i d n ey; l ess than 1 0% u n c h a n g ed
Vasoactivity: M u ch l ess vasod i l at i o n t h a n p roca i n e ; g reater
than m e p ivaca i n e and p r i l o ca i n e
pKa: 7 . 7
pH: 3.3 to 5.5
Onset: 2-3 m i n utes
H a lf- L ife : 1 .6 h o u rs (96 m i n utes)
To pical Prepa rations: 2% to 1 0% fo rm u l at i o n s
Preg nancy Categ o ry: 8
� La
• • � � ��: �� a.i l � � � � .i � � �e� �t. � i� k: �: �r� i � � � a.u� i ��
a i
• • • . IIi
 CHAPTER 5 DENTAL LOCAL ANESTHETIC DRUGS
• 49

Lidocaine-induced overdose reactions may differ from Relative Potency

other amides in that the initial excitatory phase may be Lidocaine is twice as potent as its predecessor, procaine, equal
short-lived or nonexistent (DeToledo, 2000). For more de­ in potency to mepivacaine and prilocaine, approximately
tailed information on MRD values, see Chapter 7, "Dose two-thirds as potent as articaine, and approximately one-fourth
Calculations for Local Anesthetic Solutions." as potent as bupivacaine (see Figures 5-2 • and 5-3 •).

1 0 0 % rep resents
a n equal value to th e g i ven d ru g

Exa m p l e :
" E q u a l l y as potent a s "

200% represents
a va l u e two times g reate r tha n
the g iven d rug.

Exam p l e :
"Twice as toxi c as"

50% represents
a va l u e one-half the g i ven drug

Exam p l e :
" H alf as vasoactive as"

1 40% rep rese nts

a val ue 40% g reater tha n
t h e g iven d rug

Exa m p l e :
"40% more potent, toxic,
vasoactive than"

F I G U R E S-2 Comparison Values. This scale will be applied for the purpose of discussion and comparison of
potency, toxicity, and vasoactivity.
50 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•
tl l l lt tl l l lt tl l l lt tl l l lt
0 100% 200 % 300 %
FIGURE 5-3 Relative Potency. Potency values for local anesthetic drugs
compared with lidocaine.
Many dental procedures require extended durations
of profound anesthesia that are often significantly longer
than for many medical procedures. These extended dura­
tions may be unpleasant and may increase the risk of self­
inj ury. As is the case with all the local anesthetic drugs,
lidocaine is not ideal in this respect; however, it has a ther­
apeutic potency that balances the need for profound and
durable dental anesthesia without excessive duration.
Relative Toxicity
Lidocaine is approximately twice as toxic as procaine and
prilocaine, similar in toxicity to mepivacaine and articaine,
and far less toxic (approximately one-fourth) compared
with bupivacaine (Jastak, Yagiela, & D onaldson, 1 9 9 5 ;
Tetzlaff, 2000) (see Figure 5-4 •) .
These statements are accurate but, similar to toxic­
ity statements for other local anesthetic drugs, do not com­
pletely address lidocaine's relative toxicity in all areas. For
example, although reported to be similar to articaine in toxic
potential, lidocaine has been demonstrated in studies to have
greater toxic potential (Oertel, Berndt, & Kirch, 1996; Simon
et al., 1997) . Lidocaine is more toxic to the central nervous
Lidoca i n e
Arti c a i n e
B u p ivac a i n e
M e p ivacai n e
Pri l oc a i n e
P roc a i n e
400 %
system (CNS) and cardiovascular system (CVS) than prilo­
caine but far Jess toxic than prilocaine in patients with blood
oxygenation deficiencies, such as methemoglobinemia. These
deficiencies are discussed in Chapter 10, "Patient Assessment
for Local Anesthesia." Lidocaine is approximately equal in
toxicity to mepivacaine and is considerably less toxic than
bupivacaine (approximately four times less) (Levsky &
Miller, 2005; Septodont, 2013b) (see Figure 5-4).
All local anesthetic drugs, if administered intravas­
cularly, may be potentially life threatening, particularly if
they are administered rapidly. The relative toxicity values
of the drugs discussed in this chapter assume that drugs
have not been administered intravascularly. Comparisons
take into account the normal mechanisms of metabolism.
For example, the drug procaine, which will be discussed
later in this chapter, is the least toxic of all drugs men­
tioned. If administered intravascularly, however, it may be
as toxic as the other drugs discussed.
Metabolism
Lidocaine is metabolized by hepatic enzymes also known
as oxidases and amidases (Tetzlaff, 2000). This process is
 CHAPTER 5 DENTAL LOCAL ANESTHETIC DRUGS
• 51

Lidoc a i n e

Arti c a i n e

B u p ivacai n e

Mep ivacai n e

Prilocaine

P roca i n e

100% 200 % 300 %

FIGURE 5-4 Relative Toxicity. Toxicity values for local anesthetic drugs
as compared with lidocaine.

complex and involves multiple steps. Hydrolysis accounts

for about one-third of lidocaine elimination ( Jastak,
Yagiela, & D onaldson, 1995; Tetzlaff, 2000). Several of
lidocaine's byproducts ( metabolites ) are pharmaco­
logically active. For example, lidocaine's primary initial Patie nts m a y s o m et i m e s ask a b o ut o r refe r to sou rces of
metabolite, monoethylglycinexylidide (MEGX), retains i nfo rmation that te n d to i n d i ct certa i n p h a rm a ceutica l s .
most of the pharmacological activity of lidocaine. Another These s o u rces m a y i g n o re, m isstate, exa g g e rate, o r
of lidocaine's biotransformation products, 2, 6-xylidine, has m o d ify scie ntifica l ly based evi d e n ce , especi a l ly re g a rd i n g
t h e dose-re l ated n a t u re o f d r u g toxicity. Lidoca i n e, fo r
raised concerns in the past and has been investigated as
a carcinogen in rats ( Jastak, Yagiela, & Donaldson, 1995)
exa m p l e , h a s b e e n m e n t i o n e d as a ca rci n o g e n fro m t i m e

( see Box 5 2 •).

-
to t i m e b e c a u s e of i t s d e m o nstrated t e n d e n cy to cause
m a l i g n a nt t u m o rs i n rats . It i s i m po rtant to n ote that the
i n d u ct i o n of m a l i g n a nt n a s a l t u m o rs i n rats occu rred o n ly
Excretion after very large doses were a d m i n iste re d . N ot o n ly wo u l d
Less than 1 0 % of lidocaine is excreted unchanged by the co m p a ra b l e dosi n g i n h u m a ns fa r exceed m a n ufactu rers'
kidneys. reco m m e n d e d m a xi m u m doses, but concerned patie nts
Higher excretion rates may be more common when can b e rea s s u red that t h e re is no evi d e n ce to s u p p o rt
the pH of urine is low ( Tetzlaff, 2000) ( see Box 5-3 •). s i m i l a r carci n o g e n i city in h u m a n s (J astak, Ya g i e l a , & •

na s · 1 9 )
Vasoactivity
: �� �� �� :: :
. . . . • • • • • • • • • • • • • • • • • • • • • • • • • • •
Lidocaine is a potent vasodilator with a very short dura­ greater compared with prilocaine and mepivacaine, which
tion when administered without a vasoconstrictor. It is limits its use to very short procedures if used without a
a less potent vaso dilator compared with procaine but vasoconstrictor ( see Figure 5-5 •).
52 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•

pKa

The pKa of lidocaine is 7.7.

H i g h e r co n ce ntrations of n o n m etabol ized l o c a l a n esthetic
m o l ecu l es i n u r i n e confi rm that h i g h e r p e rcentages of the
drugs h ave avoided m eta b o l i c b re a kdown, re n d e r i n g t h e m
potentia l ly m o re toxic. L o w u r i n e p H va l u es ca n be p resent
i n a s u rprisi n g n u m b e r of co n d itions, m a ny of which do n ot
p recl u d e denta l treatment. For exa m p l e , low uric pH va l u es
may be p resent in a n o rexia a n d sta rvati o n , e m p hyse m a ,
go ut, d i a rrhea, p e rsistent fever, fre q u e n t kidney sto n e
fo rmation, i nfections, a n d hyperka l e m i a (increased l eve ls of
potassi u m in the b l ood). S o m e vegeta rians a l o n g with other
denta l patie nts with susp ected o r confirmed n utriti o n a l
deficiencies m a y b e a ffected, as we l l as i n d iv i d u a l s ta k-
i n g drugs such as c h l o roth iazide d i u retics, m ethen a m i n e
m a n d e l ate, a m m o n i u m ch l o ride, a n d a l dostero n e . I n
additi o n , u n co ntro l led d i a b etics a n d those with m eta b o l i c
syn d ro m e , i n g e n e r a l , can h ave low u r i c p H va l u es (Ka m e l ,
Cheema-D h a d l i , & H a l perin, 2002; Luthra e t a l . , 2004;
Values for pKa in dentistry range from 3.5 for benzocaine to
9.3 for procaine. pKa is a valuable measurement of the rela­
tive numbers of neutral base and cationic molecules initially
available in local anesthetic solutions as affected by their
pH. The most useful pKa range for inj ectable anesthetics
falls between 7.6 and 8 . 1. Drugs with pKa values in this
range provide more rapid onsets of anesthesia. Lidocaine,
mepivacaine, and prilocaine all have pKa values of 7.7, whereas
articaine's is 7.8 and bupivacaine's is 8.1 (Carestream Health,
Inc. (2013); Malamed, 2013) (see Table 5-2 •).
pH
The pH of lidocaine plain solutions is 6.5.
The pH of lidocaine solutions with vasoconstrictors
ranges from 3.3 to 5.5.

� �:
• �. . . � �I�, :��7� �� � � : � � � : �� � � � ��0�).' . IIi
a l uf e k s h t a . , o ; e z a ff
. . . . . :
When a vasoconstrictor is added, the pH of local anesthetic
drugs is decreased.

lidoc a i n e

Arti c a i n e

B u p ivac a i n e

M e p ivacai n e

Pri l oc a i n e

P roc a i n e

100% 200 % 300 % oOO%

FIGURE 5-5 Relative Vasoactivity. Vasodilation activity for local anesthetic

drugs compared with lidocaine.
 CHAPTER 5 DENTAL LOCAL ANESTHETIC DRUGS
• 53

Table 5-2 Comparative pKa and pH Values

Drug pKa Onset Time pH

Articaine6 w/ epinephrine 1:100,000 7.8 Infiltration: 1 -2 mins 4.4 -5.2

Block: 2-21Jz mins

Articaine6 w/ epinephrine 1:200,000 7.8 Infiltration: 1 -2 mins 4.6 -5. 4

Block: 2-3 mins

Bupivacaine5 w/ epinephrine 8.1 Up to 6 -10 mins 3.0-4.5

Lidocaine1 w/ epinephrine 7. 7 2-3 mins 3.3 -5.5

Mepivacaine4 plain 7. 6 2-4 mins 4.5-6.8

Mepivacaine4 w/ levonordefrin 7. 6 11/z-2 mins 3.0-3.5

Prilocaine3 plain 7. 7 2-4 mins 6.0-7.0

Prilocaine2 w/ epinephrine 7.9 2-4 mins 3.0-4.0

Procaine 7 w/ vasoconstrictor 9.1 6 -10 mins 3.5-5.5

Sources: Product inserts for 1Xylocaine®, 2Citanest®, 3Citanest Forte®, 4Carbocaine®, 5Marcaine® and 6Septocaine® and for procaine, Malamed, S. F. :
Handbook o f Local Anesthesia, 6th ed ., St. Louis, Elsevier Mosby, 2013; National Library of Medicine, 2013.

Solutions containing vasoconstrictors are more acidic
in order to preserve the vasoconstrictors, which would
otherwise oxidize, shortening shelf life considerably. Car­
tridges with vasoconstrictors that are approaching their
shelf-life expirations typically experience an additional de­
crease in pH value that reflects the ongoing and selective
oxidation of bisulfite preservatives over the vasoconstric­
tors (see Table 5-2 ) . In addition to potentially compro­
mising their effectiveness, this decrease in pH can cause
increased burning sensations upon administration.
Onset of Action
The onset of action of lidocaine is approximately 2-3
minutes.
The onsets of most inj ectable amides available in dentistry
are considered to be rapid. There is little clinically notice­
able difference in onset between the amides, with the ex­
ception of bupivacaine, which has a much slower onset.
Vasoconstrictor
Lidocaine is available with epinephrine in dilutions of
1 :50,000 and 1 : 100,000.
A general pharmacological principle holds that when­
ever a drug maintains its therapeutic value in lower con­
centrations its use should be considered. Lidocaine with
a 1 : 5 0 , 0 0 0 dilution of epinephrine contains twice the
quantity of vasoconstrictor drug as a 1 : 100,000 dilution.
Although there may be therapeutic benefit to higher
concentrations at times, such as when more vigorous
hemostasis is desired in order to control bleeding, there is
questionable rationale for the routine use of dilutions of
1 :50,000 epinephrine (Jastak, Yagiela, & Donaldson, 1995).
Half-Life (t1f2)
The elimination half-life of lidocaine is 1.6 hours
(96 minutes).
The elimination half-lives of all dental local anesthetic
drugs are considered to be relatively short. Some bisphos­
phonates prescribed for osteoporosis and malignancies, for
example, have half-lives approximating 10 years.
The half-life of lidocaine falls between the much
shorter half-life of articaine and the much longer half-life
of bupivacaine (see Table 5-3 •).
Topical Preparations
Lidocaine is effective as a topical anesthetic. It is available
for use in concentrations ranging from 2% to 1 0 % in vari­
ous ointments, viscous solutions, and mixtures. When used
topically, the onset of anesthesia occurs within 1-2 minutes,
with peak effects available from 2 to 5 minutes (Daniel &
Harfst, 2007; Jastak, Yagiela, & Donaldson, 1995 ) . For
further discussion on topical preparations see Chapter 8,
"Topical Anesthetics."
Pregnancy Category
Lidocaine is in FDA Category B.
Lidocaine, in all formulations, is safe to use in pregnancy
once a patient's physician has confirmed that there are no
54 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•

Table 5-3 Elimination Half- life Values

Drug H alf-Life (h rs) Compa risons

Lidocaine 1. 6

Articaine* 0. 75*

Bupivacaine 2. 7-3. 5

Mepivacaine 1.9

Prilocaine 1. 6

= 1 Hour
Procaine 0. 1 \1.1

- = Time l a psed H r/M i n

- = U n used T i m e

*Septocaine product insert

Source: ADAIPDR (2009) and Tetzlaff (2000).

exceptional risks. The FDA Pregnancy Category B rating Table 5-4 Summary of F DA Pregnancy Ratings for
does not suggest that there are no risks to the use of a cate­ Dental Local Anesthetic Drugs
gory B drug; rather, it suggests that the risks are acceptable
in most circumstances ( ADA/PDR, 2009; Meadows, 200 1 ) . Dental Local Anesthetic Drug FDA Pregnancy Rating
Category B status means either that:
Articaine c
1. studies have concluded that there were no demonstrated
risks in animals and no human studies available, or Bupivacaine c
2. there are demonstrated risks in animals but well­
controlled studies fail to demonstrate those same risks Lidocaine B
in the human fetus.
Mepivacaine c
A summary of local anesthetic drugs used in dentistry with
their FDA Pregnancy Category ratings may be found in Prilocaine B
Table 5-4 • · FDA Pregnancy Categories are discussed in
further detail in Table 5-5 •· Source: ADA/PDR (2009) and Meadows (2001). Current as of May 2014.
 CHAPTER 5 DENTAL LOCAL ANESTHETIC DRUGS
• 55

Table 5-5 F DA Drug Categories in Pregnancy*

U . S . Food and Drug Ad m i n istration

Category A Adequate, well-controlled studies in pregnant women have not shown an increased risk of fetal abnormalities.

Category B Animal studies have revealed no evidence of harm to the fetus; however, there are no adequate and
well-controlled studies in pregnant women. Or Animal studies have shown an adverse effect, but adequate and
well-controlled studies in pregnant women have failed to demonstrate a risk to the fetus.

Category C Animal studies have shown an adverse effect and there are no adequate and well-controlled studies in pregnant
women. Or No animal studies have been conducted and there are no adequate and well-controlled studies in
pregnant women.

Category D Studies, adequate, well-controlled or observational, in pregnant women have demonstrated a risk to the fetus.
However, the benefits of therapy may outweigh the potential risk.

Category X Studies, adequate, well-controlled or observational, in animals or pregnant women have demonstrated positive
evidence of fetal abnormalities. The use of the product is contraindicated in women who are or may become
pregnant.

Source: ADAIPDR (2009) and Meadows (2001). Current as of May 2014.

Safety during Lactation Effective Concentrations in Dentistry

Lidocaine enters breast milk (small amounts) ; use
caution (ADA/PDR, 2009) .
M o s t drugs are available in b r e a s t milk once intro ­
duce d . Product information generally states that cau­
tion must b e exercis e d when nursing after lidocaine
administration.
Artica i n e
Background
Articaine , synthesized in 1969 by H. Rusching, is the
most recent FDA-approved inj ectable local anesthetic
drug (2000) (Malamed, 20 1 3 ; S eptodont, 20 1 3 a ) . It is
roughly equivalent to lidocaine in both safety and efficacy
(Malamed, Gagnon, & Leblanc, 200 1 ). See Appendix 5-1.
Although classified as an amide, articaine has a dis­
tinctly different aromatic ring structure with an ester
component attach e d . This unique configuration pro­
vides several beneficial pharmacologic behaviors. Un­
like other amides, the addition of the ester component
promotes rapid biotransformatio n . The presence of a
sulfur atom within the ring structure makes it highly
lipophilic, easing articaine's p a s s a g e through neural
membranes.
Offsetting these pharmacologic advantages is artic­
aine's controversial association with a higher than typical
incidence of postoperative nerve injury (paresthesia) , par­
ticularly during inferior alveolar nerve block inj ections.
This concern will be discussed more in depth in Chapter
17, " Local Anesthesia Complications and Management."
Articaine is provided in the following formulations:
4% articaine with 1 : 100,000 epinephrine
(see Figure 5-6A •)
4 % articaine with 1 :200,000 epinephrine
(see Figure 5-6B •)
New local anesthetic drugs are required to be as s afe
and as effective as 2 % lidocaine. Although articaine
c o n centrations o f l e s s than 4 % w o u l d certainly be
desirable from a safety standpoint, they are not as reliably
effective as 2% lidocaine.
Duration of Action
4 % articaine with 1 : 100,000 epinephrine
Intermediate duration = 60-75 minutes pulpal;
180-360 soft tissue
4% articaine with 1 :200,000 epinephrine
Intermediate duration = 45-60 minutes pulpal;
120-300 soft tissue
Although the product insert indicates a slightly decreased
duration with 1 :200,0 00 epinephrine solutions, they are
roughly clinically equivalent to durations with 1 : 1 00,0 00
solutions.
Similarity to Other Local Anesthetics
Articaine is most similar to prilocaine. It has few similari­
ties to the other dental local anesthetic drugs, however,
including prilocaine.
A detailed discussion of articaine's properties follows,
with a brief summary of properties, dosing recommendations,
56 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•

Septocaine" with epinephrine I : I 00,000

I: /00,000 Injection
Articaine hrdrochloride 4% with Epinephrine
•

isulltte.
Conta ins sodeum metab
of .nsert lor delatls.
See warnlflgS section

so cartridges: 1 . 7 ml each

H 3COOC

methyl 4-methy l -3 - ( 2-propy l a m i n opropanoy l am i n o ) t h i ophene-2-carboxy l ate hydroch l oride

(A)

ne I :200,000
Septocain e" with epinephri
1 :200,000 lnJe<:tJOn
.
4% \lith Epinephrine
Articaine hrdrochloride

Con tains sodtum metabis

ulfite.
,
of tnsert fOt" detaJis.
See wamJOQS seclion

50 cartridges: t 7 mL
each

H 3COOC

methy I 4-methy 1 - 3 -( 2-propy lam i nopropanoy lam i n o ) th i ophene-2 -carboxyl ate hydroc h Iori de

(B)
F I G U R E 5-6 A - 4% Articaine, 1:100,000 Epinephrine. B - 4% Articaine, 1:200,000 Epinephrine
Source: Courtesy of Dentsply Pharmaceutical .

and uses provided in Box 5-4 •· Appendix 5-3 provides a
complete reference table for articaine and a maximum
dose reference is provided in Appendix 7-3.
M RD
3.2 mg/lb (7.0 mg/kg) ; no absolute maximum provided
(previously 500 mg absolute maximum)
Relative Potency
Articaine is more than twice as potent as procaine, ap­
proximately one-third more potent than lidocaine, mepi­
vacaine, and prilocaine, and approximately one-third as
potent as bupivacaine (Malamed, 20 13) (see Figure 5-3).
Even though articaine is more potent than lidocaine,
its potency does not necessarily translate into increased
clinical efficacy. As with all drugs, variability in response
among individuals can offset any predicted benefits based
upon pharmacological activities.
Relative Toxicity
Articaine is more toxic to the CNS and CVS than procaine,
slightly more toxic than prilocaine, slightly less toxic than
mepivacaine and lidocaine, and far less toxic compared
with bupivacaine (Jastak, Yagiela, & D onaldson, 1995;
Oertel, B erndt, & Kirch, 1996) (see Figure 5-4).
While articaine is considered nearly equal in toxicity
to lidocaine, it has been characterized as being less toxic
than lidocaine in intraoral administration and as causing
less severe reactions when overdoses have been induced
(Jastak, Yagiela, & Donaldson, 1995; O ertel, B erndt, &
Kirch, 1996).
Relative Toxicity: Special Considerations
with Articaine
In addition to potential CNS and CVS toxicity, articaine
may induce methemoglobinemia when used in higher
than therapeutic doses (Haas & Lennon, 1995; Septodont,

Formulations fo r Use in Dentistry: 4% with 1 : 1 00,000
e p i n e p h ri n e ; 4% with 1 :200,000 e p i n e p h ri n e
D u ration o f Action: I nterm e d i ate, 4% with 1 : 1 00,000
e p i n e p h ri n e , 60-75 m i n utes p u l p a l ; 1 80-360 soft tiss u e ;
4% w i t h 1 : 200,000 e p i n e p h ri n e , 45-60 m i n utes p u l p a l ;
1 20-300 m i n utes soft tissue
M RD: 3 . 2 mg/lb (7 .0 m g/kg); n o a b s o l ute m axi m u m
p rovided (previ o u s l y 500 m g a b s o l ute m axi m u m)
Relative Pote ncy: Twice p roca i n e ; 1 . 5 t i m es l id o ca i n e a n d
m e p ivaca i n e ; m u c h l ess t h a n b u p ivaca i n e
Relative Toxicity: S i m i l a r t o l i doca i n e a n d m e p ivaca i n e ;
m u ch l ess t h a n b u pivaca i n e
M eta b o l ism: 90%-95% p l a s m a c h o l i n este rase;
5%-1 0% l iver
Excretio n : K i d n ey; very l ittl e excreted u n c h a n g ed
Vasoactivity: S i m i l a r vaso d i l at i o n co m p a red with l i d o ca i n e
p Ka : 7 . 8
p H : 6.0-7 .0 p l a i n ; 3 . 0-4.0 with e p i n e p h ri n e
Onset: 1 -2 m i n utes (infiltration); 2-3 m i n utes ( b l o ck)
H a lf- L ife: 43 . 8 m i n utes ( - 6 . 5 ca rtri d g es); with 1 : 1 00,000
e p i n e p h ri n e 44.4 m i n utes ( - 6 . 5 ca rtri d g es); with 1 : 200,000
e p i n e p h ri n e
To pical Prepa rations: N o n e i n d e ntistry
Preg n a n cy Category: C
�
•
La
.
� � ��� ��a: l � � � � .i � � �e.a �t- � i� k: �:� r� i �� � a.u� i ��
a i
• •
20 13a). Articaine has also been associated with a higher­
than-typical incidence of nerve damage (paresthesia) but
the actual tendency is unknown. Some experts have sug­
gested relatively low rates for all paresthesias, including
those that are transient, possibly as low as 3 per million
for articaine, which is the highest rate when considering all
inj ectable dental local anesthetic drugs (Haas & Lennon,
1995; Harn & Durham, 1990; Hawkins, 2006; Xylocaine
hydrochloride). Pogrel and Thamby have suggested that
the incidence of permanent nerve damage may be much
greater than previously thought, at between one in 26,762
and one in 160,571 in inferior alveolar blocks, for all drugs,
including articaine (Pogrel & Thamby, 2 0 0 0 ) . The true
neurotoxic potential of all the local anesthetics, including
articaine, is unknown at this time (Park et al., 2005 ; Pogrel
et al., 2003).
PAR E STH E S IA Paresthesia may be defined as a variable
set of symptoms resulting from nerve inj ury that may be
further defined as prolonged temporary or permanent,
CHAPTER 5 DENTAL LOCAL ANESTHETIC DRUGS
• 57
partial or complete loss or alteration of sensation. Fortu­
nately, the vast maj ority of paresthesias are transient.
Many clinicians are concerned that paresthesia will
develop after the use of 4% drugs in dentistry (articaine
and prilocaine ). It is possible that risk may be lessened by
reducing volumes administered, adhering to slow injection
rates, and avoiding inferior alveolar nerve blocks although
consensus on these and other strategies to lessen risk are
far from confirmed. In addition to these uncertainties,
there is considerable debate on the extent of the risk or
that the increased risk actually exists (D ower, 2003 ; Haas
& Lennon, 1995; Malamed, 20 13).
Since it is known that an inferior alveolar block is the
primary technique associated with paresthesia, avoiding
this block when administering articaine is recommended
by some authorities, not due to any proven increased in­
cidence of paresthesia with articaine ( s e e B ox 5-5 •
and Chapter 17) but due to the opinion that articaine
may cause paresthesia more frequently than other drugs
(Dower, 2007; Haas & Lennon, 1995).
Metabolism
Compared with other amide drugs, articaine has a rapid
half-life. Not only is additional dosing safer but should ad­
verse toxic reactions occur, they generally resolve quickly
(Atanasov, Popivanova, & Yochev, 198 1 ; Jastak, Yagiela, &
Donaldson, 1995; Chan, 2007; Oertel et al., 1999; Septodont,
20 13a; Vree et al., 1988).
Articaine's metabolism is unique. Five to ten percent
is metabolized via hepatic p450 enzymes. The maj ority of
articaine's removal is accomplished by rapid plasma cho­
linesterase metabolism to articainic acid, its inactive pri­
mary metabolite, before reaching the liver. Articaine is
• • • further metabolized to articainic acid glucuronide, a minor
metabolite, also considered to be pharmacologically inert
(van Oss et al., 1988, 1989).
Desp ite the exte nsive sco p e of one retrospective s u rvey, it
is i m po rtant to n ote that n ot a l l stu d i es h ave d e m o n strated
statist i c a l i n creases in the i n c i d e n ce of p a resth e s i a due to
a rtica i n e ( H a a s & Le n n o n , 1 995). S o m e h ave d e m o n strated
even g reater risk ( P o g re l & T h a m by, 2000) . Oth e rs, s u c h
as a 200 1 ra n d o m ized, d o u b l e-b l i n d i n vesti g a t i o n of the
safety of a rtica i n e i n 1 ,325 su bj ects, d i d n ot d e m o n strate
any except i o n a l risks. Two-th i rds of the s u bj e cts received
a rtica i n e and o n e-th i rd re ceived l i d o ca i n e fo r i nfe rior
a l veo l a r n e rve b l ocks. T h e i nvestigators rep o rted that " the
tota l n u m be r of su bje cts w h o re p o rted these sym pto ms
[of p a resth esia] 4-8 d ays after the proce d u re was eight
( 1 %) fo r t h e a rtica i n e g ro u p and five ( 1 %) fo r t h e l i d o ca i n e
g ro u p " ( M a l a m e d , G a g n o n , & Le b l a n c, 2000) .
•
For a m o re deta i l e d d i s c u s s i o n of p a resth e s i a a n d •
.
a
: :� � :
a ne
��
. : :� �
e
.
a pt r 1 7
• • • • : • • • • • • • • • • • • • • • • • • • • • .
58 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•
Excretion
Very little articaine, about 2 % , is excreted unchanged
(Septodont, 2013a). Metabolites excreted in urine include
articainic acid and small amounts of articainic acid gluc­
uronide (Septodont, 2013a). As with other local anesthetic
drugs, higher excretion rates are more common when the
pH of urine is low.
Vasoactivity
Articaine is approximately equal in vasodilating activity
compared with lidocaine, greater compared with mepi­
vacaine and prilocaine, and much weaker compared with
procaine and bupivacaine (see Figure 5-5).
B ecause of this activity, articaine is not considered to
be useful without the addition of a vasoconstrictor; how­
ever, a recent study of 4% articaine plain found it to be
as effective as 4% articaine, 1 : 100,000 epinephrine when
used for single tooth mandibular extractions. Four percent
articaine, 1 :400,000 epinephrine was investigated in a dif­
ferent study and found to be equivalent in effectiveness
to 1 : 100,000 and 1 :200,000 epinephrine solutions. In both
studies, the new formulations were described as safe, al­
though it should be noted that the durations of action with
the plain and reduced epinephrine concentrations were
briefer compared with 1 : 1 00,000 and 1 :200,000 epineph­
rine (Daublander et a!. , 20 12; Kammerer et a!. , 2012).
pKa
The pKa of articaine is 7.8.
Articaine's pKa is slightly higher than lidocaine's (7. 7 ) ,
which translates t o somewhat fewer base molecules avail­
able initially. Articaine is more lipophilic, however, and
its base molecules have higher affinities for nerve mem­
branes, which may contribute to a reported slightly faster
onset of anesthesia than lidocaine (see Table 5-2).
pH
The pH of articaine with 1 : 1 00,000 epinephrine
ranges from 4.0 to 5.2.
The pH of articaine with 1 :200,000 epinephrine
ranges from 4.6 to 5.4 (see Table 5-2).
Onset of Action
The onset of action for articaine in infiltration anes­
thesia is 1-2 minutes.
The onset of action for articaine in nerve block anes­
thesia is 2-3 minutes.
Articaine's onset of action is variable depending upon
the technique, although in all techniques, articaine pro­
vides a rapid onset (Malamed, 2 0 1 3 ) . In infiltrations, ar­
ticaine provides the most rapid onset of all five inj ectable
drugs in dentistry, 1-2 minutes. In nerve blocks, articaine's
onset is comparable to lidocaine but slightly slower than
mepivacaine's, 1.5-2 minutes.
Vasoconstrictor
Articaine is currently available in North America with
epinephrine in dilutions of 1 : 1 00,000 and 1 :200,000.
B o t h of t h e s e f o r m u l a s p r o v i d e c l i n i c a l l y u s e fu l
vasoconstriction (see B o x 5-4).
Half-Life (t1f2)
At 476 mg ( -6.5 cartridges) with 1 : 100,000
epinephrine articaine tVz 43.8 minutes
=
At 476 mg ( -6.5 cartridges) with 1 :200,000
epinephrine articaine tVz 44.4 minutes
=
A recent study suggests that the elimination half-life of
articaine may be age- and dose-dependent (Oertel et a!. ,
1999). When administering 60-120 mg or approximately
0.8-1.5 cartridges using common dental local anesthetic
techniques, the observed half-life of articaine was re­
ported to range from about 16 to 20 minutes, depending
on the age of the recipient ( O ertel et a!. , 1999; O ertel,
Rahn, & Kirch, 1997). Although not as specific, product
inserts agree that articaine's half-life may be age- and/
or dose -dependent ( S eptodont, 20 1 3 a ) . Until 2 0 0 6 , a
worldwide supplier of articaine listed its half-life as 1.8
hours. The revised half-life value in product inserts since
2006 represents a major adjustment to this value that con­
tinues to impact clinical dose decision making (Septodont,
20 13a). See Appendix 5-1 and Table 5-3.
Topical Preparations
Articaine is not available as a topical anesthetic.
Pregnancy Category
Articaine is in FDA Pregnancy Category C.
Category C suggests that there should be strong rationale
for the use of a drug before administering it in pregnancy
(ADA/PDR, 2009; Meadows, 200 1).
Safety during Lactation
Caution is recommended. S afe use in lactation has not
been established (Malamed, Gagnon, & Leblanc, 200 1).
Mepivaca i n e
Background
Mepivacaine was introduced in Sweden (1957) as an alter­
native to lidocaine by A. F. Eckenstam. The pharmacology
of mepivacaine is similar to lidocaine's despite its closer
chemical resemblance to bupivacaine (Malamed, 20 1 3 ;
Septodont, 2009). Its duration, onset o f action, potency,
 CHAPTER 5 DENTAL LOCAL ANESTHETIC DRUGS
• 59

and toxicity are all similar to lidocaine's (Tetzlaff, 2000) Formulations for Use in Dentistry
(see Figure 5-6 and Appendix 5-1 ). Mepivacaine is provided in the following formulations:
Unlike lidocaine, mepivacaine is a weak vasodilator
and is effective for short durations without a vasocon­ 3% mepivacaine plain (without vasoconstrictor)
strictor. The 3% formulation without vasoconstrictor, for (see Figure 5-7 A •)
example, is capable of providing approximately 20-40 2% mepivacaine with 1 :20,000 levonordefrin
minutes of pulpal anesthesia compared with plain solu­ (see Figure 5-7B •)
tions of 2 % lidocaine, which provide only 5-10 minutes of
(Levonordefrin is a vasoconstrictor used to increase
pulpal anesthesia. In individuals for whom vasoconstric­
the safety and duration of mepivacaine.)
tors are contraindicated, 3% mepivacaine solutions are
particularly useful.
Duration of Action
As with lidocaine, mepivacaine has been noted to
have anticonvulsant properties and has been used to ter­ 3 % mepivacaine plain
minate seizures or decrease their durations (Malamed, Short duration = 20-40 minutes pulpal; 120--180 soft tissue
20 1 3 ) . Similar to other local anesthetics with anticonvul­
sant properties, mepivacaine acts to prevent or terminate 2 % mepivacaine with 1 :20,000 levonordefrin
seizures by decreasing the excitability of cortical neurons Intermediate duration = 60 minutes pulpal; 180-300
(raising seizure thresholds) (Malamed, 20 13). minutes soft tissue

- _,.... -- -- ·-

� ICAl
PHARMAC EUT

ee
3 % P o l oc a i n
DE NTA L
"""

US P)
HC I ln iection ,
-·

[Me p .tv OCO ·I ne

30 m g/ mL
erature
Store 91 room t�mp
(71 F). STERIL E A��lli'eCTION
belOW 2s·c
T TO FREEZE
00 NO RMI T SOLUTI ON
16
PE
Rx only D!NT5flY f.,der 1. 3�1
ml oo<h
SO (mtridges, J .l
-(2,6-di methylphenyl )- 1 -melhyl-piperidine-2-carboxamide

(A)

_;;;:;:;::: -::!!§:=
:; =

N-(2,6-dimcthy lpheny 1 ) - 1 -mcthyl-pipcridine-2-carboxamide

(B)
F I G U R E 5-7 A - 3% Mepivacaine Plain. B - 2% Mepivacaine, 1:20,000 Levonordefrin.
Source: Courtesy of Dentsply Pharmaceutical; Carestream Health Inc.
60 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•

Mepivacaine provides durable, short-term anesthesia in Relative Potency

both infiltrations and nerve blocks without added vaso­ Mepivacaine is twice as potent as procaine, equal in po­
constrictors. Mepivacaine prepared with a vasoconstrictor tency to lidocaine and prilocaine, two-thirds as potent as
provides durations similar to lidocaine with a vasoconstric­ articaine, and approximately one-fourth as potent as bupi­
tor (ADA/PRA, 2009; Malamed, 20 13). vacaine (see Figure 5-3).

Similarity to Other Local Anesthetics Relative Toxicity

Mepivacaine is chemically similar to bupivacaine. Despite Mepivacaine is twice as toxic as procaine, approximately
this similarity, mepivacaine lacks the duration of action of twice as toxic as prilocaine, similar in toxicity to articaine
bupivacaine. (equal to or slightly more toxic), similar in toxicity to li­
A detailed discussion of mepivacaine's properties fol­ docaine (equal to or slightly less toxic) , and far less toxic
lows, with a brief summary of properties, dosing recom­ compared with bupivacaine (approximately one-fourth as
mendations, and uses provided in Box 5-6 •· Appendix 5-4 toxic as bupivacaine) (see Figure 5-4).
provides a complete reference table for mepivacaine and a Solutions of mepivacaine without vasoconstrictor are
maximum dose reference is provided in Appendix 7-3. available only in 3% concentrations for minimal effective­
Mepivacaine is most similar to lidocaine in its pharmaco­ ness. There is 50% more drug in each cartridge of any 3 %
dynamic and pharmacokinetic behaviors. For example, both drug compared with 2 % drugs.
drugs express anticonvulsant properties (Malamed, 20 13). S o m e published m aximum r e c o m m e n d e d d o s e s
for mepivacaine reflect a higher toxicity compared with
M RD lidocaine (Tetzlaff, 2000). Mepivacaine tends to produce
3.0 mg/lb (6.6 mg/kg), 400 mg absolute maximum higher blood levels than lidocaine initially after inj ection;
(previously 2.0 mg/lb; 4.4 mg/kg; 300 mg absolute however, studies suggest that patients tolerate higher lev­
maximum) els of mepivacaine before toxic effects become evident
(Jastak, Yagiela, & Donaldson, 1995).
Studies suggest that both prilocaine and articaine are
tolerated better than mepivacaine largely because of their
avoidance of liver metabolism (Jastak, Yagiela, & Donald­
Formulations fo r Use i n Dentistry: 3% p l a i n , 2% with
son, 1995; Oertel, B erndt, & Kirch, 1996; Septodont, 2009;
1 :20,000 l e vo n o rdefri n
Tetzlaff, 2000).
D u ration of Action: S h o rt, 3% p l a i n 20-40 m i n utes p u l p a l ;
I nterm e d i ate: 2 % with 1 :20,000 levo n o rd efri n 6 0 m i n utes Metabolism
p u l p a l ; 1 80-300 m i n utes soft tiss u e M epivacaine is metabolized in the liver but the path­
M R D : 3 . 0 m g / l b (6.6 m g/kg); 400 m g a b s o l ute m a xi m u m ways are different compared with lidocaine. Unlike li­
(previ o u s l y 2 . 0 m g / l b ; 4 . 4 m g/kg; 300 m g a b s o l ute docaine, amidase activity is insignificant. Its elimination
m a xi m u m ) half-life of 1.9 hours reflects its less efficient metabolic
p athway (Jastak, Yagiela, & D onaldson, 1 9 9 5 ; Tetzlaff,
Relative Potency: Twice p roca i n e ; s i m i l a r t o l i d o ca i n e a n d
p ri l oc a i n e ; l ess t h a n a rtica i n e ; m u ch l ess t h a n b u p ivaca i n e
2000).

Relative Toxicity: Twice p roca i n e ; g reater t h a n p r i l o c a i n e ; Excretion

s i m i l a r to l i d o ca i n e a n d a rtica i n e ; m u c h l ess t h a n
Excretion is variable with anywhere from virtually none to
b u p ivaca i n e
up to 16% excreted unchanged. As is true with other local
M eta b o l ism: Liver, oxidases, i n s i g n ificant a m i d a s e a ctivity anesthetic drugs, higher excretion rates are more common
Excretio n : K i d n ey; l ess t h a n 1 6% u n c h a n g ed
when urine pH is low.

Vasoactivity: Wea kest vaso d i l ator of a l l 5 a m i d e s Vasoactivity

p K a : 7 .6 Mepivacaine is a weak vasodilator, characterized as pro­
ducing only slight vasodilation, which allows it to be used
p H : 4 . 5-6 . 8 p l a i n ; 3 .0-3 . 5 with levo n o rd efri n
without vasoconstrictors. It is the weakest vasodilator of
Onset: 1 .5-2 m i n utes the five inj ectable drugs available in dental cartridge form
H a lf- L ife : 1 .9 h o u rs (1 1 4 m i n utes)
and provides useful short-term durations in both infiltra­
tions and nerve blocks in plain (no vasoconstrictor) solu­
To pical Prepa rations: N o n e in dentistry tions (see Figure 5-5).
Preg n a n cy Categ o ry: C
pKa
: La ctation: Ava i l a b l e i n b reast m i l k; exercise cauti o n
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . •• The pKa of mepivacaine is 7.6 (see Table 5-2) .

pH
The pH of 3% mepivacaine plain solutions ranges
from 4.5 to 6.8.
The pH of 2% mepivacaine solutions with vasocon­
strictor ranges from 3.0 to 3.5.
In certain situations, 3% plain solutions of mepivacaine
may have an advantage over other drugs because of their
higher pH. This distinction is further discussed in Chapter 16,
" Troubleshooting Inadequate Anesthesia," B ox 1 6-7,
"A Theory on the Use of 3 % Mepivacaine in the Presence
of Lowered pH." These advantages may also extend to plain
solutions of prilocaine (see Table 5-2).
Onset of Action
The onset of action for mepivacaine is approximately
1.5-2 minutes.
Mepivacaine's onset of action is rapid and similar to
most of the other available inj ectable drugs in dentistry.
S o m e clinicians elect to administer 3 % mepivacaine
plain as an initiating drug before the administration of
bupivacaine, which has a much slower onset. This tech­
nique allows treatment to begin while bupivacaine is
taking effect.
Vasoconstrictor
2 % mepivacaine with levonordefrin is available in a
dilution of 1 :20,000.
With the addition of levonordefrin, the 2% formulation
of mepivacaine provides adequate depth and duration of
pain control for most dental procedures equivalent to the
anesthetic effect of 2% lidocaine with 1 : 1 00,000 epineph­
rine. Levonordefrin, however, is far less effective as a he­
mostatic agent and epinephrine remains the drug of choice
for that purpose.
Half-Life (t1f2)
The elimination half-life of mepivacaine is 1.9 hours
( 1 14 minutes).
The elimination half-life of mepivacaine is prolonged com­
pared with lidocaine (96 minutes), prilocaine (96 minutes),
and articaine (44-45 minutes) (see Table 5-3).
Topical Preparations
There are no topical solutions containing mepivacaine for
dental application.
Pregnancy Category
Mepivacaine is in FDA Category C.
Category C suggests that there should be strong rationale
for the use of a drug before its administration in pregnancy
(ADA/PDR 2009; Meadows, 200 1 ) .
CHAPTER 5 DENTAL LOCAL ANESTHETIC DRUGS
• 61
Safety during Lactation
It is not known whether mepivacaine is excreted in human
milk. Caution is recommended.
Pri loca i n e
Background
Prilocaine was first prepared by Lofgren and Tegner
in 1953 and approv e d by the FDA in 1 9 6 5 . Pharma­
cologically, prilocaine is very similar to mepivacaine
(D entsply Pharmaceutical, 20 1 0b ; Malamed, 20 1 3 ) . See
Appendix 5-l.
Prilocaine entered the market with the promise of
providing similar clinical effectiveness to lidocaine with
significantly decreased toxicity (Tetzlaff, 2000). Unfortu­
nately, prilocaine can reduce the blood's oxygen-carrying
capacity, which may lead to a specific anemia known as
methemoglobinemia. This will be discussed further under
"Relative Toxicity" and in Chapters 10 and 17.
Formulations for Use in Dentistry
Prilocaine is provided in the following formulations:
4% prilocaine plain (without vasoconstrictor)
(see Figure 5-8A •)
4 % prilocaine with 1 :200,000 epinephrine
(see Figure 5-8B •)
Duration of Action
4 % prilocaine plain
Short duration (infiltration) = 10-15 minutes pulpal;
90-120 soft tissue
Intermediate duration (block) = 40-60 minutes;
120-240 soft tissue
4% prilocaine with 1 :200,000 epinephrine
Intermediate duration = 60-90 minutes pulpal;
180-480 soft tissue
D espite prilocaine's weak vasodilative properties, it is not
effective at providing long durations in infiltrations without
a vasoconstrictor. This phenomenon, whereby infiltrations
are far less effective compared with nerve blocks, has also
been observed in more potent drugs such as bupivacaine.
It is suggested that the 4% formulation with 1 :200,000 epi­
nephrine be considered whenever prilocaine is to be used
for longer procedures with infiltration anesthesia.
Similarity to Other Local Anesthetics
Prilocaine's aromatic ring is linked to a secondary amine,
unlike lidocaine, mepivacaine, articaine, and bupivacaine,
which all are linked to tertiary amines.
A detailed discussion of prilocaine's properties fol­
lows, with a brief summary of properties, dosing recom­
mendations, and uses provided in Box 5-7 •· Appendix 5-5
62 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•
(A)
(B)
F I G U RE 5-8 A - 4% Prilocaine Plain, B - 4% Prilocaine, 1:200,000 Epinephrine.
Source: Courtesy of Dentsply Pharmaceutical.
provides a complete reference table for prilocaine and a
maximum dose reference is provided in Appendix 7-3.
M RD
4.0 mg/lb (8.8 mg/kg ) , 600 mg absolute maximum
(previously 2.7 mg/lb; 6.0 mg/kg; 400 mg absolute
maximum )
Overdose reactions with prilocaine are uncommon. Prilo­
caine at 4% contains twice the amount of drug as 2% solu­
tions and 1.5 times that found in 3% solutions.
Relative Potency
Prilocaine is twice as potent as procaine, equal in potency
to lidocaine and mepivacaine, two-thirds as potent as ar­
ticaine, and approximately one-fourth as potent as bupiva­
caine ( Malamed, 20 1 3 ) ( see Figure 5-3).
N -(2-methylphenyl)-2-propylamino-propanamide
- 4"C;t;�i0rie""J'Jr....::= ·
- ;·.=:=··· · ···-
N-(2-methylphenyl )-2-propylami no-propanamide
Relative Toxicity
Prilocaine is approximately twice as toxic as procaine,
slightly less toxic than articaine and mepivacaine, and ap­
proximately half as toxic as lidocaine. It is far less toxic
compared with bupivacaine ( approximately one-fifth or
less as toxic as bupivacaine ) ( Jastak, Yagiela, & Donaldson,
1995; Tetzlaff, 2000 ) ( see Figure 5-4 ) .
When considering CNS and CVS toxicity, prilocaine
is reportedly less toxic compared with lidocaine largely
because of the availability of multiple extrahepatic meta­
bolic pathways ( Dentsply Pharmaceutical, 20 10b; Tetzlaff,
2000 ) .
Relative Toxicity: Special Considerations
with Prilocaine
As previously described in the toxicity discussion of li­
docaine, not all toxicity is related to the effects on the

Formulations fo r Use in Dentistry: 4% p l a i n , 4% with
1 : 200,000 e p i n e p h r i n e
D u ration o f Action: I nterm e d i ate, 4 % p l a i n 1 0-1 5 m i n utes
p u l p a l (i nfi ltrati o n ) ; 40-60 m i n utes p u l p a l ( b l ock); 1 20-240
soft tissue 4% with e p i n e p h ri n e 60-90 m i n utes p u l p a l ;
1 80-480 m i n utes soft tissue
M RD: 4.0 mg/lb (8 .8 m g/kg), 600 m g a b s o l ute m a xi m u m
(previ o u s l y 2 . 7 m g / l b ; 6 . 0 m g/kg; 400 m g a b s o l ute
m axi m u m )
Relative Pote ncy: Twice p roca i n e ; s i m i l a r t o l i d o ca i n e
a n d m e p ivaca i n e; l ess t h a n a rtica i n e ; m u ch l ess t h a n
b u p ivaca i n e
Relative Toxicity: Twice p roca i n e ; l ess t h a n a rtica i n e ; h a lf
l i d o ca i n e a n d m e p ivaca i n e ; m u ch l ess t h a n b u p ivaca i n e
M eta bolism: S i m p l e r l iver m eta b o l is m t h a n l i doca i n e a n d
m e p ivaca i n e; m u c h o f t h e d r u g is c l e a red b efo re it is a b l e
t o re ach t h e l iver
Excretio n : K i d n ey; very s m a l l p e rcenta g e u n c h a n g e d
Vasoactivity: We a k vas o d i l ator
p Ka : 7 . 9
p H : 6.0-7 .0 p l a i n ; 3 . 0-4.0 with e p i n e p h ri n e
Onset: 2-4 m i n utes
H a lf- L ife: 1 . 6 h o u rs (1 1 4 m i n utes)
To pical Preparations: In co m b i n at i o n with oth e r d r u g s ,
p r i m a r i l y l i d o ca i n e
Preg n a n cy Category: B
� La
. . � � ��: �� : � � � � � : � � � � �:� � �� � � ��
a i a l �
.
i ea t
. -
i k r i au i
. •
CNS and CVS. B ecause of prilocaine's metabolite ortho­
toluidine (a-toluidine), some individuals are at increased
risk of developing a potentially life-threatening anemia
known as methemoglobinemia. Cautions apply when
treating patients at risk for methemoglobinemia as well
as any patients with oxygenation difficulties, especially
those taking medications that are independently capable
of inducing methemoglobinemia (Hj elle, Grauer, 1986;
Prescott, 1996). More in-depth discussions regarding met­
hemoglobinemia may be found in Chapter 8, " Topical
Anesthetics," Chapter 10, "Patient Assessment for Local
Anesthesia," and Chapter 17.
Metabolism
Prilocaine has a simpler hepatic metabolism compared
with lidocaine and mepivacaine. Much of the drug, how­
ever, is cleared before it is able to reach the liver (Jastak,
Yagiela, & Donaldson, 1995 ) . The lungs and kidneys are
CHAPTER 5 DENTAL LOCAL ANESTHETIC DRUGS
• 63
alternate sites of metabolism when the liver is not utilized
(Jastak, Yagiela, & Donaldson, 1995; Dentsply Pharmaceu­
tical, 20 10b ).
Excretion
Only small percentages of prilocaine and its metabolites
are found in the urine (Jastak, Yagiela, & Donaldson, 1995).
As with other local anesthetic drugs, higher excretion rates
are more common when the pH of urine is low.
Vasoactivity
Prilocaine is a weak vasodilator, making it effective with­
out the addition of vasoconstrictors, although prilocaine
is a stronger vasodilator compared with mepivacaine (see
Figure 5-5).
pKa
The pKa of prilocaine is 7.9 (see Table 5-2).
pH
The pH of prilocaine plain solutions is 6.0-7.0.
The pH of prilocaine solutions with 1 :200,000 epi­
nephrine is 3.0--4.0 (see Table 5-2).
Onset of Action
The onset of action for prilocaine is 2--4 minutes.
Prilocaine has a slightly slower onset of action compared
with lidocaine, mepivacaine, and articaine as might be pre­
dicted from its pKa.
Vasoconstrictor
Prilocaine is available with epinephrine in a dilution
• • • • of 1 :200,000 epinephrine.
B ecause of prilocaine's weak vasodilative effects, less vaso­
constrictor is required. Dilutions of 1 :200,000 epinephrine
are sufficient to provide profound and durable infiltration
and nerve block anesthesia (see Box 5-8 •).
Half-Life (t1f2)
The elimination half-life of prilocaine is 1.6 hours
(96 minutes).
Drugs with 1 : 200,000 e p i n e p h ri n e d i l ut i o n s co m p a red with
those with 1 : 1 00,000 fo rm u l at i o n s ca n b e b e n efi c i a l when it
is n ecess a ry to l i m it vasoconstrictor doses. S o m e situations
i n w h i c h vasoconstricto rs s h o u l d b e l i m ited o r avo i d e d
a ltogeth e r i n c l u d e s i g n ificant card i ovascu l a r co m p ro m ise,
tricyc l i c a nt i d e p ressant use, and i n s u l i n -res ista nt d i a b etes
• •
: � � � : : � : � � � : �� � : � : � �
.
i h nde l i
. • •
r ov cu a
. .
s se
. :
• • • • • • • • • • • • •
64 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•
Although similar to lidocaine and mepivacaine half-lives,
the initial amount of drug becomes a factor in this calcula­
tion because each cartridge of prilocaine delivers 72 mg
of drug, twice as much as 2% lidocaine solutions and one­
fourth more than 3% mepivacaine plain solutions (see
Table 5-3).
Topical Preparations
Topical use of prilocaine is found only in combination with
other drugs, typically lidocaine. Concentrations of 2.5 %
lidocaine with 2.5 % prilocaine are found in two popular
products, Oraqix (D entsply Pharmaceutical, 20 1 0a) and
EMLA (Astra Pharmaceuticals, 1999). See Chapter 8.
Pregnancy Category
Prilocaine is in FDA Pregnancy Category B.
B oth inj ectable and topical solutions of prilocaine are
classified as Pregnancy Category B (ADA/PDR, 2009;
Meadows, 200 1 ) .
Safety during Lactation
It is unknown whether prilocaine is excreted in human
milk. Caution is recommended.
B u pivaca i n e
Background
Bupivacaine was prepared by A. F. Ekenstam in 1957 and
approved by the FDA in 1972. It is related structurally to
lidocaine and mepivacaine (Malamed, 20 1 3 ; Septodont,
2013b ). See Appendix 5-1. B ecause of its long durations,
bupivacaine may not be appropriate in many clinical situa­
tions, but it does have several important clinical indications:
1. When extended postoperative pain control is needed
(bupivacaine can provide up to 12 hours of relief).
F I G U R E S-9 0.5% Bupivacaine, 1:200,000 Epinephrine.
Source: Courtesy of Carestream Health Inc.
2. In situations where profound and durable anesthesia
have proven to be difficult, if not impossible, to achieve
with all the other available drugs.
3. For extended procedures requiring longer than 60- to
90-minute durations.
Self-injury is an important consideration when using
bupivacaine, particularly if the individuals are at higher
risk of self-inflicted postoperative trauma such as young
children (see Box 5-5).
Formulations for Use i n Dentistry
Bupivacaine is provided in the following formulation:
0.5 % bupivacaine with 1 :200,000 epinephrine
(see Figure 5-9 •)
The strength of bupivacaine's receptor site binding allows
for lower concentrations of epinephrine to be used.
Duration of Action
0.5 % bupivacaine with 1 :200,000 epinephrine
Long duration = up to 12 hours; pulpal and soft tissue
D espite bupivacaine's intense vasodilating characteristics,
it is capable of producing prolonged anesthesia due to its
strong protein receptor binding in sodium channels. When
used for lengthy dental procedures, pulpal and soft tissue
anesthesia may last up to 12 hours. Bupivacaine may pro­
vide sufficient anesthesia to relieve pain overnight and is
often used for that purpose when postoperative pain is an­
ticipated. In patients who metabolize other drugs quickly
and in those requiring extended management of postop­
erative pain, or for unusually long treatment times, bupiva­
caine has proven quite effective (see Box 5-9 •) .
Similarity to Other Local Anesthetics
Bupivacaine is chemically similar to mepivacaine.
CH3
1 -butyi-N-(2,6-d imethylphenyl) piperid ine-2-carboxam ide

Postoperative Pain M a n a g e ment: B u p ivaca i n e i s
fre q u e ntly a d m i n istered fo r p a i n m a n a g e m e n t w h e n
s i g n ificant posto p e rative p a i n i s anticipated. I n t h e s e
s i t u a t i o n s , it is a d m i n istered after treatment h a s b e e n
com p l eted . The va l u e of t h i s strategy i s that t h e patient
can b e n efit fro m a n exte n d e d p e r i o d of pain re l i ef, u p to
1 2 h o u rs . T h i s ca n a l low t i m e fo r o r a l pain m e d i cati o n s to
take e ffect.
Postoperative Self- I nj u ry: An i m po rtant fa ctor w h e n
co n s i d e ri n g t h e use of b u p ivaca i n e is that it i s n ot
• a p p rop ri ate fo r i n d ivi d u a l s fo r w h o m t h e re is s i g n ifi cant risk •
: • • . � � � � : �� � :� � � �� ��� �� :
of s l - n u r
.
ro o n g
. • • .
a t s a.
• • • • • • • • • • •
A detailed discussion of bupivacaine's properties fol­
lows, with a brief summary of properties, dosing recommen­
dations, and uses provided in Box 5-10 •· Appendix 5-6
provides a complete reference table for bupivacaine and a
maximum dose reference is provided in Appendix 7-3.
M RD
(
90 mg absolute maximum United States: no body
)(
weight information Health Canada FDA equiva­ [ Onset: 6-1 0 m i n utes
)
lent 0.9 mg/lb; 2.0 mg/kg ) H a lf- L ife :
(
previously 0.6 mg/lb; 1.3 mg/kg; 90 mg absolute
maximum ) Preg n a n cy Categ o ry: C
Bupivacaine will not metabolize as quickly in the presence
of a compromised CVS. Overdoses tend to be more severe
and less easily reversed because of bupivacaine's greater
(
cardiotoxicity circulation is more likely to be compro ­
mised and cannot reduce blood levels as quickly, prolong­
ing the overdose . ) ment, which slows the removal of bupivacaine from the
Relative Potency
Bupivacaine is eight times more potent than procaine, four
times more potent than lidocaine, mepivacaine, and prilo­
caine, and nearly three times more potent than articaine.
This helps explain the dilute concentration available in
(
dentistry, 0.5 % see Figure 5-3).
Relative Toxicity
B upivacaine is nearly eight times more toxic than pro­
caine, five to six times more toxic than prilocaine, and
nearly four times more toxic than lidocaine, mepivacaine,
and articaine.
Bupivacaine toxicity is nearly equal to both the CNS
(
and CVS Levsky & Miller, 2005). In overdoses, two main
factors contribute to the increased risk versus other drugs,
bupivacaine's lengthy half-life and early CVS involvement
(see Figure 5-4).
Reports of overdose have been characterized as un­
common but when they do occur, these events tend to be
CHAPTER 5 DENTAL LOCAL ANESTHETIC DRUGS
• 65
Formu lations fo r Use i n Dentist ry: 0.5% with 1 :200,000
epinephrine
D u ration o f Action: Lo n g : va ri a b l e , u p t o 1 2 h o u rs p u l p a l
• a n d soft tissue
M R D : 90 m g a b s o l ute m a xi m u m ( U n ited States : n o body
w e i g h t i nfo rmation) ( H e a lth Canada [ F DA e q u iv a l e nt]
0.9 m g / l b ; 2 . 0 m g/kg) (prev i o u s l y 0 . 6 m g / l b ; 1 . 3 m g/kg;
90 m g absol ute m axi m u m)
Relative Potency: F o u r t i m e s l i d o c a i n e , p r i l o c a i n e , a n d
m e p ivaca i n e ; l ess t h a n t h ree t i m es a rtica i n e
• Relative Toxicity: Less t h a n fo u r t i m e s l i d o ca i n e a n d
m e p ivaca i n e
M eta b o l ism: Liver a m idases
Excretion: K i d n ey; 1 6% excreted u n c h a n ged
Vasoactivity: G reater vaso d i l at i o n t h a n a l l five a m i d e s but
l ess t h a n p roca i n e
pKa: 8 . 1
p H : 4 . 5-6 .0
2.7 h o u rs (1 62 m i n utes)
To pical Prepa rations: N o n e in dentistry
more difficult to reverse because of early CVS involve­
(
circulation Levsky & Miller, 2005).
In dentistry, adverse events have been rare with bu­
pivacaine for two important reasons: easier tracking of
total doses with cartridges and lower MRD s compared
with medicine where MRDs run as much as 2.5 times
(
greater Jastak, Yagiela, & D onaldson, 1995; Levsky &
Miller, 2005 ; Younessi & Punnia-Moorthy, 1 9 9 9 ) . Al­
though precautions based on toxicity are recommended
when considering bupivacaine, there should be no hesita­
tion to use it when circumstances clearly indicate an ad­
vantage over the other drugs, such as inadequate duration
or the need for longer periods of pain relief Younessi & (
Punnia-Moorthy, 1999).
Metabolism
B upivacaine's metabolism is complex. The liver provides
j
the ma or amidase metabolic pathway Malamed, 20 1 3 ) . (
Biotransformation of bupivacaine is much slower com­
pared with the other local anesthetic drugs Tetzlaff, (
2000).
66 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•
Excretion
Very little, to up to 16 % , is excreted in the urine un­
changed (Tetzlaff, 2000). As with other local anesthetic
drugs, higher excretion rates are more common when the
pH of urine is low.
Vasoactivity
B upivacaine is a very potent vasodilator; nevertheless it
has long durations due to its strong protein receptor bind­
ing strength (see Figure 5-5).
In contrast to lidocaine, mepivacaine, articaine, and prilo­
caine, bupivacaine is a more aggressive vasodilator. It is distin­
guished not only as being the second most potent vasodilator
of those discussed in this chapter (procaine is the most potent)
but as the most durable of all drugs in dentistry, as well.
pKa
The pKa of bupivacaine is 8.1.
Bupivacaine's higher pKa translates into slower onset times.
When bupivacaine is to be used, other rapid onset drugs
such as mepivacaine and lidocaine may be administered first
in order to allow treatment to begin sooner (see Table 5-2).
pH
The pH of bupivacaine solutions with 1 :200,000
epinephrine 3.0-4.5.
=
See Table 5-2.
Onset of Action
The onset of action for bupivacaine is 6-10 minutes.
B upivacaine has the slowest onset of all the inj ectable
drugs in dentistry and is up to five to ten times slower than
mepivacaine and articaine in some situations.
Vasoconstrictor
Bupivacaine is available with epinephrine in dilutions
of 1 :200,000.
Bupivacaine in dentistry is prepared with epinephrine be­
cause of its vigorous vasodilative activity.
Despite inducing vigorous vasodilation in tissues, bu­
pivacaine requires minimal epinephrine concentrations
due to its potency.
Half-Life (t1fz)
The elimination half-life of bupivacaine is 2.7-3.5
hours (162-210 minutes).
B upivacaine has the longest half-life of all dental inj ect­
able local anesthetics (see Table 5-3).
Topical Applications
There are no topical applications of bupivacaine available
in dentistry.
Pregnancy Category
Bupivacaine is in FDA Pregnancy Category C.
As previously stated, bupivacaine is not appropriate for
routine use in dentistry, including in pregnancy (ADA/
PDR, 2009; Meadows, 20 0 1 ) . Careful consideration and
compelling rationale are necessary before using any
Category C drug.
Safety in Lactation
It is unknown whether or not bupivacaine is excreted in
human milk. Caution is advised (see Table 5-4).
Proca i n e
Background
Procaine was introduced by Alfred Einhorn in the early
1900s as an alternative to cocaine due to the desire to
eliminate addictive tendencies when using local anesthetic
drugs as well as the systemic toxicity and local tissue injury
that too often accompanied cocaine's use (Tetzlaff, 2000).
See Appendix 5-1.
Procaine is no longer available in dental cartridges;
however, it is included in this discussion to represent the
ester class of local anesthetics, none of which is currently
packaged for dental administration. Procaine's proprietary
name, Novocaine, has been synonymous with dental anes­
thesia for many years (Malamed, 20 13).
In the rare event a patient is allergic to all of the amide
dental local anesthetic drugs, procaine or other selected esters
may be substituted. Although not packaged for dentistry,
procaine and other esters may be obtained in medical vials
for use with hypodermic needles (see Figure 5-10 •).
Formulations for Use i n Dentistry
Although not currently available in dental cartridges,
procaine can be obtained in medical vials in the following
formulations (Malamed, 20 13):
2 % procaine plain (without vasoconstrictor)
4% procaine plain (without vasoconstrictor)
2% procaine with 1 : 100,000 epinephrine
4% procaine with 1 : 100,000 epinephrine
Duration of Action
2 % procaine plain (without vasoconstrictor)
4% procaine plain (without vasoconstrictor)
Very short duration = no pulpal, 15-30 minutes soft
tissue
2% procaine with 1 : 100,000 epinephrine
4% procaine with 1 : 100,000 epinephrine
Intermediate duration = 60 minutes pulpal
Procaine is a vigorous vasodilator and is rapidly metabo­
lized by plasma cholinesterase. D e spite the 60-minute

F I G U RE 5-1 0 2% Procaine, Epinephrine 1:100,000, by prescription only.
duration that may be available when combined with a
vasoconstrictor, results have been variable with a greater
number of individuals experiencing incomplete pain
control during dental appointments compared with
lidocaine. When considered along with procaine's relatively
high incidence of inducing allergic reactions, procaine's
disappearance from the dental market is understandable.
Similarity to Other Local Anesthetics
Procaine is similar to tetracaine. Both are esters. As is true
of many of local anesthetics, procaine is an anticonvulsant
(Tetzlaff, 2000).
M RD
Consult product insert.
The potential for overdose is very low as long as solu­
tion is not deposited in vessels and doses do not exceed
the MRD (Tetzlaff, 2000).
Relative Potency
Procaine is significantly less potent compared with all of
the inj ectable amides in dentistry (Malamed, 20 1 3 ) . This
property, along with procaine's relatively high incidence of
inducing allergic reactions (see Relative Toxicity discus­
sion), accounts for the decision by manufacturers to cease
preparing procaine in dental cartridges by 1989.
It is half as potent as lidocaine, mepivacaine, and prilo­
caine, and approximately one-third as potent as articaine.
It is only about 1 2 % as potent as bupivacaine. Except for
situations in which no amides may be used, procaine is not
desirable in dentistry (see Figure 5-3).
Relative Toxicity
Procaine is significantly less toxic compared with all of the
amides in dentistry. Its rapid metabolism and complete
avoidance of liver metabolism make it the safest drug of
the six. Despite this advantage, however, if high plasma
levels are reached quickly, as may happen in successive
intravascular administrations, procaine has the ability to
CHAPTER 5 DENTAL LOCAL ANESTHETIC DRUGS
• 67
/ C,H;
1-1 2
-o- COOCI-I 2C l-12 -- N
�
C,H ;
2 - ( d i et h y l a m i n o )ethyl 4-aminobenzoate
inhibit plasma cholinesterase activity, which may actu­
ally increase its potential for toxicity (Tetzlaff, 2000) (see
Figure 5-4).
Procaine is a derivative of para-aminobenzoic acid
(PABA), which is also its primary metabolite. PABA is
thought to be responsible for procaine's relatively high
rate of allergenicity (Jastak, Yagiela, & Donaldson, 1995).
The recorded incidence of allergy to procaine is significant
more for its rate of occurrence compared with the amides,
than for its high overall rate of occurrence (Fuzier et al.,
2 0 0 9 ; Gall, Kaufmann, & Kalveram, 1 9 9 6 ; Gonzalez­
Delgado et al., 2006; Wilson et al., 2000).
Metabolism
Procaine is rapidly metabolized via plasma cholinesterase.
There are no hepatic pathways for its biotransformation
(Malamed, 20 13; Tetzlaff, 2000).
Excretion
More than 2 % is excreted unchanged by the kidneys
(Malamed, 20 1 3 ) . Higher excretion rates are more com­
mon when the pH of urine is low.
Vasoactivity
Procaine is a potent vasodilator (see Figure 5-5).
pKa
The pKa of procaine is 9.1.
As might be expected from procaine's high pKa value, on­
set of anesthesia is slow. Few base molecules are available
initially. In addition to the availability of fewer base mol­
ecules, procaine has poor lipid solubility (Tetzlaff, 2000)
(see Table 5-2).
pH
The pH of procaine plain is 5.0-6.5.
The pH of procaine with a vasoconstrictor is 3.5-5.5.
68 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•
Procaine is virtually worthless as a plain preparation in
dentistry; therefore, its higher pH in plain form is not sig­
nificant. When vasoconstrictors are added, pH levels drop
to those approximating pH levels in other similar solutions
(see Table 5-2).
Onset of Action
The onset of action for procaine is 6-10 minutes.
The onset of action of procaine is similar to bupivacaine.
Procaine's pKa is high at 9.1.
Vasoconstrictor
Procaine can be obtained with epinephrine in dilu­
tions of 1 : 100,000.
Half-Life (t1fz)
The elimination half-life of procaine is 6 minutes.
B ecause of its rather rapid hydrolysis via plasma cho­
linesterase, procaine is one of the safest drugs available
(Tetzlaff, 2000). The elimination half-life is shortest of all
dental local anesthetic inj ectable drugs (see Table 5-3).
Topical Applications
There are no topical applications for procaine in dentistry
(Tetzlaff, 2000).
Pregnancy Category
Procaine is in FDA Pregnancy Category B.
Procaine is equal in safety during pregnancy to lidocaine
and prilocaine. (ADA/PDR, 2009; Meadows, 200 1 ) .
Safety during Lactation
It is unknown whether or not procaine is excreted in hu­
man milk. Use with caution (ADA/PDR, 2006).
CAS E MA N A G EME N T
Elena Gagarin
W h i l e m ost d r u g s may be fo u n d in b reast m i l k, th is is
n ot seen as a p a rti c u l a r p rob l e m . Amides a re fi rst pass
d ru g s , w h i c h m e a n s they pass t h ro u g h the l iver fi rst
a n d o n ly l esser q u a ntities wo u l d be ava i l a b l e in breast
m i l k. Even though the a d m i n istration of loca l a nesthetic
d rugs to n u rs i n g mothers is not t h o u g ht to be s i g n ifi­
cant, mothers who a re co ncerned can be reass u red if
a rtica i n e is used because a rtica i n e possesses the a n es­
thetic efficacy of the oth e r a m ides, yet it is m u c h m o re
q u ickly biotra nsformed by pseudocholinesterase.
Case Discussion : The h a lf- l ife of a rtica i n e , eve n w h e n
m a xi m u m safe d o s e s have b e e n a d m i n iste red , is a p ­
p roxi m a t e l y 4 5 m i n utes . W h e n l e s s t h a n m a xi m u m
F D A P reg n a n cy Categ o ries
In determining the safe u s e o f a drug i n pregnancy, FDA
guidelines and prescribing information should be con­
sulted. The FDA provides guidance in the form of drug
categories in pregnancy (ADA/PD R, 2 0 0 9 ; Meadows,
200 1 ) . This information can be readily accessed online at
http://www.fda.gov.
The following interpretations describe the categories
for local anesthetic drugs included in this chapter:
Category A - No demonstrated increased risk of fetal
abnormalities
Category B - No demonstrated increased risk in animal
studies but no studies available in humans or animal
studies have shown an increased risk, but well-controlled
studies in humans failed to demonstrate any risk
Category C - Not enough information to determine
at this time
A complete list of FDA Pregnancy Categories and their
rationale is included in Table 5-5 .
D ental local anesthetic drugs, including topical anes­
thetics, generally fall within Categories B and C. Inj ectable
and topical lidocaine and prilocaine fall within Cate­
gory B although it should be noted that both drugs are
at most only minimally effective in infiltrations without
epinephrine. Articaine, benzocaine, bupivacaine, mepiva­
caine, and levonordefrin are Category C drugs, similar to
epinephrine.
What does this mean? In pregnancy, lidocaine and pri­
locaine have demonstrated no increased risk of inducing
or contributing to fetal abnormalities and, although not
proven absolutely safe, are considered safe to use. Articaine,
bupivacaine, levonordefrin, mepivacaine, and epinephrine,
although not necessarily unsafe, cannot refer to studies in
pregnant women demonstrating fetal safety, and they may
actually have caused harm in animal studies. Careful con­
sideration must be given before using any Category C drug.
safe d o s e s h a ve b e e n a d m i n istered i n t ra o r a l ly, t h e
h a lf- l ife h a s b e e n d e m o n strated to b e e v e n l e s s . I n
3 h o u rs , reg a r d l ess, l eve l s d ro p to a fract i o n o f w h at
t h ey w e re i n it i a l ly (o n l y a b o u t 1 /8 to 1 / 1 6 t h e i n it i a l
d o s e ) . T h i s co m p a res w i t h l i d o ca i n e w h e re t h e re is
nea rly h a lf the i n itial d ose p resent at 3 h o u rs . The p e r­
c e n t a g e of a n y d r u g th a t a ctu a l ly e n t e rs b re a st m i l k
i s u n known a n d probably va ria b l e . I f n u rs i n g mothers
ti m e th e i r d e n ta l a p p o i ntme nts ca refu l ly a n d a rtica i n e
i s u s e d , o n l y i n s i g n ifi c a n t t r a c e s wo u l d b e p re s e n t
o n ce n u rs i n g co m m e n ce s . If b l o c ks of t h e m a n d i b l e
a re n e e d e d , G o w - G a te s o r Va z i r a n i - A k i n o s i t e c h ­
n i q ues a re reco m m e n d e d beca use o f t h e possi b l e i n ­
creased risk o f p a resthesia i n i nfe rior a lveo l a r b l ocks .
 CHAPTER 5 DENTAL LOCAL ANESTHETIC DRUGS
• 69

Chapte r Q uestio n s 8. Arrange the inj ectable local anesthetic drugs in de­
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
scending order of overall CNS and CVS toxicity .
1 . The definition of the maximum recommended dose a. B upivacaine, mepivacaine, lidocaine, prilocaine,
(MRD ) of a drug best fits which one of the following articaine
definitions? b. B upivacaine, mepivacaine, lidocaine, articaine,
a. A safe dose to administer in all situations prilocaine
b. A dose that a 150-lb individual can have c. B upivacaine, mepivacaine, articaine, lidocaine,
c. A d o s e t h a t c a n n o t be e x c e e d e d u n d e r any prilocaine
circumstance d. B upivacaine, lidocaine, mepivacaine, articaine,
d. A s a fe g u i d e l i n e w h e n a d m i n i s t e r i n g l o c a l prilocaine
anesthetic drugs
2. Which one of the following best describes articaine's
metabolism? Refe re n ces
a. Articaine is metabolized approximately 25 % in the
ADA/PDR guide to dental therapeutics ( 5th ed. ) . ( 2009) .
liver.
Montvale, NJ: Thompson PDR Corporation.
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Astra Pharmaceuticals. (1999). EMLA Cream and Anesthetic
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most appropriate for this patient when you are anes­ xylesterase in the serum of viral hepatitis patients. Folia Med
thetizing the maxillary right quadrant? (plovdiv), 23(3-4), 61 -63.
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Daniel, S. J., & Harfst, S. A. ( 2007) . Dental hygiene concepts,
4. A periodontist requires hemostasis on palatal tissues cases, and competencies ( 2nd ed. ) . St. Louis: Mosby.
in the maxillary left quadrant before elevating a surgi­ Daublander, M., Kammerer, P. W., Willershausen, B. , Leckel,
cal flap. Which one of the following drugs would fur­ M., Lauer, H. C., Buff, S., et al. ( 2012) . Clinical use of an epi­
nish the most vigorous hemostasis? nephrine-reduced ( 1/400,000) articaine solution in short-time
a. 2% mepivacaine, 1:20,000 levonordefrin dental routine treatments - a multicenter study. Clinical Oral
Investigation, 16(4), 1289-1295.
b. 4% prilocaine, 1:200,000 epinephrine
Dentsply Pharmaceutical. ( 2010a ) . Oraqix (lidocaine and pri­
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locaine periodontal gel), Rev. 09110, prescription information.
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5. Which characteristic of a local anesthetic drug deter­ www.dentsplypharma.com
mines how well it works without a vasoconstrictor? Dentsply Pharmaceutical. ( 2010b ). Prilocaine hydrochloride
injection and prilocaine hydrochloride and epinephrine
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York, PA: Author. Retrieved January 19, 2014, from www.
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beta-blocker, which one of the following drugs would
from www.dentsplypharma.com
be most appropriate to administer?
De Toledo, J. C. ( 2000) . Lidocaine and seizures. Therapeutic
a. 2% lidocaine, 1 : 1 00,000 epinephrine Drug Monitoring, 22, 320-322.
b. 2% mepivacaine, 1:20,000 levonordefrin Dower, J. S. ( 2003, February ) . A review of paresthesia in association
c. 3 % mepivacaine plain with administration of local anesthesia. Dentistry Today, 8--13.
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Anesthetic study questioned. Journal of the American Dental
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Gall, H., Kaufmann, R . , & Kalveram, C. M. (1996). Adverse
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 CHAPTER 5 DENTAL LOCAL ANESTHETIC DRUGS
• 71

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Visit www.pearsonhighered.com/healthprofessionsresources to access the student resources that accompany

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S u m m a ry of De nta l Loca l An esth eti c D ru g s*
Relative Relative
Local Anesthetic Half-Life Soft Tissue Potency Toxicity

(Reference value = lidocaine @ l 00%

Drugs MRD MRD MRD t� Pulpal Anesthesia Anesthesia Duration
Color Coded Box (mg/lb) (mg/kg) Absolute pH minutes) (in minutes) (in minutes) Vasoconstrictor Category

4% Articaine 3.2 7.0 4.4-5 .2 30 75 1 80-300 1 50% 1 00%

1 : 100,000
Epinephrine Intermediate
(w/ vaso)

3.2 7.0 4.4-5 .2 30 45 120-300 150% 1 00%

1 :200,000
Epinephrine Intermediate

90 3.0-4.5 270 90- 1 80 240-540 400% Less than 400%

1 :200,000
Epinephrine Long

3.2 7.0 500 6.5 96 5-10 60- 1 20 None 1 00% 1 00% Very short

3.2 7.0 500 3 . 3-5 .5 96 60 1 80-300 1 00% 1 00%

1 :50,000
Epinephrine Intermediate

3.2 7.0 500 3 . 3-5 .5 96 60 1 80-300 1 00% 1 00%

1 : 100,000
Epinephrine Intermediate

3.0 6.6 400 4.5-{;.8 1 14 20-40 1 20- 1 80 None 1 00% 1 25% Short

3.0 6.6 400 3 .0-3 .5 1 14 60 1 80-300 1 00% 125%

1 :20,000
Levonordefrin Intermediate

4.0 8.8 600 4.5-{;.8 96 10-15 infiltration(!) 90-1 20 (I) 1 00% 85%
40-{iO block (B) 1 20-240 (B)
None Short (!)
Intermediate (B)

4.0 8.8 600 3 .0-4.0 96 60-90 1 80-480 1 00% 85%

1 :200,000
Epinephrine Intermediate

*FDA maximum recommended dose and drug insert information for each drug should be consulted prior to use.

* * * No FDA weight-based recommendation, MRD ; 90 mg. Health Canada weight-based recommendation 0.9 mg/lb or 2.0 mglkg.
* * No FDA absolute maximum recommended dose.
Lidocaine-D rug Facts

Proprietary Names Alphaca i ne, Octocai ne, Xyloca ine

Formulations/Durations of Action (pulpal ) 2% lidocaine, 1:100,000 epinephrine 60 minutes (intermediate )

2% lidocaine, 1:50,000 epinephrine 60 minutes (intermediate )

MRD 3. 2 mg/lb 7.0 mg/kg 500 mg absolute maximum

Relative Potency 2X procaine

1 X mepivacaine and prilocaine
2/3 X articaine
l/4X bupivacaine

Relative Toxicity 2X procaine

1 X mepivacaine and articaine
l/4X bupivacaine

Metabolism Liver (oxidases and amidases; several active metabolites )

Excretion Kidneys (less than 10% unchanged )

Vasoactivity Weaker vasodilator than procaine

Stronger than mepivacaine and prilocaine

pKa 7. 7

pH 3. 3-5.5

Onset of Action 2-3 minutes

Half-Life 1.6 hours (96 minutes )

Topical Preparation 2% to 10%; 1- to 2-minute onset; - 2- to 5-minute effect

Pregnancy Category B

Lactation Enters breast milk (use caution )

Source: Courtesy of Dentsply Pharmaceutical.

73
Articaine-D rug Facts

Proprietary Names Articadent, Orabloc, Septocai ne, Zorcaine

Formulations/Durations of Action (pulpal ) 4% articaine, 1:100,000 epinephrine 60-75 minutes (intermediate )

= Septocainc•
- e �==.::�:·::.:-::. _.

4% articaine, 1:200,000 epinephrine 45 -60 minutes (intermediate )

MRD 3.2 mg/lb 7.0 mg/kg no absolute maximum provided

Relative Potency 2X procaine

3/2X lidocaine, mepivacaine, and prilocaine
113 X bupivacaine

Relative Toxicity More toxic than procaine

Slightly more toxic than prilocaine
Slightly less toxic than mepivacaine and lidocaine
1/4 X bupivacaine

Metabolism 5%-10% Liver

90%-95% via cholinesterase

Excretion Kidneys (very little excreted unchanged )

Vasoactivity Similar to lidocaine

Stronger vasodilator than mepivacaine and prilocaine
Much weaker vasodilator than procaine and bupivacaine

pKa 7. 8

pH 4.0-5.2 1:100,000 epinephrine

4.6 -5.4 with epinephrine

Onset of Action 1 -2 minutes infiltration

2-3 minutes nerve block

Half-Life 0.44 hours ( 43.8 minutes 1:100,000 epi.; 44.4 minutes 1:200,000 epi.
after 6.9 successive cartridges administered )

Topical Preparation None available in dentistry

Pregnancy Category c

Lactation Enters breast milk (use caution )

Source: Courtesy of Dentsply Pharmaceutical.

74
M epivacaine-D rug Facts

Proprietary Names Arestocaine, Ca rboca i ne, lsoca i ne, Polocai ne, Scandonest

Formulations/Durations of Action (pulpal) 3% mepivacaine plain 20-40 minutes (short)

2% mepivacaine, 1:20,000 levonordefrin 60 minutes (intermediate)

MRD 3.0 mg/lb 6.6 mg/kg 400 mg maximum

Relative Potency 2X procaine

1 X lidocaine and prilocaine
2/3 X articaine
l/4X bupivacaine

Relative Toxicity 2X procaine and prilocaine

1 X lidocaine and articaine
l/4X bupivacaine

Metabolism Liver (primarily oxidases; slower than lidocaine)

Excretion Kidneys (up to 16% unchanged)

Vasoactivity Weakest vasodilator of all 5 amides

pKa 7. 6

pH 3%: 4.5-6.8; 2%: 3.0-3.5

Onset of Action 1.5-2 minutes

Half-Life 1.9 hours (114 minutes)

Topical Preparation None available in dentistry

Pregnancy Category c

Lactation Enters breast milk (use caution)

Source: Courtesy of Dentsply Pharmaceutical.

75
Pri locaine-D rug Facts

Proprietary Names Citanest, Citanest Forte

Formulations/Durations of Action (pulpal) 4% prilocaine, plain Block: 40-60 minutes (intermediate)

4% prilocaine, plain Infiltration: 10-15 minutes (short)

4% prilocaine, 1:200,000 epinephrine 60-90 minutes (intermediate)

MRD 4.0 mg/lb 8.8 mg/kg 600 mg maximum

Relative Potency 2X procaine

1 X lidocaine and mepivacaine
2/3 X articaine
1/4X bupivacaine

Relative Toxicity 2X procaine

Slightly less than mepivacaine and articaine
1/5X bupivacaine

Metabolism Liver (much of prilocaine is cleared before it can reach the liver)
Kidneys
Lungs

Excretion Kidneys (very little excreted unchanged)

Vasoactivity Weak vasodilator, although not as weak as mepivacaine

pKa 7.9

pH 6.0-7.0 plain; 3.0-4.0 with epinephrine

Onset of Action 2-4 minutes

Half-Life 1.6 hours (96 minutes)

Topical Preparation 2.5% in combination with other drugs (usually lidocaine)

Pregnancy Category B

Lactation Enters breast milk (use caution)

Source: Courtesy of Dentsply Pharmaceutical.

76
Bupivacaine-D rug Facts

Proprietary Name M a rca ine

Formulations/Durations of Action (pulpal) 0.5% bupivacaine, 1:200,000 epinephrine 90-120 minutes (long)
(may provide up to 12 hours of non-pulpal
anesthesia)

MRD 0.9 mg/lb* 2.0 mg/kg* 90 mg maximum

Relative Potency S x procaine

4X lidocaine, mepivacaine, and prilocaine
3 X articaine

Relative Toxicity 8X procaine

5-6 X prilocaine
4X lidocaine, mepivacaine, articaine

Metabolism Liver (amidase; slow)

Excretion Kidneys (up to 16% unchanged)

Vasoactivity Strong vasodilator

pKa 8.1

pH 3.0-4.5

Onset of Action 6-10 minutes

Half-Life 2.7 hours (162 minutes)

Topical Preparation None available in dentistry

Pregnancy Category c

Lactation Enters breast milk (use caution)

* No F DA weight based recommendation, MRD = 90 mg. Health Canada weight based recommendation 0.9 mg/lb or 2.0 mg/kg.
Source: Courtesy of Dentsply Pharmaceutical.

77
··························································· ® ··························································

Vasoco n stri cto rs i n De ntistry

OBJECTIVES KEY TERMS

• Defi n e a n d d i scuss the key terms in t h i s cha pter. a d re n e rg i c 79

adverse events 8 1
• D i scuss the overa l l s i m i l a rities a n d d iffe re n ces between
e p i n e p h ri n e 79
vasoco n strictors. catech o l a m i n e 79
• D i scuss and identify c l i n ica l situ ations i n which the ch o ice of fe lypress i n 86
vasoco n strictor may d i rectly affect a n esth etic su ccess. l evo n o rd efri n 79
•
n o re p i n e p h ri n e 79
D i scuss and d eterm i n e situations in w h i ch specific vasoco n ­
p h e n y l e p h r i n e 86
stri cto rs may be i n d i cated or contra i n d icated .
sym path o m i m etic 79
• Describe the diffe rence in pote n cy between e p i n e p h ri n e a n d vasop ressors 79
l evo n o rd efri n .
• D i sti n g u ish between c l i n ica l s i g n s a n d sym pto m s o f vasoco n ­
stri cto r overd ose a n d a nxi ety/fea r responses.

CAS E S T U DY
Elena Gagarin
E l e n a G a g a r i n re cently started a n ew p rescri ption
fo r a tri cyc l i c a nt i d e p ressa nt t h a t s h e ta kes d a i ly.
She s u bse q u e ntly fra ct u red a cusp o n # 1 4 that has
a l a rg e rest o r a t i o n . S h e i s exp e ri e n c i n g no p a i n
a n d h a s n o oth e r d e ntal p ro b l e m s .
Introd u ction
Vasoconstrictors enhance local anesthetic drugs i n a num­
ber of important ways (Agency for Healthcare Research
and Quality [AHRQ] , 2002; Jastak, Yagiela, & Donaldson,
1995; Yagiela, 1999) . They constrict local vessels, increasing
safety by slowing systemic absorption. This constriction
also prolongs the local actions of the drugs, provides he­
mostasis, and increases profoundness of anesthesia (Jastak,
Yagiela, & Donaldson, 1995).
Vasoconstrictors are p articularly useful in dental
s e ttings where long durations a n d more profound
anesthesia are routinely require d . Th eir u s e fulness,
however, requires an understanding of their physiological
and pharmacological considerations. A 1999 report pre­
pared for the American D ental Association, for example,
states that vasoconstrictors have been associated with
more drug interactions than any other drugs in dentistry
(Yagiela, 1999) . A frequently overlooked fact is that the
systemic uptake of vasoconstrictors is increased by the
vasodilating properties of the local anesthetic drugs with
which they are combined (Yagiela, 1999) . In other words,
while vasoconstrictors decrease the risk of systemic toxicity
of local anesthetic drugs, local anesthetic drugs increase the
risk of toxicity of vasoconstrictors (Yagiela, 1999) .
When clinicians are knowledgeable about the physi­
ological and pharmacological effects of vasoconstrictors
and administer them appropriately, the benefits usually
outweigh the risks and they remain an essential part of the
practice of pain control in dentistry.
This chapter will discuss the pharmacology of vaso­
constrictors used in dentistry with an emphasis on epi­
nephrine and levonordefrin.
Vasoco n stricto rs in Dentistry
There are two vasoconstrictors, also known as vasopressors,
that are routinely included in dental local anesthetic
drugs in North America - epinephrine and levonordefrin.
Epinephrine represents the benchmark for vasoconstric­
tors in dental local anesthesia. Levonordefrin is a suitable
substitute.
Adrenergic Actions of Vasoconstrictors
Epinephrine is a naturally occurring catecholamine or neu­
rotransmitter, along with norepinephrine and dopamine.
CHAPTER 6 VASOCONSTRICTORS IN DENTISTRY
• 79
Unlike epinephrine, Ievonordefrin is a synthetic catechol­
amine. B oth epinephrine and levonordefrin stimulate
adrenergic receptors, the targets of the catecholamines
within the tissues. They belong to a larger group of drugs
that includes both catecholamine and non-catecholamine
adrenergic stimulators known as sympathomimetic amines
(see Table 6-1 •) (Malamed, 20 13) .
Epinephrine (adrenaline) is both a hormone and a
neurotransmitter, one of many vasoconstricting substances
that are referred to as sympathomimetic drugs, which
means they mimic sympathetic nervous system mediators
such as norepinephrine. Other sympathomimetic drugs
used in local anesthetic solutions include levonordefrin
(Neo-Cobefrin) and phenylephrine.
S y m p a t h o m i m e t i c d r u g s m a y be c l a s s i fi e d a s
direct-acting, indirect-acting, o r mixed-acting. These clas­
sifications refer to the manner in which the drugs exert
their influence on adrenergic receptors. An example of ad­
renergic receptor activity is found in their effects on the
smooth muscle walls of peripheral blood vessels. An initial
adrenergic (sympathomimetic) receptor effect on these
structures results in vasoconstriction, slowing the uptake
of anesthetic drugs into vessels (see Table 6 2 •). -
Direct-acting drugs are similar to endogenous epi­
nephrine and norepinephrine, providing direct stimulation
of adrenergic receptors on susceptible cells and tissues.
Examples of direct-acting sympathomimetic drugs include
synthetic or exogenous epinephrine and norepinephrine,
levonordefrin (Neo-Cobefrin), dopamine, isoproterenol,
methoxamine, and phenylephrine.
Indirect- acting drugs generally block the removal
or recycling of epinephrine and norepinephrine, result­
ing in a buildup of both in synapses, which in turn causes
overstimulation of adrenergic recep tors. In addition
to decreased reuptake, indirect- acting mechanisms for
the accumulation of these neurotransmitters in the syn­
apses may include a stimulation in their synthesis, an in­
crease in their release, and a decrease in their metabolic
breakdown. Indirect-acting drugs include amphetamine,
methamphetamine, and hydroxyamphetamine. Cocaine,
Table 6-1 Common Sympathomimetic Amines
Catecholami nes Non-catechola m i nes* *
Epinephrine* Amphetamine
Norepinephrine* Methamphetamine
Levonordefrin Ephedrine
Dopamine* Phenylephrine
*Naturally occurring chemicals
**All are examples of chemicals found in street drugs, diet pills, and cold
medications.
Source: Malamed (2013).
80 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•
Table 6-2 Sympathomimetic Drug Influence on Adrenergic Receptors
D i rect Acting I n d i rect Acti ng
Epinephrine Tyramine
Norepinephrine Amphetamine
Levonordefrin Methamphetamine
Isoproterenol Hydroxyamphetamine
Dopamine
Methoxamine
Phenylephrine
Source: Malamed (2013).
an ester-type local anesthetic drug, also has significant
indirect adrenergic stimulating effects.
Mixed-acting drugs have both direct and indirect ef­
fects on adrenergic receptors. Mixed-acting drugs include
metaraminol and ephedrine.
Vasoconstriction is provided by the temporary actions
of these drugs on smooth muscle walls of blood vessels.
In areas where local anesthetic drugs with vasoconstric­
tors are deposited, the slowing of vascular uptake allows
more time for drugs to enter nerve membranes and block
receptor sites. This increases the duration of anesthesia.
In addition to enabling more efficient activity of local an­
esthetic drugs within nerve membranes, there is at least
some direct action of epinephrine that results in decreased
sensation (Tetzlaff, 2000) . This effect may contribute to the
profoundness of the anesthesia.
Two types of adrenergic receptors were identified
by Ahlquist in 1948, alpha ( a ) and beta (/3) (Ahlquist,
1948) . Since that time, subcategories have been identi­
fie d that explain spe cific actions of vasoconstrictors
based on differences in their locations and functions
(Malamed, 20 1 3 ) . Alpha ( a ) receptors are responsible
for smooth muscle contraction in peripheral arterioles
and veins throughout the body (peripheral vasocon­
striction) (ADA/PD R, 2009 ) . B eta 1 (/31) receptors are
responsible for cardiac stimulation and B eta 2 (/3 2 ) re­
ceptors are responsible for the smooth muscle relaxation
that results in bronchodilation and vasodilation (ADA/
PDR, 2009) . B oth a and f3 receptors contribute to the
potential for cardiac dysrhythmias (ADA/PDR, 2009 ) .
A summary of selected effects and affected organs can
be found in Table 6-3 •·
Use or Avoidance of Vasoconstrictors
The use of vasoconstrictors in some situations remains
a controversial topic (Agency for Healthcare Research
and Quality, 2002) . Avoiding vasoconstrictors based on
M ixed Acting
Metaraminol
Ephedrine
their impact on blood pressure alone, for example, may
be misguided. Plain drugs, such as 3% mepivacaine, may
not always provide profound and/or durable anesthesia.
A lack of profound anesthesia can result in unmanageable
pain that in turn can lead to unpredictable spikes in blood
pressure due to the endogenous release of epinephrine.
Although unlikely, endogenous release can exceed admin­
istered doses of epinephrine.
When discussing vasoconstrictors, it is helpful to
remember that dental appointments can be stressful and
that endogenous epinephrine released from the adre­
nal glands may increase before and during appointments.
Endogenous release can compound the adverse adren­
ergic effects of exogenous (inj ected) epinephrine. It has
been suggested that exogenous epinephrine may actually
stimulate endogenous release by its direct action on ad­
renergic receptors of the adrenal glands (Takahashi et al.,
2005 ) . This type of release might occur, for example, if a
patient who is particularly fearful of dental appointments
is given modest amounts of epinephrine yet displays signs
and symptoms of an epinephrine overdose where none
technically exists. The endogenous release can be signifi­
cant enough to be responsible for any excessive amounts
of epinephrine in circulation. Current protocol recognizes
that exogenous epinephrine from dental cartridges causes
more significant stimulation than endogenous release
(Malamed, 20 13). The impact of the potential endogenous
release is far less predictable because of the difficulty in
anticipating quantities that might be released (Cryer, 1980;
Lipp et al., 1993; Yagiela, 1991 ) .
Adrenergic vasoconstrictors u s e d in dental proce­
dures typically d o not produce noticeable effects but
are capable of causing undesired local and systemic
reactions (Yagiela, 1999) . Local effects may include isch­
emia and necrosis, whereas systemic effects may include
changes in arterial blood pressure, palpitations, dys­
rhythmias, and even permanent inj ury or de ath due to

Table 6-3 Selected a and f3 Adrenergic Effects o n CVS and Respiratory Systems*
Cardiovascu lar System
Receptors Affected
Heart rate
Contractile force
Coronary arterioles
Peripheral resistance
Respi ratory System
Bronchiole smooth muscle
Pulmonary arterioles
ventricular fibrillation, heart attack, or stroke (Yagiela,
1999). Overdose, intravascular administration, and drug
interactions and intolerance increase the risks of these ad­
verse events (Yagiela, 1999).
Fortunately, most adverse events associated with the
use of vasoconstrictors are short-lived. This is due to their
efficient reuptake in synapses and the rapid removal and
biotransformation of any residual portions that enter the
bloodstream (Jastak, Yagiela, & D onaldson, 1995 ) . The
term adverse events refers to the undesired effects that
occur in response to the physiological and pharmacolog­
ical actions of a drug, including the events surrounding
its administration.
Although highly unlikely, clinicians must be aware of
the possibility of more serious consequences when using
these drugs. A j oint statement on vasoconstrictors of the
American Dental Association and American Heart Asso­
ciation provides the following advice:
Vasoconstrictor agents should be used only when it is
clear that the proce dure will be shortened or the anal­
gesia rendered m ore profoun d . When a vasoconstrictor
is indicate d , extreme care should be taken to avoid
intravascular injection. The minimum possible amount of
vasoconstrictor should be used. (Malamed, 20 13)
Epi n ephr i n e
A s previously mentioned, epinephrine i s a naturally occur­
ring catecholamine. Epinephrine is used in dentistry as a
potent vasoconstrictor that both enhances profound an­
esthesia and increases the safety of local anesthetic drug
administration.
CHAPTER 6 VASOCONSTRICTORS IN DENTISTRY
• 81
Action(s)
Increased (may be blocked or reversed by vagal reflex activity)
Increased
Constriction/Dilation (subject to local control)
Increased/Decreased
Relaxation
Constriction/Dilation (subject to local control)
In both medicine and dentistry, epinephrine has other
important uses, including the reversal of generalized ana­
phylaxis and bronchospasm. In ophthalmology and op­
tometry, epinephrine-induced mydriasis (dilation of the
pupils) augments diagnosis and treatment.
Epinephrine provides nearly equal a and {3 effects,
however not at the same time. Initial a vasoconstriction of
peripheral vasculature allows time for anesthetic drugs to
bind to receptor sites. Later, {32 vasodilation predominates.
This has been observed after surgery where epinephrine
has been administered. Initially, a effects enhance pro­
found, durable anesthesia and reduce hemorrhaging at
surgical sites. Postoperatively, the dominant {32 effects can
result in increased bleeding approximately 6 hours after
surgery (Malamed, 2013; Sveen, 1979).
B ecause of its nearly equal effects on both a and {3
adrenergic receptors, epinephrine is the drug of choice in
responding to generalized anaphylaxis. Anaphylaxis pres­
ents as peripheral vasodilation and bronchial constriction.
Epinephrine's a adrenergic stimulation provides periph­
eral vasoconstriction (reversing the vigorous vasodilation)
and its {3 adrenergic stimulation provides bronchodilation
(relieving breathing difficulties).
Vasoconstrictor concentration is expressed as a dilu­
tion ratio of milligrams of drug to milliliters of solution
(mg/mL) into which it is dissolved. A dilution ratio of
1 : 1000 epinephrine is equivalent to one gram in one liter,
expressed as 1,000 mg/1,000 mL 1 mg/mL. A dilution
=
ratio of 1 : 100,000 is equivalent to 1 gram in 100 liters, ex­
pressed as 1,000 mg/100,000 mL 1 mg/1 0 0 mL or 0.0 1
=
mg/mL.
Epinephrine is added to local anesthetic solutions in
North America in concentrations of 1 :50,000, 1 : 1 0 0,000,
82 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•
FIGURE 6-1 Epinephrine Dilutions. Epinephrine is added to local anesthetic solutions in dilutions of 1:50,000,
1:100,000, and 1:200,000.
Source: Modified courtesy of Dentsply Pharmaceutical .
and 1 :200,000 (see Figure 6-1 •). Dilutions of 1:50,000 con­
tain four times the quantity of vasoconstrictor as 1 :200,000.
Although there may be therapeutic benefit at times, such as
the more vigorous hemostasis provided by this higher con­
centration to control bleeding during surgical procedures,
there is questionable rationale for the use of dilutions of
1 :50,0 0 0 epinephrine in a maj ority of clinical situations
(Malamed, 20 1 3 ) . Its use may be more common in dental
specialties. All dilutions contribute to profound and dura­
ble anesthesia in combination with local anesthetic drugs.
The maximum dose of epinephrine for use in dentistry
in healthy individuals has been determined to be 0.2 mg per
appointment (Budenz, 2000; Special Committee of the New
York Heart Association, 1955; Working Conference of ADA
and AHA on Management of Dental Problems in Patients
with Cardiovascular Disease, 1964). In significant cardiovas­
cular compromise (ASA categories III & IV), the maximum
dose is reduced to 0.04 mg, which is 20% of the standard
maximum dose of epinephrine (Special Committee of the
New York Heart Association, 1955; see Chapter 7, "Dose
Calculations for Local Anesthetic Solutions"; see Chapter
10, "Patient Assessment for Local Anesthesia") . However,
application of this maximum value in all significant car­
diovascular (CV) compromise is not necessarily optimal.
Clinicians should consider all relevant factors when deter­
mining safe doses of vasoconstrictors for these individuals,
including an increased potential for endogenous release of
epinephrine. In some categories of CV compromise, shorter
appointments, conscious sedation, as well as the use of stress
reduction protocols help reduce risks (Rose et al., 2002) .
The following statement appeared in a recent issue of the
Journal of the Canadian Dental Association (Davis, 20 10) : *
Unfortunately, n o current recommendation regarding
the maximum amount of epinephrine that can be safely
*Excerpt from "What dose of epinephrine contained in local anesthesia
can be safely administered to a patient with underlying cardiac disease
during a dental procedure ? " by Ben Davis from Journal of the Canadian
Dental Association, 76:a36. Published by Canadian Dental Association.
HO
��"
� OH
(R)-4-(1 -hyd roxy-2-( methylamine)ethyl) benzene-1 ,2-diol
administered to a cardiac p atient undergoing den­
tistry is based on sound scientific evidence. Given the
population and the risk of an untoward event, ethical
considerations likely preclude a study to obtain such
evidence.
Other dose reductions may apply in selected situa­
tions, including elderly populations and in the presence
of a number of specific drug interactions (Lindquist &
Ettinger, 2003 ; Special Committee of the New York Heart
Association, 1955; Yagiela, 1999).
Summary of Actions on Specific Systems
and Tissues
Myocardium: Increased cardiac output and heart rate
Pacemaker cells: Increased incidence of dysrhythmias
Coronary arteries: Increased coronary artery blood
flow
Blood pressure: Increased systole; decreased diastole
(except increased in higher doses)
CVS: Decreased cardiac efficiency
Vasculature: a vasoconstriction in skin and mucous
membranes; {3 2 vasodilation in skeletal muscle vascu­
lature (lower doses); a vasoconstriction (higher doses)
Hemostasis: a vasoconstriction initially (higher
doses), then {32 vasodilation after 6 hours
Respiratory: {32 vasodilation of bronchiole smooth
muscle
CNS: In therapeutic doses, not a potent stimulant
Other noncardiac effects: Increased oxygen consump­
tion in all tissues may occur
In addition, epinephrine can decrease the hypogly­
cemic effects of insulin, resulting in elevated blood sugar
levels (see Box 6-1 •) .

Oth e r i m po rtant co n s i d e rati o n s b efo re t h e use of vaso­
constrictors i n c l u d e eva l u ati o n fo r situati o n s w h e re specific
tissues of t h e body a re m o re s u scepti b l e to i nj u ry due to
vasoconstrict i o n . For exa m p l e , t h i s may b e the case w h e n
t h e re is a h istory of stro ke, ra d i at i o n t h e ra py, o r u n co n ­
tro l l e d (britt l e) d i a betes w i t h u n d erlyi n g ca rd i ovascu l a r
disease.
A h i story of a cere b rovascu l a r accident (CVA) o r
stro ke i n creases t h e r i s k of exp e r i e n c i n g a s u bs e q u e nt
CVA d u e to i n creases i n b l oo d p ress u re i n res p o n s e to
vasoconstrictors.
R a d i a t i o n t h e ra p y i n cre a s e s the risk of oste o n e c ros i s
(a l s o k n o w n a s oste o ra d i o n e c ro s i s a ft e r i rr a d i a t i o n of
the b o n e) d u e to a res u l t a n t co m p ro m i s e of the vas­
cu l a r b e d . Va s o c o n st r i ctors can fu rt h e r co m p ro m i s e
t h e v a s c u l a r b e d d e p r i v i n g t h e b o n y t i s s u es of oxyg e n ,
n u t r i e nts, a n d b o n e -fo r m i n g ce l l s n e e d e d to m a i nt a i n
vita I i ty.
E p i n e p h ri n e c a n d e cre a s e t h e h y p o g lyce m i c effe cts
of i n s u l i n . T h i s m a y be a p a rt i c u l a r p ro b l e m in i n d ivi d u a l s
w i t h d i a b etes t h a t req u i re l a rg e d o s e s o f i n s u l i n , p re v i ­
o u s l y refe rred to a s brittle diab etics, e s p e c i a l l y t h o s e
w i t h s i g n ifi c a n t c a r d i ovascu l a r d i s e a s e . I n d i vi d u a l s w i t h
u n co n t ro l l e d d i a b etes h a ve d iffi cu lty m a i n ta i n i n g co n ­
s i st e n t b l o o d s u g a r l e v e l s a n d c a n a l t e r n ate b etwe e n
severe h y p o - a n d h y p e r g l y ce m i c e p i s o d e s . A co n s u lta­
tion with t h e p a t i e nt's p h ys i c i a n c a n h e l p d e t e r m i n e t h e i r
stat u s . E p i n e p h r i n e c a n g e n e ra l l y b e g iv e n to i n d iv i d u ­
a l s w h o s e d i a b etes i s we l l c o n t ro l l e d with o u t s p e c i a l
p reca uti o n s .
F I G U RE 6-2 Levonordefrin Dilutions. Levonordefrin is added to local anesthetic solutions in a dilution of 1:20,000.
Levonordefrin is much weaker than epinephrine and is formulated in a dilution that is five times more concentrated
(less diluted ) to provide similar efficacy of the local anesthetic drug.
Source: Modified courtesy of Dentsply Pharmaceutical.
CHAPTER 6 VASOCONSTRICTORS IN DENTISTRY
• 83
Termination of action: Reuptake by adrenergic nerves
and once absorbed, catechol-0-methyltransferase
(COMT) and monoamine oxidase (MAO) inactivation
Effect on endogenous epinephrine release: The
exact mechanism is unknown although it has been
suggested by some that adrenomedullary stimulation
by exogenous epinephrine on presynaptic {3-receptors
may be responsible for endogenous releases
(Takahashi et al., 2005 ) .
Sources:Jastak, Yagiela, and Donaldson ( 1995), Malamed (2013),
Sveen (1979), and Takahashi et a!. (2005).
Levo n o rd efri n
Levonordefrin is the only synthetic catecholamine available
in dental cartridges in North America. It is considered to
have about one-sixth the potency of epinephrine and there­
fore more concentrated dilutions are needed in dental car­
tridges (Malamed, 20 1 3 ) . Formulated as 2 % mepivacaine,
1 :20,000 levonordefrin (the only dental solution available),
this drug is considered to be equal in both clinical and sys­
temic effects to 2 % lidocaine, 1 : 1 0 0,000 epinephrine. It
provides no systemic advantage over 1 : 1 00,000 epineph­
rine concentrations (Hargreaves & Cohen, 20 1 1 ) . Some
patients sensitive to epinephrine, however, may not be sen­
sitive to levonordefrin. It also differs from epinephrine in
its actions on adrenergic receptors. Unlike epinephrine's
50% a and 50% f3 effects, levonordefrin's action is primar­
ily a, 75 % versus 25 % f3 (Jastak, Yagiela, & D onaldson,
1995 ) . As a weak stimulator of beta adrenergic receptors,
it is similar to norepinephrine, which is approximately 90 %
a (Jastak, Yagiela, & Donaldson, 1995 ) . Despite levonor­
defrin's major effect on a receptors, epinephrine is a more
powerful vasoconstrictor of peripheral vasculature, thus
providing good hemostasis (control of bleeding).
4-[(1 5 ,25)-2-amino- 1 -hydroxy-propyl)benzene-1 ,2-diol
84 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•
Levonordefrin is less potent compared with epineph­
rine and is formulated in dilutions of 1 :20,000, which are
five times more concentrated ( less diluted ) than 1 : 100,000
epinephrine solutions ( see Figure 6-2 •) . Two percent
mepivacaine with 1 :20,000 levonordefrin provides a good
alternative to 2 % lidocaine with 1 : 1 00,000 epinephrine in
most clinical situations, and in specific situations in which
epinephrine may be contraindicated, including when other
specific drugs ( such as beta-blockers ) are being taken
( Zhang et al., 1999).
Summary of Actions on Specific Systems
and Tissues
In general, levonordefrin has less effect on the adrenergic
receptors of the cardiovascular and cardiopulmonary
systems compared with epinephrine ( Jastak, Yagiela, &
Donaldson, 1995; Malamed, 20 13). The lack of significant
{3 stimulation tends to negate the advantages of levonor­
defrin's weaker adrenergic stimulation and its inability to
significantly dilate the smooth muscles of the bronchioles
precludes its use for anaphylaxis. Epinephrine also pro­
vides much better hemostasis, as previously mentioned. In
the concentrations found in the single dental formulation
(2 % mepivacaine, 1 :20,0 00), levonordefrin provides an
equivalent duration of local anesthetic activity compared
with 1 : 100,000 epinephrine.
Myocardium: Increased cardiac output and heart rate
but less than epinephrine
Pacemaker cells: Increased incidence of dysrhythmias
but less than epinephrine
Coronary arteries: Increased coronary artery blood
flow but less than epinephrine
Blood pressure: Increased systole but less than epi­
nephrine. D ecreased diastole, except increased in
higher doses
CVS: Decreased cardiac efficiency
Vasculature: a vasoconstriction in skin and mucous
membranes but less than epinephrine; {32 vasodila­
tion in skeletal muscle vasculature ( lower doses ) ;
a vasoconstriction ( higher doses ) but less than
epinephrine
Hemostasis: Much less effective than epinephrine
Respiratory: Vasodilation of bronchiole smooth mus­
cle but much less than epinephrine
CNS: In therapeutic doses, a less potent stimulant
compared with epinephrine
Metabolism: Elevated blood sugar but less than epi­
nephrine. Increased oxygen consumption in all tissues
but less than epinephrine
Termination of action: Reuptake by adrenergic nerves
and COMT inactivation
Effect on endogenous epinephrine release: Unknown
mechanism but less than epinephrine
Dosa g e D i scussion
D etermining the dose o f vasoconstrictor drug i n a given
volume of solution requires an understanding of dilution
ratios, standard cartridge volumes, the defined maximum
recommended dose for each drug, and relevant patient
health factors.
A thorough discussion of methods for calculation of
vasoconstrictor doses can be found in Chapter 7, "Dose
Calculations for Local Anesthetic Solutions."
Toxi city a n d B i otra n sfo rmation
of Vasoco nstricto rs
Vasoconstrictor toxicity results from excessive stimula­
tion of adrenergic receptors. High plasma levels of epi­
nephrine have been described as inevitable soon after
administration and typically result in increased heart rate
and systolic blood pressure ( Clutter et al., 199 1 ; Tetzlaff,
2000; Tolas, Pflug, & Halter, 1982). Peak plasma concen­
trations, for example, have been shown to occur within
the first few minutes ( Jastak, Yagiela, & D onaldson,
1 9 95 ) . Outward signs and symptoms of transient high
plasma levels are only occasionally noted clinically but
tend to be quite frightening when they occur ( Jastak,
Yagiela, & D onaldson, 1995 ) . These signs and symptoms
include nausea, restlessness, a racing heart, severe head­
aches, palpitations, tremors, and shakiness. Fortunately,
these unpleasant effects are usually short-lived because
of the efficiency of vasoconstrictor metabolism ( Jastak,
Yagiela, & Donaldson, 1 9 9 5 ) . Levonordefrin is similar
to epinephrine in this respect although to a lesser extent
( Jastak, Yagiela, & D onaldson, 1995). Table 6-4 • dem­
onstrates typical signs and symptoms of vasoconstrictor
overdose and adverse events. Note that many of the signs
and symptoms of overdose mimic those observed in anxi­
ety and fear as discussed in Chapter 2, "Fundamentals of
Table 6-4 Adverse Events in Vasoconstrictor
Overdose
Compa rison of S i g n s a n d Sym pto ms
Vasoconstricto r Overdose versus Anxiety and Fea r
-------
Vasoconstrictor Overdose Anxiety/Fear Responses
Nausea Nausea
Restlessness Restlessness
Heart racing Heart racing
Intense anxiety Intense anxiety
Weakness Weakness
Tremor Tremor
Severe headache Headache
Hyperventilation Hyperventilation
Palpitation Palpitation
Shakiness Shakiness
Fainting

Pain Management," and Chapter 18, "Insights for Fearful
Patients."
The absorption of vasoconstrictors from areas of
deposition is slowed by their own actions and may take
several hours (Jastak, Yagiela, & Donaldson, 1995). Once
absorbed, however, biotransformation of adrenergic va­
soconstrictors is rapid with expected plasma half-lives of
only about 1-2 minutes (ADA/PDR, 2009).
Epinephrine is recycled in the synaptic j unctions. The
enzyme catecholamine - 0 - methyltransferase (COMT)
is responsible for the biotransformation of any epineph­
rine that is not recycled. Further breakdown may oc­
cur via monoamine oxidase (MAO ) (Jastak, Yagiela, &
D onaldson, 1995, Malamed, 20 1 3 ) . Levonordefrin is also
biotransformed by COMT; however, it is not subj ect to
significant MAO metabolism due to its chemical struc­
ture (Jastak, Yagiela, & D onaldson, 1 9 9 5 ) . Its systemic
effects and the termination of its actions are similar to
epinephrine's (Jastak, Yagiela, & D o naldson, 1 9 9 5 ) .
Responses t o suspected overdoses o r other reactions to
vasoconstrictors and local anesthetic drugs are discussed
in Chapter 17, " Local Anesthesia Complications and
Management."
D espite the administration of only very small doses
of vasoconstrictors, signs and symptoms of overdose
or other adverse events may occur in some individuals
either during or shortly after administration. These ef­
fects pass rather quickly. Individuals affected in this way
may state or record on h e alth histories that they are
Some confu s i o n exists a m o n g patie nts re g a rd i n g t h e i r
exp e r i e n ces w i t h e p i n e p h r i n e a n d w h a t constitutes a n
a ctu a l a l l e rg i c res p o n s e . Wh i l e a l l ergies h ave occu rred to
exo g e n o u s e p i n e p h ri n e preparations, t h ey a re c h a ra cter­
ized as h a v i n g b e e n extre m e l y rare a n d l i ke l y d u e to t h e
s pecific form u l at i o n that was used, e i t h e r e p i n e p h r i n e
hydroch l o r i d e o r e p i n e p h ri n e b ita rtrate (Ko h a s e & U m n io,
2004) . These e p i n e p h r i n e-re l ated a l l ergies i n d e nta l set­
t i n g s a re n e a rly u n h e a rd of. It is fa r m o re l i ke l y that i n d ivid­
uals re p o rti n g past expe r i e n ces of e p i n e p h ri n e a l l ergies in
d e n t a l sett i n g s h ave a ctu a l ly expe r i e n ced a hyper- res p o n s e
to the d r u g . The term hyper-response refers to overdose
m a n ifestati o n s to doses that typ ica l ly wo u l d n ot res u lt in
n oticea b l e e ffe cts . I n these i n d iv i d u a l s , t h i s is their n o rm a l
res p o n s e t o doses that oth e rwise fa l l wit h i n a ccepted
g u i d e l i n es fo r m ost.
H y p e rs e n s itivity refe rs to an a l l e rg i c p rocess that i n ­
volves h u m o r a l , ce l l - m e d i ated, a n d/or a nt i g e n-antibody
rea ct i o n s . Tru e a l l e rg i c res p o n ses a re n o t dose-re l ate d .
CHAPTER 6 VASOCONSTRICTORS IN DENTISTRY
• 85
Table 6-5 Contrasting Overdose versus Allergic
Responses
Compa rison of S i g n s a n d Sym pto ms
Vasoconstricto r Overdose versus A l l e rgy
-------
Vasoconstrictor Overdose Allergic Response*
Nausea Hives
Restlessness Rash
Heart racing Bronchospasms
Intense anxiety Vasodilatation
Weakness
Tremor
Severe headache
Hyperventilation
Palpitation
Shakiness
*Allergic response to epinephrine is nearly impossible; signs and
symptoms of allergy may be in response to other contents of the
cartridge.
" allergic" to the " adrenaline" in the anesthetic. Although
it is possible this was the result of intravascular deposi­
tion, it may actually reflect a hyper-response to absorbed
doses, particularly if it has occurred on repeated occa­
sions (see B ox 6-2 •) . It is important to note that this
type of sensitivity is not allergenic because it lacks hu­
moral, cell-mediated, and/or antigen-antibody reactions
(see Table 6-5 •) . Instead, it relates to a rapid, direct,
and vigorous stimulation of adrenergic receptors. These
events can be dramatic and frightening and provide con­
vincing rationale for limiting or avoiding epinephrine­
containing local anesthetics in these individuals. They do
not, however, reflect a true epinephrine allergy, which
is not possible because epinephrine in local anesthet­
ics is identical to endogenous epinephrine (Pickett &
Terezhalmy, 2006).
Othe r Vasocon strictors U sed
in Dentistry
Norepinephrine, phenylephrine, and felypressin are not
currently available in dental local anesthetic preparations
in North America; however, all three vasoconstrictors
have been in use in other regions of the world for many
years.
Norepinephrine
Norepinephrine is a n atural-occurring catecholamine
whose activity on adrenergic receptors is approximately
9 0 % a (Malamed, 20 1 3 ) . It is similar to levonordefrin
in its actions o n t h e s e receptors and quite different
compared with epinephrine in that norepinephrine's
v a s o c o nstrictive acti o n s lack significant {3 2 activity;
thus, they are virtually unoppo s e d (Jastak, Yagiela, &
86 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•
D o naldson, 1 9 9 5 ; Malamed, 20 1 3 ) . The vigorous and
sustained vasoconstriction ( h e m o s t a s i s ) induced by
norepinephrine may induce necrosis, especially on the
palate (Malamed, 20 1 3 ) .
Phenylephrine
Phenylephrine is a synthetic non-catecholamine with
weak vasoconstrictive effects, approximately 95 % a ac­
tivity (Malamed, 20 1 3 ) . It is formulated in much higher
concentrations ( 1 :2,500) compared with epinephrine and
levonordefrin in order to overcome its weaker vasocon­
strictive effects (Malamed, 20 1 3 ) . It has been described as
an excellent drug with few significant side effects; however,
plasma levels of lidocaine were found to be elevated when
phenylephrine was administered for epidural block com­
pared with similar solutions with epinephrine (Malamed,
20 13; Stanton-Hicks, B erges, & Bonica, 1973 ) . This directly
relates to its weak vasoconstrictive action. Phenylephrine
was previously available in North America in a 4% pro­
caine, 1 :2,500 dilution. With the elimination of procaine as
a primary local anesthetic in dentistry, this formulation is
no longer available.
Felypressin
Felypressin is a synthetic hormone that has vasoconstric­
tive properties with more smooth muscle effects on the
venous, rather than the arteriolar, microcirculation. It has
a wide margin of safety, with little to no effect on the myo­
cardium and no adrenergic nerve influence. It is therefore
safe to use for patients with dysrhythmias or hyperthyroid­
ism, and for patients using tricyclic antidepressant medica­
tion (Inagawa, Ichinohe, & Kaneka, 2005; Jastak, Yagiela,
& D onaldson, 1995; Malamed, 20 1 3 ) . Felypressin is not
available in the United States.
For additional information on norepinephrine, phen­
ylephrine, and felypressin, the clinician is urged to consult
the references for this text.
.�.h. �. P..t.E! � . 9.LJ.E!��.i.e>.". � ........................................... .
1 . Which one of the following vasoconstrictors is most
useful in providing hemostasis?
a. Phenylephrine
b. Epinephrine
c. Levonordefrin
d. Felypressin
2. A patient has significant cardiovascular disease and
requires a restorative procedure on tooth #5. Retrac­
tion cord and hemostasis are needed in order to keep
the restorative site dry. Which one of the following
drugs would be most indicated in this situation?
a. 4% articaine, 1 :200,000 epinephrine
b. 2% mepivacaine, 1 :20,000 levonordefrin
c. 2% lidocaine, 1 :50,000 epinephrine
d. 4% prilocaine plain
CAS E MA N A G EME N T
Elena Gagarin
Because of p reca utions surro u n d i n g tricycl i c a ntide­
p ressa nt u s e , i t i s d e c i d e d t h a t a d r u g w i t h o u t a
v a s o c o n st r i ct o r o r w i t h l i m i t e d v a s o c o n st r i ct o r
d oses w i l l be used . T h e fi rst c h o ice, 4% p r i l o ca i n e
p l a i n , fa i l ed t o p rovi de a d e q u ate a n esthesia o r d u ­
ration fo r a crow n , w h i c h was t h e treatm ent a g reed
u p o n . The s e co n d c h o i c e , 3 % m e p ivaca i n e , p ro ­
v i d e d p rofo u n d a n esthesia of # 1 4 but it l asted o n ly
5 m i n utes. F o u r p e rc e n t a rtica i n e with 1 : 2 0 0 , 0 0 0
e p i n e p h ri n e was s e l e cted, because it p rovides a d ­
e q u ate p rofo u n d n ess a n d d u rati o n , it h a s a v e ry
s h o rt h a lf- l ife , a n d it h a s t h e l e ast a m o u n t of e p i ­
n e p h ri n e p e r m i l l i m eter ava i l a b l e .
Case Discussion : A severe s p i ke i n b l ood p ressu re
a n d refl exive b ra d yca rd i a c a n o cc u r in t h e p res­
e n ce of tricyc l i c a n t i d e p ressants if vasoconstrictors
a re u s e d . The r i s k with l evo n o rd efri n i s a p p roxi­
m a t e l y five to t e n times t h e n o rm a l r i s k and with
e p i n e p h r i n e the r i s k i s a p p roxi m at e l y two t i m e s
t h e n o r m a l r i s k . I f a v a s o c o n st r i ct o r i s n e e d e d ,
l evo n o rd e fr i n s h o u l d b e a vo i d e d a n d e p i n e p h ­
r i n e m ay be a d m i n istered b u t t h e tota l q u a ntities
s h o u l d b e l i m it e d . A 1 : 2 0 0 , 0 0 0 d i l u t i o n i s s a fe r
t h a n a 1 : 1 00,000 d i l ution because it conta i n s
h a l f t h e a m o u n t o f e p i n e p h ri n e . T h ree d r u g s a re
p a c k a g e d i n t h i s d i l u t i o n : 4% p r i l o c a i n e , 0 . 5 %
b u p i v a c a i n e , a n d 4 % a rt i c a i n e w i t h 1 : 2 0 0 , 0 0 0
e p i n e p h ri n e . A n y o f t h e th ree m i g h t w o r k i n t h i s
situati o n , h oweve r, i f E l e n a is sti l l n u rs i n g , t h e h a lf­
l ife of p r i l o ca i n e ( 1 . 6 h o u rs) a n d b u p ivaca i n e (2 . 7
h o u rs) a re s i g n ifica ntly g reater t h a n t h e h a l f- l ife of
a rtica i n e (l ess t h a n 45 m i n utes) .
3. Which one of the following statements is true?
a. Levonordefrin is more potent compared with
epinephrine.
b. Cardiac stimulation from levonordefrin is greater
compared with epinephrine.
c. Cardiac stimulation from levonordefrin is less com­
pared with epinephrine.
d. Levonordefrin is equal in potency compared with
epinephrine.
4. Epinephrine's metabolism is relatively rapid after
local anesthesia administration.
a. True
b. False
5. Metabolic enzymes for epinephrine include which of
the following?
a. COMT and MAO
b. Hepatic isoenzymes

c. Renal isoenzymes
d. COMT only
6. A diabetic patient requires periodontal therapy on
the upper and lower right quadrants. She is well
controlled and otherwise healthy. Which one of the
following represents the safest and most effective lo­
cal anesthesia regime?
a. 4 cartridges of 2 % lidocaine, 1 : 1 00,000 epinephrine
b. 2 cartridges of 2% lidocaine, 1 : 1 00,000 epinephrine
and 2 cartridges of 3% mepivacaine plain
c. 2 cartridges of 2% lidocaine, 1 : 100,000 epinephrine
and 2 cartridges of 4% articaine, 1 :200,000 epinephrine
d. 2 cartridges of 2 % lidocaine 1 : 1 00,000 epineph­
rine and 2 cartridges of 2% mepivacaine, 1 : 20,000
levonordefrin
Refe re n ces
ADAJPDR guide to dental therapeutics (5th ed.). (2009). Montvale,
NJ: Thompson PDR.
Agency for Healthcare Research and Quality. (2002, March).
Cardiovascular effects of epinephrine in hypertensive dental
patients. Summary, Evidence Report/Technology Assessment
Number 48, AHRQ Publication Number 02-E005. Rockville,
MD: Author.
Ahlquist, R. P. (1948). A study of the adrenotropic receptors.
American Journal of Physiology, 153, 586 -600.
Budenz, A. W. (2000, August). Local anesthetics and medically
complex patients. Journal of the California Dental Association,
28(8), 611 -619.
Clutter, W. E., Bier, D. M., Shah, S. D., & Cryer, P. E. (1991).
Epinephrine plasma metabolic clearance in healthy volunteers
and in patients having third molar surgery. British Dental
Journal, 1 70, 373-376.
Cryer, P. E. (1980). Physiology and pathophysiology of the hu­
man sympathoadrenal neuroendocrine system. New England
Journal of Medicine, 303, 436-444.
Davis, B. (2010). What dose of epinephrine contained in local
anesthesia can be safely administered to a patient with under­
lying cardiac disease during a dental procedure? Journal of the
Canadian Dental Association, 76, a36.
Hargreaves, K. M., Cohen, S. (2011). Cohen's Pathways of the
Pulp (lOth ed.). St. Louis: Mosby Elsevier.
Inagawa, M., Ichinohe, T., & Kaneka, Y. (2005). Felypressin con­
tained in dental local anesthetics aggravates myocardial oxygen.
Tokyo Dental College: Chiba-shi Chiba, Japan. Retrieved July
26, 2007,from http://iadr.confex.com/iadr/2005Balt/techprogram/
abstract_63639.htm
Jastak, J. T., Yagiela, J. A., & Donaldson, D. (1995). Local
anesthesia of the oral cavity. Philadelphia: Saunders.
Jones, J. H., & Mason, D. K. (1990). Oral manifestations of sys­
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complimentary study tools created for this specific title.
CHAPTER 6 VASOCONSTRICTORS IN DENTISTRY
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Kohase, H., & Umino, M. (2004). Allergic reaction to epineph­
rine preparation in 2% lidocaine: Two case reports. Anesthesia
Progress, 51, 134 -13'Z
Lindquist, T. J., & Ettinger, R. L. (2003). The complexities in­
volved with managing the care of an elderly patient. Journal of
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Lipp, M., Dick, W., Daublander, M., Fuder, H., & Stanton-Hicks,
M. (1993). Exogenous and endogenous plasma levels of epi­
nephrine during dental treatment under local anesthesia.
Regional Anesthesia and Pain Medicine, 18, 6 -12.
Little, J. W., Falace, D. A., Miller, C. S., & Rhodus, N. L. (2013).
Dental management of the medically compromised patient
(8th ed.). St. Louis: Mosby Elsevier.
Malamed, S. F. (2013). Handbook of local anesthesia (6th ed.).
St. Louis: Elsevier Mosby.
Mosby's medical, nursing, and allied health dictionary (4th ed.).
(1994). St. Louis: Mosby-Year Book, Inc.
Pickett, F. A., & Terezhalmy, G. T. (2006). Dental drug reference
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of the American Dental Association, 133(Supplement 1 ),
37s -44s.
Special Committee of the New York Heart Association. (1955).
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Stanton-Hicks, M., Berges, P. U., & Bonica, J. J. (1973). Circulatory
effects of peridural block. IV. Comparison of the effects of
phenylephrine and epinephrine. Anesthesiology, 39, 308-314.
Sveen, K. (1979). Effect of the addition of a vasoconstrictor
to local anesthetic solution on operative and postoperative
bleeding, analgesia, and wound healing. International Journal
of Oral Surgery, 8, 301 -306.
Takahashi, Y., Nakano, M., Sano, K., & Kanri, T. (2005). The
effects of epinephrine in local anesthetics on plasma catechol­
amine and hemodynamic responses. Odontology, 93, 72-79.
Tetzlaff, J. E. (2000). Clinical pharmacology of local anesthetics
(1st ed.). Woburn, M A: Butterworth-Heinemann.
Tolas, A. G., Pflug, A. E., & Halter, J. B. (1982). Arterial plasma
epinephrine concentrations and hemodynamic responses after
dental injection of local anesthetic with epinephrine. Journal
of the American Dental Association, 1 04, 41 -43.
Working Conference of ADA and AHA on Management of
Dental Problems in Patients with Cardiovascular Disease
(1964). Journal of the American Dental Association, 68, 333-342.
Yagiela, J. A. (1991). Epinephrine and the compromised heart.
Orofacial Pain Management, 1, 5-8.
Yagiela, J. A. (1999). Adverse drug interactions in dental practice:
Interactions associated with vasoconstrictors, Part V of a se­
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Zhang, C., Banting, D. W., Gelb, A. W., & Hamilton, J. T. (1999).
Effect of {3-adrenoreceptor blockade with nadolol on the
duration of local anesthesia. Journal of the American Dental
Association, 130(12), 1773-1780.
· · ······ ·············· · ················ · ········· · ······ · ·· 0 ······· ······ · · · ·· · · ··········· · · · · ······ ········ · · · · ·····

Dose Ca l cu l ati o n s fo r
toea I Am estf.l e�i·e �a l l!J�i·o·m s

OBJECTIVES KEY TERMS

• Defi n e a n d d i scuss the key terms in t h i s cha pter. ca rd i a c dose 94

cartri d g e vo l u m e 90
• Defi n e a n d d i scuss the s i g n ifica n ce of the maxi m u m
C l a rk's R u l e 95
reco m m e n d ed dose o f a d ru g . d i l uti o n ratios 92
• List m axi m u m recom m e n d ed doses fo r each l oca l a n esth etic d r u g co n ce ntratio n 90
d ru g and vasocon strictor. d r u g p e rcenta g e 90
•
d r u g ratio 94
Id e n tify a n d d iscuss the re l eva nt i nfo rmation a n d
l i m it i n g d r u g 94
m athematica l operati o n s req u i red t o ca l c u l ate d ru g doses.
maxi m u m reco m m e n d e d
• Id e n tify re l evant i nfo rmation n ecessa ry to co m p ute reco m ­ d o s e ( M RD) 8 9
m e n d e d d ru g doses. Yo u n g 's r u l e 95
• Ca lcu l ate the reco m m e nded doses of fo r local a n esth etic
d ru g s and vasocon stri cto rs i n c l i n ica l situati o n s .
• Ca lcu l ate the reco m m e nded d o s e s when m u lt i p l e d ru g s with
d iffe ri n g concentrations a re a d m i n iste red .
• D i scuss recom m e n d e d d ose mod ifications fo r vasoco n strictors
i n patients with s i g n ificant ca rd i ovascu l a r co m p rom ise.
C a l cu l ate the recom m e n ded doses of fo r local a n esth etic
ugs and vasoco n strictor fo r patients with s i g n ificant
r co m p rom ise.
c rfe nded doses of local a n esthetic d ru gs
l a rk's R u l e a Rule.

88
 CHAPTER 7 DOSE CALCULATIONS FOR LOCAL ANESTHETIC SOLUTIONS
• 89

CAS E S T U DY
lliana Gagarin
After a d m i n istering one ca rtridge of 4% priloca i n e with
1 : 200,000 e p i n e p h r i n e fo r a crown o n # 1 4, which l i m its
the tota l a m o u nt of e p i n e p h ri n e a d m i n istered to ! I ia n a
G a g a r i n , i t w a s later decided that a d d ition a l a n esthetic
wo u l d be necessary because # 1 4 was beco m i n g sensi­
tive d u ri n g the p l acement of a te m pora ry crow n .
T h ree p e rcent m e p ivaca i n e p l a i n w a s selected fo r
two reaso n s . The fi rst is that it h a s no vasoco nstrictor
a n d t h e seco n d is t h a t t e m p o r a ry fa b ri c a t i o n wo u l d
req u i re o n ly brief a d d itio n a l a n esth esi a .
! I i a n a G a g a r i n w e i g h s 1 2 0 l b s a n d i s ot h e rw i s e
h e a l t h y. C a l c u l a t e t h e t o t a l v o l u m e o f 3 % m e p i ­
vaca i n e t h a t s h e can receive at h e r a p p o i ntment.
H ow m a n y m i l l i g ra m s o f d r u g d o e s t h i s re p re s e n t ?
W h a t is t h e tota l dose of e p i n e p h ri n e t h a t s h e
rece i v e d ?

Introd u ction Definition o f Maximum Recommended Doses for

Treatment planning and accurate documentation o f local
anesthetic agents require careful calculation and recording
of drug doses. Local anesthetic solutions used in dentistry
contain one or more drugs (a local anesthetic drug with or
without a vasoconstrictor) . The maximum recommended
dose for each solution is dependent on the drug which
limits the total volumes that may be delivered.
Local Anesthetic Drugs
As introduced in Chapter 4 , "Pharmacology B a sics,"
maximum recommended dose (MRD ) represents the
maximum quantity of drug that can be safely administered
during an appointment in most situations. Dose recom­
mendations are provided by the FDA and manufacturers
in product inserts.
Table 7-1 • provides MRD values for all five inj ect­
able dental local anesthetic drugs.

Ca lcu lati n g Local An esthetic
D ru g Doses
Calculations in the previous edition of t h i s t e x t used
values that added an additional level of safety, despite
sometimes conflicting with manufacturer recommenda­
tions. The calculations have been adj usted throughout
this edition of the text to conform to current U.S. Food
and Drug Administration (FDA) -approved maximum
recommended doses (MRD ) . Clinicians should note that
current recommendations are significantly different for
some drugs than previous recommendations in this text.
Factors Required for Drug Dose Calculations
Clinicians commonly express and document doses of local
anesthetic drugs as the number of cartridges, milliliters of
solution, and/or milligrams of drug administered. Regard­
less of the manner in which they are expressed, these doses
are all calculated based upon milligrams.
Table 7-1 F DA-Approved Maximum Doses of Local
Anesthetic Drugs

Clinicians who prefer to use previous, more conservative

Maxi m u m Dose per Appoi ntment
recommendations to guide their clinical decision mak­
Based on Loca l Anesthetic Drug O N LY*
ing regarding dosing can continue to do so because the
previous recommendations do not exceed FDA-approved Drug mg/lb mg/kg mg per appt. *
MRDs. Administering the least amount of drug that pro­
vides the desired level of anesthesia is advised by all man­ Articaine 3. 2 7. 0 NA
ufacturers in product inserts.
An understanding of the following information is Bupivacaine 0.9'' 2.0" 90mg
necessary in order to calculate the recommended doses
and/or to determine the dose of local anesthetic drugs Lidocaine 3.2 7. 0 500 mg
administered:
Mepivacaine 3. 0 6.6 400 mg
1. Concentration for the selected anesthetic drug
Prilocaine 4.0 8.8 600 mg
2. Dilution percentages for vasoconstrictors
3. Standard cartridge volumes '
Note: "per appt ." values represent dosages for healthy individuals;
values must be adjusted for children, elderly, and medically
4. Defined maximum recommended dose for each drug compromised individuals.
5. Relevant patient factors, such as weight and general "Canadian recommendations. No U.S. recommendations available.
health status, including medications Source: FDA, ADA/PDR, 5th ed ., 2009; Malamed, 6th ed ., 2013.
90 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•

The drug concentration of a local anesthetic in a

cartridge is expressed as a p ercentage, 0 . 5 % , 2 % , 3 % ,
or 4 % . The percentages refer to the number of grams in
100 mL of solution; for example, a 2% solution contains
1 00% s o l uti o n = o n e g r a m (1 ,000 m g) of d r u g p e r m i l l i l iter 2 grams of drug in each 100 mL and a 3% solution contains
of s o l u t i o n = 1 ,000 m g/m l 3 grams in each 1 0 0 mL. The drug percentage is there­
1 0% s o l uti o n = o n e-te nth t h e m i l l i g ra m s (1 00 m g) of d r u g fore an expression of the relative amount of drug in a
p e r m i l l i l iter of s o l u t i o n = 1 00 m g/m l cartridge. A 4 % drug contains twice as much drug as a
1 % s o l uti o n = o n e - h u n d redth t h e m i l l i g ra m s ( 1 0 m g ) of 2 % drug.
� • • • • • • •
u
•
.•
e
• � � : � : � : � �: � : �
il il t f s o u ti o = 1 0
. . . • . .
• •
� :��� • .li In order to understand the percentages on which the
contents of local anesthetic drug solutions are based, it may
be helpful to begin with a 100% solution, which, by defini­
tion, contains 1 gram or 1,000 mg of drug per milliliter of
solution. This may be expressed as 1,000 mg/mL. A 1 0 %
solution therefore would contain one-tenth the milligrams
per milliliter, expressed as 100 mg/mL, and a 1 % solution
would contain one-hundredth the milligrams per milliliter
T h e re is n o i nt e r n a ti o n a l sta n d a rd re g a rd i n g ca rt r i d g e or 10 mg/mL ( see Box 7-1 •) . Considering that a stan­
vo l u m e . C a rt r i d g e s d i st r i b u t e d i n N o rt h A m e r i c a a re dard North American cartridge contains 1.8 mL of solu­
d e s i g n e d to c o n t a i n 1 . 8 m l of s o l u t i o n . I n m a n y c a s e s ,
tion, not 1.0 mL ( see Box 7-2 •), at a concentration of 1 % ,
t h e m a n ufact u re r 's i n s e rt, i n co m p l i a n ce w i t h F D A re g u ­
one cartridge would contain 1 8 m g o f drug ( 1 0 mg/mL X
l a t i o n s , w i l l state t h a t t h e c a rtri d g e l i q u i d c a p a city i s
1.8 mL/cartridge 18 rug/cartridge ) . =
1 . 7 m l. T h i s re p re s e nts a m a n ufactu r i n g v a r i a t i o n o f
± 0 . 1 m l a n d a s s u res t h a t n o less than 1 . 7 m l i s p re s ­
Box 7-3 • and Appendix 7-1 •, " Local Anesthetic
e n t i n e a c h c a rt r i d g e . T h i s w i l l n o t a l t e r t h e b a s i c Solutions - D ose Calculation Facts," provide a compre­
fo rm u l a s fo r ca l c u l at i o n a n d a l l ows fo r vo l u m es u p t o hensive summary of key factors for determining drug
1 . 8 m l o f s o l u t i o n (wh i c h m a y b e p re s e n t i n a n y sta n ­ dosages.
d a rd c a rt r i d g e , e v e n if it i s n o t g u aran teed to b e t h e re ) . Inj ectable local anesthetic drugs for use in dentistry
T h e sta n d a rd fo r ca l cu l a t i n g d o s a g e s i s c o n s i d e re d to b e are provided in concentrations of 0.5 % , 2 % , 3 % , and 4 % .
1 . 8 m l. T h i s i s a n a s s u m pt i o n t h a t i n cre a s e s safety b e ­ Compared with a 1 % solution with 1 0 mg/mL o f drug, a
c a u s e t h e ave r a g e vo l u m e of s o l u t i o n i n d e n t a l c a rtri d g e s 0.5 % solution, for example, contains half this quantity, or
h a s b e e n fo u n d to b e 1 . 7 6 m l; i n oth e r w o r d s , a n y p a rt i c­ 5 mg/mL of drug. A 2% solution contains twice this quan­
u l a r c a rtri d g e is l i ke l y to d e l ive r l ess t h a n b u t n ev e r m o re
tity, or 20 mg/mL; a 3 % solution contains three times this
t h a n 1 . 8 m l of s o l u t i o n ( R o b e rtso n et a l . , 2007) .
quantity, or 30 mg/mL of drug; and a 4% solution contains
Cartri d g e s i n t h e U n ited K i n g d o m a n d Austra l i a typ i­
ca l ly conta i n 2 . 2 ml of s o l u ti o n . In J a p a n , s o m e h ave b e e n
40 mg/mL of drug. To determine the dose of drug per 1.8
n oted to b e 1 .0 m l. De nta l c l i n i c i a n s m ust b e awa re of t h e mL cartridge, multiply the mg/mL by 1.8 ( see B ox 7-3 ) .
ca rtri d g e capa cities i n t h e cou ntries i n w h i c h t h ey p ra ctice Appendix 7-3 •, "Estimating D rug Volumes," provides

� •
. . . .
d o s c rd n g 1
� �� � � � �: �: � �� : �
an c c la e r
. . . . . . • • • • • • • • • • • • • .li
visual cues for determining total volumes of solution
administered.

Drug dose an d "per cartridge " facts:

1 ml = 1 cc
1 ca rtri d g e = 1 . 8 ml s o l uti o n (1 . 8 cc)
1 % sol ution = 1 0 m g/m l
1 ca rtri d g e of a 1 % l oca l a n estheti c = 1 0 m g/m l X 1 . 8 m Ucartri d g e = 1 8 m g/ca rt

Common Dental Concentrations: Ca rtrid g e Conversions:

0.5% s o l ution m l/ca rtri d g e = 5 m g/m l 0 . 5 m g/m l X 1 .8 = 9 m g/ca rtri d g e

2% s o l uti o n m l/ca rtri d g e = 2 0 m g/m l 20 m g/m l X 1 . 8 = 36 m g/cartri d g e
3% s o l ut i o n m Uca rtri d g e = 30 m g/m l 30 m g/m l X 1 . 8 = 54 m g/cartri d g e
'
: 4% so l ut i o n m l/ca rtri d g e 40 m g/m l 40 m g/m l X 1 . 8 = 72 m g/cartri d g e
•
=

: . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
 CHAPTER 7 DOSE CALCULATIONS FOR LOCAL ANESTHETIC SOLUTIONS
Calculating Local Anesthetic Drug Doses
Methods used to determine the number of milligrams
of local anesthetic drug delivered vary among clinicians.
A common method will be demonstrated for the follow­
ing situation. Assume that two cartridges of 2% lidocaine
plain have been administered to a 100-lb patient. The first
step in calculating the dose is to identify the key factors.
For this situation these factors are:
1. In a 2 % solution, there are 36 mg of drug per cartridge.
2. Two cartridges have been delivered.
3. The MRD for lidocaine is 3 . 2 mg/lb or 5 0 0 mg
maximum.
4. The patient's weight is 100 lbs.
Milligrams Delivered
To calculate the milligrams of drug delivered, first multiply
the total number of cartridges by the total mg of drug in
each cartridge for 2% drug:
2 (cartridges) x 36 mg = 72 mg
This patient received 72 mg of lidocaine.
Dose Related to M RD
To determine the maximum dose for this patient, multiply
the MRD for this drug by the patient's weight:
3.2 mg/lb X 100 lbs = 320 mg
The MRD for lidocaine for this patient is 320 mg.
Although the absolute MRD for lidocaine is 500 mg, when
adjusted for weight, this patient may receive only 320 mg
of drug. The maximum dose should not exceed 500 mg
for lidocaine, regardless of body weight. This would mean
that an individual weighing more than about 156 lbs could
receive no more than 500 mg of lidocaine.
Appendix 7-2 •, "Local Anesthetic and Vasoconstric­
tor Dose Reference," provides a comprehensive look-up
table for determining total cartridges of drug by body
weight. A conversion formula for kilograms to pounds is
also included in Appendix 7-2.
Calculating Additional Doses of the Same Drugs
This patient has received 72 mg of lidocaine and can safely
receive a maximum of 320 mg. Subtract the total dose
already delivered from the MRD for this patient to deter­
mine the additional allowed dose:
320 mg - 72 mg = 248 mg
An additional 248 mg of lidocaine may be delivered.
Converting Milligrams to Cartridges
To convert this number (248 mg) into clinically useful
terms, determine the number of cartridges this would rep­
resent. To do this, divide the additional mg allowed by the
mg per cartridge:
• 91
248 mg + 36 mg/cartridge of 2 % lidocaine =
6.8 cartridges
This patient may receive 6. 8 additional cartridges of
lidocaine.
Calculating Additional Doses of Different Drugs
The following discussion assumes that the toxic effects of
local anesthetic drugs in combination may be synergistic.
When considering additional administrations of differ­
ent drugs, the toxic risks would be greater than the sum
of the individual toxic risks of the drugs. In addition to
administering 0.5 % bupivacaine after administering 3 %
mepivacaine plain, for example, there would b e a greater
potential risk associated with their combined use than
simply the sum of the individual risks.
It may be s af e s t to a s s u m e , t h e r e fore, t h a t t h e
potential toxic risks of local anesthetic drug combinations
are synergistic rather than additive, which would have the
effect of increasing the combined toxic potential beyond
that which would ordinarily be expected when using
more than one drug at a single appointment (Pickett &
Terezhalmy, 2006). Although the extent of this synergy (if
it exists) is not known at this stage, clinicians are advised
to use caution and to follow closely the recommendation
of using the absolute maximum dose of the most toxic
drug when calculating maximum doses of combinations
(Pickett, 2006). In other words, this assumes that all drugs
delivered are as toxic as the most toxic drug. It is impor­
tant to remember that manufacturers are not obligated to
supply information on the risks of additional administra­
tions of different local anesthetic drugs.
Assume therefore that 4 % prilocaine plain will be
added to the two cartridges of 2% lidocaine plain that
were administered in the previous example. B efore adding
another drug, additional key factors are:
1. The 1 0 0 - l b p at i e n t initially r e c e i v e d 72 m g o f
lidocaine.
2. The MRD for lidocaine for this patient is 320 mg.
3. In a 4 % s o lu t i o n , t h e r e are 72 mg of drug p e r
cartridge.
4. The MRD for prilocaine is 4 mgllb or 400 mg maxi­
mum for this patient.
When multiple drugs are administered with different
MRDs, the lowest MRD (most toxic drug) is applied when
calculating total drug doses. To determine the MRD of pri­
locaine for this patient, multiply the MRD for this drug by
the patient's weight:
4 mg/lb X 100 lbs = 400 mg
The MRD for prilocaine for this patient is 400 mg.
Although the MRD for prilocaine is 600 mg, when ad­
justed for weight, this patient may receive only 400 mg. In
this example, the absolute MRD for lidocaine (the most
toxic drug) is 500 mg, which is lower than the MRD for
92 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•

prilocaine (600 mg ) and will be used for calculating dose Table 7-2 Examples of local Anesthetic Doses in
limits. Total mg per Cartridge(s)
This patient has received 72 mg of lidocaine. Since the
MRD for lidocaine will limit this example, they can safely % Loca l An esthetic D r u g
receive a maximum of 248 mg of drug. Subtract the total
dose already delivered from the MRD for this patient to 0. 5 % 2% 3% 4%
determine the allowed additional dose: Cartridge = Volume ( x 5 mg) ( x 20 mg) ( x 3 0 mg) ( x 40 mg)

320 mg - 72 mg = 248 mg
1 = l.S mL 9 mg 36 mg 54 mg 72 mg
For this patient, 248 mg of 4% prilocaine can be
delivered. 2 = 3.6 mL 18 mg 72 mg 108 mg 144 mg
To convert this number (248 mg ) into clinically use­
3 5.4 mL 27 mg 108 mg 162 mg 216 mg
ful terms, determine the number of cartridges this would =

represent. Divide the additional mg allowed by the mg per

cartridge:
248 mg + 72 mg/cartridge of 4% prilocaine = -3.4 cartridges
This patient may receive 3. 4 cartridges of 4% prilocaine
in addition to the two cartridges of 2 % lidocaine
already delivered.
It is important to note that individuals do not react
in the same manner to drugs. Some respond to so-called
safe doses with signs and symptoms of overdose ( hyper­
responders ) . These doses, for these individuals, are not
safe. Others respond to administered overdoses as if safe
doses had been delivered ( hypo-responders ) . These doses,
for these individuals, are, indeed, safe. Others fall within
these extremes but do so with wide variations of response.
It cannot be assumed that s afe doses are necess arily
safe for an individual patient, nor can it be assumed that
exceeding a maximum dose for another individual will
result in an overdose.
Alternate Method for Calculating Doses Delivered
Another approach to calculating doses of local anesthetic
drugs administered applies only the mg/mL values previ­
ously discussed for 0.5 % , 2 % , 3 % , and 4% drugs. After
determining the total volume in milliliters of solution ad­
ministered, multiply the total volume by the mg/mL for
the concentration of drug used. For example:
1. A 2 % solution contains 20 mg of drug per milliliter.
2. A 4% solution contains 40 mg of drug per milliliter.
3. Two cartridges of 2 % lidocaine ( 3 . 6 mL ) and - 3 . 4
cartridges o f 4 % prilocaine ( -6.2 mL) are allowed.
4. Total of 2% lidocaine = 20 mg X 3.6 mL = 72 mg.
5. Total of 4% prilocaine = 40 mg X -6.2 mL = -248 mg.
Given the prevision example, 72 mg of lidocaine were
delivered, and 248 mg ofprilocaine are allowed.
Milligrams Delivered
To calculate the milligrams of drug delivered, first multiply
the total number of cartrid g e s by the total mL p e r
cartridge:
2 X 1.8 mL = 3.6 mL
4 = 7.2 mL 36 mg 144 mg 216 mg 288 mg
Now, multiply this result by the mg/mL based on the drug
percentage (2 % drug = 20 mg )
3.6 mL X 20 mg = 72 mg
This patient received 72 mg of a 2 % drug.
For one-half cartridge, the calculation would be:
0.9 mL X 20 mg = 18 mg
For two-thirds cartridge, the calculation would be:
1.2 mL X 20 mg = 2.4 mg
Table 7-2 • provides a summary of the milligrams of
drug based on drug concentrations and cartridges delivered.
Ca lcu lati n g Vasoco nstricto r Doses
Determining the dose of vasoconstrictor in a given volume
of solution requires an understanding of dilution ratios
or percentages, standard cartridge volumes, the defined
MRDs for epinephrine and levonordefrin, and relevant
patient factors such as general health status.
Calculations of vasoconstrictor doses are different
compared with those used to determine local anesthetic
drug doses. The main differences are that vasoconstrictors
are expressed as dilution ratios rather than concentration
percentages and maximum doses of vasoconstrictors are
not weight dependent.
Definition of Maximum Recommended Doses for
Vasoconstrictor Drugs
Limits on vasoconstrictor doses ( MRDs ) are based on rec­
ommendations of the 1954 Special Committee of the New
York Heart Association and subsequently the American
Heart and D ental Associations, for patients with ische­
mic heart disease ( Budenz, 2000; Finder & Moore, 2002;
Malamed, 20 1 3 ; Special Committee of the New York
He art Association, 1955; Working Conference of ADA
and AHA on Management of Dental Problems in Patients
with Cardiovascular Disease, 1964). Table 7-3 • provides
values for epinephrine and levonordefrin.
 CHAPTER 7 DOSE CALCULATIONS FOR LOCAL ANESTHETIC SOLUTIONS
• 93

Table 7-3 M aximum Safe Doses for Epinephrine and medicine and in some non-North American dental jurisdic­
Levonordefrin tions). Compared with a 1 :100,000 solution with 0.018 mg of
drug, a 1 :20,000 solution contains five times the quantity or
Maxi m u m Safe Dose per Appoi ntment 0.09 mg of drug; a 1 :50,000 solution contains twice the quan­
tity or 0.036 mg of drug; and a 1 :200,000 solution contains
Drug Ratio Healthy Patient Ischemic Heart Disease half the quantity or 0.009 mg of drug (see Box 7-4 •).

Epinephrine Calculating Vasoconstrictor Drug Doses

In order to calculate the total milligrams of vasoconstric­
1:50,000 0.2 mg 0.04 mg
tors in local anesthetic solutions that are administered ,
1:100,000 0.2 mg 0.04 mg
start b y identifying the k e y factors. Assume that two car­
tridges of 2% lidocaine with 1 : 100,000 epinephrine have
1:200,000 0.2 mg 0.04 mg been administered to a 1 0 0-lb female. For this situation
these factors are:
Levonordefrin
1. For a 1 : 100,000 dilution there are 0.0 18 mg of vaso­
constrictor drug per cartridge.
1:20,000 l mg 0.2 mg
2. Two cartridges have been delivered.
Source:Special Committee of the New York Heart Association (1955) 3. The MRD for epinephrine in a he althy p atient is
and Working Conference of ADA and AHA on Management of Dental
Problems in Patients with Cardiovascular Disease (1964). 0.2 mg.
4. The MRD for 2 % lidocaine is 3 . 2 mg/lb or 5 0 0 mg
Vasoconstrictor Dilutions maximum.
To understand vasoconstrictor dilutions, ratios are ex­
Milligrams Delivered
pressed as milligrams to milliliters. A dilution ratio of
1 : 1 ,000 epinephrine is equivalent to 1 gram in 1 liter, ex­ From the previous local anesthetic drug calculation, it was
pressed as 1 ,000 mg/1 ,000 mL 1 mg/mL. A dilution ratio
=
determined that this patient received 72 mg of lidocaine.
of 1 : 1 00,000 is equivalent to 1 gram in 100 liters, expressed To calculate the milligrams of vasoconstrictor delivered,
as 1 ,000 mg/1 00,000 mL 1 mg/100 mL, or 0.0 1 mg/mL
=
multiply the total number of cartridges by the total mg of
(see Box 7-4 •). drug in each cartridge for a 1 : 1 00,000 solution:
Since each cartridge contains 1.8 mL of solution, one 2 X 0.018 mg = 0.036 mg
cartridge with 1 : 1 00,000 epinephrine contains 0.0 18 mg of This patient received 0. 036 mg of epinephrine.
epinephrine (0.0 1 mg/mL X 1.8 mL!cartridge 0.018 mg =

per cartridge). Vasoconstrictor dilutions used in dentistry DETERM I N I N G T H E LIM ITI NG DRUG In the previous edition
are provided in ratios of 1 :20,000, 1 :50,000, 1 : 100,000, and of this text, MRDs for some local anesthetic drugs were
1 :200,000 (currently, 1 :400,000 epinephrine is available in lower than current FDA-accepted maximum doses that

Drug dose and "per cartridge" facts:

The re l ative a m o u nts of vasoco n strictors i n ca rtri d g e s a re co m m o n ly refe rred to as d i l ut i o n ratios.
1 : 1 ,000 = 1 g o r 1 ,000 m g of vasoconstrictor p e r 1 ,000 ml s o l ution = 1 m g/m l
1 : 1 0,000 = 1 m l of 1 : 1 ,000 vasoco nstrictor + 9 m l water = 0 . 1 m g/m l
1 : 1 00,000 = 1 m l of 1 : 1 0,000 vasoconstrictor + 9 m l water = 0.01 m g/ca rtr i d g e
8 m l cartri d g e of 1 : 1 00,000 = 0.01 m g/m l X 1 .8 m l = 0.01 8 m g/ca rtridge
Common Dental Concentrations
1 :20,000 = 0.05 m g/m l or 0.05 X 1 .8 m l = 0.09 m g/ca rt
1 :50,000 = 0.02 m g/m l or 0.02 X 1 .8 m l = 0.036 m g/ca rt

� .
1 : 1 00,000 = 0.01 m g/m l or 0.01 X 1 .8 m l = 0.01 8 m g/ca rt
:� � �� �- �� 5 �:��� � r �- ��5. � 1 �8 �: �. �- ��9. �:/c� rt
1 0 �0 .=. . • • • • • • • • • • • • • • • • • • • • • • • •

. . . . .
94 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•

have been adopted in this edition. The limiting MRD for Table 7-4 Maximum Cartridge Calculations per
each anesthetic solution was typically the local anesthetic Product Inserts"'
drug. The number of cartridges that could be administered
for a he althy adult based on the epinephrine content Local Anesthetic Limited by Local Lim ited by
was greater than for the local anesthetic drug content. Drugs Anesthetic Vasoconstrictor
Previously, for example, when calculating the dose for a
healthy adult, 150 lbs or greater, a maximum of approxi­ 0.5% Bupivacaine
mately 8.3 cartridges of 2% lidocaine, 1 : 100,000 epineph­ w/ 1:200,000 epi 10
rine could be administered (150 lbs X 2 mgllb 300 mg
=

absolute maximum 7- 36 mg lidocaine/cartridge -8.3

=
2% Lidocaine
cartridges ) . Eleven cartridges could be administered based w/ 1:50,000 epi 5.5
on the epinephrine content alone (0.2 mg maximum in the
same healthy adult 7- 0.018 rug/cartridge - 1 1 cartridges ) .
= 2% Lidocaine
Fewer cartridges based on the lidocaine content could be w/ 1:100,000 epi 11
administered; therefore, the limiting drug was lidocaine.
When calculating using current recommendations, the 2% Mepivacaine
limiting drug in the same situation has reversed. For exam­ w/ 1:20,000 levo 11 11
ple, at a weight of 150 lbs the current MRD would be 480
mg or - 1 3 cartridges (150 lbs X 3.2 mgllb lidocaine 480 = 3% Mepivacaine
mg maximum; 480 mg 7- 36 rug/cartridge -13 cartridges
=
Plain 7
based on the lidocaine content ) . The epinephrine is the
same at - 1 1 cartridges in both calculations since vasocon­ 4% Articaine
strictor recommendations have not changed for 1 : 100,000
w/ 1:100,000 epi 6.5
epinephrine dilutions; therefore, the limiting drug is now
the epinephrine (11 is less than 13). 4% Articaine
Maximum cartri d g e v a l u e s for local a n e s th e t i c
w/ 1:200,000 epi 6.5
a n d vasoconstrictor drugs prepared for u s e in dentistry
illustrate this point and may be found in Table 7-4 • ·
4% Prilocaine 8
Consult Table 7-1 for M R D s in milligrams for local
anesthetic drugs and Table 7-3 for maximum safe doses Plain 8
for epinephrine and levonordefrin.
4% Prilocaine
M RD Related to Both Local Anesthetic and w/ 1:200,000 epi 8 8
Vasoconstrictor
Examples in this table are calculated for a healthy, 150-lb person and are
It was determined that the MRD for lidocaine for this pa­ rounded down to half cartridge volumes based on the limiting drug.
<I>Administering the maximum number of cartridges as listed in this
tient was 480 mg. Assuming this is a healthy patient, the
established recommended dose for epinephrine is 0.2 mg table for routine clinical procedures is not recommended . All product
per appointment. inserts make similar statements recommending that clinicians administer
the lowest dosage needed to provide effective anesthesia .
It has been calculated that the patient received 0. 036 mg
of epinephrine, which is well under the established
recommended dose for epinephrine of 0.2 mg. dose of epinephrine (0. 164 milligrams ) into clinically use­
ful terms, determine the number of cartridges this would
Calculating Additional Doses of Same
represent. Divide the additional mg allowed by the mg per
Vasoconstrictor cartridge:
This patient received 0.036 mg of epinephrine and can
0. 164 mg 7- 0.018 rug/cartridge 9 cartridges
safely receive a maximum of 0.2 mg. Subtract the total dose =

already delivered from the recommended dose for this
patient to determine the allowed additional dose:
0.2 mg - 0.036 mg = 0.164 mg
This patient may receive an additional 0. 1 64 milligrams of
epinephrine.
Converting Milligrams to Cartridges
It was determined that this patient may receive an ad­
ditional 0. 164 milligrams of epinephrine. To convert the
This patient may receive an additional nine cartridges
based on epinephrine.
Cardiac Considerations for Vasoconstrictors
Vasoconstrictor doses for patients with ischemic heart dis­
ease are restricted as previously noted. This reduced value
or amount, also referred to as the cardiac dose, is 0.04 mg
per appointment for epinephrine and 0.2 mg levonorde­
frin. Table 7-5 • states the maximum number of cartridges
this represents for each drug ratio.
 CHAPTER 7 DOSE CALCULATIONS FOR LOCAL ANESTHETIC SOLUTIONS
• 95

Table 7-5 Cardiac Doses of Vasoconstrictors by Drug Ratio

Ca rd i a c Doses of Vasoco nstrictors by D r u g Ratio

Tota l M i l l ig ra m s Ava i l a b l e
Ca rd i a c Dose = 0 . 04 m g e p i n e p h ri ne, 0 . 2 m g l evon o rdefrin
Shaded boxes indicate excessive doses of the drug by total cartridges

N u m ber of Epi nephrine Epinephrine Epinephrine Levonordefrin

Cartridges 1 : 50,000 1 : 1 00,000 1 :200,000 1 :20,000

1 0.036 mg 0.018 mg 0.009 mg 0.09 mg

2 0.072 mg 0.036 mg 0.018 mg 0.18 mg

3 0.108 mg 0.054 mg 0.027 mg 0.27 mg

4 0.144 mg 0.072 mg 0.036 mg 0.36 mg

Source: ADAIPDR (2006), Davis and Vogel ( 1996), and Malamed (2013).

Ca lcu lati n g Ped iatric Doses
Calculating drug doses for children applies the same
principles as determining adult doses; however, there may
be some exceptions with obese children (see Box 7-5 •) .
The k e y to correct dosing for children is to determine
their actual weight rather than rely on "guessing." Clini­
cians can deliver overdoses to children both by failing to
make appropriate adj ustments based on weight and by
making erroneous estimates of weight. An available scale
can eliminate any problems due to overestimating a child's
weight.
There are two approaches frequently used for deter­
mining pediatric drug doses in addition to the calculation
methods already discussed. These are Clark's Rule and
Young's Rule; Clark's rule is applied in this text.
As of 2014, the American Academy of Pediatric Dentistry
(AAPD) recommends lower MRDs compared with current
FDA-approved maximum recommended values (American
C h i l d h o o d obes ity m ay pose a u n i q u e c o n cern w h e n
ca l cu l at i n g safe d r u g d o s e s . R e l y i n g s o l e l y o n a c h i l d 's
w e i g h t to esta b l is h safe doses i n obese c h i l d re n ca n b e
p rob l e m atic. Ass u m pt i o n s that these ch i l d re n can re ceive
doses that corres p o n d to t h e i r w e i g h t d o not take i nto
acco u n t the i m m atu rity of t h e i r o rg a n deve l o p m ent. An
obese 7-yea r- o l d , fo r exa m p l e , ca n n ot m eta b o l ize d r u g s
as effi ciently as a 20-yea r-o l d of t h e s a m e w e i g h t (Ba l l &
B i n d l e r, 2008) . I n t h i s situati o n , it m ay be u s efu l to c o n s u l t
sta n d a rd p e d i atric a g e s pecific h e i g ht-w e i g h t c h a rts
(see Ta b l e 7-6 •l . For fu rt h e r discuss i o n see C h a pter 1 9,
" I ns i g hts fro m P e d i atric Dentistry, " Box 1 9-1 , " S p e c i a l
Academy of Pediatric Dentistry, 2009). These values are used
in the following examples as listed in Table 7-7 •·
Clark's Rule
Clark's Rule is based upon a child's weight and states that
the child's weight (in pounds) is divided by 150 to get the
approximate fraction of the adult dose to give to the child.
For example, to calculate the maximum safe dose for a
6-year-old, 50-lb child, using 2 % lidocaine:
1. 50 -:- 150 = 0.33 (113)
2. 300 mg X 0.33 = 100 mg (child's dose)
The dose would be approximately 113 of the adult MRD of
300 mg (8 cartridges), and the child's dose would be 100 mg,
or about -2.8 cartridges (100 mg/36 mg per cartridge = -2.8,
which rounds down to 2 . 5 ) . It is important to remember
that this is a maximum dose for this example, not a routine
or recommended dose.
This method is most similar to the methods discussed
previously. Knowing the child's weight and the MRD in milli­
grams per pound allows for easy calculations. For example, for
2% lidocaine the MRD is 2.0 mgllb, for a 50-lb child this is:
2.0 mg/lb X 50 lbs = 100 mg
The MRD based on the standard method for 2 % lidocaine
for this child is 1 0 0 mg.
Young's Rule
Young's Rule is based on a child's age regardless of weight.
This "rule of thumb" states that the child dosage is equal to the
adult dosage multiplied by the child's age in years, divided by
the sum of 12 plus the child's age. For example, to calculate the
dose for a 6-year-old, 50-lb child, the adult MRD for 2% lido­
caine would be 300 mg. The calculation would be:
1. 300 mg X 6 = 1800

� ��
2. 1800 -:- (12 6) = 100
.li
+

�: �� � :� � �� � : : :
n s i d a ti o n il st ·
. . • . • . . • • • • • • • • • • • • • • • • The child's dose would be 1 00 mg.
96 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•

Table 7-6 Child and Adolescent H eight-Weight Average*

Male Female

Age Height Weight Age Height Wei g ht

(yea rs) (inches) (pounds) (yea rs) (inches) (pounds)

1 year old 28-29 22 1 year old 28-29 - 22

2 years old 31 - 28 2 years old 30 - 28

3 years old 33 33 3 years old 33 -31

4 years old 37 35-3 7 4 years old 37 -35

5 years old 40 - 42 5 years old 40 - 40

6 years old 42 - 46 6 years old 41 - 46

7 years old 44 - 51 7 years old 43 - 51

8 years old 45 -57 8 years old 45 - 57

9 years old 49 - 62 9 years old 47 - 64

10 years old 51 - 70 10 years old 51 - 70

11 years old 52 77 11 years old 52 - 80

12-13 years old 58-62 85-100 12-13 years old 60-63 95-105

14-15 years old 63 -66 105-125 14-15 years old 63 -64 105-115

16 -17 years old 67-70 130-150 16 -17 years old 64 115-120

18-20 years old 68-70 150-160 18-20 years old 66 125-130

'This data is based on averages from CDC tables for child and adolescent height-weight averages (2000 CDC Growth Charts for the United
States: Methods and Development, http://www.cdc.gov/growthcharts) and is provided only as a conservative average for making clinical judgments
of appropriate dosages of local anesthetic drugs for children.

Table 7-7 AAP D Maximum Recommended Doses

Maxi m u m Reco m m ended Dose per Appointment

D r ug Ba sed on Loca l An esthetic D r u g O N LY*

mg!lb mg/kg M g per appt. *

Articaine 3.2 7.0 500 mg

Bupivacaine 0. 6 1.3 90 mg

Lidocaine 2. 0 4. 4 3 00 mg

Mepivacaine 2. 0 4. 4 3 00 mg

Prilocaine 2. 7 6.0 400 mg

'Values adopted for children by the American Academy of Pediatric Dentistry (2009),
current as of April 20 14. Dose should be based on child's weight and should never exceed
maximum recommended limits.
 CHAPTER 7 DOSE CALCULATIONS FOR LOCAL ANESTHETIC SOLUTIONS
• 97

CAS E MA N A G EME N T
lliana Gagarin
l l i a n a w e i g h s 1 2 0 l b s . S h e received o n e ca rt r i d g e of No m o re t h a n 400 mg of m e p ivaca i n e is a l l owed
4% p r i l o ca i n e with 1 : 200,000 e p i n e p h ri n e , w h i c h h a s reg a rd l ess of weight.
a maxi m u m d o s e o f 4 . 0 m g p e r l b . B a s e d o n this l i m it,
/Iiana, however, weighs 1 20 lbs; therefore,
/Iiana can receive up to 480 mg of prilocaine ( 1 20 lbs X
she can have only 360 mg of mepivacaine
4 . 0 mg/lb MRD).
( 1 20 lbs X 3.0 mg!lb MRD).
/Iiana received 72 mg of prilocaine (the mgs
Each c a rtri d g e of 4% p r i l o ca i n e c o n ta i n s 7 2 mg
contained in one cartridge).
of d r u g . 3 6 0 m g ( m e p iv a ca i n e M R D)-7 2 m g (i n it i a l
Switc h i n g to 3% m e p iv a ca i n e m e a n s t h a t a b s o ­ p r i l o ca i n e d ose) = 2 8 8 m g (a d d iti o n a l d ose a l l owed) .
l ute maxi m u ms m ust be identified fo r b o t h d ru g s a n d T h i s is t h e a d d itio n a l n u m be r o f m i l l ig ra m s o f m e p iva­
t h e l owest m u st b e s e l e cted w h e n d r u g s a re c o m ­ ca i n e I I i a n a can h ave fo l l owi n g the d ose of priloca i n e .
b i n e d . The a bsol ute maxi m u m fo r m e p ivaca i n e is 400 To b e c l i n i c a l l y u s efu l , t h i s i n fo r m at i o n c a n b e
m g , a n d the a b s o l ute m a xi m u m fo r p r i l o ca i n e is 600 converted t o ca rtri d g e s by t h e fo l l owi n g ca l c u l ati o n :
m g p e r a p p o i ntment. The lower maxi m u m of 400 mg 2 8 8 m g (ava i l a b l e ) + 5 4 m g ( d o s e i n a 1 . 8 - m l ca r­
(3 . 0 m g/l b) fo r m e pivaca i n e wi l l be used fo r all ca l c u ­ tridge of 3% m e p ivaca i ne) = 5 . 3 a d d itio n a l cartrid g es
l a t i o n s after the i n itia l d ose of p r i l o ca i n e . of 3% m e pivaca i n e .

5. A n individual has received 4 cartridges of

-�.h. ()_ p_t_� r.. 9.l1.��� _i_().rl � . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2% lidocaine, 1 : 100,000 epinephrine, and is not
1 . All of the following are correct when considering profoundly anesthetized. How many cartridges of
MRDs, except: 4% articaine, 1 :200,000 epinephrine, may be adminis­
a. Articaine (3.2 mg/lb, 7.0 mg/kg )
=
tered if the individual weighs 160 lbs?
b. Bupivacaine 90 mg (0.9 mg/lb, 2.0 mg/kg )
=
a. 2.5
c. Lidocaine 600 mg ( 4.0 mg/lb, 8.0 mg/kg )
=
b. 3.5
d. Mepivacaine 400 mg (3.0 mg/lb, 6.6 mg/kg )
=
c. 4.5
d. 5.5
2. Relevant information and mathematical operations
required when calculating drug doses for local 6. How many cartridges of 4 % articaine, 1:200,000
anesthetics and vasoconstrictors include all but which epinephrine may be administered to an individual
one of the following? with significant cardiovascular compromise?
a. Dilution percentages a. 1
b. Standard cartridge volumes b. 2
c. Defined MRD for each drug c. 3
d. Height and weight d. 4

3. Which one of the following is not related to the MRD 7. Which one of the following accurately describes
for 2% lidocaine, 1 : 100,000 epinephrine? available formulations?
a. - 1 1 cartridges absolute maximum a. 2 % lidocaine, 1 : 1 00,000 epinephrine; 3 % lidocaine,
b. - 1 3 cartridges absolute maximum 1 :200,000 epinephrine
c. 3.2 mg/lb b. 2% lidocaine, 1 : 1 00,000 epinephrine; 4% lidocaine,
d. 500 mg absolute maximum 1 :200,000 epinephrine
c. 2% lidocaine, 1 : 1 00,000 epinephrine; 2% lidocaine,
4. What is the MRD for vasoconstrictors when admin­ 1 :50,000 epinephrine
istering 2% lidocaine, 1 : 100,000 epinephrine to a d. 2% lidocaine, 1 :200,000 epinephrine; 2% lidocaine,
healthy individual? 1 :20,000 levonordefrin
a. 0.02 mg
b. 0.1 mg
c. 0.2 mg
d. 1 mg
98 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•
8. The maximum dose per weight of 4 % articaine,
1 : 100,000 epinephrine for children is:
a. 2 mg/lb
b. 3 mg/lb
c. 2.2 mg/lb
d. 3.2 mg/lb
9. 0.5 % bupivacaine, 1:200,000 epinephrine con­
tains how many milligrams of anesthetic drug per
cartridge?
a. 9
b. 1 8
c. 36
d. 5 4
Refe re n ces
2000 CD C Growth Charts for the United States: Methods and
Developments. Available at http://www. cdc.gov/growthcharts/
cdc_charts. htm. Accessed January 25, 2014.
ADA/PDR guide to dental therapeutics ( 5th ed. ) . ( 2009 ) .
Montvale, NJ: Thompson PDR .
American Academy of Pediatric Dentistry. ( 2009) . Guideline
on use of local anesthesia for pediatric dental patients.
Available at: www.aapd.org/media/Policies_Guidelines/
G_LocalAnesthesia.pdf. Accessed January 25, 2014.
Visit www.pearsonhighered.com/healthprofessionsresources to access the student resources that accompany
this book. Simply select Dental Hygiene from the choice of disciplines. Find this book and you will find the
complimentary study tools created for this specific title.
Ball, J. W., & Bindler, R. C. ( 2008) . Pediatric nursing, caring for
children ( 4th ed. ) . Upper Saddle River, NJ : Pearson Prentice
Hall.
Budenz , A. W. ( 2000, August ) . Local anesthetics and medically
complex patients. Journal of the California Dental Association,
28(8), 611 -619.
Davis, M. J., & Vogel, L. D. ( 1996) . Local anesthetic safety in
pediatric patients. New York State Dental Journal, 62(2) , 32-35.
Finder, R. L., & Moore, P. A. ( 2002) . Adverse drug reactions
to local anesthesia. Dental Clinics of North America, 46( 4) ,
747-757.
Malamed, S. F. ( 2013) . Handbook of local anesthesia ( 6th ed. ) .
St Louis: Elsevier Mosby.
Pickett, F. A., & Terezhalmy, G. T. ( 2006) . Dental drug reference
with clinical applications. Baltimore: Lippincott Williams &
Wilkins.
Robertson, D., Nusstein, J., Reader, A., Beck, M., & McCartney,
M. ( 2007) . The anesthetic efficacy of articaine in buccal
infiltration of mandibular posterior teeth. Journal of the
American Dental Association, 138(8), 1104-1112.
Special Committee of the New York Heart Association. ( 1955) .
Use of epinephrine with procaine in dental procedures.
Journal of the American Dental Association, 50, 108.
Working Conference of ADA and AH A on Management of
Dental Problems in Patients with Cardiovascular Disease
1964. Journal of the American Dental Association, 68, 333-342.
Local Anesthetic So lutions-Dose Calculation Facts

Local Anesthetic Drugs-Volume of Drug per Cartridge

Loca l a nesthetic d rugs used i n dentistry a re d i l uted and com mo n ly referred to as a concentra tion

Drug dose and "per cartridge" facts: 1 mL = 1 cc

(all facts based on 1.8 mL cartridge volumes )

1 cartridge = 1.8 mL solution (1.8 cc )

1 % solution = 10 mg/mL

1% = 10 mg/mL X 1.8 mL!cartridge = 18 mg/cart

Common Denta l Concentrations-1 .8 m L Cartridge Conversions:

Concentration Drug per mL Drug per cartridge

0.5% solution � 5 mg/mL � 0.5 X 1.8 = 9 mg/cartridge

2% solution � 20 mg/mL � 20 X 1.8 = 36 mg/cartridge

3% solution � 30 mg/mL � 30 X 1.8 = 54 mg/cartridge

4% solution � 40 mg/mL � 40 X 1.8 = 72 mg/cartridge

Vasoconstrictor Drugs-Volume of Drug per Cartridge

Vasoconstricto rs used i n d e ntistry a re d i l uted and com m o n ly refe rred to as a ratio

Drug dose and "per cartridge" facts:

1 : 1 ,000 1 g or 1 ,000 mg of vasoconstrictor per 1 ,000 mL solution (1 mg/mL)

1 :10,000 1 mL of 1 : 1 ,000 vasoconstrictor + 9 mL water = 0.1 mg/mL

1 : 100,000 1 mL of 1 : 10,000 vasoconstrictor + 9 mL water = 0.018 mg/cartridge

1 : 100,000 = 0.01 mg/mL X 1.8 mL = 0.018 mg/cartridge

Common Dental Ratios-1 .8 m L Cartridge Conversions:

Ration Drug per mL Drug per cartridge

1 :20,000 � 0.05 mg/mL � 0.05 X 1.8 mL = 0.09 mg/cart

1 :50,000 � 0.02 mg/mL � 0.02 X 1.8 mL = 0.036 mg/cart

1 : 100,000 � 0.0 1 mg/mL � 0.01 X 1.8 mL = 0.018 mg/cart

1 :200,000 � 0.005 mg/mL � 0.005 X 1.8 mL = 0.009 mg/cart

(Continued)
99
1 00 SECTION II PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•

Append ix 7-1 Loca l Anesth etic Sol utions-Dose Ca l cu l ation Facts (Continued)
Maxi m u m Doses for Vasoconstrictors
Doses Based SOLELY on Vasoconstrictor

Epinephrine Levonordefrin

Healthy patient - 0. 2 mg/appointment Healthy patient - 1 mg/appointment

= 10 mL of 1:50,000 = 20 mL of a 1:20,000

= 20 mL of 1:100,000 " Cardiac Dose" - 0.2 mglappointment

= 40 mL of 1:200,000 = 4 mL of a 1:20,000 (2 cartridges)

" Cardiac Dose" - 0.04 mglappointment

= 2 mL of 1:50,000 (1 cartridges)

= 4 mL of 1:100,000 (2 cartridges)

= 8 mL of 1:200,000 (4 cartridges)

Note: " Cardiac Dose" 20% (115) of healthy pt. dose

=

"Reduce" for Compromised/Geriatric Patients

(based on professional judgment)
Local Anesthetic and Vasoconstrictor
Dose Reference
Previous Recommendations Updated Recommendations 2013
*
articaine 3.2 mg/lb 500 mg articaine 3.2 mg/lb
*
bupivacaine 0.6 mg/lb 90 mg bupivacaine 90 mg
lidocaine 2.0 mg/lb 300 mg lidocaine 3.2 mg/lb 500 mg
mepivacaine 2.0 mg/lb 400 mg mepivacaine 3.0 mg/lb 400 mg
prilocaine 2.7 mg/lb 600 mg prilocaine 4.0 mg/lb 600 mg
*No recommendation provided
LA Drug A bsolute MRD Vasoconstrictor MRD
Limiting Drug Cardiac Vasoconstrictor MRD*
Healthy Individual
epinephrine= 0.04 mg
Plain formulations are limited by pt. epinephrine= 0.2 mg
levonordefrin = 0.2 mg
weight, health status, and local anesthetic levonordefrin = 1.0 mg
drug mgllb. epinephrine 1: 50,000 = 1 cartridges
1:50,000 & 1:100,000 epinephrine 1:200,000 = 2 cartridges
Formulations w/ vasoconstrictors are
The MRD for LA drugs is frequently met epinephrine 1:200,000 4 cartridges
limited by pt. weight, health status, and =

before the MRD for vasoconstrictor with epinephrine 1:200,000 = 8 cartridges

vasoconstrictor concentration.
these formulations.
Most formulations reach the MRD for the 1------1 levonordefrin 1:20,000 = 2 cartridges
vasoconstrictor before meeting the limits 1:200,000; 1:400,000
for the local anesthetic drug. These maximums are calculated solely on
The MRD for LA drugs will be met well
vasoconstrictor. Individual pt. weight may
Converting Pounds to Kilograms
before the MRD for vasoconstrictor with
restrict doses even lower. These doses are
lbs --+ kg lbs + 2.2 these formulations; therefore, the MRD
= rounded down to nearest 112 cartridge.
kg --+ lbs = kg X 2.2 for epinephrine will never be approached.

2% lidocaine 4% articaine
3.2 mg/lb = 7 mg/kg 3.2 mg/lb = 7 mg/kg
Absolute MRD = 500 mg Absolute MRD =Not Provided
2% = 20 mg/mL= 36 mg/cartridge 4% = 40 mg/mL = 72 mg/cartridge
vasoconstrictor epinephrine vasoconstrictor epinephrine
Formulations Formulations

w/o vasoconstrictor! w/ epi 1:50,000 w/ epi 1:100,000 w/ epi 1:200,000 w/ epil 1:400,000

!Provided for comparison only, not currently available in the United States2013
2% mepivacaine 3% mepivacaine plain
3 mg/lb = 6.6 mg/kg 3 mg/lb = 6.6 mg/kg
MRD =400mg MRD =400mg
2% = 20 mg/mL= 36 mg/cartridge 3% = 30 mg/mL =54 mg/cartridge
vasoconstrictor levonordefrin vasoconstrictor = none
Formulations Formulations
w/levonordefrin 1:20,000 I · I I

4% prilocaine 0.5% bupivacaine

4.0 mg/lb = 8 mg/kg 0. 9 mg/Jb+ = 2.0 mg/kg+
MRD =600mg MRD =90mg
4% = 40 mg/mL= 72 mg/cartridge 0.5% = 5 mg/mL = 9 mg/cartridge
vasoconstrictor epinephrine vasoconstrictor epinephrine
Formulations Formulations
--------�
w/o vasoconstrictor w/ epi 1:200,000

+No U.S. recommendation available;

Canadian recommendation= 0.9 mg/lb, 2.0 mg/kg
Estimating Drug Volumes

Visual Cues for 11Guestimating" Volumes Delivered

Total Drug Volume = 1.8 ml

1.6 • • • •
1.2 0.8 0.4

Drug Volume Expelled by 1 stopper= 0.2 ml

Partial Cartridge to ml Volumes

1 full 3/4 1/2 1/4

cartridge cartridge cartridge cartridge

ml 1.8 ml 1.35ml 0.9 ml 0.45 mL ml

ml 1.8 ml 1.2 ml 0.6 ml ml

1 full 2/3 1/3

cartridge cartridge cartridge

Source: Courtesy of Dentsply Pharmaceutical.

102
································ ·························· ® ··························································

Topical Anesthetics

OBJECTIVES KEY TERMS

• Define and discuss the key terms in this chapter. benzocaine 106
butamben 112
• Demonstrate and discuss the most common methods of
compounded drugs 105
application of topical anesthetic drugs.
dyclonine hydrochloride 110
• Identify and discuss indications and contraindications of topi­ eutectic mixture 112
cal anesthetic drugs. lidocaine 110
tetracaine 111
• Discuss dose and application considerations when maximum
recommended doses of topical anesthetics are not provided
by manufacturers.

• Describe and recognize the signs and symptoms of adverse

topical anesthetic drug reactions, both local and systemic.

• Discuss the properties of eutectic mixtures that determine

their effectiveness.

• Discuss the FDA guidelines for formulation and use of

compounded drugs.
104 SECTI O N I PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•
CAS E S TUDY
Elena Gagarin
E l e n a Gag a r i n b e l ieves that s h e h a s a h i g h t o l e ra n ce
fo r p a i n . Desp ite t h i s b e l i ef, w h e n p a l ata l i nj e cti o n s
w e re n e cessa ry fo r t h e p l a c e m e n t of a r u b b e r d a m
c l a m p o n the r i g h t poste rior p a l atal tissues, s h e cried
I ntrod uction
Whether used alone o r i n combination, topical anesthetic
agents have many applications and are important options in
current pain control strategies (see Figure 8-- 1•). Their benefits
are many and include minimizing apprehension, managing
injection discomfort, and decreasing the need for injections.
Topical anesthetic preparations used in dentistry
are included as a separate discussion for several reasons
(ADA/PDR, 2009; Tetzlaff, 2000):
1. The maj ority of inj ectable anesthetics are ineffective
for topical use in dentistry in safe concentrations.
2. Ester local anesthetic drugs are both useful and popu­
lar in topical formulations.
3. Some agents, such as dyclonine hydrochloride, that
have no inj ectable counterparts or are too toxic for
inj ection can nevertheless provide capable and safe
topical anesthesia.
4. Paraben preservatives such as methylparaben, banned
in inj ectable preparations, are necessary in multiuse
topical preparations.
Topical anesthetic agents have many uses in dentistry.
The most common is for penetration site anesthesia before
needle insertions. Topicals are also useful for discomfort
related to radiographic film placement, periodontal evalu­
ation and treatment, procedures confined to superficial
mucosa, the placement of retraction cord and rubber dams
(when anesthesia has not been established before place­
ment) , and controlling gag reflexes.
FIGURE 8-1 A Variety of Common Topical Anesthetic
Products and Preparations.
d u ri n g t h e i nj e cti o n . S h e s a i d t h a t s h e was fi n e at
t h e t i m e b u t req u ested an a ltern ative to t h e p a l ata l
i njections at s u bseq uent visits, if possi b l e .
Topical agents are widely accepted based o n a n exten­
sive history of safe and effective use. Despite this history,
there have been rare deaths associated with the excessive
use of topical preparations. Adverse reactions are primar­
ily seen in medicine, and the inherent dangers of excessive
self-application are illustrated in an incident before laser
hair removal (see Box 8-1 •) .
Generally formulated in concentrations exceeding
those approved for use in inj ectable local anesthetic drugs,
topical preparations are potentially more toxic. This is com­
plicated by the wide variety of application methods and the
lack of reliable methods for determining doses applied.
This chapter will discuss the most common topical
anesthetic drugs in dentistry and some promising applica­
tions currently under development. Special attention will
be given to describing common signs and symptoms of
adverse events, the benefits of topical drug combinations,
and guidelines for the use of compounded formulations.
(01 /1 8/0 5-RALEIG H)-A yo u n g wom a n ' s fa m i ly says she
was on her way to h ave l aser h a i r-rem ova l treatment i n
R a l e i g h w h e n someth i n g went terribly wro n g . Doctors say
the you n g wom a n suffered bra i n d a m a g e and heart fa i l u re
d u e to h i g h l eve ls of l idoca i n e i n her blood.
. . . December 28th, [the you n g woman] had a n
appointment f o r laser h a i r rem ova l, b u t she n ever m a d e it
to the treatm ent.
She had been given tubes of l idoca i n e cream to apply
i n preparation for that treatment . . . [It is known] that she ap­
plied some of the cream on the morning of December 28th.
About 4 5 m i n utes before the sched u l e d treatm ent,
a member of the DOT's M otorist Assista nce Patro l fou n d
[th e yo u n g woman] i n h e r car, on t h e s i d e o f Interstate 40
havi n g a seizu re .
[The] death certificate i n d i cates a cause o f death was
e l evated b l ood lidocaine levels .
. . . a . . . drug i nformation speci a l ist, says lidoca i n e is
com m o n l y used as a loca l a nesthetic, but it comes with a
warn i n g .
Excerpt from: "Commonl y Used Drug Leads to Mysterious Death"
by Angela Hampton. Copyri g ht © by Disney ABC Tel e vi s i o n
: Group. Used by permi s si o n of Disney ABC Televi s ion Group. ••
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
 CHAPTER 8 TOPI C AL ANESTHETICS
• 105

Genera l Considerations
Unlike their injectable counterparts, maximum dose recom­
mendations for many topical products do not exist (Yagiela,
2005 ) . Even when manufacturers provide maximum rec­
ommended dose (MRD) information, clinicians often have
difficulty determining how much drug was dispensed or ab­
sorbed. Compared with injectable administrations with cali­
brated cartridges containing specific concentrations of drugs,
determining topical dosages can be problematic. Patches and
metered sprays offer more precise calculations, as do some
single-dose application systems. Liquids and gels in multi­
use containers, and unmetered sprays present problems even
when maximum doses are known because there is no easy
way to determine how much was dispensed or how much was
absorbed before being washed away in saliva.
When choosing to use topical agents from com pounding
pharmacies, it is important to be fa m i l i a r with the FDA
Modernization Act of 1 997. This legislation states: "The
compounded product m ust be individu a l ly prescribed for
a n identified patient" (FDA, 1 997) .Th is language may be
interpreted to mean that it is contra ry to the act to acq u i re
a m u ltidose package intended for use on patients yet to
be identified. An exa m p l e of one interpretation of this rule
wou ld be that a product shared with a d ifferent office cou l d
n o t be used in that office, because those patients were not
identified when the prescription was fi lled. Copies of the act
� y e t i
� �
• �� . . � � �� � �� � ��� �� � � ���� �
t b si t , h t /
� . . • . :: - .:..• Ji
d a g o v.

Another factor in topical anesthetic application is that

there is no rationale for excessive durations of application.
When there is no therapeutic benefit, exceeding peak uptake
intervals (the period during which the majority of absorption
occurs) should be avoided because the longer topical anes­
thetics contact mucosa the greater the risk of tissue damage.
Application methods include the use of cotton swabs,
sprays, air inj ection systems, and subgingival delivery
systems with blunt-tipped devices (see Figure s 8 - 3 •,
8-4 • and 8-5 •) .

(
All standard commercial topical preparations should
be accompanied by a set of instructions specific for their
intraoral use. In addition, instructions for compounded
drugs, formulated based on prescription by compound­
ing pharmacies (see Figure 8-2•) , should state that they
are intended for use only on what the Food and D rug
Administration (FDA) describes as identified patients (see
Box 8-2 •). Strict adherence to all instructions accompa­
nying these preparations is recommended.
Factors that may affect topical anesthetic toxicity in­
clude concentration, the relative ability to penetrate tissue,
the speed of systemic absorption, and the total area of cov­
erage. Any situation that slows the metabolism of topical
anesthetics increases their toxic potential.

Com mon App l ication Methods (A)

Available in a variety of commercial forms, topical anesthetics
may be dispensed as liquids, gels, creams, ointments, metered
and unmetered sprays, and subgingival dual-phase systems.

(B)
FIGURE 8-3 Various Topical Anesthetic Application
Methods. A- Topical anesthetic agents are applied by a
FIGURE 8-2 Example: Compounded Topical variety of methods. B- Delivery systems vary mostly based
Anesthetic Product. on the viscosity of the product and desired application sites.
106 SECTI O N I PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•

Topical anesthetics in liquid form have been used for

many years. Liquid rinses can provide widespread topical
effects, for example, controlling gag reflexes before ex­
posing radiographs or taking impressions. This form has
proven less useful before needle penetration because it
is difficult to maintain site-specific, durable coverage of
tissue. Gels, on the other hand, are less useful for wide­
spread pain control or controlling the gag reflex but are
more useful in smaller areas, such as before needle pen­
etration. Creams may contain single drugs or mixtures of
drugs. Ointments provide excellent topical anesthesia and
have been used for years. Metered sprays have significant
benefit over unmetered sprays when considering toxicity.
FIGURE 8-5 Secondary Syringe Delivery Applicators.
One product, a subgingival liquid-to-gel system, is easily
applied because of its liquid state at room temperature
and its rapid transformation to a gel-like state once placed
subgingivally. In addition to providing excellent tissue an­
esthesia and occasional pulpal anesthesia, this system has
wide margins of safety, a known MRD, and easily quan­
tified volumes dispensed because of its packaging in car­
tridge form ( Oraqix®, D entsply Pharmaceuticals, York,
PA) . Another unique formulation delivers the drug in a
varnish gel (see Figure 8-9 •) that forms an insoluble film
upon contact with moist tissue (BeeGentJe®, CAO Group,
20 10).
Typical application methods for gels include cotton
swabs and single-dose commercial applicators (see Fig­
ure 8-4) . Sprays include disposable intraoral tips and are
either metered (the dose is related to the length of time
the nozzle is depressed) or unmetered (unknown quanti­ FIGURE 8-6 Commercial Spray Delivery Applicators.
ties are administered) (see Figure 8-6 •) . Interestingly,
some sprays call for depressing the nozzle only one-half
second per application. This rather limited spray interval
is difficult to accomplish clinically, and applications may
routinely exceed the half-second interval.

FIGURE 8-7 Patch Administration of Benzocaine.

drugs, which will be discussed individually and in combina­

FIGURE 8-4 Single-Dose Commercial Applicators. tion according to their approved formulations: benzocaine,
dyclonine hydrochloride, lidocaine, tetracaine hydrochlo­
ride, butamben, and prilocaine.

Common Top i ca l Agents Benzocaine

A number of drugs can be used alone and in combinations Benzocaine, an ester, is one of the most widely used topi­
to provide effective topical anesthesia for common den­ cal anesthetic agents (Jastak, Yagiela, & Donaldson, 1995;
tal procedures. These preparations include the following B eutlich ) . Existing ne arly 1 0 0 % in the base form, it is
 CHAPTER 8 TOPI C AL ANESTHETICS
• 107

FIGURE 8-9 Varnish Delivery System B eeGentle™

administers benzocaine topical in a varnish medium.

FIGURE 8-8 A Variety of Common Topical B enzo­

caine Preparations.

poorly absorbed into the systemic circulation, which gives

it a very low potential for systemic toxicity. It may be ac­
quired in gel, liquid, and spray forms in concentrations
ranging from 6% to 20% ( see Figure 8-8 •). The most
commonly used concentration is 20 % , which provides ad­
equate topical effect in 30 seconds, with a peak effect oc­
curring at 2 minutes. Durations range from 5 to 15 minutes.
When delivered in a unique time-release varnish prepara­
tion, longer durations may be obtained as drug is released
at a constant rate for up to 30 minutes ( see Box 8-3 •).
Similar to prilocaine, benzocaine can induce methe­
moglobinemia and should be avoided in individuals who
are at risk. It is best to avoid both drugs in this situation
( see Table 8-1 •). On May 5, 20 1 1 , the FDA issued a con­
sumer warning about the use of over-the-counter ( OTC )
benzocaine liquids and gels marketed to reduce teething
BeeGentle™ (CAO G roup, 201 0) is a u n i quely form u l ated,
honey-flavored 20% benzocaine topica l . BeeGentle com­
bines benzoca ine in a water-insol uble materi a l (ethanol­
based solvent) that forms a n inso l u b l e fi l m upon contact
with moist tissue. This a l l ows the topical agent to adhere to
the oral m u cosa where placed. After i n itial a d m i n istration
with a thi n-tipped dispensing syri nge, it will form a wh ite sur­
face coati ng that provides a visible "target" when applied at
an appropriate penetration site. BeeGentle is a unique d u ra­
ble, time-release varnish that provides longer-l asti ng topica l
anesthesia compared with conventional water-so l u b l e prod­
ucts. Accord ing to the product insert, benzoca ine is re leased
at a consta nt rate for u p to 30 m i n utes. The coati ng remains
in place until physica lly removed or until slowly d issolved by
s l va ( e e F u r
: . � : . . � • • :� . � ��9. �);
• • • • • • • • • •• • • • • • • • • • • • •

pain in very young children, noting an increase in the in­

cidence of methemoglobinemia. Box 8-4 • provides more include tetracaine and butamben ( butyl 4-aminobenzoate )
details for this alert. also known as butylcaine.
Similarity to other topical anesthetics Effective concentrations in dentistry
B enzocaine is an ester. B enzocaine is formulated in 6% to 20 % preparations.
It has been characterized as nonionic and remains nearly Onset of action
1 0 0 % nonionic ( in its neutral base form ) even if swal­ The onset of anesthesia for benzocaine is 0.5 minutes,
lowed ( Tetzlaff, 20 0 0 ) . Other ester topical anesthetics with peak effect at 2 minutes.

Table 8-1 Dental Single Drug Topical Anesthetic Preparations

Effective Onset of Action Duration of FDA Pregnancy

Drug Class Concentrations (minutes) Action (minutes) M RD (mg) Category*

benzocaine ester 6-20% 0.5-2 5-15 unknown c

dyclonine ketone 1% up to 10 30 200 c

lidocaine amide 2-5% 1-2 15 200-300 B

tetracaine ester 0.25-0.5 up to 20 slow ( ) 20-60 20 c

*During lactation all of these drugs should be used with caution.

108 SECTI O N I PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•
On May 5, 201 1 , the FDA issued a consumer warn ing about
the use of over-the-counter benzocaine liqu ids and gels
marketed to reduce teething pain in very young ch i l d ren in
response to reports of methemoglobinemia with a l l strengths
of benzocaine gels and liqu ids in ch ildren aged 2 or younger.
Methemoglobinemia is a condition that greatly reduces
the amount of oxygen carried in the bloodstream and in
the most severe cases can be life-th reatening (discussed
in Chapter 1 0, " Patient Assessment for Loca l Anesthesia,"
and Chapter 1 7, " Local Anesthesia Complications and
Management"). In addition to liqu ids and gels, benzoca ine
is a lso available in lozenges and spray sol utions. The main
ingredient, benzocaine, is commonly packaged in 7 . 5% and
1 0% preparations for use in ch i l d ren and is found in numer­
ous brand name prod ucts (see Table 8-2 •).
The FDA repo rts describe m eth e m o g l o b i n e m i a as
being associated with all strengths of benzoca i n e gels a n d
l i q u ids i n c l u d i n g conce ntrations as l o w as 7 . 5%, with most
cases occu rri ng in ch i l d ren aged 2 or you n g e r who were
treated with a gel for teeth i n g d iscomfort.
Signs and sym ptoms usua l ly appear with i n m i n utes to
h o u rs a n d include p a l l o r or g rayn ess, shortness of breath,
fatigue, confusion, l i g htheadedness, and in crease i n h e a rt
rate. If any of these sym ptoms occu rs, the FDA recommends
seeki n g i m m e d iate medical atte nti o n .
The F D A states t h a t benzoca i n e p roducts s h o u l d not
be g iven to ch i l d re n you n g e r than age 2 u n l ess u n d e r the
supervision of a hea lthcare p rofession a l . The American
Academy of Ped iatrics reco m m ends givi n g ch i l d ren with
teeth i n g p roblems a c h i l l e d teeth i n g ring, or gently rub­
bing the c h i l d ' s gums with a finger.
The FDA offers these tips for parents:
• • If benzoca i n e p ro d u cts a re used, watch ca refu l ly for
signs and sym ptoms of m eth e m o g l o b i n e m i a , i n cl u d i n g
p a l e, g ray, o r b l ue-co l o red s k i n , l i ps, and n a i l beds. Also,
shortness of b reath, fatigue, confusion, headache, l i g ht­
headedness, a n d rapid heart rate a re sym ptoms of a
reactio n . If any sym ptoms occu r, seek medical attention
i m mediately.
• Keep i n m i n d that p roblems caused by benzoca i n e can
show u p after a single a d m i n istration of the p roduct.
• Use benzoca i n e gels and l i q u ids spari n g ly, and o n ly
when needed, a n d not m o re than fou r times a day.
Side effects s h o u l d be reported i m m e d i ately to the FDA
M edwatch progra m .
Although the onset of action with benzocaine i s rapid,
a more reliable time elapse in terms of comfort before
inj ection is 1-2 minutes.
Duration of action
The average duration of anesthesia for benzocaine is
5-15 minutes.
Fifteen minutes is seldom needed before inj ection, but
once the initial 5 minutes have elapsed, there is no guar­
antee that an acceptable topical effect is still present. Re­
application should be considered after 5 minutes if the
inj ection has not occurred during that time.
MRD (maximum recommended dose)
There is no established MRD for benzocaine.
It is recommended that clinicians follow manufacturer's
r e c o m m e n d a t i o n s w h e n e v e r a v a i l ab l e . With s p r a y
preparations of benzocaine, n e v e r e x c e e d a 2-second
administration period (ADA/PDR, 2009) .
Toxicity
Toxic reactions to benzocaine in dentistry are rare.
Precautions incre ase when tissues are highly abraded,
when used in children and adults of very low weight, and
when applied to large areas of tissue (see Box 8-5 •).
Although uncommon, this potential nevertheless ex­
ists, especially if sprays are used in larger volumes, such
as might occur from excessive numbing of the oral cav­
ity before exposing radiographs or taking impressions.
Although unlikely, methemoglobinemia has occurred
when excessive doses in spray form have been adminis­
tered (FDA, 2006) . The risk of methemoglobinemia is in­
creased in small children, probably due to their low body
weight (Tetzlaff, 2000) . Although by no means typical, it
is important to point out that benzocaine gel for teething
pain has resulted in symptomatic methemoglobinemia in
the past (Tetzlaff, 2000).
B enzocaine has also been reported to be an antagonist
to the actions of the sulfonamide antibacterials (Alston,
1992).
As an ester, benzocaine metabolizes to para-amino­
benzoic acid (PABA), which is an FDA-identified antigen.
Allergies are more frequent to ester agents. In the case
of topical anesthetics, allergic reactions, although not re­
stricted to local areas of tissue, tend to involve delayed re­
sponses and are usually limited to areas of contact only.
B enzocaine allergies are almost always restricted to these
areas. Lidocaine topical is an appropriate substitute should
this occur.
Metabolism
B enzocaine is metabolized by ester hydrolysis (via
cholinesterase) .
Principal metabolites include PABA a n d ethanol, which
may further metabolize to carbon dioxide and water.
Excretion
B enzocaine is excreted as PABA, ethanol, carbon
dioxide, and water in var iable ratios.
Pregnancy category
B enzocaine is in FDA Category C.
 CHAPTER 8 TOPI C AL ANESTHETICS
• 109

Table 8-2 Topical Anesthetic Products Containing Benzocaine for Oral Use*

Aerosols Creams
• Hurricane 20% • B enzocaine 5 %
• Americaine 20% • Oraj el PM Maximum Strength 20%

Gels
• HDA Toothache 6.5 % • Anbesol Maximum Strength 20%
• B aby Anbesol 7. 5 % • ComfortCaine 20 %
• B aby Oral Pain Reliever 7. 5 % • B enzocaine Topical Anesthetic Gel 20%
• Detane 7. 5 % • D entapaine 2 0 %
• Oraj el B aby Happy Smiles Kit 7. 5 % • Gingicaine 20 %
• Oraj el Teething Medication 7.5 % • Americaine Anesthetic Lubricant 20%
• Oraj e11 0 % • Kank-A Soft B rush Lubricant 20 %
• B aby Oraj el Nighttime 1 0 % • Oral Anesthetic 20 %
• Teething Baby Medicine 1 0 % • Orabase-B 2 0 %
• Zilactin B aby Extra Strength 1 0 % • Oraj el Maximum Strength 20%
• Zilactin B 10% • Oraj el Mouth Aid 20%
• Oraj el Denture Plus 15 % • Topex 20%
• Oraj el Ultra Mouth Sore 15 % • Topicale 20%
• Hurricaine 20%

Gel Patch Gum

• Topicale GelPatch 36 mg/patch • D ent's Extra Strength Toothache 20%

Swabs Liquid Solutions

• Oraj el B aby Teething Swabs 7. 5 % • Orasept 1.53 %
• Den temp Oral Pain Relief 1 0 % • Gumsol 2 %
• Gingicaine One SwabStick 20% • B abee Teething Lotion 2.5 %
• Hurricaine 20% • Rid-A-Pain 6.5%
• Orajel Medicated Mouthsore Swab 20 % • Miradyne-3 9 %
• Orajel Medicated Toothache Swab 20 % • Tanac Liquid 1 0 %
• Topex 20% • Anbesol Maximum Strength 20%
• Zilactin Toothache Maximum Strength 20 % • Gingicaine 20 %
• Hurricaine 20%
• Kank-A 20%
• Topex 20%

Ointments Lozenges
• Anacaine 1 0 % • Chloraseptic Sore Throat 6 m g
• B enzodent 1 0 % • Cepacol Extra Strength 10 m g
• Cora-Caine 20 % • Spec-T 10 mg
• Red Cross Canker 20 % • Bi-Zets 15 mg
• Topicale 20%

*Product list current as of April 2013. This list provides samples only and is not intended to be inclusive of all available products.

Lactation
Caution is recommended in nursing.
M o s t drugs are available in breast milk o n c e intro­
duced. Product information generally states that cau­
B roken skin a n d inflamed or d a m a ged m u cosa, such as tion must be exercise d when nursing after benzocaine
the l i n i n gs of diseased periodontal pockets, a re m o re administration.
easily penetrated because the d rugs bypass the p rotec­
tive epith e l i a l b a rrier, m ovi n g d i rectly to exposed b l ood Proprietary names by application category
vessels i n the co n n e ctive tissue and fro m there i nto the (variable concentrations)
syste m i c ci rcu l ati o n . Topical a n esthetics applied i n this
Some prescription and over-the-counter products
containing benzocaine are listed in Table 8-2 •·
•
manner m ust be considered m o re ca refu l l y when m o n itor- •

i f s
: . �: �� � ���� � • • • • • • • • • • • • • • • • • • • • • • • • • • • • • Sources: FDA, 2006; Tetzlaff, 2000.
110 SECTI O N I PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•
Dyclonine Hydrochloride
Dyclonine hydrochloride, formerly available as Dylcone
(0. 5 % solution) , is a nonester, nonamide, ketone topical
anesthetic (the aromatic and amino ends are j oined by
a ketone linkage) (Jastak , Yagiela, & D onaldson, 1995 ) .
D yclonine provides a relatively s afe and very durable
topical effect. It also possesses some b actericidal and
fungicidal properties. With a slow o n s e t of between
2 and 10 minutes and duration of about 30 minutes, it is
particularly useful when amides and esters may not be
used. Dyclonine is marketed as 1 % and 0.5 % solutions
and is occasionally available as a spray (see Figure 8-10 •).
It can also be found in OTC products such as Sucrets Chil­
dren's, Regular Strength, and Maximum Strength lozenges
and Cepacol S ore Thro at Lozenges and Sprays ( s e e
Figure 8-1 1 •) (Malamed, 20 1 3 ) . It w a s formerly avail­
able as Dylcone before the product was withdrawn from
the market. The U.S. FDA issued the following statement
in 2004, 3 years after the product was withdrawn: "The
Food and Drug Administration (FDA) has determined
that dyclone (dyclonine hydrochloride [HCl] ) 0.5 % and
1.0 % Topical Solutions were not withdrawn from sale for
reasons of safety or effectiveness."
FIGURE 8-10 Dyclonine Hydrochloride by Prescription.
FIGURE 8-11 OTC Source of Dyclonine Hydrochloride. OTC
oral anesthetic lozenges containing dyclonine hydrochloride.
Similarity to other topical anesthetics
Dyclonine is a ketone.
It is chemically unique c o m p a r e d with o t h e r l o c a l
anesthetics used i n dentistry and medicine.
Effective concentrations in dentistry
Dyclonine is commonly formulated in 1 %
preparations.
Onset of action
The onset of anesthesia for dyclonine is up to 10
minutes.
Duration of action
The average duration of anesthesia for dyclonine
is about 30 minutes (effects may last as long as
1 hour) .
MRD
The MRD for dyclonine is 200 mg, or 20 mL of a 1 %
solution; 40 m L of a 0.5 % solution.
Doses are reduced for children and medically compro­
mised adults as well as for situations in which tissues are
heavily abraded before application. Safe doses have not
been determined for children under age 12. Allergic reac­
tions are uncommon.
Toxicity
Although toxicity is unlikely and the toxic potential of
dyclonine is very low because of poor water solubility, in
excessively large doses it may affect sensitive neural tis­
sues similar to other local anesthetic agents, resulting in
progressive signs and symptoms of central nervous system
(CNS) and cardiovascular system (CVS) depression.
Metabolism
No information is available on dyclonine
metabolism.
Excretion
No information is available on dyclonine excretion.
Pregnancy category
Dyclonine hydrochloride is in FDA Category C.
Lactation
Caution is recommended in nursing.
Most drugs are available in breast milk once introduced.
Product information generally states that caution must be
exercised when nursing.
Proprietary names and available preparations
S o m e prescription and OTC products containing
dyclonine hydrochloride are listed in Table 8-3 •·
Lidocaine
Lidocaine is an effective topical anesthetic drug and an ex­
cellent alternative to esters when esters are contraindicated

Table 8-3 Topical Anesthetic Products Containing
Dyclonine for Oral Use
Solution
• Dyclonine hydrochloride 1 % and 0.5 % (compounded
only)
Lozenges
• Sucrets lozenges:
• Children's 1.2 mg
• Regular Strength 2 mg
• Maximum Strength 3 mg
Source: Tetzlaff (2000) and Wynn (2012-2013).
(Jastak, Yagiela, & D onaldson, 1995 ) . The most common
preparation of lidocaine topical is as an ointment in multi­
use jars (see Figure 8-12 •). It is also available in 2% to 5 %
concentrations primarily i n liquid and gel forms. Toxic re­
actions, although uncommon, have occurred with lidocaine
topical, particularly in the spray form (see Box 8-1) . Dental
preparations of lidocaine in spray form are available from
Canadian distributors (20 13). Onset times vary between 2
and 10 minutes with an expected duration of 15 minutes.
Lidocaine is available as a predominantly acid salt prepa­
ration (lidocaine hydrochloride) or as a neutral base for­
mulation (lidocaine base) . Base preparations have lower
systemic absorptions in comparison to acid salt formu­
lations and therefore are less toxic (Mehra, Caiazzo, &
Maloney, 1998).
Similarity to other topical anesthetics
Lidocaine is most similar to prilocaine compared with
other topicals in dentistry.
Effective concentrations in dentistry
Lidocaine topical is commonly formulated in 2% to
5 % preparations.
FIGURE 8-12 Lidocaine Topical Cream.
CHAPTER 8 TOPI C AL ANESTHETICS
• 111
Onset of action
The onset of anesthesia for lidocaine is 1-2 minutes;
peak effects may take up to 5-10 minutes.
Duration of action
The typical duration is 15 minutes.
MRD
The MRD for lidocaine topicals is reported to be 200 mg.
Overdose reactions are similar to overdoses from injectable
forms of lidocaine with typical progression to CNS depres­
sion without initial excitation, although overdoses are very
unlikely when using lidocaine topical alone.
Toxicity
Lidocaine topical is a CNS depressant; however, toxic
reactions are rare.
Precautions incre ase when tissues are highly abraded,
when used in children and adults of very low weight, and
when applied to large areas of tissues.
Metabolism
Lidocaine is metabolized in the liver by hepatic
oxidases and amidases.
Excretion
Less than 10% of lidocaine is excreted unchanged by
the kidneys.
Pregnancy category
Lidocaine is an FDA Category B.
Lactation
Caution is recommended in nursing.
Most drugs are available in breast milk once introduced.
Product information generally states that caution must be
exercised when nursing.
Proprietary names by application category
Some prescription and OTC products containing
lidocaine are listed in Table 8-4 •·
Sources: ADAIPDR (2009), Jastak, Yagiela, and Donaldson (1995),
and Malamed (2013).
Tetracaine Hydrochloride
Tetracaine is a potent ester topical anesthetic. In dentistry, tet­
racaine is used only in combination with other topical anes­
thetics, but a new product currently in clinical trials, Kovacaine
Mist ™ (St. Renatus, Fort Collins, CO), makes use of a spray
application to provide both soft tissue and pulpal anesthesia.
Historically, it replaced cocaine as an equally effective yet
less irritating substitute when applied to the eyes. Repeated
or long-term eye contact is now discouraged. Excessive dos­
ing and too frequent application may result in serious adverse
reactions, including those requiring resuscitation.
Similarity to other local anesthetics
Tetracaine is an ester similar to benzocaine and
butamben.
112 SECTI O N I PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•
Table 8-4 Some Topical Anesthetic Products Containing lidocaine for Oral Use
Ointment (base formulation)
• Octocaine 5 % (50 mg/mL)
• Xylocaine 5% (50 mg/mL)
Solution (base formulation)
• Zilactin - 2.5 %
Source: ADAIPDR (2009) and Jastak, Yagiela, and Donaldson (1995).
* Product list current as of May 2013. This Jist provides samples only and is not intended to be inclusive of all available products.
Effective concentrations in dentistry
Tetracaine is commonly formulated in 0.25 % to 0.5 %
preparations.
Onset of action
The onset of anesthesia for tetracaine is slow and
variable, with peak effects taking up to 20 minutes.
Duration of action
The average duration of anesthesia for tetracaine is
20-60 minutes.
MRD
The MRD for tetracaine is 20 mg (1 mL of a 2 %
solution) .
Tetracaine is rapidly absorbed through mucous mem­
branes with a very slow metabolism. Precautions increase
when tissues are highly abraded and when used in smaller
children.
Toxicity
Tetracaine is the most potent of the dental topical an­
esthetics. Serious adverse reactions have occurred in
conjunction with tetracaine topical anesthesia, partic­
ularly in medicine. Excessive doses and too frequent
administrations should be avoided. Extreme caution
has been urged with the use of tetracaine because of
its potential for systemic toxicity.
Metabolism
Tetracaine undergoes hydrolysis via plasma
cholinesterase.
Primary metabolites of tetracaine include PABA and
diethylaminoethanol, both of which have an unspecified
activity.
Excretion
Tetracaine is excreted by the kidneys.
Pregnancy category
Tetracaine is an FDA Category C.
Lactation
Caution is recommended in nursing.
Most drugs are available in breast milk once introduced.
Product information generally states that caution must be
exercised when nursing.
Gel (hydrochloride salt formulation)
• Xylocaine 2% Jelly (lidocaine hydrochloride)
Oral Topical Solution
• Lidocaine 2 % Hydrochloride Oral Topical Solution USP (Viscous)
• Lidocaine 4% Hydrochloride Topical Solution USP
Table 8-5 Nondental Examples of Topical Anesthetic
Products Containing Tetracaine
Solution
• Pontocaine 0.25 % and 0.5% topical solutions
Nebulized Spray
• Pontocaine 0.5 %
Source: ADAIPDR (2009), Jastak, Yagiela, and Donaldson (1995), and
Wynn (2012-2013).
Tetracaine in combination will be discussed later as "Benzocaine,
Butamben, and Tetracaine combination."
Proprietary names by application category
Some nondental prescription products containing
tetracaine are listed in Table 8-5 .
Sources: ADAIPDR (2009), Jastak, Yagiela, and Donaldson (1995),
Malamed (2013), Patel, Chopra, and Berman, (1989).
Topical Drug Com binations
Topical anesthetics may be formulated i n combinations
to provide enhanced onsets and durations beyond the
properties of each drug individually. These combinations
are formulated to provide more useful clinical ranges of
onset and duration for optimal therapeutic effect.
S o m e are designed for enhanced effectiveness in
specific applications. For example, prilocaine is found
in combination with lidocaine for topical use in den­
tistry. This combination of anesthetic drugs is known as
a eutectic mixture (Jastak, Yagiela, & D onaldson, 1995 ;
Tetzlaff, 2000) . Prilocaine and lidocaine mixtures are de­
scribed later in this chapter in the discussion of eutectic
mixtures.
Benzocaine, Tetracaine, and Butamben (Combination)
When formulated in combination, these three ester drugs
provide a much more useful range of topical anesthesia
compared with any of the individual drugs acting alone:
14 % benzocaine ( short-acting, fast-onset) ,
2 % tetracaine (long-acting, slow-onset) , and
2% butamben (intermediate-acting,
intermediate-onset) .

This particular example, Cetacaine® (Cetylite Industries
Inc. , Pennsauken, NJ) , enables a rapid onset and a very
long duration of topical anesthesia (see Figure 8-13 •).
Similarity to other topical anesthetics
All three drugs are esters.
Effective concentrations in dentistry
Tetracaine, butamben, and benzocaine are commonly
formulated with 2% tetracaine, 2% butamben, and
14% benzocaine.
Onset of action
The onset of action of tetracaine, butamben, and
benzocaine combinations is about 30 seconds.
Duration of action
The duration of the combination may be as much as
45 minutes.
MRD
See product inserts for specific MRDs for this
combination.
Toxicity
Overdose reactions are similar to overdoses from
inj ectable esters with signs and symptoms of CNS
depression followed by CVS toxicity. Precautions
increase when tissues are highly abraded, when used
in children and adults of very low weight, and when
applied to large areas of tissue.
FIGURE 8-13 Cetacaine® Topical Preparations­
B enzocaine, Butamben, and Tetracaine (combination) .
CHAPTER 8 TOPI C AL ANESTHETICS
• 113
Metabolism
Esters are metabolized via cholinesterase.
Excretion
Excretion occurs primarily through the kidneys.
Pregnancy category
B enzocaine, Butamben, and Tetracaine are all in FDA
Category C.
Lactation
Caution is recommended in nursing women.
Most drugs are available in breast milk once introduced.
Product information generally states that caution must be
exercised when nursing.
Proprietary names by application category
Some prescription and OTC products containing
benzocaine, butamben, and tetracaine combined are
listed in Table 8-6 •·
Sources: ADAIPDR ( 2009) , Jastak, Yagiela, and Donaldson (1995) ,
and Malamed ( 2013) .
Eutectic M ixtu res
Eutectic mixtures of local anesthetics provide a more
rapid onset on skin and a greater depth of topical penetra­
tion on both skin and mucosa compared with any of the
ingredients acting alone. This is the result of very specific
properties of the mixture.
In preparing eutectic mixtures, powdered drugs are
suspended in water and oil to form a cream (Tetzlaff,
20 0 0 ) . Concentrations of the drugs are typically higher
than those used in inj ectable forms and are present in the
cream largely as base molecules (Tetzlaff, 2000).
Enhanced properties of eutectic mixtures result from
higher concentrations of base molecules, the homoge­
neous nature of the cream, and the lower melting point
of the mixture compared with any of the melting points
of the individual components. These properties assure in­
creasing depths of anesthesia, an even distribution, and
a faster onset on skin compared with other topicals but
Table 8-6 Examples of Topical Anesthetic Products
Containing Benzocaine, Tetracaine, and Butamben
Spray
• Cetacaine (14 % , 2 % , 2 % )
Liquid
• Cetacaine (14 % , 2 % , 2 % )
Gel
• Cetacaine gel (14 % , 2 % , 2 % )
Source: ADAIPDR ( 2009) , Jastak, Yagiela, and Donaldson (1995) , and
Cetylite Industries Inc., 2014.
*Products current as January 2014 Cetylite Inc. Cetacaine topical. Cetylite
Inc .. Prescribing information. Cetylite Inc.,Pennsauken, NJ www.cetacaine.
com/dental/about/prescribing-information. Accessed April 12, 2014.
114 SECTI O N I PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•

not on mucosa, where most individual topicals have simi­

lar onsets. The longer the mixtures are left in contact with
skin or mucous membranes, however, the deeper their
penetration . Contact on skin for 2 hours will typically
yield a greater penetration of anesthesia compared with
1 hour.
Compared with mucosa, skin is a more significant bar­
rier to diffusion of topical drugs and requires longer appli­
cation times, typically 60 minutes or longer. As previously
stated, onsets of eutectic mixtures on mucous membranes
are considered rapid compared with skin but still require
(A)
similar time compared with other commonly available
topical agents. A eutectic's advantage on mucosa over any
faster-acting topicals is the depth of topical anesthesia it
is able to provide. The difference is considerable enough,
in fact, that eutectic mixtures have been used as the sole
method of anesthesia, especially in pediatric dentistry
where their enhanced depth may be sufficient to provide
pulpal anesthesia in the youngest patients (Malamed,
(B)
20 1 3 ) . Pulpal effects were found to be less reliable for
adults and older children (Malamed, 20 13). FIGURE 8-15 Oraqix® D elivery System Syringe Safety

Two common eutectic mixtures of local anesthetic
drugs commercially available are Eutectic Mixture of Local
Anesthetics (AstraZeneca, 20 10) and Oraqix® (D entsply
Pharmaceuticals, York, PA) (see Figure 8-14 •). EMLA
is formulated for skin but has been used successfully on
mucous membranes in both medicine and dentistry. It is
approved only for medical use, however, and specific in­
structions for use in dentistry do not exist. It is a combi­
nation of lidocaine and prilocaine. Oraqix, also a mixture
of lidocaine and prilocaine, is formulated for subgingival
application although it has a uniquely different method of
application. Because of the inclusion of prilocaine, the risk
of methemoglobinemia exists in both preparations.
Lidocaine and Prilocaine Periodontal Eutectic Mixture
O raqix is a eutectic mixture designed for " intrapocket"
use in dentistry (ADA/PDR, 2009; O raqix) . It is a liq­
uid at room temperature that thickens to a gel-like con­
sistency (dual-phase) when placed subgingivally. The
Features A - Assembled syringe system.
B - Components of the Oraqix syringe system.
Oraqix delivery system includes a syringe-type carrier
(see Figure 8-15 •) that holds a specialized cartridge and a
blunt-tipped applicator (see Figure 8-16 •). The drugs are
applied, rather than injected, into the sulcus via the blunt­
tipped applicator (see Figure 8-17 •). The product insert
suggests a wait of 20-30 seconds after initial application
in the gingival sulcus before deeper application into peri­
odontal pockets. Deeper application is discontinued once
the gel becomes visible at the gingival margin. Features en­
hancing the safety of Oraqix include:
1. Low systemic toxicity with only 20 % to 40 % of the
dispensed drug available systemically.
2. E a s e of d o s e tracking compared with multi d o s e
p ackaging common with other topicals. (S tandard
calculation methods can b e used with the 1 . 7-mL
cartridges.)
3 . A specialized safety collar (see Figure 8-18 •) prevents
accidental placement of the cartridge into standard
aspirating syringes, avoiding accidental submucosal
inj ection of the drugs.

FIGURE 8-14 Examples of Eutectic Mixtures. Oraqix® FIGURE 8-16 Oraqix® Delivery System Cartridge
lidocaine and prilocaine periodontal gel topical (front) and Needle.
and a generic EMLA product. Source: Modified courtesy of Dentsply Pharmaceutical.

(A)
(B)
FIGURE 8-17 Oraqix® Subgingival D elivery A- The needle
tip is angled subgingivally similar to a periodontal probe; the
mixture is deposited at the base of the sulcus. B - The needle
tip (top) is not sharp like a standard inj ection needle (bottom)
and is not intended to penetrate tissues.
Oraqix can substitute for inj ectable local anesthetics
in some situations, although pulpal anesthesia is not
expected but may be provided to some extent (Oraqix) .
Similarity to other topical anesthetics
Lidocaine and prilocaine are amides.
Lidocaine is similar to etidocaine and prilocaine is similar
to articaine. There is no equivalent combination to Oraqix
because of its unique liquid-to-gel transformation at physi­
ologic temperatures.
Effective concentrations in dentistry
Lidocaine and prilocaine in eutectic mixtures for
topical use are commonly formulated with 2.5 %
lidocaine and 2.5 % prilocaine.
Onset of action
The onset of anesthesia for topical lidocaine and
prilocaine combinations is about 1 minute.
CHAPTER 8 TOPI C AL ANESTHETICS
• 115
(A)
(B)
FIGURE 8-18 Oraqix D elivery System Cartridge Safety
Features. A - Oraqix has a unique "crosshatched"
colored band (top) similar to the drug identification
color bands on standard dental cartridges (bottom).
B - Each Oraqix cartridge has a white plastic safety
collar over the end cap and needle penetration end
(right) when compared with standard local anesthetic
cartridges (left) to prevent insertion into standard
syringes and inadvertent submucosal inj ection.
Duration of action
The overall duration of action of Oraqix is 20 minutes
(ranging between 14 and 31 minutes).
D uration is variable and d e p e n d s upon the time of
application and the type of tissue on which Oraqix is applied.
MRD
The MRD for topical lidocaine and prilocaine in a
eutectic mixture is five cartridges per appointment
(Oraqix).
Toxicity
Only about 20% to 40% is absorbed systemically.
O v e r d o s e r e a c t i o n s are s i m i l a r to o v e r d o s e s fro m
inj ectable amides with signs and symptoms of CNS
depression followed by CVS toxicity. Prilocaine increases
the possibility of the development of methemoglobinemia
in individuals with congenital and idiosyncratic tendencies.
116 SECTI O N I PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•
Metabolism
Lidocaine is metabolized by hepatic oxidases and
amidases.
Prilocaine is metabolized in the liver by amidases, and in
the lungs and kidneys.
Excretion
Excretion occurs primarily through the kidneys.
Pregnancy category
Lidocaine and prilocaine are both in FDA Category B.
Lactation
Caution is recommended in nursing women.
Most drugs are available in breast milk once introduced.
Product information generally states that caution must be
exercised when nursing.
Source: Oraqix.
Lidocaine and Prilocaine Eutectic Mixtures
Another eutectic mixture of lidocaine and prilocaine is
available as EMLA. The same concentration of drugs
found in Oraqix is available in EMLA , 2 . 5 % lidocaine
and 2.5 % prilocaine; however, EMLA is not a dual-phase
system (see AstraZeneca, 20 10). EMLA is also available in
generic preparations (see Figure 8-19 •).
In pediatric dentistry, EMLA may provide complete
pulpal anesthesia for some procedures because of its
significant depth of penetration (Munshi, Hegde, & Latha,
20 0 1 ) . As with Oraqix, EMLA has gained popularity by
providing deep topical effects (Malamed, 20 1 3 ) . Although
not originally recommended for dental use, clinical trials
have demonstrated that it can be effective in dentistry
(B ernardi, S e cco, & B enech, 1 9 9 9 ; Munshi, Hegde, &
Latha, 200 1 ) . Product information accompanying EMLA
does not include specific information regarding its use on
oral mucous membranes.
Similarity to other topical anesthetics
Lidocaine and prilocaine are amides.
NIIC 01 8&0357-30
II only
tQ!IEiera •
LIDOCAINE and
PRILOCAINE CREAM, 2.5%12.5%
FIGURE 8-19 Lidocaine and Prilocaine Eutectic Mixture
(Generic EMLA).
EMLA is not approved by the FDA for dental use. For
this reaso n, there a re no denta l-specific instructions
included with the product. O n the other hand, the FDA
has n ot banned it from use i n dentistry. So-ca l l e d off- l a b e l
u s e i m p l ies knowledge on the p a rt o f c l i n icians i n t h e
appropriate a n d reason a b l e u s e o f such p ro d u cts.
Th e direction s for m edica / u s e include th e following:
Apply 1 -2 grams in each 1 0 cm2
Suppl ied in 5- and 30-g ram tubes and as a n a d h esive
Ji
� an t
•• � �
i
� � � �� � � • • • • • • • • • • • • • • • • • • • • • • • • • • • •
Lidocaine is similar to etidocaine and prilocaine is
similar to articaine.
Effective concentrations
No information is available for intraoral applications.
Effective concentrations and application have been estab­
lished for medical use only (see Box 8-6 •).
MRD
0-3 months or less than 5 kg (body weight) = 1 gram
3-12 months or greater than 5 kg = 2 gram
1-6 years or greater than 10 kg = 10 grams
7-12 and greater than 20 kg = 20 grams
Typically, up to 5-10 grams must be applied on genital
mucosa for effective topical anesthesia.
Overdose reactions are similar to overdoses from inj ect­
able amides with signs and symptoms of CNS depression
followed by CVS toxicity. Prilocaine increases the possibil­
ity of the development of methemoglobinemia in individu­
als with congenital and idiosyncratic tendencies.
Toxicity
Approximately 1120 the amount of the lidocaine ap­
plied on skin is absorbed systemically, whereas approxi­
mately 1136 the amount of the prilocaine applied on skin is
absorbed systemically.
When 10 grams were applied to genital mucosa, the ab­
sorbed doses of lidocaine and prilocaine, respectively, were
148--641 nanograms/mL (ng/mL) and 40--346 ng/mL, which is
well below the concentrations anticipated to give rise to sys­
temic toxicity (5,000 ng/mL for both lidocaine and prilocaine ).
Onset of action
Five to 10 minutes are required on genital mucosa for
sufficient anesthesia. No information is available on oral
mucosal uses.
The longer EMLA is held against the tissues, the
greater the depth of anesthesia it provides. Applications
on skin are usually adequate in 1 hour.

Duration of action
No information is available for intraoral
applications.
MRD
No information is available for intraoral
applications.
Toxicity
No information is available for intraoral
applications.
Metabolism
Lidocaine is metabolized by hepatic oxidases and
amidases.
Prilocaine is metabolized in the liver by amidases, and in
the lungs and kidneys.
Excretion
Excretion occurs primarily through the kidneys.
Pregnancy category
Lidocaine and prilocaine eutectic mixtures are in
FDA Category B.
Lactation
Caution is recommended in nursing women
(see AstraZeneca, 20 10).
Most drugs are available in breast milk once introduced.
Product information generally states that caution must be
exercised when nursing.
Source: AstraZeneca, 2010.
Considerations i n the Ad m i n i stration
of Top ica ls
Although toxic reactions are rare, the higher concentra­
tions of many topical anesthetics compared with inj ectable
agents give them a potentially greater risk of toxicity. As
these agents become more popular and gain acceptance
as alternatives to traditional inj ectable anesthesia, it is im­
portant to consider the increased risks when using them.
Administered volumes, peak uptake intervals between
successive applications, and areas of coverage are all im­
portant considerations.
Local Adverse Reactions
Local reactions with topical agents include tissue slough­
ing, edema, delayed hypersensitivity, redness, pain, and
burning at the sites of application. Increased likelihood of
adverse events follows application on abraded or broken
tissue, including that caused by trauma during applica­
tion, prolonged contact with skin or mucosa, and undiag­
nosed hypersensitivities to any of the ingredients. These
reactions generally respond well to palliative strategies
CHAPTER 8 TOPI C AL ANESTHETICS
• 117
FIGURE 8-20 Local Adverse Reaction. Local edema
following application of a benzocaine topical.
and discontinuation of the agent. Localized edema follow­
ing an allergic reaction is shown in Figure 8-20•·
Systemic Reactions
Topicals are readily absorbed through oral and bronchial
mucosa but only weakly absorbed through GI mucosa.
Swallowing does not promote significant systemic uptake
(Malamed, 20 13).
Allergic reactions to ester topical agents are rare but
not impossible, whereas allergies to amide topicals have
been described as virtually unknown (Yagiela, 2005). Some
multiuse amide topicals, however, may contain methyl­
paraben. These preparations benefit from methylparaben's
antioxidant, bacteriostatic, and fungistatic properties, par­
ticularly in a container that is repeatedly opened and closed,
compared with sealed sterile cartridges, which are designed
to be used once and then discarded (Malamed, 20 13) .The
FDA ordered the removal of methylparabens from dental
cartridges in 1984, in response to increasing reports of al­
lergenicity and the absence of a continued need for their in­
clusion. The order did not affect topicals (Malamed, 20 13).
It is recommended that product information be consulted
for the possible inclusion of methylparaben.
Despite the very low risk of systemic allergic reaction,
systemic reactions are possible and have occurred. These
have typically been overdose reactions and have ranged
from subclinical to life-threatening. Overdoses may mani­
fest as mild CNS depression (restlessness, agitation, and
increased heart rate) or more severe CNS and CVS de­
pression (unconsciousness, convulsions, decreased force of
myocardial contraction, respiratory collapse, and cardio­
vascular collapse).
When systemic signs and symptoms occur because of
methemoglobinemia, they may manifest as lethargy, cya­
nosis, and respiratory difficulty (Malamed, 20 13). Adverse
methemoglobinemic events have occurred because of dif­
ficulties in determining applied doses, particularly in spray
forms. B enzocaine, for example, one of the most widely
used and certainly one of the safest topicals, has been
linked (in excessive volumes in spray form) to serious met­
hemoglobinemia (Abu-Laban et al. , 200 1 ) . The following
118 SECTI O N I PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•

excerpt appeared in the FDA Patient S afety News: Ad­

visory on B enzocaine Sprays and Methemoglobinemia
Show #50, April 2006:

The FDA recently issued a public health advisory to remind

health care professionals that the overuse of benzocaine
anesthetic sprays can cause methemoglobinemia, a poten­
tially life-threatening condition that can result in cyanosis,
confusion, hemodynamic instability and coma . . . . Patients
with methemoglobinemia can suffer effects ranging from
headache to cyanosis (turning blue due to lack of oxygen)
that can be life-threatening in the most severe cases.

The link to methemoglobinemia also applies to prilocaine in

(A)
both topical and inj ectable forms (MMWR, 1994). 1 t is im­
portant to point out that FDA warnings were prompted by
the results of excessive application related to the removal of
leg hair and before intubation (FDA, 1997). Nevertheless, the
potential exists for life-threatening adverse reactions follow­
ing the inappropriate and excessive use of spray topicals be­
fore exposing radiographs, for controlling gag reflexes, and for
widespread topical anesthesia in dental hygiene procedures.
In some circumstances, particular caution is advisable.
Underlying conditions that may predispose to methemo­
globinemia according to the April 2006 FDA Advisory
include : " . . . patients with bre athing problems, such as
asthma or emphysema, patients with he art disease, and
those who smoke. . . . "
A number of other medications, such as acetamino­ (B)
phen and sulfonamides, and some additives and dyes are
FIGURE 8-21 Pre-anesthesia "Jet" Injection A - Palatal
also linked to methemoglobinemia. Methemoglobinemia
pre-anesthesia administered with a Syrijet device. B - Facial
is discussed in depth in Chapter 5, "D ental Local Anes­
infiltration administered with an Injex Device.
thetic Drugs," Chapter 10, "Patient Assessment for Local
Anesthesia," and Chapter 17, "Local Anesthesia Complica­
tions and Management." 20 1 3 ) . They may also be used to provide deeper topical
anesthesia before needle penetration (see Figure 8 21 •) . -

Their greatest advantage appears t o arise from the ability to

Jet Injection Devices
Jet inj ection devices, which propel solution into tissues using
air, may be particularly useful in needle-phobic individuals
and children. Technically, they inject anesthetics, effecting
complete local anesthesia for some procedures (Malamed,
propel solutions into tissues at significant depth without the
use of needles, deep enough at times to provide pulpal anes­
thesia. According to a 200 1 evaluation of 100 children, the
degree of pulpal anesthesia provided was deemed "com­
pletely successful" and there was a statistically significant

CAS E MA N A G EME N T Case Discussion: Some patients are adamant regarding

Elena Gagarin
Adeq u ate topica l a n esthesia can desensitize the m ax­
i l l a ry p a l ata l tissues in a reas being treate d . S l ow i njec­
tion and expressing a few d rops of a n esthetic sol ution
a h e a d of t h e n e e d l e often works we l l , but E l e n a re­
q uested n o need les i n the p a l ate. Some topica ls such
as E M LA ca n p rovide g reater d e pths of p e n etrat i o n
co m p a red w i t h oth e r to p i c a l s a n d d o n ot u s u a l ly re­
q u i re i nj e cti o n s afterwa rd in o rd e r to p l a ce comfort­
a b l e rubber d a m c l a m ps .
not wanti ng to receive p a l ata l i njections. This attitude
often arises from painfu l injections in the palate d u ri n g
previous denta l visits. Placement o f topica l a h e a d o f i n ­
jection with enough t i m e t o diffuse through the su rface
layer, the a p p l ication of press u re in the a rea to fu rther
" pren u m b " the tissues, and very slow deposition rates
wi l l h e l p p revent fea r of p a i n fro m p a l ata l i njecti o n s .
W h e n these g u i d e l i nes have n o t b e e n observed i n t h e
past, i t is sometim es necessary t o re ly on topica l a n es­
thetics or i nterpa p i l l a ry i njections orig i n ating from the
b u cca l aspects of teeth i n order to desensitize p a l ata l
tissues.
 CHAPTER 8 TOPICAL ANESTHETICS
• 119

bias in favor of the use of a needleless jet syringe over con­

ventional syringes in children (Munshi, Hegde, & B ashir,
200 1 ) . Other authors have referred to these devices as inad­
equate substitutes for traditional needles and syringes and
as providing primarily topical anesthesia (Malamed, 20 13).
The impact of j et-propelled solutions, themselves,
is obj ected to by some and well tolerated by others
(Malamed, 20 13). There is often some local tissue damage
at the site of inj ection in the form of transient bruising, es­
pecially in the palate.
D e spite the costs of these devices, some will find
them invaluable in the treatment of children and in other
patients with greater dental anxieties, including needle
phobias.
Currently available devices include the Syrij et Mark
II Needleless Inj ector (Mizzy Division, Keystone Indus­
tries, Cherry Hill, NJ) , the MadaJet XL (MADA Medi­
cal Products Inc. , Carlstadt, NJ) and the Inj ex (INJEX
Pharma USA, Miami, FL) . These devices are further dis­
cussed in Chapter 9, "Local Anesthetic Delivery D evices."
FIGURE 8-22 Future Developments in Topical
Future Developments in Topical Local Anesthesia Anesthetics Refrigerants, similar to the cryo-anesthetics
Current research may result in a dental application of a ( "cold spray" ) used in medicine, are being explored for
refrigerant (similar to those used for pulp testing) to
provide fast-acting topical anesthesia (see Figure 8-22 •).
future applications in dentistry.

A study comparing the use of a refrigerant as a topi­
cal anesthetic versus more time-consuming gel topicals
found that pain was significantly reduced when the refrig­
erant was administered (Kosaraj u & Vendewalle, 2009) .
The refrigerant used was 1 , 1 , 1 ,3 ,3 -pentafluoropropane/
1 , 1 , 1 ,2-tetrafluoroethane ( G ebauer Comp any, 2 0 0 9 ) .
In arriving at that favorable comp aris on, only a 5 - to
1 0-second application of the refrigerant was necessary.
Additional clinical trials are needed to verify the previ­
ously described dental application method.
Medical uses of refrigerants as topicals on skin have
demonstrated similar results in immunizations compared
with patch preparations. Adverse inflammatory reactions
on skin, which can apparently alter pigmentation patterns
under exposed areas, were described as not having been
identified specifically for mucosa. The manufacturer indi­
cates that the product should not be used on diabetics or
those with poor circulation or on any skin with a sensitivity
deficit. In addition, cautions include the possible develop­
ment of postoperative discomfort, irritation, and frostbite .

.�.h. �.P..�.� �. 9.l1.� ��.i.�.� � ........................................... .
1 . Eutectic mixtures have which of the following
characteristics?
a. They work more rapidly than most other topicals.
b. They penetrate more deeply on skin than mucosa.
c. Their melting points exceed that of their ingredi­
ents acting alone.
d. Their formulations facilitate deeper and more ef­
ficient penetrations of tissues compared with their
ingredients acting alone.
2. Which of the following lists is most accurate when
describing topical anesthetic uses?
a. B efore exposing radiographs, before inj e ctions,
before placing retraction cord
b. B efore dental hygiene therapy and in subgingival
tissues
c. In procedures confined to mucosa and before tak­
ing impressions
d. All of the above
3. Which one of the following statements is incorrect
regarding maximum recommended doses of topical
anesthetics?
a. They are sometimes difficult to track.
b. MRDs are not always provided.
c. Spray forms have easy-to-track dosing.
d. Oraqix has easy-to-track dosing.
4. Generous quantities of topical and inj ected anesthe­
sia have been administered, when the patient begins
to shake and appears agitated and anxious. Is there a
reason for concern?
a. Y e s , b e cause these may be e arly signs of CNS
depression.
b. No, because this is a very nervous patient and he or
she hates dental appointments.
c. No, because the doses of inj ectable anesthetic were
within safe guidelines.
d. Yes, because the patient is a dental phobic.
120 SECTI O N I PHARMACOLOGY OF LOCAL ANESTHETIC PAIN CONTROL
•
5. Topical anesthetic mixtures may be of benefit in all
but which one of the following ways?
a. Combinations may increase therapeutic ranges.
b. Combinations may increase penetration depths.
c. Mixtures may allow drugs to be used as topicals
that are not suitable when used alone.
d. Mixtures decrease the potential for adverse reaction.
6. All of the following statements are true regarding
compounded drugs, except:
a. Compounded drugs are formulated for individuals
for whom they are prescribed.
b. Compounded drugs may be used on other individu­
als as long as the use is the same as the original use.
c. Compounded drugs may contain much larger quan­
tities of drug compared with multiuse commercial
preparations.
d. Compounded topicals are dispensed by prescription.
7. The predominantly base form of lidocaine topical
anesthetic is safer than the predominantly hydrochlo­
ride salt.
a. True b. False
8. Dyclonine hydrochloride is an excellent and very du­
rable topical anesthetic and belongs to which one of
the following classes of anesthetic?
a. Amide c. Ester
b. Ketone d. None of the above
References
Abu-Laban, R. B . , Zed, P. J. , Purssell, R. A., & Evans, K. G . (200 1 ,
January). Severe methemoglobinemia from topical anesthetic
spray: Case report, discussion and qualitative systematic
review. Canadian Journal of Emergency Medicine, 3(1), 5 1-56.
ADA/PDR guide to dental therapeutics (5th ed.). (2009) .
Montvale, NJ: Thompson PDR.
Alston, T. A. (1992). Antagonism of sulfonamides by benzocaine
and chloroprocaine. Anesthesiology, 76, 375--476.
AstraZeneca. (20 10, May Rev. ) . EMLA. AstraZeneca, prescrip­
tion information. Mississauga, Canada: Author. Retrieved
January 25, 2014, from www.astrazeneca.ca
B ernardi, M., Secco, F. , & Benech, A. (1999) . Anesthetic efficacy
of a eutectic mixture of lidocaine and prilocaine (EMLA)
on the oral mucosa: Prospective double-blind study with a
placebo. Minerva Stomatal, 48, 9--43 .
Beutlich LP Pharmaceuticals. Hurricane topical 20% benzocaine
oral anesthetic spray. (HSDF 458-0 109), Beutlich LP Pharma­
ceuticals Product information. Beutlich LP, Pharmaceuticals,
Waukegan, IL; www.beutlich.com/documents/hurricaine/
hurricaine_spray_drug__facts.pdf.com. Accessed April 12, 2014.
CAO Group. (20 10, June Rev.). BeeGentle. CAO Group, prescrip­
tion information. West Jordan, UT: Author. Retrieved January
25, 2014, from http://www.caogroup.com.
Visit www.p earsonhighered.com/he �lthprofessionsresources to access the student resources that accompany
. .
thts b�ok. Stmply select D ental Hygiene from the choice of disciplines. Find this book and you will find the
comphmentary study tools created for this specific title.
Centers for Disease Control and Prevention (CDC). (1994,
September 9). Prilocaine-induced methemoglobinemia­
Wisconsin, 1993. MMWR (Morbidity and Mortality Weekly
Repor0, 43(35), 655-657.
Cetylite Inc. Cetacaine topical. Cetylite Inc .. Prescribing infor­
mation. Cetylite Inc. , Pennsauken, NJ www.cetacaine.com/
dental/about/prescribing-information. Accessed April 12, 2014.
FDA Modernization Act of 1997. Accessed January 25,
2014, http://www.fda.gov/Regulatoryinformation
/Legislation/FederalFoodDrugandCosmeticActFDCAct
/SignificantAmendmentstotheFD CAct/FDAMA
FDA Patient Safety News. (2006). Advisory on benzocaine sprays
and methemoglobinemia: Show #50. Accessed http://www.
accessdata.fda.gov/scripts/cdrh/cfdocs/psn/printer.cfm?id=4.
Gebauer Company. (2009). Gebauer's Pain Ease, topical aerosol
skin refrigerant. Retrieved January 25, 2014, from Techni-
cal data document: www.gebauerco.com/Contentpages/
ResourceCenter/PDFs/TechSheets/PETS_ENGPdf
MMWR (Morbidity and Mortality Weekly Report) Centers for
Disease Control and Prevention (CDC), Prilocaine-induced
methemoglobinemia - Wisconsin, 1993: September 09, 1994,
43(35) ; 655-7.
PDR Network, LLC. PDR, prescription information.
Montvale, NJ: Author. Retrieved January 25, 2014,
from www.pdr.net/drug-summary/hurricaine-topical­
anesthetic-spray?druglabelid=2182
Jastak, J. T. , Yagiela, J. A., & Donaldson, D. (1995). Local
anesthesia of the oral cavity. Philadelphia: Saunders.
Kosaraju, A., & Vendewalle, K. S. (2009). A comparison of a
refrigerant and a topical anesthetic gel as preinjection anesthetics.
Journal of the American Dental Association, 140, 68--72.
Malamed, S. F. (20 13). Handbook of local anesthesia (6th ed.).
St. Louis: Elsevier Mosby.
Mehra, P., Caiazzo, A., & Maloney, P. (1998). Lidocaine toxicity. Jour­
nal of the American Dental Society of Anesthesia, 45(1), 38--41.
Munshi, A. K., Hegde, A., & Bashir, N. (200 1 ) . Clinical
evaluation of the efficacy of anesthesia and patient preference
using the needle-less jet syringe in pediatric dental practice.
Journal of Clinical Pediatric Dentistry, 25, 131-136.
Munshi, A. K., Hegde, A. M., & Latha, R. (20 0 1 ) . Use of EMLA:
Is it an inj ection free alternative. Journal of Clinical Pediatric
Dentistry, 25, 215-219.
Oraqix (lidocaine and prilocaine periodontal gel) , (Rev.
09/10), DENTSPLY Prescription information available
from DENTSPLY Pharmaceutical, USA, York, PA; www.
dentsplypharma.com. Accessed January 25, 2014.
Patel, D., Chopra, S., & B erman, M . D. (1989). Serious sys­
temic toxicity resulting from use of tetracaine in upper
endoscopic procedures. Digestive Diseases and Sciences,
34(6), 882-884.
Tetzlaff, J. E. (2000). Clinical pharmacology of local anesthetics
(1st ed.). Woburn, MA: Butterworth Heinemann.
Wynn, R. L. (20 12-20 13). Drug information handbook for
dentistry (18th ed.). Hudson, OH: Lexicomp.
Yagiela, J. A. (2005, May). Safely easing the pain for your
patients. Dimensions, 3(5), 20-22.
Benzocaine-Drug Facts

Proprietary Name Benzocaine

Formulations/Durations of Action Topical: 6% to 20 % formulations

Duration: 5- to 15-minute duration

MRD Not available

Relative potency One-half lidocaine

Relative toxicity Very low

Metabolism Cholinesterase

Excretion Kidneys

Vasoactivity Strong vasodilator

Onset of action 30 seconds to 1 minute

Half-life Not established

Topical preparation Gel and combinations

Pregnancy category c

Lactation Enters breast milk ( use caution )

12 1
Dyclonine-Drug Facts

Proprietary Name Dyclonine

Formulations/Durations of Action Topical: 1 % formulations

Duration: 30- to 60-minute duration

MRD 200 mg or 20 mL of a 1 % solution

Relative potency Not available

Relative toxicity Very low

Metabolism NA ( nonamide, non-ester-ketone linkage )

Excretion Kidneys

Vasoactivity Not available

Onset of action From 2 to 10 minutes

Half-life Not available

Topical preparation Dyclonine is a formulated topical anesthetic

Pregnancy category c

Lactation Enters breast milk ( use caution )

122
Lidocaine-Drug Facts

Proprietary Name Lidocaine

Formulations/Durations of Action Topical: 2% to 5% formulations

Duration: 15 minutes

MRD Refer to individual production insert

Relative potency Similar to prilocaine and benzocaine

Much less than tetracaine

Relative toxicity Greater than prilocaine and benzocaine

Much less than tetracaine

Metabolism Liver

Excretion Kidneys

Vasoactivity Vasodilator

Onset of action 1-2 minutes

Half-life 96 minutes

Topical preparation Gels, ointments, patches, combinations

Pregnancy category B

Lactation Enters breast milk ( use caution )

12 3
Tetracaine-Drug Facts

Proprietary Name Tetracaine

Formulations/Durations of Action Topical mixtures:

2 % tetracaine HCL; 14% benzocaine; 2 % butamben
Duration: Long-lasting 20--60 minutes
Intranasal*: 3% tetracaine, 0.05 % oxymetazoline
(HCL Kovacaine Mist - in development)

MRD (Tetracaine, butamben, benzocaine mixture) 400 mg (combination)

0.4 mL (of the mixture/concentrations described above)
(Not Available for Kovacaine Mist*)

Relative potency 4 X lidocaine

Relative toxicity Much greater than lidocaine (CNS)

2X lidocaine (CVS)

Metabolism Cholinesterase

Excretion Kidneys

Vasoactivity Not available

Onset of action 30 seconds

Half-life Not established

Topical preparation Tetracaine, benzocaine, butamben combination

Pregnancy category c

Lactation Enters breast milk (use caution)

* Kovacaine Mist (intranasal delivery local anesthetic) in FDA Phase III clinical trials (2013)

124
Butamben-Drug Facts

Proprietary Name Butamben (butyl-4-aminobenzoate)

Formulations/Durations of Action Topical (found only in mixtures):

2% butamben; 14% benzocaine; 2 % tetracaine
Duration: 30-60 minutes (combination)

MRD Not available

Relative potency Not available

Relative toxicity Not available

Metabolism Cholinesterase

Excretion Kidneys

Vasoactivity Not described

Onset of action 30 seconds

Half-life Not available

Topical preparation Tetracaine, benzocaine, butamben combination

Pregnancy category c

Lactation Enters breast milk (use caution)

12 5
This page intentionally left blank
C h a pter 9 Loca l An est h et i c D e l ivery Devi ces

C h a pter 1 0 Pati e n t Assess m e n t for Loca l A n est h e s i a

Chapter 1 1 F u n d a m e nta ls fo r Ad m i n istration o f Loca l Anesthetic Agents

··························································· ® ··························································

Local Anesthetic Delivery Devices

OBJECTIVES KEY TERMS

• Define and discuss the key terms in this chapter. armamentarium 129
bevel 136
• List and explain the purpose of each item in the basic
breech-loading 130
armamentarium for anesthetic injections.
carpule 140
• List and discuss the different types of syringes available for cartridge 140
local anesthetic injections. cartridge-type syringe 130
computer-controlled
• Identify and explain the function of each component of a local
local anesthetic delivery
anesthetic syringe.
(CCLAD) 147
• Identify the components of a needle. devices 129
• Discuss the factors to consider when selecting needles. diaphragm 140
end cap 140
• Describe the components of a local anesthetic cartridge.
Engineering Controls
• List and describe the purpose of the contents in a cartridge. (EC) 138
• Identify local anesthesia cartridges according to the American finger grip 7 32
Dental Association (ADA) color code system. gauge 135
harpoon 134
Discuss and demonstrate safe needle recapping and disposal
harpoon-type aspirating
p dures.
syringe 130

128
 CHAPTER 9 LOCAL ANESTHETI C DELI V ERY DEVICES
• 129

KEY TERMS (contin ued)

h u b 7 36 self-aspirati ng syri nge 7 30

i ntravasc u l a r a d m i n istration 7 30 sh aft 7 36
jet i njection 7 50 s h a n k 7 36
l u m en 7 36 sto pper 7 40
medical devices 7 2 9 syri n g e 7 30
needle a d a ptor 7 34 syri nge a d a ptor 7 36
needle caps 7 38 syri nge ba rre l 7 3 7
needles 7 35 th u m b ring 7 33
penetrating e n d 7 36 w i n d ow 7 3 7
piston 7 33 Wo rk- Practice Co ntro ls (WPC) 138
scoop tech n i q u e 7 38

Armamenta ri u m for Denta l

CAS E S TUDY
Elena Gagarin
W h e n t h e c l i n i c i a n a p p ro a c h e d t h e o p e ra t o r's
c h a i r, t h e patient h a d a l re a d y b e e n seated a n d a
cotto n -ti p p e d a p p l icator with to p i c a l a n est h et i c
w a s p rotrud i n g fro m h e r m o uth . The assista nt h a d
pre loaded the syri nge w i t h 2% l idoca i n e , 1 : 1 00,000
e p i n e p h r i n e before leavi n g . She had a lso displ ayed
the res u lts of the m ost recent hea lth h isto ry on the
m o n itor to s h ow that t h e re were n o contra i n d ica­
t i o n s to l id o ca i n e o r e p i n e p h r i n e and that t h e p a ­
t i e n t h a d rece ived both d ru g s p revi o u s l y w i t h n o
adverse reactions.
Aft e r re m ov i n g the cotto n -t i p p e d a p p l i c a ­
t o r a n d r i n s i n g t h e p a t i e nt's m o ut h , t h e c l i n i c i a n
p ressed l i g htly o n t h e tissues u n d e r t h e a p p l i cator
to test fo r s e n s itivity. T h e patient res p o n d e d that
she d i d n 't fee l a t h i n g . The need l e was posit i o n e d
ove r t h e p e n etrati o n site a n d was a d v a n ce d b e ­
n e at h t h e m u co s a w i t h o u t p a i n , c o n ti n u i n g t h e
p e n et r a t i o n u n t i l t h e t a r g e t a re a w a s re a c h e d .
The c l i n ician p u l l ed b a c k s l i g htly o n the th u m b
r i n g t o create n e g ative p ress u re i n t h e c a rtri d g e
i n o r d e r to a s p i rate. N o s i g n s o f b l o o d a p p e a red
in the ca rtri d g e and the c l i n i c i a n d e p ressed t h e
t h u m b r i n g to d e p o s i t s o l u t i o n b u t n ot i c e d t h a t
t h e p l u n g e r d i d not m ove, n o m atte r h o w h a rd i t
w a s p u s h e d . The syri n g e w a s withd rawn fro m t h e
mouth.
Loca l Anesthesia
After determining which procedures will be performed,
the inj ection techniques and devices that will best meet
the anesthetic requirements of the procedures can be se­
lected . The term devices specifically refers to medical
devices in accordance with the Federal Food, Drug, and
Cosmetic (FD &C) Act, section 20 1 (h). (See Box 9-1 •.)
These include syringes, cartridges, needles, and recapping
and disposal items (National Institute for Occupational
Safety and Health, 2002) . The term armamentarium re­
fers to all equipment, materials, devices, and methods used
during the delivery of local anesthetic agents. For histori­
cal perspective on the armamentarium use for dental local
anesthesia, see Box 9-2 •·
The Federa l Food, Drug, a n d Cosmetic (FD&C) Act defi nes
a device as " . . . a n instru m e nt, apparatus, i m p l e m e nt,
m a ch i n e, contriva n ce, i m p l a nt, in vitro reagent, or oth er
similar or re lated a rticle, including any component, part or
accessory, which is i ntended for use i n the d i a g n osis of d is­
ease o r other con d itions, or in the cure, m itigation, treat­
ment, or p revention of d isease, in m a n or other a n i m a ls, or
intended to affect the structu re of a ny function of the body
and which does not achieve its primary intended pu rpose
thro u g h chemical a cti on and which is not dependent upon
being m eta bol ized for the achievem ent of its p ri m a ry i n ­
tended pu rposes. "

Source:�Secti o n 201 (h) of the Federal Food, Drug, and Cosmetic Act
a t d
•

I ntrod uction : . : � :� :::� � � ; �� • • • • • • • • • • • . • • • . • • • • • • • • • .

This chapter discusses devices required for the delivery
of local anesthetic agents. A thorough knowledge of these
devices is necessary for appropriate selection and use.
Practices for safe handling and disposal of the devices will
also be discussed.
Basic armamentarium appropriate for dental local an­
esthetic injections includes (see Figure 9-3 •):
1. mouth mirror (may also include a cheek retractor)
2. devices for safe needle recapping and disposal
130 SECTI O N Il l I N JECTI O N FUNDAMENTALS
•

3. syringe devices Dental Local Anesthetic Syringes

4. cotton pliers or hemostat A local anesthetic syringe is a device for inj ecting anes­
5. gauze squares for drying tissues and enhancing thetic agents submucosally or subcutaneously. Standard
syringes are metallic or plastic piston pump devices into
which disposable glass cylinders ( cartridges ) of anesthetic
retraction
6. cotton swabs for application of topical anesthetic agents
solution are inserted. After attaching a needle to the sy­
and predetermination of penetration sites and angles
ringe and activating gentle pressure on a plunger, the de­
7. needles of appropriate gauge and length vice is used to administer local anesthetics.
8. cartridges of drugs S everal different typ e s of syring e s are available
9. topical anesthetic agents in dentistry, including those that are sterilizable stain­
l e s s s t e e l or plastic, disp o s able plastic, manual and
Syringes, cartridges, n e e dles, and recapping and
disposal devices and their variations will be discussed in
the following sections.

FIGURE 9-1 Local Anesthetic Syringe and Needle Set, FIGURE 9-2 Local Anesthetic Syringe, circa
circa late nineteenth century. mid-1 930s.
Source: Used with permission. The Dr. Samuel D. Harris, Na­ Source: Used with permission. The Dr. Samuel D. Harris,
tional Museum of Dentistry, University of Maryland. National Museum of Dentistry, University of Maryland.

I n a d d ition to the local a n esthetic drugs themse lves, Because of reports of hepatitis transm ission through
t h e i r m ethod of d e l ive ry has a lso u n d e rg o n e exte nsive contaminated need les, d isposable, sta inless steel need les
i m p rove ment over the years. The deve l o p m e n t of hypo- were introduced in 1 959, which effectively e l i m inated the
derm i c syr i n g es i n the 1 8 50s s i m p l ified the d e l ivery of need for the steril ization and reuse of need les (J asta k,
coca i n e a n d oth e r d r u g s o l utions (J asta k & Ya g i e l a , 1 98 1 ) . Yagiela, & Donaldson, 1 995). T h e self-aspirating syringe was
D u r i n g Wo rld Wa r I, Dr. H a rvey Cook, who was an a rmy developed to provide an easy way of determ ining whether or
surgeon, developed a breech-load i n g , cartridge-type not the tips of needles a re located with in blood vessels.
syri n g e that functi o n e d s i m i l a rly to a breech - l o a d i n g rifle Computer-contro l l e d local a n esthetic d e l ivery
(see Fi g u re 9-1 •) . Replacing more cumbersome early de- (CCLAD) devices were i ntroduced i n 1 997 . The fi rst of
signs (see Figure 9-2 •), this syr i n g e h e l d a g l ass cartri d g e these, the Wa n d (M i l esto ne Scie ntific, N J ) , w a s fo l l owed
conta i n i n g a local a n esthetic d r u g . B oth the syr i n g e a n d b y t h e CompuDent®, a n d has n o w b e e n rep l a ced b y the
cartrid g e were i ntro d u ced i n 1 92 1 by D r. Cook' s n ewly Wa nd STA Single Tooth Anesthesia System® Instru ment,
formed co m p a ny, Cook La b o ratories. which has a u n i q u e pressu re sensing tech no logy known as
In 1 947, the N ovocol C o m p a n y deve l o p e d the fi rst Di rect Pressu re Sensi ng (DPS).
asp i rati n g syri n g e , which red u ced the risk of i njecti o n Anoth er CCLAD device i n u s e in N o rth America, how-
i nto b l o o d vessels, known as i ntravascu lar admin istra- ever no longer m a rketed, is the Comfort Co ntro l Syringe
t i o n . Un l i ke the syri n g es used tod ay, it made use of a (Dentsply I nternational, PA). Internatio n a l ly the Quick-
screw-based tech n o l ogy for secu ri n g cartri dges. The Sleeper (Denta l H i Tech, Fra n ce), Anaeject (J M o rita, N a -
harpoon-type aspirat i n g syri n g e i n cu rrent use was de- s h i ka Line, J a p a n), and Calaject (R0NVIG Denta l Mfg. A/S.
veloped by Cook-Wa ite Labo rato ries i n 1 9 57 (ori g i n a l ly Denma rk) a re m a rketed . CCLAD devices ava i l a b l e i n N o rth
Cook La b o rato ries). Today, p ro d u cts a re s o l d u n d e r the America a re d iscussed i n deta i l later i n this chapter a n d
•
Coo k-Wa ite l a b e l as p a rt of Ca restre a m H e a lth I n c . , i n Appendix 9-5, "Comp uter-Contro l l e d Local Anesthetic •

oda Den a l s t lv r ·'

: � �
. • • · · · � . . :� ��� .• • • • • • • • • • • • • • • • • • • • • • • • • • • • • �� � � : : • • • • • • • • . • • • . . • • • • • • • • • . • . • • • • • • •

FIGURE 9-3 Inj ection Armamentarium. A - cheek retractor or B - mouth mirror, C - safe needle recapping device,
D - syringe, E - cotton pliers or F - hemostat, G - gauze squares, H - cotton swabs, ! - needle, J - anesthetic cartridge,
and K- topical anesthetic.
self-aspirating, ratcheted for delivering small doses under
pressure, needleless, and computer-controlled. Figure 9-4 •
provides examples. Most types have one or more designs
available. Preference and availability will usually determine
which type is selected.
The most common design in dentistry is the steriliz­
able, breech-loading, cartridge-type, aspirating syringe
because inadvertent intravascular inj ection is a primary
hazard of local anesthetic inj ections. This syringe has
easy-to-master aspirating capabilities to allow testing and
visual inspection before drugs are administered.
Anatomy of a Dental Syringe
Syringes for dental local anesthesia consist of a syringe
barrel, finger grip portion (with spring and guide bearing) ,
sliding piston with thumb ring and harpoon, and needle
adaptor. Figure 9-5 • shows a disassembled syringe and its
individual components. The function of each component is
discussed next.
Syringes have traditionally come in two standard de­
signs and sizes (see Figure 9-6 •). Those with winged thumb
rests are somewhat longer than wingless "petite" designs.
Several variations in size are now available to accommodate
CHAPTER 9 LOCAL ANESTHETI C DELI V ERY DEVICES
• 131
small to large hand sizes (Figures 9-7 • and 9-8 •). Syringes
distributed in North America accommodate standard
1.8-mL cartridges.
Although manual aspiration syringes are more com­
mon, some clinicians prefer self-aspirating hybrids, which
differ from manual syringes in that they do not have har­
poons and they do not require thumb movements in a
direction away from deposition sites in order to aspirate
(see Figure 9-9A •). When using self-aspirating syringes,
all accompanying instructions must be followed for proper
aspiration testing (see Box 9-3 •) . An extra step is fre­
quently required in order to initiate aspiration before in­
j ection (see Figure 9-9B•) .
The syringe barrel (Figure 9-SG) i s designed t o hold
glass cartridges of local anesthetic solutions. The most
common style has a large side opening allowing breech­
loading of cartridges into syringe barrels. This large side
opening (window) also provides for direct visibility of
cartridges throughout inj ections. Although less common,
some syringes load from the end of the barrel. The finger
rest portion articulates open to provide entry into the end
of the barrel. Figure 9-10 • shows examples of breech­
loading and articulating devices.
132 SECTI O N Il l I N JECTI O N FUNDAMENTALS
•

FIGURE 9-4 Various Dental Local Anesthetic Syringes. Syringes are selected based
on technique and clinician preference. They include a number of manual and computer­
controlled devices.

FIGURE 9-5 The Anatomy of a Syringe. Syringe components are identified as follows:
A - thumb ring, B - finger grip, C - spring, D - guide bearing, E - piston with attached
F - harpoon, G - syringe barrel, and H - needle adaptor.

The finger grip (Figure 9-S B ) component encircles on the finger grip to balance and control movements of
the diameter of the syringe barrel and the piston passes the syringe. There are two basic styles of finger rests,
through the middle of the finger grip. During use, clini­ winged and wingless. See Figure 9-6 for examples of
cians hold the syringe with the index and middle fingers winged and wingless finger rests. The spring (Figure 9-S C)

FIGURE 9-6 Commonly Used Syringes. These
examples are breech-loading, manual aspiration,
cartridge-type devices. The syringe on the left is a
"wingless" design and the one on the right is "winged. "
FIGURE 9-7 Syringe Size and D esign. Syringes vary in
size and design; clinician preference may be based on
hand size.
and guide be aring ( Figure 9-S D ) slide into the finger
grip when the syringe is loaded, which provides tension
on the cartridge. At least one syringe is now available
with a silicone-coated finger grip and thumb ring, which
may improve grip and stability during aspiration ( s e e
Figure 9-1 1 •).
A thumb ring ( Figure 9-SA) is attached to the ex­
ternal end of the piston. Clinicians place their thumbs
in the ring to advance or retract pistons. Traditionally,
thumb ring components have been available in one stan­
dard size and shape, which has been problematic for cli­
nicians with small hands. Current syringes are available
CHAPTER 9 LOCAL ANESTHETI C DELI V ERY DEVICES
• 133
FIGURE 9-8 Small, Medium, and Large Syringes. Septodont
USA has redesigned their syringes to accommodate small,
medium, and large hands. Note the graduated sizes of the
thumb ring.
Source: Courtesy of Septodont, U S A.
Syri nges designed to self-aspi rate do not h ave h a rpoons
on their pistons because negative pressu re is not depen­
dent on m a n u a l " p u l l-back" motions o n stoppers. These
syri nges h ave a "th u m b d isk" on the piston above the
• fi nger grip. Befo re i n itial i njection, c l i n icians press a g a i nst
the t h u m b disk to activate the aspiration test (Fi g u re 9-9B).
N e g ative press u re is created by the el astic recoi l of the car­
tridge d i a p h ragm when the cartridge is pushed a g a i nst the
hub i n the base of the syri nge. D u ri n g the i njection, aspira­
tion is acco m p l ished by gently applying brief pressure on
the piston a n d re leasi n g . I n this situ ation, aspiration occu rs
when the clinician re l eases the pressu re on the stopper
•
(Aspiject™; Astra P h a rm a ceutical Pro d u cts, Inc., R0NVIG •
n � f S n ar )
: � � �� �
. � :� . :�
a
��
� ���� : · . � .� . � : • • • • • • • •• • • • •
in a variety of thumb ring designs in order to provide
for ease of aspiration for all hand sizes. Oval designs re­
quire shorter distances to engage the inside of the thumb
ring for aspiration. For a comparison of round and oval
thumb rings see Figure 9-12 •· Other syringes have
smaller thumb rings. As noted previously, some newer
designs have a textured silicone coating to enhance grip
( see Figure 9-1 1 ) . Figures 9-6 through 9-12 display a
number of syringe options.
The piston ( Figure 9-SE) passes through the finger
grip complex and is attached on one end to the finger ring
and on the other end to the harpoon tip. B efore loading
134 SECTI O N Il l I N JECTI O N FUNDAMENTALS
•
(A)
FIGURE 9-9 Self-Aspirating Syringes. A- Self-aspirating syringes do not have
harpoons to seat into stoppers. B- Some designs require an additional step. The
thumb disks must be pressed in order to activate aspiration before injection.
FIGURE 9-10 Breech-loading Syringe. Top - An
example of a breech-loading device (most commonly
used today) ; B ottom - An example of an articulating
device. Note the hinge j oint just below the finger grip,
the lack of a thumb ring and lack of a harpoon.
FIGURE 9-11 Silicone-Coated Finger Grip and Thumb
Ring Designs. Silicone coatings (top view) may reduce
"slipping" during aspiration procedures and are avail­
able on both standard and petite syringes.
(B)
syringes, pull-back movements of the piston create tension
on the spring, retracting the bearing guide to allow inser­
tion of cartridges into syringes.
Advancing the piston engages the harpoon in the
cartridge stopper to deposit solution and facilitate aspi­
ration tests. The steps for aspiration tests are discussed in
Chapter 1 1 , "Fundamentals for Administration of Local
Anesthetic Agents."
With smaller (petite) syringe designs, the pistons may
be shortened to accommodate shorter distances needed to
activate aspiration tests. It is important to note that it may
be impossible to expel the entire contents of a 1.8-mL car­
tridge when pistons are shortened.
The harpoon (Figure 9-SF) is the part of the piston
inside the barrel that penetrates the stopper. Embedding
harpoons into cartridge stoppers allows for retraction of
stoppers to create a slight negative pressure inside the car­
tridge during aspiration tests. Harpoons are very sharp and
can cause injury if syringes are mishandled.
S e lf-aspirating syri n g e s do n o t have h a rp o o n s ;
therefore, other methods are implemented to cre­
ate n e g ative p r e s s u r e s r e q u i r e d f o r aspiration tests.
B o x 9-3 • explains how self- aspirating syringes create
this pressure. Figure 9-1 0 shows syringes with and with­
out harpoons.
The needle adaptor (Figure 9-SH) is the threaded
surface at the end of the barrel onto which needles are
attached. This component is sometimes referred to as
the hub or tip of the syringe. The needle adaptor may be
permanently attached or replaceable. For adaptors that
can be unscrewed, care should be taken to avoid inadver­
tent removal and disposal of the needle adaptor when the
needle is removed from the syringe.
Syringes should be inspected regularly to assure
proper function of each component of the device.
 CHAPTER 9 LOCAL ANESTHETI C DELI V ERY DEVICES
• 135

FIGURE 9-12 Thumb Rings Designs. A - An example of

round thumb rings; B - An example of oval thumb rings. Note
the distance from the piston to the upper inside surface of the
ring.
Dental Local Anesthetic Needles
Needles u s e d for dental local anesthesia are slender
hollow, sterile stainless steel devices with sharp p oint�
intended to be attached to a syringe to inj ect local an­
esthetic solutions. All needles are disposable, single­
patient devices. Needles are identified by their lengths
and by their diameters, also referred to as their gauge,
and are selected based on the inj ection techniques to be
used. Removable plastic needle caps protect the needle
from contamination before and after use. Needle caps
are color-coded for ease of identification of lengths and
gauges, although there is no standard for this (see Fig­
ure 9-1 3 •) . Although the needle cap has an important
role in protection from n e e dlestick inj uries, it should
FIGURE 9-13 Dental Local Anesthetic Needles.
Needles from various manufacturers have colored caps
that designate needle length. There is no uniform color­
coding system for needles.
not be considered the primary safety device for needle­
stick protecti o n . If n e e d l e s are m i s h a n d l e d or b e n t
their caps c a n easily be pierced as demonstrated in Fig�
ure 9-14 •· Careful attention to needle handling and re­
capping is required . Whenever needles are unsheathed,
n e e dl e s tick p r e v e n t i o n p r o t o c o l s should remain in
effect.
Anatomy of a Local Anesthetic Needle
Needles for dental local anesthesia consist of a shaft (with
beveled tip and cartridge penetrating end) , a syringe adap­
tor, and a "hub."

(A) (B)
FIGURE 9-14 Needle Puncture Risks. Needle caps alone cannot prevent needlestick injuries.
Close attention to needle use guidelines and Work-Practice Controls must be observed. In this
example, a bent needle was not adequately resheathed and the needle tip penetrated the cap.
Source: Courtesy of Albert "Ace" Goerig DDS, MS.
13 6 SECTI O N I N JECTI O N FUNDAMENTALS
Ill •
Each needle has a flexible, hollow, stainless steel shaft.
This one-piece shaft, also referred to as a shank, extends
from the tip of the needle through the syringe adaptor
and hub, to what is known as the cartridge penetrating
end (Figure 9-15 •). The hollow portion of the needle is
referred to as its lumen, which runs through the entire
length of the shaft. The diameter of the lumen determines
the gauge of the needle. Smaller gauges are identified by
larger numbers and larger gauges by smaller numbers.
Needle gauges will be discussed in more detail later. Some
needles are coated with silicone to aid insertion through
tissues.
The bevel is the diagonal cut that makes the point
of a needle (Figure 9-15B ) . It is designed to facilitate
atraumatic penetration through mucosal and cutaneous
tissues.
The cartridge penetrating end of the needle shaft op­
posite the bevel end pierces through the center of the dia­
phragm of the local anesthetic cartridge (Figure 9-15C).
The syringe adaptor of the needle is the plastic or
aluminum hub through which the nee dle shaft passes
(Figures 9-15D and 9-16 •) . Hubs are either self-thread­
ing or prethreaded (see Figure 9-16) and attach the nee­
dle to the syringe. Self-threading adaptors must be pushed
D- -E
FIGURE 9-15 Anatomy of a Needle. Needle components
are identified as follows: A - needle shaft with beveled tip B
and cartridge penetrating end C, D - syringe adaptor, and
E - "hub," F - needle cap.
FIGURE 9-16 Needle Hub Variations. Needle hubs
are either metal or plastic, and either prethreaded or
self-threading.
and turned onto syringes to seat the needle. Once seated,
these plastic adaptors can be adjusted slightly to reorient
bevel directions when desired. Most prethreaded adap­
tors anchor in one position only, locking bevels in one
orientation.
Some syringe adaptors have an indicator mark that al­
lows for easy identification of the orientation of the needle
bevel. Examples of bevel indicators are shown in Figures
9-17A • and 9-17B •·
The hub of a needle is the point at which the shaft
j oins and s e cures the n e e d l e to the syringe adaptor
(Figure 9-15E) . Clinicians commonly refer to the entire
syringe adaptor/hub complex as "the hub."
A
8
c
(A)
t
(B)
FIGURE 9-17 A - Needle Attachment and Bevel Indicators.
To attach the needle: A- the cartridge penetrating end is
inserted through the cartridge diaphragm; B- the needle is
screwed onto the syringe with firm pressure; C- once seated,
check the bevel orientation. Some needles have dots, arrows, or
other markings on their hubs D that correspond to the locations
of the bevel lumens or openings E. B - B evel Indicators. When
checking bevel orientations, keep needle tips shielded by caps to
prevent needle stick injury.
Source: (A) Modified courtesy of Dentsply Pharmaceutical.
 CHAPTER 9 LOCAL ANESTHETI C DELI V ERY DEVICES
• 13 7

Common Needle Lengths in Dentistry

The length of needle is selected based on the depth of pene­
tration necessary to achieve successful anesthesia. Local anes­
thetic needles in dentistry are usually identified as long, short,
and extra-short. Although needle lengths vary slightly among
manufacturers, typical lengths (shown in Figure 9-18 •) are:
1. long needles average -32 mm (1llz inches)
2. short needles average -25 mm (1 inch)
3. extra-short needles average - 12 mm (liz inch)
FIGURE 9-19 Needle Gauge Indicators. A common
Short needles are frequently used for inj ections that
do not require significant depths of penetration, such as system for indicating gauge size is: Red caps = 25-gauge
infiltrations and maxillary block techniques. Long needles needles, Yellow caps = 27-gauge needles, and Blue caps =
are used when deposition sites are at greater distances 30-gauge needles.
from penetration sites, such as mandibular block tech­ Source: Courtesy of Dentsply Pharmaceutical.

niques. Extra-short needles can be used when penetrations

are shallow such as in palatal inj ections.
Regardless of the injection technique used, clinicians are
cautioned to avoid inserting needles to their hubs. Needle
breakage, although rare, is more likely to occur at the hub
when excessive lateral pressure is exerted against hub/shaft
interfaces (Brunton, Lazo, & Parker, 2006) . For this reason,
changing the direction of a needle when deeply embedded
within tissue is not recommended. The best practice when a
needle must be redirected is to withdraw at least half the in­
serted length before establishing a new pathway (Malamed,
2004) . Needle breakage is further discussed in Chapter 17,
"Local Anesthesia Complications and Management."
Common Needle Gauges in Dentistry
Needles in dentistry are available in 25, 27, and 30 gauge
sizes (see Figure 9-19 •). Selection of the gauge to be used
is based on the depth of penetration necessary to reach
deposition sites, on the relative risks of what is known as
positive aspiration, and on clinician preference. Factors
impacting this choice are related to needle deflection, ease
and accuracy of aspiration, and perceived patient comfort.
In inj ections such as inferior alveolar blocks, which re­
quire deep penetrations through dense tissue, smaller gauge
needles deflect less. Higher gauge needles (30 gauge) are the
most flexible and have demonstrated the greatest deflection.
Figure 9-20 • shows an example of needle pathways for 27-
and 30-gauge needles. Some clinicians prefer 25-gauge nee­
dles for injections where the risks of positive aspiration are
greater. Examples include inferior alveolar, posterior supe­
rior alveolar, and mental and incisive nerve blocks.
Many clinicians believe that inj ections administered
with 27- or 30-gauge needles cause less discomfort during
insertion compared with 25 -gauge needles despite com­
parisons in clinical studies that have demonstrated that

32 mm 20 m m 1 0 mm
& & &

II
i
I• ��-1I
I
I

I
I
_I

FIGURE 9-20 Needle Deflection. Examples of nee­

FIGURE 9-18 Needle Lengths. Common needle
lengths used in dentistry are: long ( average -32 mm/1\-2
inches ) , short ( average -25 mm/1 inch ) , and extra-short
( average -12 mm/Vz inch ) .
Source: Modified courtesy of Dentsply Pharmaceutical.
dle deflection with: A - traditional "straight" insertion
technique, and B - bidirectional rotation technique
during needle penetration using Wand® handpieces
and needles. Note the greater deflection with the
straight insertion pathway and with 30-gauge needles.
138 SECTI O N I N JECTI O N FUNDAMENTALS
Ill •

patients are unable to differentiate between larger and Figure 9-21 •) . A needle cap must not be handled until
smaller gauge needles (Evers, 1993 ; Malamed, 2004). the point of the needle is protected by the sheath. Care
must be taken to avoid contaminating the needle during
N E E D L E C A P S Needle caps and hubs are individually
this process, especially if it may be used again. It is perhaps
color coded by manufacturers to identify needle gauges
more convenient to hold the cap with a forceps or hemo­
and lengths. Although there is no standardized system,
stat while inserting the needle in order to avoid dragging it
over the tray cover. (See Figure 9-22 •.)
many manufacturers use a similar set of criteria to identify
needle gauge. See Figure 9-19 for an example.
Engineering Controls (EC) are designed to provide
Each needle cap is fixed to a needle in a manner that
added protection when handling and recapping needles.
requires breaking a seal before using the needle. This step
A variety of devices is available, as demonstrated in
Figure 9-23 • and Appendix 9-4, " Suggested Needle
assures sterility.

Needle Safety for Patients and Clinicians

Needlestick injuries present a significant risk for the trans­
mission of infectious diseases to dental healthcare per­
sonnel (HCP). Inadvertent needlesticks during intraoral
inj ections put HCP at risk for contracting hepatitis and ac­
quired immunodeficiency syndrome (HIV-AIDS). Atten­
tion must be focused on careful handling of dental needles
during each step of an inj ection.
Both the Centers for Disease Control and Prevention
and OSHA have published specific guidelines and standards FIGURE 9-2 1 CDC Suggested Needle Recapping
for recommended techniques ( Work-Practice Controls ­ Work-Practice Controls. The "scoop-method" is a
WPC ) and/or devices ( Engineering Controls - EC ) to be simple one-handed method of recapping a contaminated
implemented for the prevention of needlestick inj uries. needle. Care must be taken to avoid contact with the
According to OSHA, "recapping or needle removal must be tray while passing the needle into the needle cap.
accomplished through the use of a mechanical device or a
one-handed technique" ; therefore, clinicians are prohibited
from managing needles with two-handed manual recapping
techniques. Information on accessing these guidelines and
standards is provided in Box 9-4 •·
There are a number of methods for safely managing
needles. The scoop technique is a recommended WPC
maneuver (CD C, 2003 ) . This technique requires that cli­
nicians slide uncapped needles into needle caps (sheaths)
while the caps are lying on instrument trays or tables (see

FIGURE 9-22 Modified "Scoop-Method. " Stabilizing

the needle cap can improve access for ease of insertion in
a modified "scoop-method."

Specific g u i d e l i n es a n d sta n d a rds for the m a nagement of

needles in the denta l workp lace can be a ccessed at:
ProTector
CDC G u idelines for I nfection Contro l i n Dental MIMitSh ntiiPlDf
O�lllle OH-HIMM R"""'
H ealth-Care Settings-2003 MMWR, December 1 9,
2003/52(R R 1 7); 1 -61 ....., ...., � ,.,.

http://www. cdc.gov/m mwr/preview/ m m wrhtm l/

rr5 2 1 7 a 1 . htm

Note: Updates to these guidelines are expected in 20 1 4.

OSHA Bloodborne Pathogens and Need lestick Prevention

Reg u l ations (Sta nda rds-29 C F R), B l oodborne

path ogens.-1 91 0.1 030
FIGURE 9-2 3 Needle Recapping Devices. Many different
http://www. os h a . g ov/S LTC/b lood b o r n e pat h oge ns/

� . IIi
nde h safe recapping devices are available, including single-use and
• • • : • • � � ��� • • • • • • • • • • • • • • • • • • • • • • • • • • •
sterilizable devices.
 CHAPTER 9 LOCAL ANESTHETI C DELI V ERY DEVICES
• 139

Recapping Techniques - 'B est Practices:" The EC should

provide a barrier between the tip of the needle and the
fingers of the HCP throughout the recapping procedure.
These devices prevent accidental needlesticks when prop­
erly used as demonstrated in Figure 9-24 •· Clinicians
should never recap needles with their opposite hand or in
the hand of an assistant. All clinicians must assure that re­
capping controls are in place and functioning properly.
Once needles are removed from syringes they must be
placed in appropriate sharps containers for containment
and disposal as demonstrated in Figure 9-25 •·
Another device to consider for reducing risks as­
s o ciated with removing and disposing of needles is a
disposable safety syringe system where needles are not
removed; rather, they are covered with sliding she aths
after use. This eliminates the need for further handling of
contaminated needles, which increases the risk of injury.
FIGURE 9-2 4 Engineering Controls ( EC ) for Recapping
D isposable safety syringe systems are discussed later in
Needles. The EC provides a barrier between the tip of the
this chapter.
needle and the fingers throughout the recapping procedure and
recapping can be one-handed.

(A)

(B) (C) (D)

FIGURE 9-25 Needle Disposal. A-Needles must be disposed of in appropriate sharps containers, using a
one-handed method. Hands and fingers should not be in front of sharp ends at any time. B - This sharps box
allows for one-handed needle insertion into the container. C- The needle hub is grasped with a plier device
on the box to detach the needle. D- The needle drops into the box without the use of hands.
140 SECTI O N I N JECTI O N FUNDAMENTALS
Ill •
FIGURE 9-2 6 Standard Local Anesthetic Cartridge for
Dentistry. Cartridge components are identified as follows:
A- cylindrical glass tube, B - stopper, C- aluminum cap,
D- diaphragm.
Local Anesthetic Drug Cartridges
The dental cartridge is a glass cylinder that holds local an­
esthetic drugs and other contents in solution for inj ection
into oral tissues. It is commonly referred to as a carpule,
which is actually a trademark term of Cook-Waite Labora­
tories. Purity and sterility of anesthetic solutions are more
easily managed in single-unit, glass cartridges. The clear
glass also provides easy monitoring of delivered doses and
unobstructed views of aspiration tests. Cartridges used in
the United States contain up to 1.8 mL of solution. Volumes
in other countries vary from 1.0 mL in Europe, 1.5 mL
in Jap an to 2.2 mL in the United Kingdom. Syringes in
these countries are specifically designed to accommodate
the differences in cartridge volume and size.
Anatomy of Dental Drug Cartridges
The dental cartridge has four components: a cylindrical
glass tube; a rubber (or silicone) stopper; an aluminum
end cap; and a rubber diaphragm (see Figure 9-26 •).
The cylindrical tube contains local anesthetic drugs
and other ingredients in solution . It is most commonly
made of glass (see Figure 9-26A) .
The stopper (or bung) is made of silicone-treated, non­
latex rubber to improve ease of movement through the cyl­
inder (see Figure 9-26B). The syringe harpoon is engaged
Latex a l l e rgies a re beco m i n g m o re a n d m o re com m o n
a n d s h o u l d be considered when u s i n g l o c a l a nesthetic
devices. Alth o u g h local a n esthetic sol utions do not conta i n
l atex, the d i a p h ragms a n d stoppers o f s i n g l e u n it dental
cartridges a n d m u ltidose vials may be made of l atex. The
American Academy of A l l e rgy a n d I m m u n o l ogy Task Fo rce
on All ergic Reactions to Latex suggests the fo l l owing p ro­
tocol when l atex a l l e rgy is suspecte d : " M ed ications stored
u n d e r l atex closures s h o u l d not be used if a su bstitute is
ava i l a b l e in a non-l atex-cove red storage via l " (see R0NVIG
Denta l Mfg. A/S.). To avoid the possib l e associated risks,
m a n ufactu rers h ave vo l u ntarily rep l a ced l atex stoppers in
: � � �� : :� � : �� : � : : ��
e n a l r r g e w t h n o a x a lt e n a i s
• . . . . .•• .•• . :••••••••••
• Disti l l e d water (th e d i l u ent-majo rity of s o l ution)
• Loca l a n esth etic drug
• • Vasoconstrictor drug (if p resent)
: • Su lfite p reservative (when vasoconstrictor p resent)
:
Sod u
: .••• .
� i
: � �� �: �� :f� �� �� � � � � ��; � � � � :
r i t i i su c
. . . .
a i iiy
•• . IIi
into the stopper and pushed by the piston to deposit solu­
tion. The stopper also creates an airtight seal in the cartridge.
The aluminum end cap on the other end of the cylin­
der fits tightly around the neck of the cartridge (see Fig­
ure 9-26C) and holds the diaphragm (or septum) in place
(see Figure 9-26D) . The diaphragm is a semipermeable bar­
rier that is centered in the cap. The penetrating end of the
needle pierces the center of the diaphragm. As long as the
needle does not puncture at an angle, the diaphragm acts as
a seal to prevent anesthetic from leaking around the needle.
Until recently, stoppers and diaphragms for dental car­
tridges were made of latex products. Because latex allergies
have become more common, many manufacturers have vol­
untarily replaced the stoppers and diaphragms with nonlatex
materials. For further discussion on latex allergies and local
anesthetic devices, see Box 9-5 • (Shojaei & Haas, 2002).
Contents of Anesthetic Cartridges
Each cartridge contains a local anesthetic drug in solution,
and most also contain a vasoconstrictor drug. To create
an inj ectable aqueous solution, powdered local anesthetic
drug is mixed with hydrochloric acid to create an acidic
salt for better water solubility. The hydrochloride salt of
the drug is then added to distilled water (the diluent) ,
which makes up the maj ority of the solution.
When vasoconstrictors are included, sodium bisulfite (a
food and drug preservative) is added to the solution to pro­
long the shelf life and efficacy of the vasoconstrictor drug. So­
dium bisulfites increase the acidity of the solution, which can
result in a burning sensation when administered. Additionally,
sodium chloride is included to improve tissue compatibility
(isotonicity). These contents are summarized in Box 9-6 •·
As noted previously, dental cartridges distributed for
use in North America are designed to hold 1.8 mL of solu­
tion. Although all cartridges are capable of holding 1.8 mL,
some package inserts state that the cartridge holds 1.7 mL.
In stating that a cartridge is guaranteed to hold 1.7 mL,
a manufacturer is protected against occasions in which a
cartridge might contain slightly less than 1.8 mL.
When calculating drug dosages, the standard volume
of 1.8 mL is used in all calculations regardless of manufac­
turers' minimum guarantees of 1.7 mL. This is a valuable
practice because any particular cartridge that is guaran­
teed to contain at least 1.7 mL may contain up to 1.8 mL,
averaging 1.76 mL as noted in Chapter 7, "D ose Calcula­
tions for Local Anesthetic Solutions."
 CHAPTER 9 LOCAL ANESTHETI C DELI V ERY DEVICES
• 141

Total Drug Vol ume = 1 .8 ml

-
-
The ADA crite ria for Loca l Anesthetics Color-Co d i n g states

11 1.6 - 1.2 11 11 11 0 .8 0 .4
that:
• The color code consists of a band 3 ± 0.5 mm wide at
- a d ista n ce of 1 5 ± 5 mm from the stopper end of the
Drug Vol ume Expel led by 1 stopper = 0.2 ml cartridge.
• The e n d cap of the cartrid g e m ay be either color coded
to m atch the ADA Color-Cod i n g System or g iven a sil­
FIGURE 9-2 7 Dosage Calculation Tips. Each stopper displaces
ver co lor.
approximately 0.2 mL of solution from a 1 .8-mL cartridge. • The stopper w i l l n ot be color coded a n d s h o u l d n ot be
Monitoring stopper movement can be used to determine drug i n d i cative of the drug or co lor code.
doses delivered. • Letteri n g o n the cartridge s h a l l be b l a ck a n d font size
s h o u l d fo l l ow FDA l a b e l i n g g u i d e l i nes (head i n gs at l east
The volume of drug expelled by one cartridge stopper 8-point type a n d text at l east 6-point type).
• Letteri n g s h a l l be i n d u ra b l e print that will n ot be re­
length is a standardized unit that can be used for easy cal­
culation of volumes of solution delivered. moved by normal office h a n d l i n g .
Each stopper displaces approximately 0.2 mL of solu­ These criteria a re demonstrated i n F i g u res 9-28
tion. Monitoring the distance the stopper moves can be a n d 9-29 •·

� S.o �r�:: ���.d ��t:p�y��:r�� ���/�a���a��a ::f�:t�e.n�f:t: :s; . IIi

used to determine the portion of solution expelled from
a 1.8 mL cartridge. For example, when the stopper is ad­ •

vanced three times its length, 0 . 6 mL of solution have

been expelled. Figure 9-27 • demonstrates the use of
stopper lengths for quick dosage calculations, and Appen­ Each cartridge should be examined before inj ection
dix 7-3 , "Estimating Drug Volumes," provides other use­ in order to confirm that the appropriate anesthetic and
ful visual cues. vasoconstrictor are being administered and that the so­
lution has not expired. It should never be assumed that
Cartridge Labeling and Color Coding
another individual has loaded a syringe properly. This re­
Every cartridge is wrapped in a secure, a polyester film sponsibility rests solely with the individual who adminis­
label. Each label provides information on the local an­ ters the drug.
esthetic and vasoconstrictor drugs contained in the car­ Since June of 2 0 0 3 , manufacturers have b e e n re­
tridge. B oth trade and generic drug names are provided, quired to apply a uniform cartridge color-coding system
along with drug concentrations and dilutions of vasocon­ for identifying specific local anesthetics and local anes­
strictor, the manufacturer, an expiration date, a local an­ thetic/vasoconstrictor combinations. Box 9-7 • describes
esthetic drug color code band, and the lot number and this color-coding system, and Figures 9-28 and 9-29
bar code (see Figure 9-28 •) . demonstrate the label requirements and color codes for
the dental local anesthetic drugs distributed in North
America.
== 2% B ra n d N a m e Effective April 26, 2006, the FDA published the final
-- with Epinephrine Bar Code Label Requirements for Human Drug Products
-
and Biological Products regulation. Although this rule is
intended to improve patient safety in hospital settings by
NDC 668 1 26 40 1 4 8 m l
reducing medication errors, it requires pharmaceutical
2 % B ra n d N a m e
manufacturers to include bar codes on all drug packages.
with Epinephrine Bar codes can be seen on dental local anesthetic cartridges
1 : 1 00,000 as demonstrated in Figure 9-28.
( l idocaine and epinephrine
injection U SP)
Integrity of Cartridges and Contents
Man ufactures Name
Lot 1 28 468 Exp 1 1 /1 3 B e cause of high standards for packaging, shipping, and
delivery, cartridges generally arrive intact. During normal
FIGURE 9-28 ADA Label Standards and Cartridge Label usage, cartridge integrity is protected by a polyester film
Information. Cartridge labels provide trade and generic drug label, which serves as both a protective sleeve and a sur­
names, drug concentrations, dilutions of vasoconstrictor, the face for printing product label information.
name of the manufacturer, and an expiration date. Each drug is Problems with cartridges may include excessive air
identified with color code band and each batch with a lot number. bubbles, leaking around the cap or stopper, distortion of
142 SECTI O N I N JECTI O N FUNDAMENTALS
Ill •

Articaine 4% with Epi 1 : 1 00,000

Articaine 4% with Epi 1: 200,000

Bupivicaine 0.5% with Epi 1 : 200, 000

lidocaine 2% Plain

Lidocaine 2% with Epi 1: 50,000

lidocaine 2% with Epi 1 : 1 00,000

Mepivicaine 3% Plain

FIGURE 9-30 Air Bubbles in Cartridges. No air bubbles are

visible in cartridge A or B. Cartridge C contains a large air bub­
Mepivicaine 2% with Leva 1 : 20,000
ble. Note the intruded stopper in cartridge A and the extruded
stopper in cartridge C.
Prilocaine 4% Plain

Cartridges should be discarded when larger bubbles

(A) Prilocaine 4% with Epi 1 : 200 ,000
are noted below the cap when held vertically. Large bub­
bles can result when solutions have been frozen or con­
taminated (see Figure 9-30 •) .

Leakage a t the Cap

(B)
FIGURE 9-29 ADA Local Anesthetics Color-Coding System.
A - All dental local anesthetic cartridges manufactured in
North America comply with this labeling system. The intent is to
reduce risks of inadvertently administering an unintended drug.
B - Shown here are actual cartridges that have been available in
North America, included are examples of Oraqix and Ora Verse
to contrast their unique safety features.
stoppers, difficulty advancing stoppers, and j amming of
cartridges in the barrel.
Air Bubbles in Cartridges
During manufacturing, small air bubbles (1 to 2 mm) are
frequently trapped under the diaphragm when the alumi­
num cap is placed on the cartridge. Clinicians are usually
not able to see this bubble because it is very small and
concealed by the cap. The bubble is of little consequence
because it will never pass through the needle.
Although it is recommended that cartridges be seated in
syringes before attaching needles, many clinicians routinely
assemble syringes by screwing the needle on first. This usu­
ally does not present a problem; however, when higher
gauge needles (such as 30 gauge) are used, there is an in­
creased risk of leakage. Because of the flexibility of higher
gauge needles, deflection of the cartridge penetrating end
can occur when cartridges are loaded into a syringe. This
deflection may cause tearing of the diaphragm and leaking
of solution when pressure is applied to the stopper. Insert­
ing cartridges in the syringe when loading, before screwing
on needles, can reduce the incidence of this type of damage.
Leakage at the Stopper
When pressure is applied to the syringe piston in a prop­
erly assembled syringe, slight expansion of the stopper
occurs. This expansion creates even contact between the
inner surface of the glass cylinder and the stopper, which in
turn prevents leakage from the cartridge. When a syringe
piston is damaged or bent, the stopper tips away from the
side of the cylinder under the pressure. This allows anes­
thetic solution to leak.
Displacement of Stoppers
When stoppers are partially extruded from cartridges, it
is possible that freezing occurred during shipping or stor­
age or that contamination occurred during storage in dis­
infectant solution. Disinfectant solutions are able to seep
into cartridges and displace stoppers. Affected cartridges
should be discarded. Figure 9-30C • shows an extruded
stopper caused by freezing.

Cartridge Handling, Storage, and Expiration
Millions of anesthetic cartridges are used worldwide every
year. Purity and sterility of drugs are assured through com­
plicated manufacturing processes in carefully controlled
environments. Continuous evaluation of samples from
each lot (which are set aside for 6 months) helps to main­
tain a high level of quality control. In addition, every indi­
vidual cartridge is inspected before shipment.
If solutions have been overheated during shipping and
handling, the contents of the cartridge may appear cloudy
or sediment may be visible. If there is any question regard­
ing the contents of a cartridge, it should be discarded.
Although damage during shipment rarely occurs, it is
important to visually examine each cartridge before admin­
istering its contents. Cartridges should be inspected for:
1. integrity
2. clarity of the solution
3. presence of large air bubbles
4. damaged or tarnished caps
5. damaged or leaking stoppers
6. lapsed expiration dates
All local anesthetic solutions should be stored in cool
dry areas at temperatures recommended in product inserts.
Solutions containing vasoconstrictors should be stored in
the dark. Cartridges should never be stored in alcohol or
other disinfectant solutions that can leak into them, con­
taminating the solutions. If cartridges are stored in approved
warming devices, it is important to be aware that long-term
storage at temperatures higher than typical room tempera­
tures may degrade the contents more quickly. Cartridges
stored in these devices should be used as soon as possible.
Local anesthetics without vasoconstrictors have a
shelf life of approximately 24 months. Those with vasocon­
strictors have a shelf life of approximately 18 months.
Steps for Loading Syringes
Preparing and testing syringes for accurate delivery of local
anesthetic drugs should be accomplished before penetrating
mucosa. Comfortable insertion, controlled delivery rates, and
effective aspiration testing are all dependent on the proper
functioning of the syringe and its components. The follow­
ing recommended sequence of steps addresses all safety and
functional issues. These steps are demonstrated in Appendix
9-3, "Summary of Basic Steps for Loading Syringes."
1. Select the appropriate syringe needle, and cartridges
(see Appendix 9-3).
2. Remove the syringe from the sterile pack.
a. Confirm that all parts are intact and secure (im­
portant with syringes that can be disassembled) .
b. Examine the harpoon and piston for imperfec­
tions and debris.
c. Pull back on the thumb ring to fully retract the pis­
ton (this will place tension on the spring and guide
bearing) as demonstrated in Appendix 9-3, Step 1.
CHAPTER 9 LOCAL ANESTHETI C DELI V ERY DEVICES
• 143
3. Insert the cartridge into the barrel as demonstrated in
Appendix 9-3, Step 2.
a. The cap should be oriented toward the needle
adaptor and the stopper toward the harpoon.
b. Confirm that the cartridge is firmly seated in the
barrel (Appendix 9-3, Step 3 ) .
c . Release the tension on the piston (cartridge will
fit "snugly").
4. Engage the harpoon securely into the stopper.
a. Hold the syringe in the "ready for inj ection"
position.
b. Press on the thumb ring until the harpoon is
fully seated into the stopper as demonstrated in
Appendix 9-3, Step 4.
i. To confirm seating of the harpoon, gently turn
the thumb ring; the cartridge should turn freely
in the barrel.
5. Attach the needle to the syringe as demonstrated in
Appendix 9-3, Steps 5 and 6.
6. Gently pierce the cartridge diaphragm* with the pen­
etrating end of the needle shaft as demonstrated in
Appendix 9-3, Step 6.
*If cartridges have been removed and stored outside
of their protective packaging, diaphragms should be
cleaned with alcohol prior inserting needles through
the diaphragm.
a. Take care to pierce the center of the diaphragm.
b. Screw the needle securely onto the needle
adaptor.
i. For plastic hub needles that are not pre­
threaded, maintain firm pressure while attach­
ing the needle to thread it into place (the metal
will cut the thread design into the hub).
7. Establish a needle recapping technique as demon­
strated in Appendix 9-3 , Step 7 and Appendix 9-4,
and locate a sharps disposal container.
a. Scoop method (with or without guide)
1. Cap on tray, cap stabilized in forceps, and sta­
bilization card attached
b. Recapping device
i. Device prepared and/or attached
8. Confirm the needle bevel orientation (when desired)
as demonstrated in Appendix 9-3 , Step 8.
a. Gently remove the cap.
1. Examine the bevel direction, determine by
directly viewing bevel direction, or
n . Determine orientation by means of the bevel
indicator on needle hub.
b. Using appropriate one-handed recapping technique,
reseat the cap as demonstrated in Appendix 9-3 ,
Step 9.
c. If indicated, redirect the bevel by gently turning
the needle at the hub.
d. Recheck and repeat as necessary.
e. Recap with one-handed recapping technique.
144 SECTI O N I N JECTI O N FUNDAMENTALS
Ill •
9. Orient the syringe to display the large window when it
is picked up for inj ection as demonstrated in Appen­
dix 9-3 , Step 10.
a. When there is no assistant present to pass the sy­
ringe, it is helpful to set up the syringe for viewing
of the large window when first picked up. To do
this, place the syringe on the tray with the window
facing down. When ready, pick up the syringe with
the palm facing down toward the tray.
10. Retrieve the syringe and proceed with the inj ection.
a. Retrieve the syringe.
1. Once in position for the inj ection, the large
window will be facing the clinician.
b. Carefully remove the cap (when a recapping guide
is used, always keep fingers behind the guide) .
c . S e t the cap down (with guide o r i n recapping
device).
d. Proceed with the inj ection.
These steps are summarized in Box 9-8 •·
Harpoons may occasionally disengage from stoppers
during aspiration testing. The syringe must be withdrawn
from the mouth and the needle made safe. Once the nee­
dle is removed and safe, reintroduce the harpoon into the
stopper by pushing on the thumb ring. A second and less
time-consuming method may be used in which the needle
is safely capped after withdrawal from the mouth and a
quick direct blow is applied to the thumb ring with the
palm of the dominant hand while holding the syringe with
the other hand, in order to reengage the stopper. The steps
for the second method are summarized as follows:
1. Withdraw the syringe from the patient's mouth and
recap.
2. Move the syringe clear of the patient and other sup­
port individuals (b efore initiating a "blow" to the
thumb ring) .
3. Stabilize the syringe in one hand (without wrapping fin­
gers around the barrel and surrounding the cartridge).
4. Apply a quick, direct "blow" to the thumb ring. When
the blow is administered, it is not necessary to "follow
1. Select the appropriate syri nge, needle, and cartridge(s).
2. Remove the syri nge from the steri l e pack and exa m i n e .
3. I nsert t h e cartridge into the barre l .
4. Engage t h e h a rpoon securely i nto t h e stopper.
5. Attach the needle.
6. Esta b l ish the need l e reca p p i n g tech n i q u e .
7. Confirm the bevel orientation (when desired).
8. Orient the syri nge for viewi ng of the l a rge window.
� • .9� • � : � � �� � : :� �� ��� �� � �: � �� � : ��
e r v t
: .
y in a
. .
c t t i n ec i ·
. . .Ji
.
through" with the force. Instead, the hand should be
quickly withdrawn in a "forward thrust, rapid back­
ward release" sequence. Glass cartridges are less likely
to fracture if the forward thrust is only momentary and
is quickly reversed. Ideally, the stopper does not visibly
change positions in the cartridge when this maneuver
is used, minimizing hydraulic pressures on the glass.
5. Examine the stopper to confirm that the harpoon has
been reengaged.
6. If a cartridge fractures, replacement is necessary. Safe
Work Practices should be observed at all times.
Steps for Disassembling Syringes and Disposal
of Needles and Cartridges
Once an inj ection has been complete d , proper recap ­
ping and unloading of syringes is mandatory. The needle
is contaminated and primary concerns center around the
potential for needlestick inj uries and infectious disease
transmission. Because of this specific concern, the CD C
Guidelines for Infection Control in D ental Health-Care
Settings - 2003 are explicit in their instructions for han­
dling needles. Appendix 9-1 provides the text of the rel­
evant section of these guidelines.
Prevention of injuries is, of course, the best approach to
this health and safety issue. Protocol for the safe handling
of needles and for an appropriate response in the event of
a needlestick must be in place before significant exposure
occurs and must be followed at all times (Smith et al., 200 1 ) .
The first part of this protocol involves a sequence
of steps for disassembling syringes. Recommendations
include:
1. Withdraw the syringe from the oral cavity, keeping all
patient tissues and all hands in view.
2. Move the syringe to the recapping area with the nee­
dle in clear view at all times.
a. It is safest if the clinician re-sheaths the needle
rather than another individual.
3. Using appropriate one-handed Work Practice and En­
gineering Controls, reinsert the needle into its cap. A
variety of methods is demonstrated in Appendix 9-4.
4. Once the needle tip is completely enclosed within the
cap, secure the cap to the needle hub.
a. Ideally this is accomplished by applying gentle
pressure with a one-handed technique as demon­
strated in Figure 9-31 •·
5. Remove the needle from the syringe by "rocking" or
"twisting" it off the needle adaptor and moving the
exposed penetrating end away from the syringe and
any hands.
a. Be sure the needle adaptor remains on the syringe
(see Figure 9-32 •).
i. If the adaptor is accidentally removed with the
needle, it should be removed with a forceps or
hemostat. Never use unprotected fingers.
b. For needles with metal hubs, simply unthread the hub.

FIGURE 9-3 1 Recapping and Making Needles Safe. Using a
one-handed technique, completely enclose the needle in the cap
and then secure the cap to the needle hub by applying gentle
pressure.
6. Continue to move the n e e d l e to an appropriate
sharps container at a predetermined location near
chairside.
7. Holding the sheathed end of the needle and cap, insert
the needle into the receiving hole of the container ac­
cording to product instructions (see Figure 9-25) .
a. Some recapping guides will stay i n place until this
step is completed and aid in placing the needle,
sharp end first, into sharps containers.
FIGURE 9-32 Loss of Syringe Parts. When removing needles
take care that the needle adaptor does not detach from the
syringe and be disposed with the needle.
CHAPTER 9 LOCAL ANESTHETI C DELI V ERY DEVICES
• 145
8. Once the needle is safely disposed of, remove the
cartridge.
a. Pull back on the piston to disengage the harpoon.
b. Tip the syringe to the side to allow the cartridge to
fall free of the barrel.
i. Occasionally stoppers remain lodged on har­
poons. They can be removed safely with a
forceps or hemostat after the cartridge has
been removed from the syringe. Do not use
fingers at any time to dislodge stoppers from
harpoons.
ii. Empty cartridges are contaminated and the
glass may be broken. All cartridges must be
disposed of in sharps containers.
9. When needles and cartridges have been properly dis­
posed of, syringes may be sterilized along with other
contaminated instruments.
These steps are summarized in Box 9-9 •·
The second part of this protocol is related to the man­
agement of needlestick injuries. All healthcare facilities are
required to have procedures in place for the prevention of
needles tick injuries and for a standardized response if they
occur. In the event of a needles tick injury, clinicians must
report the inj ury to the designated exposure manager as
soon as possible and follow established protocol.
Attitudes can play a significant role in the safe han­
dling of needles. Changing long-standing unsafe practices
can prove challenging. Observance of standard precau­
tions during all phases of inj ection administration, how­
ever, is both ethically and medically sound.
Response to Needlesticks
If a needles tick (or other puncture injury) occurs, all anes­
thetic procedures and treatment should be terminated and
the inj ured tissues immediately and thoroughly washed
with soap and water. The facility 's exposure manager
should be notified while appropriate first aid is initiated.
According to CDC guidelines, postexposure management
should include documentation in both the patient's record
and the exposed individual's health record.
1 . Withd raw the syri nge from the oral cavity.
2. Move the syri nge to the reca p p i n g a rea.
3. Use a n appropriate one-handed Work Practice and
Eng ineering Contro ls to cap the need le.
4. Secure the cap to the need l e hub.
5. Remove the need l e from the syri nge a n d p l ace i n a n
appropriate s h a rps conta i n e r.
6. Remove the cartridge from barre l a n d d ispose i n a n
appropriate s h a rps conta i n e r.
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• .7: •
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146 SECTI O N I N JECTI O N FUNDAMENTALS
Ill •

Technique Specific Syringes

In addition to syringes based on the traditional Cook de­
sign, a number of specialized devices are routinely used
in dentistry. Some syringe devices allow for ease of access
and delivery of anesthetic solutions, while reducing physi­
cal stress on the hand when drugs are delivered under
pressure. Others facilitate controlled rates of delivery to
improve patient comfort. Additional features are designed
to regulate incremental dosing. Although used in a tradi­
tional manner, some syringes are designed as single-use
devices with specific safety features intended to reduce the
risk of needles ticks.
Five devices will be discussed, including those used for
periodontal ligament (PDL) and intraosseous inj ections,
computer-controlled local anesthetic delivery, j et inj ection, FIGURE 9-3 3 Common PDL Syringes. Two common PDL
and those whose primary goal is safety (disposable "safety syringes are the Paroj ect (top) and N-Tralig (bottom) .
syringes").

Periodontal Ligament Injection Manual Devices

In PDL inj ections, measured doses of anesthetics are de­
livered under pressure to confined spaces. Some clinicians
find hand pressures associated with PDL inj ections diffi­
cult to sustain when using standard aspirating syringes.
Specialized devices for PDL inj ections are available in
two primary designs, a "pistol grip " and a "pen type" ar­
rangement, both of which reduce hand pressures. Glass
cartridges are typically enclosed within syringe barrels
with no exposure to the outside or with very small pro­
tected windows. Should a cartridge fracture within these
syringes, there is no danger of glass falling into the mouth. FIGURE 9-3 4 N-Tralig 4 5 Degree Angle Adaptor. The 45-de­
Pressures compared with hand pressures with traditional gree angle adaptor provides appropriate insertion angles without
syringes are reduced by using mechanical advantages. De­ bending needles.
vices available for PDL inj ections include the N-Tralig
(Miltex Inc.) and the Paroj ect (Septodont USA). Some sy­
ringes are also able to deliver specific and small volumes
of drug and facilitate tracking the volumes of drug deliv­
ered. Computer-controlled devices used for PDL inj ec­
tions are discussed later in this chapter.
As discussed in Chapter 15, "Supplemental Techniques
and Adjunctive Strategies," achieving the most appropri­
ate angle for needle insertion can be challenging with
these and all syringes. For maximum safety, commercially
designed syringe adaptors are available that facilitate a
45 degree insertion angle. For example, a 45-degree angle
attachment is available for a standard N-Tralig syringe
designed for PDL inj ections. These devices are shown in
Figures 9-33 • and 9-34 •· They can eliminate the need
for bending needles, and their use does not compromise
OSHA (or other state) safety standards that prohibit
bending of contaminated needles in most situations. FIGURE 9-3 5 Stabident Intraosseous Injection Device.

lntraosseous Injection Devices
Intraosseous inj ection techniques require local anesthetic
solutions to be deposited within alveolar bone through
which they diffuse to nerves. To accomplish this, a small
penetration through alveolar bone, known as a perforation,
is necessary. A needle is then inserted and the anesthetic
delivered. These systems provide both perforator tips and
27 gauge inj ection needles (8 mm - ultra-short) .
D evices utilized for intraosseous inj ections include
the Stabident system (Fairfax Dental Inc. , FL) , the X-Tip
(Dentsply Maillefer, OK), and the IntraFlow device (Pro-Dex
Micro Motors, CA) and are shown in Figures 9-35 •, 9-36 •,

FIGURE 9-3 6 X-Tip Intraosseous Inj ection Device.
FIGURE 9-3 7 IntraFlow Intraosseous Inj ection Device.
FIGURE 9-38 QuickSleeper Intraosseous Inj ection Device.
Source: Courtesy of DENTAL Hi Tech, France.
and 9-37 •· The QuickSleeper demonstrated in Figure 9-38 •
(further discussed with the CCLAD devices) is currently
available in Europe and features a unique design as both a
CCLAD and an intraosseous injection device. Intraosseous
techniques are discussed in detail in Chapter 15, "Supple­
mental Techniques and Adjunctive Strategies."
Computer-Controlled Local Anesthetic
Delivery Devices
Computer-controlled local anesthetic delivery (CCLAD)
devices are preprogrammed, electronic delivery systems
for the administration of anesthetic inj ections. A key fea­
ture of CCLAD devices is the ability to precisely control
the rate of delivery. The initial phase of the inj ection can
start at a very slow rate of delivery for a given period
CHAPTER 9 LOCAL ANESTHETI C DELI V ERY DEVICES
• 147
of time. Following this initial deposition, the rate is in­
creased to a predetermined rate based on the inj ection
technique selected. Clinical research has shown that this
approach will produce a more consistent inj ection than
traditional techniques with manual syringes and does
not depend on clinicians to assure a slow rate of deliv­
ery. Of particular importance when performing inj ections
into dense tissues, such as the p alate, attached gingiva,
or PDL, these devices can maintain a specified rate and
controlled pressure that can eliminate patient discomfort
and adverse tissue reactions occasionally seen when us­
ing manual syringes.
Available devices are operated by means of either
manual or foot controls that start the flow of anesthetic
drugs, signal for aspiration tests, and stop the flow of so­
lution. These devices differ markedly from PDL syringes
in that they do not generate high pressures. For this rea­
son, when using one of these devices, one can deposit
greater volumes of solution at controlled lower pressures,
when compared with other PDL devices (and standard
syringes).
A second-generation CCLAD device, The Wand STA
Single Tooth Anesthesia System Instrument (Milestone
Scientific Inc. , Livingston, NJ) , designed with an innovative
technology called Dynamic Pressure Sensing Technology®,
has also been optimized for single-tooth anesthesia tech­
niques (PDLs). This is the most current CCLAD device in­
troduced to the dental market. Unlike its predecessors, this
device has real-time pressure feedback providing clinician's
immediate information to identify correct injection sites.
There are three primary devices in use in North America:
The Wand STA Single Tooth Anesthesia System Instrument
(Wand STA) and the CompuDent®fWand® Instrument (Mile­
stone Scientific Inc.), and the Comfort Control Syringe (CCS)
(Dentsply/Professional) . Although supplies for all three de­
vices are available, only the Wand STA instrument is currently
on the market. Use of CCLADs for specific inj ection tech­
niques is discussed in Appendix 9-5 and Chapters 12-15.
Comfort Control Syringe (CCS)
The Comfort Control Syringe (CCS) was marketed by
Dentsply/Professional until 20 13. The design features of the
CCS handpiece have some similarities to manual syringes
(see Figure 9-39 •) . The CCS uses standard cartridges and
needles that are attached following basic steps similar to
manual syringes. Other features of the CCS include a digi­
tal panel that displays the rate, elapsed time, and amount
of anesthetic delivered, and a clear plastic cartridge sheath
that allows complete visibility of cartridges at all times.
The CCS handpiece is considerably larger than man­
ual syringes and is controlled by buttons on its front sur­
face. It is a two-stage, controlled-rate delivery device. The
inj ection begins at a very slow rate of 10 seconds and is
programmed to increase to a faster rate of delivery, con­
sistent with the inj ection technique selected from the con­
trol panel. Clinicians with small hands may need to modify
their grasps in order to comfortably stabilize, activate, and
manage this handpiece. The CCS has five preprogrammed
148 SECTI O N I N JECTI O N FUNDAMENTALS
Ill •

FIGURE 9-3 9 Comfort Control CCLAD .

FIGURE 9-40 Wand STA Single Tooth Anesthesia System
Instrument and CompuD ent/ Wand Instrument

delivery rates, listed in Table 9-1 •· Although still in use,

this device is no longer marketed.

As with other CCLAD systems, the Wand STA Single

CompuDent/Wand and Wand STA Single Tooth
Tooth Anesthesia System Instrument and CompuD ent
Anesthesia Instruments
Instruments operate using a multistage delivery system.
Milestone Scientific was the first manufacturer to mar­ To enhance inj ection comfort, technique steps recom­
ket a CCLAD device (the Wand® Instrument) in 1997, at m e n d e d by Milestone are d e s crib e d as prepunctu re,
the same time pioneering the AMSA inj ection technique puncture, penetration, and injection . During the prepunc­
(Friedman & Hochman, 1998; Hochman et al. , 1997 ) . The ture and puncture steps, a small volume of anesthetic is
CompuD ent® Instrument was formerly marketed as the administered ahead of the needle. This " anesthetic path­
Wand Instrument. Although the Wand STA Single Tooth way" serves to minimize discomfort from needle penetra­
Anesthesia System® Instrument is currently the only tion and may eliminate the need for topical anesthetics.
device manufactured by Milestone Scientific, both are in This may be characterized as a stealth technique in which
use worldwide (see Figure 9-40 •) . the recipient is unaware of the proce dure until it is
finished.
B oth the Wand STA Single Tooth Anesthesia Sys­
tem and CompuDent instruments have similar, prepro­
Table 9-1 Comfort Control Syringe Preset Delivery Rates grammed delivery rates, listed in Table 9-2 •·
The design features of these delivery systems are
Injection Technique Delivery Rate unique compared with traditional syringes. The compo­
nents have been described as "slim-line" and are relatively
Block 0.020 mL!sec unobtrusive, which may offer a psychological benefit for
some patients (see Figure 9-4 1 • ) . Most clinicians, but
Intraosseous 0.020 mL!sec
particularly those with small hands, find it easy to grasp
and stabilize the slender ergonomic wand-like handpiece
Infiltrations 0.017 mL!sec
during inj ection. Clinicians will find that this system can
Palatal 0.008 mL!sec prevent repetitive hand-strain injury because of the over­
all system design (Murphy, 1998 ) . Additionally, with a
POL 0.007 mL!sec simple adaptation of the Wand® handpiece (see Figures
9-42 • through 9-45 •) , needle approach and insertion
Source: Comfort Control Syringe product manual REF 850155. may be achieved without stimulating a visual response in
 CHAPTER 9 LOCAL ANESTHETI C DELI V ERY DEVICES
• 149

Table 9-2 CompuDent and Wand STA Single Tooth Anesthesia System Instrument Preset Delivery Rates

CompuDent M odes Delivery Rate Wand STA M odes Delivery Rate

slow speed - 1.8 mL/50 seconds STA - 1 drop/2 seconds

1-speed mode 0.005 mL!second
Contro/Flo

fast speed - 1.8 mL/25 seconds Normal -1 drop/second

2-speed mode 0.005 mL!second
ControlFlo 0.03 mL!second
RapidFio

Turbo 0.005 mL!second

3-speed mode 0.03 mL!second
ControlFlo 0.06 mL!second
RapidFlo
TurboFlo

Source: ST A Single Tooth Anesthesia SystemTM and CompuDent® Instruments product manuals, Hochman, MN: Single-tooth anesthesia: pressure­
sensing technology provides innovative advancement in the field of dental local anesthesia, Compendium, Apri1 2007, 28(4), 186-193.

FIGURE 9-43 Adaptation of the Wand Handpiece - Step 2.

Gently "peel" the plastic tubing from the length of the Wand
handpiece.

FIGURE 9-41 Wand Handpiece. The "slim-line" Wand hand­

piece is designed specifically for use with the Wand STA Single
Tooth Anesthesia System and CompuDent Instruments.

FIGURE 9-42 Adaptation of the Wand Handpiece - Step 1 . FIGURE 9-44 Adaptation of the Wand Handpiece - Step 3.
Loosen the plastic tubing from the slot i n the side o f the Wand With a rocking motion, snap off the slim handle portion of the
handpiece. Wand handpiece, above the needle hub.
150 SECTI O N I N JECTI O N FUNDAMENTALS
Ill •
FIGURE 9-45 Modified Wand Handpiece.
FIGURE 9-46 Maxillary Buccal Infiltration with a Modified
Wand Handpiece.
FIGURE 9-47 Ultra Safety Plus XL Safety Syringe System.
Source: Courtesy of Septodont USA.
the patient as demonstrated in Figure 9-46 •· The Wand®
handpiece is also available with a specially designed nee­
dle safety device called the Safety Wand® shown in Figure
9-47 •· With both devices delivery of local anesthetics is
initiated and controlled by a foot pedal.
The slim profile of the Wand handpiece enhances
the unique insertion technique recommended. During
inj ections with standard syringes, needles deflect away
from bevel openings when needles are advanced . With
the Wand STA Single Tooth Anesthesia System and Com­
puDent instruments, deflection is avoided by rotating the
needle during insertion (known as a "pen roll" or "bidi­
rectional" rotation technique ) , a maneuver that would
be difficult, if not inherently dangerous, with standard
syringes (Hochman & Friedman, 2000). Figure 9-20 dem­
onstrates this phenomenon with both 27-and 30-gauge
needles.
A specific design feature of the Wand STA Single
Tooth Anesthesia System Instrument facilitates single­
tooth anesthesia with the STA-Intraligamentary inj ection
without associated trauma to the PDL. The Wand STA
Single Tooth Anesthesia System Instrument has patented
dynamic pressure sensing technology that provides audi­
ble and/or visual feedback to the clinician to assure the op­
timum placement of the needle throughout the inj ection.
When properly placed, intraligamentary (PDL) inj ections
can be accomplished with significantly less pressure than
when delivered by traditional PDL syringes.
CCLAD systems provide a number of advantages
over traditional, manual syringes and have a significant
place in future dental anesthesia practices.
Jet Injectors
Jet injection devices use narrow bursts of air, or "j ets " to
penetrate mucosa without needles. These spring-loaded
syringes are used primarily to establish deep prepenetra­
tion topical anesthesia, but they have also been used in in­
filtration and shallow block anesthesia with some success.
Examples of j et inj ectors are the Syrij et (Mizzy/Keystone
Products, Cherry Hill, NJ) , the Madaj et (MADA Medi­
cal Equipment International, Carlstandt, NJ) shown in
Figure 9-48 •, and the Injex (INJEX Pharma USA, Miami,
FL) shown in Figure 9-49 •·
Safety Syringes
Safety syringes are plastic single-use, or partially dispos­
able devices designed to reduce the risk of needlestick
(A) (B)
FIGURE 9-48 Safety Wand Handpiece. A - needle positioned
for injection; 8 - needle retracted into safety sleeve.
Source: Courtesy of Septodont USA.

FIGURE 9-49 Jet Injection Devices. Two common jet injection
devices are the Syrij et (top) and Madajet (bottom).
injuries associated with trapping inj ection needles. Interest
in these devices has become quite limited and many are no
longer available.
As noted previously, one such device, the Ultra Safety
Plus XL from Septodont (Figure 9-50 •) is available and
Milestone Scientific provides The S afety Wand® Hand­
piece for CompuDent and STA devices (Figure 9-46) .
CAS E MA N A G EME N T
Elena Gagarin
Case Discussio n : As the c l i nician d iscovered when the
ca rtridge was re m oved fro m the syri nge, it h a d been
loaded backwa rds and the harpoon had perforated the
d i a p h ra g m i n stead of the stopper. The patient wo u l d
need another injection because the clinician, w h o was or­
dinarily very attentive to detail, had failed to check the ar­
mamentarium that someone else had set up.
T h e re a re at l east two i m p o rtant l essons l e a r n e d
from this experience:
� h. � P.t�� 9.LJ.���.i.c:>.". � ........................................... .
. . . . . .
1 . Which one of the following statements is correct?
a. The standard aspirating syringe is designed to pro­
vide negative pressure on aspiration, unlike the
self-aspirating syringe.
b. The standard aspirating syringe is designed to pro­
vide positive pressure on aspiration, unlike the self­
aspirating syringe.
c. Neither the standard nor the self-aspirating sy­
ringes provide negative pressure on aspiration.
CHAPTER 9 LOCAL ANESTHETI C DELI V ERY DEVICES
• 151
(A)
(B)
FIGURE 9-50 Small Jet Injection Device. A-The Inj ex device
is smaller overall than other jet inj ection devices currently avail­
able. B- During inj ection, the device may be nearly concealed
in the palm of the hand.
Source: Courtesy of Betsy Simpson.
1 . A see m i n g ly neg ative aspirati o n was not eve n a n
aspirati o n .
2 . B efo re i n s e rt i n g n e e d l es i n to t i s s u e s , syri n g es
s h o u l d be checked for easy flow of sol ution in ad­
d ition to confi r m i n g that t h e co rrect d ru g s were
l o a d e d . H a d t h i s been d o n e , t h e c l i n i c i a n wo u l d
h ave known that t h e cartrid g e was l o a d e d back­
wards before penetrating any tissues.
d. The standard aspirating syringe is designed to pro­
vide negative pressure on aspiration similar to the
self-aspirating syringe.
2. Which o n e of the following is correct when address­
ing OSHA requirements for medical device safety in
dentistry?
a. Two hands are allowed as long as one hand only
secures the needle cap.
b. Contaminated needles may be bent as long as
the bend is accomplished with cotton pliers or a
hemostat.
152 SECTI O N I N JECTI O N FUNDAMENTALS
Ill •

c. Two hands are never allowed to recap needles even Astra Pharmaceutical Products, Inc. Astra Self-Aspirating
when one hand is holding a hemostat or locking pli­ Syringe, Product Insert. Westborough, MA 0 1606: Author.
ers to secure the protective caps. Brunton, L., Lazo, J. , & Parker, K. (2006). Goodman and
d. Uncontaminated needles may be bent. Gilman's the pharmacological basis of therapeutics (11th ed.).
New York: McGraw-Hill.
3. In comparing a 25-gauge needle with a 30-gauge nee­ CDC Guidelines for Infection Control in Dental Health-Care
dle, the 25-gauge needle: Settings - 2003. (2003 , December 19). Morbidity and Mortal­
1. Has better aspiration. ity Weekly Report (MMWR), 52(RR17); 1-61. Retrieved from
2. Breaks more easily. http://www.cdc.gov/mmwr/preview/mmwrhtmllrr5217al.htm
3. Is less comfortable than the 30 gauge. Centers for Disease Control and Prevention (CDC). (2003). De­
vice screening and evaluation forms. Retrieved November 1 1 ,
4. Has a smaller diameter.
2008, from www.cdc.gov/oralhealth/infectioncontrol/forms.htm
5. Can be used in highly vascular areas.
Dentsply/Professional. Comfort Control Syringe REF850155,
a. 2,4,5 Product Insert. 1301 Smile Way, York, PA 17404: Author.
b. 2,4 Evers, H. (1993). The dental cartridge system. Trosa, Sweden:
c. 1 ,3,5 Trosa Tryckeri AB.
d. 1 ,5 Federal Food, Drug, and Cosmetic (FD&C) Act, section 20 1 (h),
52 FR 30097, August 12, 1987, as amended at 59 FR 63008,
4. Long needles are approximately ____ long.
December 7, 1994; 66 FR 38799, July 25, 2001.
a. -12 to 22 mm Friedman, M. J. , & Hochman, M. N. (1998) . The AMSA inj ection:
b. -32 to 36 mm A new concept for local anesthesia of maxillary teeth using a
c. -40 to 42 mm computer-controlled inj ection system. Quintessence Interna­
tional, 29, 297-303.
5. When a stopper is extruded, what has likely caused
Hochman, M. N. , Chiarello, D., Hochman, C. B., Lopatkin, R., &
the problem?
Pergola, S. (1997). Computerized local anesthesia delivery vs.
a. The cartridge was overfilled during manufacturing. traditional syringe technique. New York State Dental Journal,
b. Freezing occurred during shipping or handling. 63, 24-29.
c. Overheating has caused pressure in the cartridge. Hochman, M. N., & Friedman, M. J. (2000). In vitro study of
d. Oxidation of sodium bisulfate has created gas in needle deflection: A linear insertion technique versus a bi­
the cartridge. directional rotation insertion technique. Quintessence Interna­
tional, 31 , 737-743 .
6. During an infiltration injection you give the patient Jastek, J.T., Yagiela J.A. 1981. Regional anesthesia of the oral
three stopper-widths of local anesthetic. How much cavity, St. Louis: CV Mosby Co.
solution have you inj ected into the patient? Jastak, J. T. , Yagiela, J. A., & Donaldson, D. (1995). Local anesthe­
a. 0.2 mL sia of the oral cavity. Philadelphia: Saunders.
b. 0.9 mL Malamed, S. F. (2004) . Handbook of local anesthesia (5th ed.).
c. 1 .8 mL St. Louis: Mosby.
d. 0.6 mL Murphy, D. (1998) . Ergonomics and the dental care worker
(p. 181 ). Washington, DC: American Public Health Association.
7. What substance is used as the preservative for epi­ ISBN: 0-87553-0233-0.
nephrine in local anesthetic cartridges? National Institute for Occupational Safety and Health. (2002) .
a. Sodium bisulfite Safer medical device implementation in healthcare facilities.
b. Sodium hypochlorite Retrieved September 17, 2002, from http://www.cdc.gov/niosh
c. Methylparaben /topics/bbp
d. Nitrogen OSHA Bloodborne Pathogens and Needlestick Prevention
Regulations (Standards -29 CFR), Blood borne pathogens-
191 0.1030 (1991). www.osha.gov/SLTC/bloodbomepathogens/
standards.html. Accessed January 25, 2014.
References Shoj aei, A. R., & Haas, D. A. (2002) . Local anesthetic cartridges
and latex allergy: A literature review. Journal of the Canadian
R0NVIG Dental Mfg. A/S. Aspiject: Product information, Dental Association, 68(10), 622-626.
Product Insert. GI. Vejlevej 57-59, DK-8721 Daugaard, Smith, A. J. , Cameron, S. 0., Bagg, J. , & Kennedy, D. (20 0 1 ) .
Denmark: Author. Retrieved January 25, 2014, from www. Management of needles ticks i n general dental practice. British
ronvig.com Dental Journal, 1 90(12), 645-650.

Visit www.pearsonhighered.com/healthprofessionsresources to access the student resources that accompany

this book. Simply select Dental Hygiene from the choice of disciplines. Find this book and you will find the
complimentary study tools created for this specific title.
Sum m ary of Sharps M anagement
Reco m mendations

CDC G u idel i nes for Infection Control i n Denta l H ealth Ca re Settings

I. Preventing Transmission o f Bloodborne Pathogens
II. Preventing Exposures to Blood and OPIM
1. General recommendations
a. Use standard precautions (OSHA's bloodborne pathogen standard retains the term standard precautions) for
all patient encounters (lA, I C) (11,13,19,53).
b. Consider sharp items (e.g., needles, scalers, burs, lab knives, and wires) that are contaminated with patient blood
and saliva as potentially infective and establish engineering controls and work practices to prevent injuries (IB,
IC) (6,13,113).
c. Implement a written, comprehensive program designed to minimize and manage DHCP exposures to blood
and body fluids (IB, I C) (13,14,19,97).
2. Engineering and work-practice controls
a. Identify, evaluate, and select devices with engineered safety features at least annually and as they become avail­
able on the market (e.g. , safer anesthetic syringes, blunt suture needle, retractable scalpel, or needle less IV sys­
tems) (IC) (13,97,110-112) .
b. Place used disposable syringes and needles, scalpel blades, and other sharp items in appropriate puncture­
resistant containers located as close as feasible to the area in which the items are used (IA, I C) (2, 7,13,19,113,115).
c. D o not recap used needles by using both hands or any other technique that involves directing the point
of a needle toward any part of the body. Do not bend, break, or remove needles before disposal (lA, I C)
(2, 7,8,13, 97,113).
d. Use either a one-handed scoop technique or a mechanical device designed for holding the needle cap when
recapping needles (e.g., between multiple inj ections and before removing from a nondisposable aspirating
syringe) (IA, I C) (2, 7,8,13,14,113).

Excerpt from: Morbidity and Mortality Weekly Report, Guidelines for Infection Control in Dental Health-Care Settings -2003,
December 19, 2003 I Vol. 52 I No. RR-17, Page 40, Centers for Disease Control and Prevention.
153
C DC Sampl e Device Evaluation Form: Dental
Safety Syringes and N eedl es
Available at www.cdc.gov/OralHealth/infection_control/forms.htm

S a m p l e Device Eva l u at i o n Form

Denta l Safety Syri nges a n d N eed l es

This form collects o p i n ions a n d observations from dental healthcare perso n n e l who have p i lot
tested a safer dental device. This form can be ada pted fo r use with m u lt i ple types of safer
devices. Do not use this form to coll ect i nj u ry data beca use it can not e n s u re confi d e n t i a l ity.

Date :�____________
Product: Name, brand, com pany .:_________________________________
N umber of times used : _____________________________________

Your position or title: _____________________________________

Your occupation or specia lty: -------

1. Did you receive training in how to use this product?

0 Yes [Go to Next Question] 0 No [Go to Question 4]

2. Who provided this instruction? (Check All that Apply.)

0 Product representative 0 Staff member O Other

3. Was the training you received adeq uate?

D Yes O No

4. Compared to others of your sex, how would you describe your hand size?
0 Small 0 Medium 0 Large

5. What i s your sex? o Female D Male

Please answer all questions that apply to your duties and responsibil ities. If a q uestion does not apply to your d uties and
responsibilities, please leave it blank .

During the Pilot Test of this Strongly Neither Agree Strongly

Disagree Agree
Device . . . Disagree nor Disagree Agree

6. The weight of the device was

2 4
similar to that of a conventional
dental syringe.

7. The device felt sta ble during

assembly, use and disassembly. 2 4

8. The device fit my hand

2 4
comfortably.

9. The anesthetic cartridges were

easy to change. 2 4

1 0. Aspiration of blood into the

2 4
anesthetic cartridge was clearly
visible.

11.
2 4
I had a clear view of the injection
site and needle tip.

1 2.
2 4
The device did not appear to
increase patient discomfort.

May, 14 2002
http://www. cd c. g ov/O ra i H ea lth/i nfection_co ntrol/forms.htm

154
 CHAPTER 9 LOCAL ANESTHETI C DELI V ERY DEVICES
• 155

Strongly Neither
During the Pilot Test of this Strongly
Disagree Disagree Agree nor Agree
Device . . . Agree
Disagree

1 3. The device performed rel iably. 2 3 4 5

14. I w a s a b l e t o give injections in all

mouth sizes and a l l areas of the 2 3 4 5
mouth .

1 5. I used the device for all of the

same pu rposes for which I use 2 3 4 5
the conventional device.

16.
2 3 4 5
Activating t h e safety feature was
easy.

17.
2 3 4 5
T h e safety feature was easy to
recognize and use.

18. T h e safety feature d i d not

2 3 4 5
activate inadvertently, causing
me to use additional syri nges or
needles.

19. T h e safety feature functioned a s

intended. 2 3 4 5

20.
2 3 4 5
The instructions were easy to
follow and complete.

21. I could have used this product

2 3 4 5
correctly without special tra i n i n g .

22. The "feel" of t h e device did not

cause me to change my 2 3 4 5
tech nique.

23.
2 3 4 5
This device meets my clin ical
needs.

24.
2 3 4 5
This device is safe f o r clin ical
use.

Additional comments for any responses of "Strongly Disagree " or " Disagree."

May, 14 2002
http : //www . c d c . g ov/Ora i H ea l th/i nfect i on_con t ro l/fo r m s . h t m

Source: Courtesy of Centers for Disease Control and Prevention.

Sum m ary of Basic Steps for Load i ng Syringes

Select appropriate syringe, needle(s), cartridge(s), and recapping method.

1. Fully retract the piston to allow cartridge to slide 2. Insert the cartridge with the stopper toward the
into the barrel. piston.

M aintai n pressure
with lh umb to keap
P u l l-back o n the
thumb ring to fully
piston retracted.

retract the piston.

3. Release the tension on the piston and confirm 4. Seat the harpoon securely into the stopper.
that the cartridge is fully seated.

Use genUa thu m b

Cartridge end c a p pressure t o seat
will sl ide forwerd into harpoon prior to
needle adapter end. attaching needle.

156
 CHAPTER 9 LOCAL ANESTHETI C DELI V ERY DEVICES
• 15 7

5. Open the needle by gently turning the cap to 6. S crew the needle securely onto the needle
break the seal. adaptor.

Sterile ca rtridge Mainta i n firm

penetrati n g end pressure for

self theading
will be exposed.
needles.

7. Prepare the n e e dl e recapping device 8. Gently loosen and remove the cap to confirm
(when applicable ) if used. bevel orientation and then orient the syringe for
viewing of the large window.

T h u m b s h o u l d o nly
Two handed procedure
be on front of card
while attaching d evice.
is acceptable O N LY for
uncapping needles.

I
I�

9. S afely r e p l a c e t h e cap with a o n e - h a n d e d 10. Orient the syringe facing down to achieve ease of
technique. retrieval with:
a. a "palm up" grasp
b. large window visible

This recapping device

serves as a prop for
the cap during the
"scoop" method .

Orient syri nge

with large window
fac ing down.
Suggested N eedle Recap ping Techniques­
" Best Practices"

Each clinician is obligated to apply safe needle handling and recapping methods based on CDC and OSHA
guidelines for their practice setting. A variety of acceptable techniques apply OSHA Work Practice and Engineering
Controls. The key to safe needle recapping is sound one-handed technique. Examples follow.

Basic "scoop" method

"Scoop" method assisted with cotton pliers as cap "Scoop" method assisted with weighted cap holder
holder

158
 CHAPTER 9 LOCAL ANESTHETI C DELI V ERY DEVICES
• 159

" S coop" method assisted with card prop device cap " Scoop" method assisted with rubber prop device cap ':
holder hcldcr

Best Practices allow for (A) removing caps with the assistance of a device, but recapping MUST be done with one
hand. With all recapping methods and devices it is important that an unprotected needle is NEVER moved toward
clinicians' hands (B) .

(A) (B)

(A) (B)
160 SECTI O N I N JECTI O N FUNDAMENTALS
Ill •

Note the unsa fe practice Note the unsa fe practice

The thumb is on the front of the device. This device aids Although the fingers are behind the card, this device is
recapping by propping up the cap for ease of entry. It is not puncture proof and is not intended for recapping in
NOT considered a barrier to needle penetration. this manner. This practice can be used to uncap needles.

Note the BEST PRA CTICES

Regardless of the method used, recapping needles with a one-handed method is the safest way to render needles
safe.
Computer-Controlled Local Anesthetic Del ivery
MARK N. HOCHMAN, DDS

OBJECTIVES
KEY TERMS
• Defi ne a n d d i scuss the key terms in this cha pte r.
bi-rotatio n a l i n serti on 1 65
• I d e ntify a n d d i scuss the tech n o l og ica l advantages of CCLAD. computer-co ntro l led
• Identify a n d d i scuss the i m pact of c l i n i cia n/patient ben efits to u s i n g local a n esthetic d e l ivery
CCLAD. (CCLAD) 1 6 1
Dyn a m i c P ressu re Sensing®
• Identify a n d d i scuss how tissue type a n d flow rate effect i njection
(DPS) 1 62
outcomes. F l u i d dyn a m i cs 1 62
• Identify a n d d i scuss the i m pact of fl u i d press u re, fl u i d flow rate, a n d vol­ fl u i d flow rate 1 62
u m e d ispensed in tissues with low tissue com p l i a nce, for exa m p l e , palate fl u i d press u re 1 62
and P D L. type 1 -l ow-density
tissue 1 62
• I d entify a n d d i scuss how l a rg e vo l u m es of a n esth etic sol ution ca n be safe l y
type 2-m oderate-d e nsity
a n d comforta bly a d m i n istered i nto pa lata l tissues w i t h contro l led l ow pres­
tissue 1 62
s u res d e l ivered by CCLAD. type 3-h i g h -de nsity
• Identify a n d d i scuss why l a rg e vo l u mes of a n esthetic sol ution ca n be a d ­ tissue 1 62
m i n i stered i n the P D L safely a n d p a i n l essly when u s i n g contro l led l ow CCLAD-contro l l e d low
pressu res performed with CCLAD. p ress u res 1 6 1

I ntrod uction
Effective maxillary and mandibular anesthesia can be
aided through the use of computer-controlled local an­
esthetic delivery (C CLAD) as seen in Figure A9.5-1 •·
Benefits of CCLAD include increased patient comfort and
reduced tissue damage for all inj ections. CCLAD is espe­
cially useful to improve comfort when performing inj ec­
tions in tissues with low tissue compliance, such as palatal
mucosa and periodontal ligament (PDL).

Backg round
CCLAD represents a n innovative and proven alternative
to traditional mechanical dental syringes for administra­
tions of local anesthetics (Ashkenazi, Blumer, & Eli, 2005 ; FIGURE A9. 5-1 Computer-Controlled Local Anes­
CRA, 1998; Hochman et a!. , 1997) . thetic Delivery (CCLAD) Offers Unique B enefits for
Patients and Clinicians.

This appendix addresses some unique features and advantages for use of Computer-Controlled Local Anesthetic Delivery (CCLAD) .
CCLAD devices available are discussed in Chapter 9, "Local Anesthetic D elivery Devices" (Figures 9-38, 9-39, and 9-40) .
161
162 SECTI O N I N JECTI O N FUNDAMENTALS
Ill •
Traditional dental syringes are simple mechanical
systems designed primarily for convenience with little focus
on patient comfort (Hoffmann-Axtheim, 1981 ) . CCLAD
systems have a technological advantage over manual sy­
ringes in that they are designed with an electro mechanical
motor regulated by a microprocessor capable of precisely
controlling the flow rate of anesthetic solutions deposited
into tissues. CCLAD advantages initially recognized in­
clude reduced subj ective pain perception, pain disruptive
behavior, and fear and anxiety (Allen et al. , 2002; Gibson
et al. , 2000; Krochak & Friedman, 1988; Nicholson et al. ,
200 1 ) . During early CCLAD use, i t became apparent that
a fundamental change to the subj ective experience and
physical outcome of a dental inj ection had occurred as a re­
sult of the precise control of the variables of fluid pressure
and fluid flow rate. Collectively, these two variables are de­
fined as the fluid dynamics (fluid pressure and fluid flow
rate) of a dental inj ection. The control of fluid dynamics of
a dental inj ection using CCLAD led to many advantages
reported early on. Among these are more effective diffu­
sion of drugs through oral tissues and an ability to deposit
larger volumes of solution into tissues without adverse re­
actions and with minimal distension (Friedman & Hoch­
man, 1997; Hochman et al., 2006). These findings led to the
development of several new dental inj ection techniques
described later in this appendix and Chapter 13, "Inj ections
for Maxillary Pain Control II - Palatal Approach," and in­
clude the AMSA, P-ASA, and a modified PDL inj ection
(Aboushala et al., 2000; Friedman & Hochman, 1998,1999;
Hochman, 2007).
CCLAD systems represent a new category of ad­
vanced subcutaneous drug delivery instruments. These
instruments were designed spe cifically for maximum
patient comfort and allow unique dental inj ections that
take advantage of this new fluid dynamic. The Wand STA
Single Tooth Anesthesia System Instrument (Milestone
Scientific, Inc. , Livingston, NJ) is a CCLAD device devel­
oped to precisely control and measure fluid pressures at
the needle tip during dental inj ections (Hochman, 2007 ) .
This patented process called Dynamic Pressure Sens­
ing® (DPS) (Milestone S cientific, Inc) allows for real­
time audible feedback of fluid pressures generated during
inj ections.
I m p l ications of F l u i d Dynam ics
and Anatom ica l Location
Research has demonstrated that different oral cavity tissue
types require different flow rates and optimum pressure
values. These tissue-specific inj ection dynamics will pro­
vide fluid pressures that result in safe and comfortable
inj ections for each specific tissue type (Hochman, et al. ,
2006 ) . The research identified three basic tissue types in
the oral cavity based on tissue compliance (distensibility) .
They are defined as follows:
Type 1 - Iow-density tissues with high tissue compli­
ance, found in buccal mucosa, retro-molar fossae, and
unattached gingiva. These tissues are more adaptive to a
range of flow rates (greater than 0.005 cc/sec and less than
0.03 cc/sec) and pressures (9 psi to 12 psi) .
Typ e 2 - moderate- density tissues with m o derate
tissue compliance, found in attached gingiva and palatal
tissues. These tissues are less adaptive and require slower
flow rates (approximately 0.005 cc/sec) and produce mod­
erate pressure (ranging from 50 psi to 75 psi) for safe and
comfortable injections.
Type 3 - high-density tissues with very low tissue com­
pliance (i.e., minimal adaptive capacity), found in the PDL.
This tissue type requires a fixed slow flow rate (0.005 cc/sec)
and produces a range of tissue pressures (225 psi to 350 psi).
In contrast to CCLAD systems, traditional manual
syringes are dependent upon subj ective pressures applied
to syringe pistons by clinicians (Hochman, 1997). To over­
come tissue resistance during manual inj ections, operators
must apply force to the syringe piston. The force applied
must be sufficient to overcome any back-pressure resis­
tance that builds up while inj ecting the anesthetic. This
force leads to increasing pressures in tissues. Manual sy­
ringes lack design features to regulate pressures or pre­
cisely control flow rates ; therefore, operators must rely
on subj ective observations and tactile sensations. These
uncontrolled variables lead to conditions where opera­
tors may not apply sufficient force to overcome b ack­
pressures generated during dental inj ections in one tissue
type, whereas in other tissue types, operator response to
high resistance may result in extremely high pressures
( 600 psi to 1 ,200 psi) (Pashley, Nelson, & Pashley, 198 1 ;
Walton & Garnick, 1982) . Limitations i n the design o f
traditional manual syringes, coupled with poor operator
technique, contributes to undesirable outcomes of pain
and adverse tissue reactions (Pertot & Dejou, 1992; Saroff,
Chasens, & D oyle, 1986; Smith & Pashley, 1983; White,
Reader, B eck, & Meyers, 1988) . The subj ective flow rates
and uncontrolled high pressures produced by traditional
mechanical syringes have been shown to produce opera­
tive and postoperative pain as well as tissue damage for
dental patients (Froum et al. , 2000). The use of CCLAD
systems is currently the only approach that takes into ac­
count that specific tissues require specific flow rates and
controlled low pressures in order to maintain comfort,
efficacy, and safety when performing dental inj ections
(Hochman et al. , 2006).
CCLAD and M a n u a l Syri nge
Com parison
A key difference between CCLAD instruments and man­
ual syringes is their respective impact on fluid dynamics.
CCLAD instruments permit fluid flow rates and fluid
pressures to be independent parameters. This is not pos­
sible with manual syringes, where increased flow rate will
result in increased pressure and decreased flow rate will
result in decreased pressure. When these two parameters

are decoupled, flow rates and fluid pressures can be in­
dividually optimized for each tissue type. This results in
improved diffusion of anesthetic solutions through soft
tissues and cortical bone, optimal patient comfort, and
minimal tissue damage (Corbett et a!. , 20 10; Kudo, 2005 ;
Nusstein et a!. , 2004).
With the introduction of CCLAD systems, two in­
j e ctions previously unreported in the dental literature
have been described, the AMSA and P-ASA (Friedman
& Hochman, 1998,1999 ) . These inj ections have certain
distinct similarities; they are both maxillary inj ections,
performed from a p alatal approach, and require large
volumes (0.9 mL to 1.4 mL) of anesthetic solutions to
be deposited into dense palatal tissue (Type 2) with low
compliance (distensibility ) . To produce pulpal anesthe­
sia of multiple maxillary teeth, 0 . 9 mL to 1.4 mL of an­
esthetic solution is required to effectively diffuse from
the p alatal soft tissue through the cortical bone to the
maxillary dental plexus without producing pain or tissue
damage.
Studies have confirmed that CCLAD systems make
it possible to provide effective pulpal and soft-tissue an­
esthesia to multiple maxillary teeth from a single palatal
approach inj ection (Bassett & DiMarco, 20 10; Fukayama,
200 1 ; Perry & Loomer, 2003 ) . These techniques are de­
scrib e d in Chapter 13, " Inj ections for Maxillary Pain
Control 11 - Palatal Approach." Studies further confirm
that CCLAD systems can deposit large volumes of anes­
thetic solutions from a palatal approach (Acharya et a!.,
20 1 0 ; Corbett et a!. , 20 1 0 ; Holtzclaw & Toscano, 2008;
Schwartz-Arad, D olev, & Williams, 2004) . Reliably com­
fortable and safe delivery of large volumes of fluid into
low compliance (non-distensible) tissues is possible with
CCLAD instruments because of their controlled fluid dy­
namics. This is due to the fact that CCLAD systems gen­
erate a distinctly different fluid dynamic (controlled rate
and pressure) compared with traditional manual syringes.
Without the ability to control tissue pressures, severe pain
and tissue damage can occur.
The Benefits of CCLAD for POL
I njections
The benefits o f CCLAD systems are also demonstrated
when performing intraligamentary (PDL) dental inj ec­
tions (Ashkenazi, Blumer, & Eli, 20 10; B erlin et a!., 2005;
Froum, et a!., 20 00). The PDL inj ection dates back to the
early 1900s and typically was used as an alternative inj ec­
tion when conventional techniques failed to produce ad­
equate pulpal anesthesia (Fischer, 1933). It was defined as
an inj ection performed using "high pressures" generated
by manual syringes (Dreyer, Van Heerden, & D e Joubert,
1983 ; Walton & Abbott, 198 1 ) . Pashley and coworkers
were the first to report on the fluid pressure exhibited dur­
ing this inj ection (Pashley, Nelson, & Pashley, 198 1 ) . Pres­
sures generated during PDL inj ections exceeded 600 psi
CHAPTER 9 LOCAL ANESTHETI C DELI V ERY DEVICES
• 163
and produced undesirable tissue changes. Later, a pistol
grip, high-pressure manual syringe was developed that ex­
erted even greater pressures (in excess of 1 ,200 psi) than
previously reported. As expected this also produced tis­
sue damage (Walton & Garnick, 1982). The vast maj ority
of negative sequelae, which included moderate to severe
pain and reversible and irreversible tissue damage, can be
attributed to the traumatic forces and high pressures gen­
erated when performing PDL inj ections with manual sy­
ringes (Pertot & Dejou, 1992) . It is now generally accepted
that Type 3 periodontal tissues generate very high pres­
sures in response to mechanical systems used to deliver
anesthetic solutions. As a result of this high back-pressure,
only a relatively small volume (0.2 mL to 0.4 mL) of an­
esthetic solution can be delivered, resulting in short dura­
tions of effective anesthesia; however, of greater concern
are the consistent reports of tissue damage and moder­
ate to severe pain (Dower & Barniv, 2004; Faulkner, 1983;
Miller, 1983).
In contrast, the fluid dynamics of CCLAD systems
produce controlled low pressures (225 psi to 350 psi ) ,
where flow rates a n d fluid pressures are maintained at
independent, specific values (Hochman et a! . , 2 0 0 6 ) .
CCLAD-controlled administration enables improved dif­
fusion of anesthetic solutions through soft tissues into the
medullary bone (Nusstein et a!. , 2004) . This improvement
is a direct result of its ability to introduce greater volumes
of anesthetic solution without increasing pressure in the
PDL space (Froum et a!. , 2000). This greater volume (0.9
mL to 1.4 mL) of anesthetic solution results in longer du­
rations of effective anesthesia, approaching 35 minutes on
mandibular molar teeth with 1.4 mL volume, from PDL in­
j ections performed with a CCLAD system (B erlin et a!. ,
2005 ) .
Histologic reports following PDL inj e ctions with a
CCLAD system in a mini-swine pig model showed that
PDL inj ections could be performed without producing ad­
verse inflammatory tissue reactions (Froum et a!. , 2000).
Previous PDL histologic studies conducted with manual
syringes demonstrated consistent and repeated tissue
damage and increased pain (Albers & Ellinger, 1988; Galili
et a!., 1984; Pertot & D ej ou, 1992; Walmsley et a!., 1989;
Walton & Garnick , 1982) . Numerous published studies
have demonstrated that there is minimal to no pain and no
tissue damage experienced when receiving PDL inj ections
with a CCLAD system (Asarch et a!. , 1999; Ashkenazi,
B lumer, & Eli, 2005; Froum et a!., 2000; Gibson et a!.,
2000; Oztas et a!. , 2005) .
Device Featu res
Dynamic Pressure Sensing
As previously noted, a unique feature of Wand STA de­
vices is their dynamic (pressure force feedback) (DPS®).
The audible and visual feedback system ( s e e Figure
A9.5-2 •) provided during PDL inj ections cues clinicians
164 SECTI O N I N JECTI O N FUNDAMENTALS
Ill •
• •
FIGURE A9. 5-2 Patented Dynamic Pressure Sensing (DPS)
on the Wand/STA Instrument Provides Real-Time Audible
and Visual Feedback of Fluid Pressures during Injections. The
example here is during a PDL inj ection, in PDL mode.
FIGURE A9. 5-3 Diffusion of Local Anesthetic Solution during Periodontal Ligament Injections with the STA
Wand Instrument.
Source: Courtesy of Mark Hochman DDS.
to optimal needle placement and fluid pressures through­
out the inj ection. When properly placed, significantly less
pressure is required for intraligamentary (PDL) inj ec­
tions compared with traditional manual PDL syringes.
The DPS feedb ack indicates that the anesthetic is dis­
tributing in the PDL space verses into the surrounding
soft tissues, ensuring that adequate volumes of anesthetic
diffuse through the medullary bone as demonstrated in
Figure A9.5-3 •· The DPS system also maintains a speci­
fied range of pressures for safe and successful intraliga­
mentary inj ections.
Multi-Cartridge Technique
The success rates of inferior alveolar nerve blocks can
be enhanced using CCLAD in conj unction with a multi­
cartridge technique that was described by Camarda et al. ,
2007. Unlike manual syringes, the basic design o f Wand
STA devices allows more than one cartridge to be adminis­
tered from a single needle insertion (see Figure A9.5-4 •)
because the cartridge holder of the device is not directly
connected to the needle. This design allows additional car­
tridges to be exchanged without removing the needle from
the deposition site during an inj ection reducing trauma as­
sociated with multiple needle insertions.
Any technique that allows increased anesthetic vol­
umes to be deposited from a single insertion has multiple
potential benefits, including reduced risk of:
1. positive aspiration and hematoma
2. trauma and local complications, such as trismus, intra­
vascular needle placement, and dysphasia from direct
contact with the lingual nerve
3. intraoperative and postoperative discomfort
 CHAPTER 9 LOCAL ANESTHETI C DELI V ERY DEVICES
• 165

FIGURE A9.5-4 Use of the Multi-Cartridge Mode on the Wand/STA Instrument

Allows for More Than One Cartridge of Anesthetic to Be Delivered Simultaneously
with a Single Needle Insertion, Reducing Associated Tissue Trauma.
Source: Courtesy of Mark Hochman DDS.

Tech n iq u e Considerations produces a reactive force that is opposite to the direction

Effective dental anesthesia can b e aided through CCLAD.
Benefits include increased patient comfort and reduced
tissue damage for all inj ections especially when perform­
ing palatal inj ections.
Inferior Alveolar Nerve Block
When performing deep penetrations for inferior alveolar
nerve blocks, the occurrence of needle deflection away
from optimal deposition sites has been reporte d . The
small, lightweight Wand® handpiece system allows clini­
cians to improve success by using a hi-rotational insertion
technique. The hi-rotational insertion technique reduces
inadequate lA blocks by eliminating needle deflection
(Hochman & Friedman, 20 00) . Mandibular block anes­
thetic techniques suggest either a 25-gauge or a 27-gauge
long needle as described in Chapter 14, " Inj ections for
Mandibular Pain Control." Needles are designed with a
long (1 IA to 1% inch) flexible, cylindrical shaft with a bev­
eled needle tip facing in one direction. The needle bevel
that the bevel faces. If a bevel is facing up, it will cause
the needle to bend downward during insertion. When ad­
vancing a needle with a manual syringe, the needle tip will
deflect in a direction that is opposite to the needle bevel.
Clinicians cannot safely rotate needles attached to manual
syringes during insertion. Wand handpiece systems use
a pen-like grasp of a lightweight, disposable handpiece
held between the index finger and thumb (see Figure
A9.5-5 •) . As the Wand handpiece is advanced, clinicians
simultaneously roll the handpiece between the finger
tips in a gentle clockwise and counter-clockwise move­
ment that minimizes needle deflection. This is referred to
as bi-rotational insertion. The needle bevel is constantly
changing directions as it is advanced; therefore, the hi­
rotational insertion technique eliminates forces that cause
needle deflection. When inserted this way, needle tips may
be positioned closer to the intended target above the man­
dibular foramen. The hi-rotational insertion technique has
been shown to improve success (Aboushala et al. , 2000)
when performing inferior alveolar nerve blocks and other
166 SECTI O N I N JECTI O N FUNDAMENTALS
Ill •
FIGURE A9. 5-5 Wand Handpiece. The unique lightweight
handpiece provides for easy use and reduced ergonomic stress
on the hands common with the use of manual syringes.
Source: Courtesy of Mark Hochman DDS.
mandibular techniques such as Gow-Gates and Vazarani­
Akinosi blocks. Additionally, mandibular anesthesia can
be improved by employing a multi-cartridge technique
with CCLAD.
AMSA and P-ASA Techniques
Clinical studies have reported that AMSA (see Figure
13-18) and P-ASA (see Figure 13-10) inj ections performed
with a CCLAD system produce a more comfortable ex­
perience for p atients compared with manual syringes.
Potential CCLAD benefits in palatal inj ections include
reduced patient anxiety, profound soft-tissue anesthesia,
improved pulpal anesthesia and tissue hemostasis, more
efficient diffusion of solution through tissues, and reduced
tissue trauma compared with manual syringes (B assett &
D iMarco, 20 10; Friedman & Hochman, 1998; Fukayama
et al., 2003 ; Lee et al. , 2004; Perry & Loomer, 2003 ) . These
results appear to be related to the ability of CCLAD sys­
tems to precisely control fluid flow rates and fluid pres­
sures irrespective of dense palatal connective tissues that
make comfortable inj ections with manual syringes difficult
to perform. CCLAD systems have specific settings (capa­
ble of maintaining low-pressure gradients during deposi­
tion) for palatal inj ections that allow increased volumes to
be deposited without causing tissue damage. Maintaining a
low-pressure gradient with a controlled fluid pressure over
a longer period of time produces more effective diffusion
within the tissues and a more comfortable inj ection.
PDL Technique Using Wand STA Single Tooth
Anesthesia System Instruments
As previously noted, PDL inj ections given with CCLADs
administer greater volumes of anesthetic solution without
increasing pressure in the PDL space. Two benefits of this
are longer duration of anesthesia (due to greater volumes)
and less trauma to the PDL (due to low pressures exerted) .
Performing P D L inj ections with Wan d STA d e ­
vices differs from manual syringes i n a number of ways
(Milestone Scientific, 20 13).
B o th may u s e 3 0 - gauge extra-short needles ( -lh
inch); however, Wand STA devices use a handpiece sys­
tem for which a bonded, pre-attached needle is required.
The Wand STA device is set to the STA Mode (utiliz­
ing 225 psi to 350 psi ) . This activates the Pressure Sens­
ing Scale (PSS) (a sequence of orange, yellow, and green
LED lights on the face of the instrument) for real-time
visual and auditory feedback to guide needle placement
at PDL. The PSS gauge will light up as the foot control
is depressed and the device begins pressure sensing (see
Figure A9.5-2).
To perform the inj ection, a pen-like grasp is used to
insert the needle into the gingival sulcus in a manner simi­
lar to a periodontal probe. Once a fulcrum is established,
flow is initiated after which the needle is advanced slowly
and gently, similar to the advancement of a periodontal
probe. The visual PSS feedback can be interpreted as
follows:
1. Orange indicates minimal pressure has built up.
2. Yellow indicates mild pressure has been achieved.
3. Green indicates moderate pressures indicative of the
PDL tissue.
Corresponding ascending tones will accompany visual
feedback from the PSS LED. A voice will report "PDL"
once the green zone is achieved and the PDL tissue is
located.
Similar to the adoption of many new technologies, a
learning curve exists when adapting to Wand STA devices.
It is normal when performing Wand STA intraligamentary
inj ections to relocate the needle tip a number of times to
find an optimal deposition site within the PDL tissues. With
feedback from the DPS technology confirming appropri­
ate placement of the needle, successful anesthesia is more
likely to result. Importantly, continuous PSS feedback
assures that the needle has not moved from its original
location during the inj ection process. Efforts should be
made to stabilize the needle in order to avoid movements
that displace the tip during deposition. If displacement
occurs, it can result in a rapid loss of pressure (noted by
the PSS LED scale moving back to yellow or orange) . If
pressure loss is confirmed, the needle should be withdrawn
and its original location reestablished or another effective
site located.
Removing needles from tissues is best accomplished
in the middle of CCLAD aspiration cycles (the time from
initiation to completion of aspiration) after automatic flow
of solution has ceased and before flow is resumed to avoid
back-spray or dripping solution into patients ' mouths.
B ack-spray or dripping of solution into the mouth is not
harmful and the solution can be flushed and suctioned out,
but anesthetics have a very bitter taste.
In contrast to manual syringes, using force to press
Wan d h a n d p i e c e s y s t e m n e e d l e tips i n t o P D L s is

unnecessary. An additional function of the DPS feedback
signals clinicians when excessive hand force is applied to
needles. Excessive hand force should be avoided because
they can result in blockages of the flow of anesthetic so­
lutions. Pressures over 450 psi result in an over-pressure
condition triggering D P S auditory and visual alarms.
Further administration of anesthetic will be prevented. If
this occurs, force applied to the needle tip the needle tip
must be reduced, and it may be necessary to reposition
the needle.
Over-pressure alarms can be triggered by excessive
hand force and/or occlusion of the needle. In either situa­
tion, the needle must be relocated.
Drug Selection
In all situations, clinicians must use current dental litera­
ture and professional judgment when selecting anesthetic
drugs and volumes. For PDL inj e ctions performed with
Wand STA devices, the following guidelines are provided
by the manufacturer:
2% Xylocaine Hydrochloride, 1:100,000 Epinephrine (or
other 2 % local anesthetics)
• A drug volume of 0.9 mL is recommended for single­
rooted teeth.
• A drug volume of 1.8 mL is recommended for multi­
rooted teeth.
• 1 :50,000 vasoconstrictor concentrations are not rec­
ommended for PDL inj ections.
4 % A r t i c a i n e H y d r o c h l o r i d e ( o r o t h e r 4 % l o c al
anesthetics)
• A drug volume of 0.5 mL is recommended for single­
rooted teeth.
• A drug volume of 0.9 mL is recommended for multi­
rooted teeth.
• 4% articaine with 1 :200,000 vasoconstrictor concen­
tration is recommended.
• 4% articaine with 1:100,000 vasoconstrictor concen­
trations are not recommended for PDL injections or
palatal injections to include the AMSA and P-ASA
injections (these injections are further discussed in
Chapter 13, "Injections for Maxillary Pain Control 11 -
Palatal Approach).
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··························································· ® ··························································

Patient Assessment for Local

�tilestmesia

OBJECTIVES KEY TERMS

• Defi ne a n d d i scuss the key terms in this cha pter. absol ute
contra i n d ications 178
• I d e ntify a n d d i scuss the respon s i b i l ities associated with the
adverse drug eve nts
d e l ivery of reg i o n a l a n esthesi a . (AD R) 181
• Descri be t h e ASA (Am erican Society o f Anesthesio l o g ists) a ltern ative medicine 1 71
Physica l Status C l a ssification Syste m categories I-VI ( P 1 -P6) . American Society of
Anesthesiologists (ASA) 170
• D iscuss patient assess m e nt too l s for the eva l u ation of physica l
ASA P hysica l Status
a n d psych o l o g i ca l to l e ra n ce to l oca l a n esth esi a .
C l a ssification Syste m 1 71
• Ana lyze a n d d i scuss t h e i m p l i cati ons o f patient eva l u ation i n atypica l p l a s m a
obta i n i n g informed consent. c h o l i n esterase 178
• I d e ntify and a p p l y contra i n d i catio n s to the use of l oca l cerebrovascu l a r accident
a n esth esi a . (CVA) 180
co m p l e mentary a n d a lte rna­
• I dentify a n d eva l uate treatment mod ificati ons that ca n be tive medicine (CAM) 1 71
m a d e to i n crease patient safety a n d comfo rt with l oca l co m p l e mentary
a n esth esi a . medicine 171
•. Eva l u ate situ ations that req u i re a m e d i ca l consu ltation before co ncom ita nt 1 72
treatment. De nta l Anxiety Sca l e
(DAS) 1 72
• Defi n e fu n cti o n a l capacity and d escri be a ctivities to m eet the
dental fea rs
4 m etabo l i c e q u iva lent of task (M ET) I l eve l . q u esti o n n a i re 1 71
• Descri be t h e dose l i m itati o n with a vasoco n strictor when fu n cti o n a l capacity 175
ca rd i ovascu l a r d i sease is reported . i nteg rative medicine 171
meta b o l i c eq u ivalent of task
• I dentify s i g n s a n d sym ptom s of u n d i a g n osed m e d i ca l
(M ET) 175
con d itions that ca n affect l oca l a nesthetic a d m i n i stratio n .
meth a m p h eta m i n e 183
• D iscuss t h e i m po rta nce o f posta nesth etic ca re . meth e m o g l o b i n e m i a 1 78

169
170 SECTI O N I N JECTI O N FUNDAMENTALS
Ill •
KEY TERMS (contin ued)
re l ative contra i n d icati ons 1 78
revers i b l e isch e m i c n e u ro l o g i c d eficit ( R I N D) 1 80
Stress red u ctio n protoco l (S R P) 1 7 1
CAS E S TUDY
Carlos Martinez
C a r l os M a rtinez, a 67-ye a r- o l d H is p a n i c m a l e , is a
new patient with exte nsive d e nt a l n e e d s . H i s h is­
tory i n c l u d es Type 2 d i a b etes and chro n i c i nfection
with h e patitis C . B l ood p ress u re is 1 42/90 and he
is a m o d e rate s m o ke r. O n fu rther q u esti o n i n g a n d
after medical consu ltatio n , h e is fo u n d t o h ave sig­
n ifi cant l iver damage, is resista nt to insu l i n thera py,
a n d is ta k i n g a new m e d i cati o n fo r hyperte n s i o n ,
C o rg a rd ( n a d o l o l ) , w h i c h h e a n d h i s p h ys i c i a n a d ­
m it has n ot yet consiste ntly bro u g h t B P va l ues t o a
n o r m a l leve l .
H e a lso h a s a fa m i ly h i story o f meth e m o g l o b i ­
nem ia, a l t h o u g h h e states t h a t h e has never h a d a n
e p isode, perso n a l ly.
H e is a m b u l at o ry a n d o t h e rwise a b l e to visit
the denta l office with out d ifficulty. Exte nsive d e nta l
a n d d e nta l hyg i e n e t h e ra p y a re p l a n n e d that wi l l
req u i re l o c a l a n est h e s i a with v a s o c o n st r i ct o r fo r
periodonta l debridement i n a l l fou r q u a d ra nts a n d
n u m erous resto rative a p p o i ntme nts.
I ntrod uction
Local anesthesia can b e physically and psychologically de­
manding for patients (Meechan, 2005; Moore & Brodsgaard,
200 1). Comprehensive patient assessment is the foundation
for safe delivery of local anesthetic drugs. In most healthy
individuals, local anesthetics can be administered accord­
ing to published dose recommendations. In individuals with
compromised health, the administration of local anesthesia is
usually safe as long as appropriate precautions are observed.
Clinicians must determine when local anesthetic solutions
can be used safely or should not be used. Patients should
always be monitored before, during, and after the adminis­
tration of local anesthetic agents. This chapter will discuss
specific considerations for local anesthesia administration
and a standardized approach to patient assessment. By ob­
serving standardized assessment criteria, limitations and con­
traindications for receiving local anesthesia can be identified.
ASA Physical Status Classification System
Applying a standardized approach to patient assessment
should be used when determining physical and psycho­
logical tolerance to proposed treatment. The assessment
thyrotoxic crisis 1 77
thyrotoxicosis 1 77
transient isch e m i c attack (TIA) 1 80
process is valuable in determining appropriate modifica­
tions to reduce the risk of adverse events and potential
medical emergencies.
According to the American Society of Anesthesiologists
(ASA), patient safety is the most important goal in the deliv­
ery of anesthesia ( American Society of Anesthesiologists,
20 12). The responsibilities associated with the delivery of
local anesthesia are described in the ASA Statement on
Regional Anesthesia* :
Anesthesiology i n all o f its forms, including regional an­
esthesia, is the practice of medicine. Regional anesthesia
involves diagnostic assessment, the consideration of indi­
cations and contraindications, the prescription of drugs,
and the institution of corrective measures and treatment
in response to complications. Therefore, the successful
performance of regional anesthesia requires medical as
well as technical expertise.
According to the ASA, clinicians who administer re­
gional local anesthesia must conform to a prescribed se­
quence of care ( see Box 1 0-1 •) . B ecause regional nerve
blocks are administered by dental professionals, these
guidelines apply when local anesthetics are administered.
Appropriate attention to anesthetic procedures and
patient responses is crucial because it has been reported
that the majority of medical emergencies in the dental
office are associated with the administration of local an­
esthesia ( Kaufman, Goharian, & Katz, 2000; Malamed,
20 1 3 ) . An example of pre-anesthetic evaluation is obtain­
ing vital signs and considering blood pressure levels before
1 . Pre-anesthetic eva l u ation of the patient
2. Prescri ption of the a nesthetic p l a n
3. Person a l p a rticipation i n the tech nical aspects o f t h e
reg i o n a l a n esthetic
4. Fo l l owing the cou rse of the a n esthetic
5. Rem a i n i n g physica l ly ava i l a b l e for the i m m e d iate
d i a g n osis and treatment of emergencies
6. Provi d i n g i n d icated post-anesthesia care
Source: "El e ments o the ASA Medical Component of Care" from
Statement on Regionalf Anesthesia. Copyright © 2007 by American
, Soci ety of Anesthesiol o gists. Used by permi s si o n of American So- ,
•
ciety of Anesthesiol o gists.
: . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . •
*Excerpt from Statement on Regional Anesthesia. Copyright © 2007 by
American Society of Anesthesiologists. Used by permission of American
Society of Anesthesiologists.
 CHAPTER 1 0 PATI E NT ASSESSMENT FOR LOCAL ANESTHESI A
• 171

administering a local anesthetic with a vasoconstrictor. emergencies (Malamed, 2007; Nield-Gehrig & Willman,
Patients must be continuously observed and assessed for 2008; Pickett & Gurenlian, 20 10). See Appendix 10-2 for a
adverse reactions following the delivery of local anesthetic suggested stress reduction protocol. For further discussion
agents, particularly because of the possibility of delayed on dental fears related to local anesthesia, see Chapter 18,
responses. Clinicians should be prepared to identify and "Insights for Fearful Patients."
manage all adverse reactions.
Comprehensive patient assessment, including the use Tools for Patient Assessment
of the ASA Physical Status Classification System, is a key
Comprehensive Patient Assessment
factor in determining the safety of local anesthesia ad­
ministration (see Box 10-2 •) . The ASA system classifies Standardized, comprehensive patient assessment is nec­
patients into six categories, ASA I-VI (also noted as ASA essary in order to minimize adverse events related to re­
P1-P6 ) , based on their overall physical health. Examples ceiving local anesthesia. Key elements for applying health
of medical conditions in each class are provided in Appen­ information to local anesthetic procedures will be high­
dix 10-1 (Malamed, 2007; Nield-Gehrig & Willman, 2008) . lighted in the following discussion. D e ntal fears ques­
The maj ority of healthy patients are classified ASA I tionnaires and the benefits of consulting with medical
or ASA II. Treatment modifications are few and serious professionals will also be discussed.
adverse events are uncommon for these patients. Patients
who are classified ASA III with severe systemic disease are Medical and Dental History
more likely to experience adverse events. These patients Information from medical and dental histories includes
may still be considered for elective dental procedures with past and current medical conditions, prescription medi­
local anesthesia; however, treatment modifications to en­ cations being taken, as well as over-the-counter products,
sure patient safety are frequently necessary. Elective den­ including dietary and herbal supplements. Prudent prac­
tal care is contraindicated for ASA IV patients. tice suggests that the best way to identify potential health
Local anesthesia is stressful for many patients, and a risks from local anesthesia administration is to take a good
common emergency situation associated with the inj ec­ medical history and to follow up positive responses thor­
tion process is syncope. Syncope is a stress-related emer­ oughly (Pickett & Gurenlian, 20 10).
gency (Malamed, 2007); therefore, the assessment process When interviewing patients, it is also important to
should include a determination of psychological tolerance inquire about the use of complementary and alterna­
in addition to physical tolerance. Anxiety and fear can be tive medicine (CAM), defined by the National Institutes
measured using dental fears questionnaires and dental of Health as "a group of diverse medical and health care
anxiety scales (DAS) (Corah, 1969; Humphris, Morrison, systems, practices, and products that are not generally
& Lindsay, 1995 ) . Most health history forms include a considered part of conventional medicine (NIH, 2014)."
question for "previous problems in a dental appointment." (For further explanation, see Box 10-3 •) . Previous expe­
A positive reply on this item indicates the need for a de­ riences with local anesthesia can provide valuable insight
termination of the cause of the event and the role of stress
(Pickett & Gurenlian, 20 10). Treatment modification with
an appropriate stress reduction protocol (SRP) can re­
duce the incidence of psychogenically generated medical

The U.S. N ational Institutes of Health defi ne complementary

and a lternative medicine (CAM) as " a group of d iverse med­
ical and hea lth ca re systems, practices, and products that a re
not genera l ly considered part of conventional medici n e . "
ASA I A normal hea lthy patient " Complementary medici n e " refers t o the u s e of
ASA II A patient with m i l d system i c d isease a non m a i nstream approach togethe r with conventi o n a l
ASA I l l A patient with severe system i c d isease medicine.
" Alternative med icine" refers to the use of CAM in
ASA IV A patient with severe system i c d isease that is a place of conventio n a l medicine.
constant th reat to l ife " I ntegrative medici ne" com b i n es treatments from
ASA V A mori b u n d patient who is n ot expected to conventio n a l medicine and CAM for which there is some
survive without the operation h i g h -q u a l ity evidence of safety a n d effectiveness. It is a lso
ASA VI A declared brain-dead patient whose organs a re ca l l ed integrated medicine. Accord i n g to the NIH, the
being removed for donor p u rposes b o u n d a ries between CAM a n d conventio n a l medicine a re
not absol ute, a n d specific CAM p ra ctices m ay, over time,
Source: " ASA Physic Status Cl a ssification System" from Physical
Status Classifi cation alSystem. (2006)
become widely accepted.
. Copyright © 2007 by Ameri c
Soci ety of Anesthesi o l o gi sts. Used by permi s si o n of Ameri can an : Source: http://nccam.nih.gov/heal t h/whati s cam. Accessed January :
: S.o � i �t: �: � n.e�t ��s:o� o.g:s:s .(�S.A:
• •

• • • • • • • • • • •• • • • • • • • •
: .2� 2.0 ;�·
.

• • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • •
172 SECTI O N I N JECTI O N FUNDAMENTALS
Ill •
regarding potential problems; for example, patients may
report difficulty getting numb, experiencing rapid heart­
beats, or feeling fatigued after inj ections. They may also
report fainting during or after receiving anesthesia or from
" shots" in any setting, staying numb for several hours, or
that they always "take a lot of Novocain," among other re­
sponses. It is important to investigate all previous adverse
reactions and to develop plans to avoid their recurrence.
B efore the administration of local anesthetic agents,
all current drugs and drug-related products that a patient
is taking must be evaluated and recorded. Attention to po­
tential interactions between these drugs and drug-related
products and the local anesthetics to be administered is im­
portant in avoiding adverse reactions (Pickett & Gurenlian,
20 10) . B ox 1 0-4 • outlines a suggested patient drug re­
cord. Drugs that are in a patient's system when local an­
esthetics are administered are referred to as concomitant.
These drugs may influence the choice of local anesthetic
drugs and the quantities administered because of their in­
fluence on the efficacy, metabolism, and/or elimination of
anesthetic drugs. In other words, some concomitant drugs
potentiate the actions or delay the metabolism of local
Docu m e nt the fo l l owing for p rescription m edica tion s:
1 . Drug n a m e : both trade and generic n a m es (such as
Cou m a d i n TM [wa rfa rin])
2. Drug cl assificatio n : intended action of drug group
(such as a nticoa g u l a nt)
3. P u rpose for taki n g the drug; this m ay d iffer from its
cl assification, for exa m p l e, a cardiovascu l a r drug (such
as propranolol) that is used to p revent m i g ra i n es
4. Prescri bed dose a n d sched u l e , note any deviations
from p rescribed and ratio n a l e
5. Side effects a n d adverse rea ctions
6. Preca utions o r contra i n d i cations
7 . Drug i nteractions
8. Treatment mod ifications i n d i cated
For n onprescription, over-th e-cou nter drugs, vita m in s,
m in erals, h e rba ls, and CAM, docum ent:
1 . Drug n a m e : both trade and generic n a m es (Advi l ™
[i b u p rofen])
2. Drug cl assificatio n : intended action of drug group
(such as a n a l gesia)
3. Pu rpose for taki n g the d rug, for exa m p l e , m i l d
headache
4. Dose a n d sch e d u l e (if a p p l ica b l e); note when doses
exceed l a b e l dose
5. Side effects o r adverse reactions
Updates should include notations reg a rd i n g any concerns
or chan ges since p revious appointments. Refere n ces a re
ava i l a b l e fo r over-th e-co u nter p roducts a n d a re integrated
: . � • • �� · · · � ; , �� • • • : . �� ��� � . ;� .� ; • • • • • • • • •
i to n y e l c ro c d e n a l c ro a s
anesthetic drugs whereas others diminish their actions or
hasten their metabolism; likewise, local anesthetic drugs
can alter the actions of concomitant drugs. For example,
ester local anesthetics can interfere with the antimicrobial
activity of sulfonamide antibacterials and epinephrine's ef­
fects can be potentiated by nonselective beta-blockers.
There are many different medical and dental history
forms available, including multilingual versions of basic
forms (see Box 1 0-5 •) . Recognizing that there are re­
gional variations in documentation and in approaches to
information gathering, formats that meet clinical expecta­
tions should be selected.
An additional tool for assessing patient anxiety and
fear is a fears questionnaire. This document can provide
helpful information about levels of dental anxiety and
fear. According to Newton and Buck, there are 15 different
measures of dental care anxiety (Newton & Buck, 2000). A
useful method for measuring anxiety in the dental setting
has been developed by Corah (Corah, 1969; Humphris,
Morrison, & Lindsay, 1995) (see Box 10-6 •) .
Clinical Examination
Obj ective information about a patient's physical condi­
tion can be obtained from an evaluation of vital signs
including blood pressure, pulse, respiration, and weight
In a u n i q u e p roject, the University of the Pacific School
of Dentistry a n d MetLife Insurance Company have cre­
ated a basic hea lth h istory form ava i l a b l e in 40 l a n g uages
(Metlife, 201 4), i n cl u d i n g Ara b i c, C h i n ese, Farsi, German,
H m o n g , J apanese, Portu g u ese, Russian, Spanish, Thai,
Vietn a m ese, a n d m a ny oth ers. These forms a re ava i l a b l e at
: . ��� · :n. :� . ;� . �:n. . . �� : · · · ��� . �� ��� �� . �� ·• • •
e en l .c und he " R ur t "t
Cora h 's Dental Anxiety Scale (DAS) is a c l i n i ca l too l for
measuri n g dental a nxiety i n a d u lts (Cora h , 1 969; H u m p h ris,
Morrison, & Lindsay, 1 99 5). Patients were ori g i n a l ly pro­
vided with fo u r exa m p l es of dental situations. A fifth situ­
ation, specifica l ly concern i n g l oca l a n esthesia, was l ater
added to the tool ( H u m p h ris, Morrison, & Lindsay, 1 99 5).
' Patients a re asked to select the response that most closely
m atches their reaction to one of the hypothetica l situ a­
tions. The responses a re a rra nged in order of i n creasing
severity, two being more severe than on e, for exa m p l e .
• Patients score betwee n 4 a n d 2 0 poi nts, with h i g h e r va l u es
i n d icating h i g h e r anxiety. Scores above 1 5 i n d i cate p h o b i c
l eve ls. D A S forms a re ava i l a b l e a t : www.denta lfearcentra l .
: . . :�rr:�d.i � /��� t.a �-��� i �t:�s.c � l � �p.d! · • • • • • • • • • • • • • • •
or

(Wilkins, 20 12). Blood pressure values directly correlate
with specific ASA classifications. Values outside normal
ranges should be investigated before administering local
anesthetics. Acceptable safe ranges for the administra­
tion of local anesthetics are listed in Appendix 10-1 , "ASA
Physical Status classification: Examples of Diseases and
Conditions." Abnormally slow or fast breathing can be an
indicator of disease, anxiety, or both. Values above 20 and
below 12 are considered to be outside the normal range.
Pulse rates may vary as well depending on general health
and fitness, anywhere from 60 to 1 0 0 beats per minute
(Wilkins, 20 12). In disease states, pulses may range from
very low to very high. As previously discussed, weight is
critical when determining appropriate local anesthetic
dosing, especially for children (see Chapter 7, "Dose Cal­
culations for Local Anesthetic Solutions").
General observations of patients can yield clues as to
their ability to tolerate local anesthetic procedures. Patients
should be rested and well nourished before appointments.
To reduce risks of hypoglycemia, it is important for patients
with diabetes to have consumed adequate food and have
taken prescribed medications before appointments.
Medical Consultation
In order to optimize safety, consultation with a patient's
physician is sometimes needed before local anesthesia.
Medical consultation may be considered when a patient
has symptoms of undiagnosed disease and/or has not had
regular medical exams. It may also be considered when
there are gaps in information provided, when pregnant, or
when other concerns suggest follow-up is necessary. Medi­
cal conditions that suggest a need for consultation include
cardiovascular conditions, recent surgeries, uncontrolled
hypertension, psychological conditions that may influence
oral procedures, compromised liver and/or kidney func­
tion, immune system compromise, and any concerns re­
garding local anesthesia and/or treatment.
U ND IAGNOSE D AND U N D I SCLOS E D M E D I CAL COND IT I ONS
B oth medical history and dental fears questionnaires are
completed by patients or their representative( s) and provide
both obj ective and subj ective information. Unfortunately,
information is limited to details that the patient or his or
her representative chooses to or is able to disclose. Ideally,
patients will be thorough and truthful about details in
medical and dental histories.
When information gained is questionable, a consult
with a patient's physician is recommended in order to
clarify details and, in some cases, to ensure safety during
anesthetic procedures. This is especially true if patients are
unable to recall or appear to be withholding important de­
tails about medical conditions or current medications. An
incomplete understanding of health status can result when
there is no history of recent medical care.
Some patients have undiagnosed medical conditions
with no obvious signs or symptoms and for whatever rea­
son do not seek heathcare or lack access to it. Undiagnosed
CHAPTER 1 0 PATI E NT ASSESSMENT FOR LOCAL ANESTHESI A
• 173
medical conditions can influence the safety of local anesthetic
drugs. Medical conditions, language barriers, cultural barriers,
mental disabilities, and physical disabilities can all limit an in­
dividual's ability to provide relevant health-related informa­
tion. Unusual signs and symptoms observed or elicited during
patient assessment serve as clues to undiagnosed medical
conditions that may need to be addressed before local an­
esthesia is administered. Uncontrolled high blood pressure
(;:o:180/110), for example, contraindicates dental treatment un­
til medical evaluation and appropriate treatment reduces the
risks for myocardial infarction and stroke. Vasoconstrictor
doses should be limited when hypertension is suspected. El­
evated vital signs are sometimes indications of undiagnosed
systemic problems. Frequent thirst and urination may be a
sign of undetected and uncontrolled diabetes. Uncontrolled
diabetes leads to cardiovascular disease. Although rare in the
dental office, hyperglycemic crisis can occur and should be
considered an emergency situation. Medical evaluations are
indicated for these and many other conditions before receiv­
ing local anesthesia with vasoconstrictors.
When patients are unable to provide adequate assess­
ment information, a family member, friend, legal guardian,
or translator must be available. This is necessary not only
during the assessment process but also when providing in­
formation about procedures and when obtaining informed
consent for proposed treatment (in the case of a child, a
mentally or physically disabled patient, or when there are
language barriers ) . See Chapter 1 1 , "Fundamentals for
Administration of Local Anesthetic Agents," for further
discussion on informed consent.
Systems Review
B efore the administration of local anesthesia, a thorough
review of systems is indicated . Appropriate follow-up
questions related to risks for oral care and administra­
tion of local anesthesia are essential (Pickett & Gurenlian,
20 10). This review includes the cardiovascular, respiratory,
nervous, metabolic, and excretory systems.
Cardiovascular System
The systemic effects of local anesthetic drugs with vaso­
constrictors include actions on both cardiac and vascular
structures. Even if ignoring the adrenergic effects of the
drugs, stress from inj ections is likely to increase blood
pressure, pulse, and possibly respiration.
This was demonstrated in a study in which blood pres­
sures were compared in anesthetized and non-anesthetized
patients undergoing routine restorative procedures. Al­
though blood pressures increased during inj ections in anes­
thetized patients the elevated pressures quickly decreased
once needles were withdrawn. Blood pressure values for
patients who received no anesthesia, on the other hand,
were elevated throughout their appointments (Gortzak,
Oosting, Abraham-Inpijn, 1992). Vital signs serve as base­
line values and are used for comparisons should adverse
events develop after local anesthetics are administered.
174 SECTI O N I N JECTI O N FUNDAMENTALS
Ill •
Most local anesthetic inj ections through tissue are
considered to be noninvasive and do not require antibiotic
premedication. The treatment planned following local an­
esthesia, on the other hand, may dictate a need for antibi­
otic prophylaxis. For most procedures, the use of a properly
administered local anesthetic to prevent pain and stress is
beneficial and provides a margin of safety in cardiac dis­
ease. In the absence of profound anesthesia, adrenaline­
induced tachycardia with increased cardiac workload and
increased oxygen requirements can precipitate coronary
ischemia and angina pectoris. In some individuals these
may progress to cardiac arrest. Stress reduction is impor­
tant in order to reduce adverse events during oral proce­
dures. Long appointments should be avoided in patients
with cardiac disease. Individuals with blood pressure below
180/1 10 mm Hg can undergo necessary dental procedures
with very little risk of adverse outcomes (Little et a!. , 20 13).
Although large doses of epinephrine can result in a signifi­
cant rise in blood pressure and heart rate, small doses (1 to 2
cartridges of 1 : 100,000) usually have minimal physiologic
impacts. The available evidence strongly suggests that ben­
efits outweigh risks when administering modest doses of
epinephrine to achieve profound pain control.
There is concern about vasoconstrictors when nonse­
lective beta-blocking agents such as propranolol are taken
to control hypertension or prevent migraines. The basis for
the concern relates to the nonselective /3-blocking action
of these drugs that inhibits the skeletal muscle vasodila­
tion of f3 receptors. Vasoconstrictors administered when
nonselective beta-blockers are in effect have resulted in
uncompensated peripheral vasoconstriction because of
the unopposed stimulation of a 1 receptors, leading to in­
creases in blood pressure and bradycardia, and headaches
Do you now h ave, or h ave you ever had or taken, a ny of the fo l l owing?
1 . Artificial heart valves or co n g e n ital heart d isease
2. I nfective endocard itis
3. R h e u m atic fever, rheumatic heart d isease, o r sca rlet fever
4. H e a rt attack, bypass s u rgery, stents, a n g i n a , or other heart problems
5. High blood pressu re o r l ow blood pressu re
6. H e a rt fa i l u re
7 . Stro ke (cerebrovascu l a r accident or tra nsient isch e m i c attack)
8. H e m o p h i l i a or cl otti ng d isorders
9. H e m ato mas fo l l owing l oca l a n esthesia
1 0. Weight loss med ications such as fen-phen
1 1 . Antibiotic premedications before dental treatment
and/or discomfort (Hersh & Giannakopoulos, 20 1 0 ) .
Significantly, a few patients with undiagnosed vascular
abnormalities in their brains are at risk of suffering cata­
strophic strokes. Because it is impossible to identify which
individuals are at risk of suffering catastrophic strokes,
some experts caution to avoid epinephrine in all individu­
als taking nonselective beta-blockers (Horn & Hansten,
2009) . Although this potential exists, small amounts of
epinephrine as commonly used in dentistry are unlikely to
be a problem (Horn & Hans ten, 2009) . Further discussion
is presented later in this chapter. Vasoconstrictors should
be avoided, if possible, in patients taking digitalis glyco­
sides (digoxin) for heart failure or other reasons. The com­
bination can precipitate arrhythmias (Little et a!. , 20 1 3 ) .
A stress reduction protocol is advisable for individuals
with heart failure.
Vasoconstrictors should be used with caution and in
low concentrations in patients prone to arrhythmia. High
doses of vasoconstrictor can precipitate arrhythmia (Little
et a!., 20 1 3 ) . Patients with hemophilia and clotting disor­
ders, and patients on blood thinning medications such as
warfarin, may require modifications to the types of inj ec­
tions, drugs, and doses of local anesthesia they may re­
ceive. Patients who have experienced recent myocardial
infarctions or cerebrovascular accidents may need to de­
lay elective dental treatment, including local anesthesia,
for appropriate periods of time (see Appendix 10-1 ) . An
important strategy when assessing risk for adverse events
during oral procedures and administration of a local anes­
thetic is to ask the right questions and follow up positive
responses thoroughly (Pickett & Gurenlian, 20 10). Exam­
ples of health history questions that focus on the cardio­
vascular system are presented in Box 10-7 •·
Yes/N o
Yes/N o
Yes/N o
Yes/N o
Yes/N o
Yes/N o
Yes/N o
Yes/N o
Yes/N o
Yes/N o
Yes/N o
 CHAPTER 1 0 PATI E NT ASSESSMENT FOR LOCAL ANESTHESI A
• 175

F U NCT I O NAL CAPA C I T Y Any pathological systemic con­ is increased when the patient is unable to meet a 4 MET
dition that impacts vital sign values poses a medical risk capacity (Fleisher, 2007). Box 10-8 • illustrates various ac­
during procedures. The assessment tool to identify when tivities and corresponding MET levels. To determine if a 4
the risk is greatest is called functional capacity. In 2007, MET capacity is reached, the patient must be able to per­
the American College of Cardiology updated published form activities listed (walk up a hill, run a short distance,
guidelines for risks when treating individuals with a his­ climb stairs, etc.) . For the patient with a history of myocar­
tory of severe cardiac disease during provision of non­ dial infarction or severe angina (pain not resolved upon
cardiac procedures (Fleisher, 2009) . These guidelines are rest) , the medical history review should include questions
intended to be used for planning oral care procedures and to establish the convalescence or recovery following the
are for nonphysician caregivers involved in preoperative, cardiac event (Pickett & Gurenlian, 20 1 0 ) . Recovery is
operative, and postoperative care of individuals who have measured by being able to complete activities in a 4 MET
a history of myocardial infarction or severe cardiovascular capacity (see Box 10-8 •) . Oral procedures and local anes­
disease who need noncardiac procedures (i.e., oral surgery, thesia should be delayed for a patient unable to attain a 4
periodontal procedures, etc.). Surgery-specific cardiac risks MET capacity until further medical testing has been com­
in noncardiac surgery are related to two important factors: pleted to quantify the level of cardiac risk for treatment.
the type of surgery or procedure itself and the degree of Requiring a written medical release when the physician
stress associated with it. Factors that help determine car­ determines oral procedures can be performed is essential.
diac risk include functional capacity, age, comorbid condi­ Noncardiac procedures, such as periodontal debridement,
tions (e.g., diabetes mellitus, peripheral vascular disease, are generally safe for individuals with functional capacity
renal dysfunction, chronic pulmonary disease) and the of 4 MET.
type of surgery to be performed. The 2007 guidelines clas­
sified surgical head and neck procedures as an intermedi­ S I C K L E C E L L A N E M I A Patients with sickle cell anemia
ate risk procedure (cardiac risk less than 5% ). Superficial should not receive local anesthesia or any dental treat­
procedures (which would include periodontal debride­ ment during a crisis. Antibiotic prophylaxis is necessary for
ment and most dental hygiene procedures) were classified procedures that may cause bacteremia. A physician con­
as having a low risk (cardiac risk less than 1% ) . Guidelines sult is recommended regarding the patient's cardiac status
include the pretreatment evaluation of functional capac­ because the disease can result in significant myocardial
ity as an important factor to determine cardiac risks in damage. Vasoconstrictors should be limited to situations
oral procedures. Functional capacity is expressed in meta· in which longer, more profound durations are necessary
bolic equivalent of task (MET) levels or simply, metabolic or when specific drugs are indicated that are formulated
equivalents. Baseline MET levels are equivalent to aerobic only with vasoconstrictors. Procedure durations should
demands for various activities. Perioperative cardiac risk be as short as possible and plain drugs are preferred

1 MET = Indivi d u a l can feed onese lf, d ress oneself, use toi l et,
wa l k one b l ock on l evel gro u n d at 2 m p h

4 MET = In d ivi d u a l c a n do l i g ht housework, move furniture, wa l k

u p a flight o f sta i rs without chest pain, wa l k u p a h i l l ,
wa l k on level g ro u n d a t 4 m p h , r u n a short d ista n ce,
p a rtici pate in activities such as dancing, go lf, bowl i n g ,
d o u b les tennis

10 MET = strenuous sports, basketb a l l , down h i l l ski i n g , s i n g l es

tennis

Adapted fro m : Fleisher LA et al. ACC/AHA (2007) G u id e l i n es on

Periope rative Cardiovascu l a r Eva l u ation a n d Care for N o n ca rd i a c S u rgery.
: Circ u l ation 1 1 6(1 7): 1 97 1 -96. •

: . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . •
17 6 SECTI O N I N JECTI O N FUNDAMENTALS
Ill •
whenever possible ( da Fonseca, Oueis, Casamassimo, 2007;
Michelson, Whitmore, 1967).
Respiratory System
The systemic effects of local anesthesia on the respiratory
system are typically minimal. Epinephrine acts on f3 recep­
tors of the smooth muscles of the bronchioles to dilate air
passages.
Asthma may be induced by allergy, including sulfite
sensitivity (a component of local anesthetic solutions with
vasoconstrictors) and physiological and psychological
stresses related to local anesthesia administration, all of
which may decrease a patient's respiratory capacity. Anxi­
ety in susceptible children typically provokes asthmatic
episodes. In adults, anxiety more commonly causes hyper­
ventilation or syncope.
Congestive heart failure (CHF) impairs lung function,
particularly in the pulmonary vessels where fluid accumu­
lates (congestion in the lungs). This leads to pulmonary hy­
pertension and compromises both heart and lung function,
which may necessitate modifications for dental treatment.
Patients diagnosed with CHF should be asked if a supine
position is comfortable. Some may prefer a semi-supine
position. Symptomatic CHF is an ASA IV risk factor and
dental treatment is contraindicated. Examples of health
history questions that focus on the respiratory system are
presented in Box 10-9 •·
Nervous System
The overall condition of a patient's nervous system has a
maj or influence on the process and outcome of local an­
esthesia. The patient's ability (or inability) to tolerate the
stress of local anesthesia is partially influenced by the
Do you now h ave, or h ave you ever had, any of the fo l lowi ng?
1 . Asthma
2. Em physe m a
3. Tu bercu losis
4. Congestive h e a rt fa i l u re
5. C h ro n i c l u n g d isease
6. Sinus or e a r problems
7 . Persistent or b l oody cough
8. Methemoglobinemia, or episodes of "turn i n g b l u e " after local a n esthesia
9. Sensitivity to su lfite preservatives i n food or i n local a n esth etics
1 0. Episodes of hyperventilation because of a nxiety or p a n i c attacks
health of their nervous system. Local anesthetics are cen­
tral nervous system (CNS) depressants. This depression is
additive to any existing CNS depression. When CNS de­
pression is suspected, careful evaluation before the use of
a local anesthetic is indicated. For example, when a patient
has taken narcotic drugs before anesthesia administration,
the local anesthetic can have a more profound effect on
the CNS.
Paresthesia is a potential complication from inj ection
technique in local anesthesia. If, during the evaluation ,
signs and symptoms o f intraoral paresthesia are evident, it
should be determined whether or not they are the result of
previous local anesthetic procedures. If so, it is important
to determine the specific inj ection(s) performed in order
to avoid inj ections that follow the same pathway. Exam­
ples of health history questions that focus on the nervous
system are presented in Box 10-10 •·
Metabolic Systems
Patients with compromised liver function may not be able
to metabolize amide local anesthetic drugs efficiently. Be­
cause the liver is the primary source of cholinesterase, es­
ter metabolism may also be compromised. When serious
compromise is suspected, a consultation with a physician
is indicated. This will help to determine appropriate limita­
tions on the type and dose of local anesthetic used. If there
has been extensive liver damage, for example, articaine
(90 % -95 % non-liver metabolism) may be preferable to
other drugs. D epending upon the degree of cholinester­
ase depletion, however, articaine may have less advantage
(Pickett & Terezhalmy, 20 10). Shorter appointments with
fewer milligrams of drug administered are recommended,
regardless of the anesthetic selected.
Yes/N o
Yes/N o
Yes/N o
Yes/N o
Yes/N o
Yes/N o
Yes/N o
Yes/N o
Yes/N o
Yes/N o

Do you now h ave, or h ave you ever had, any of the fo l lowi ng?
1 . Seizu res
2. Denta l anxiety
3. Diagnosed menta l i l l n ess
4. O bsessive-co m p u lsive disorders
5. Eati ng D isorders
6. Depression
7 . Treatment for chemical dependency
8. C h ro n i c pain
9. H e a d a ches o r m ig ra i n e
1 0. H e a d inju ries
Amide local anesthetics are broken down into inac­
tive metabolites for excretion. In the liver, they compete
for metabolic pathways with other drugs. This competition
may result in significant drug interactions that influence
the blood levels of the various drugs, as well as their half­
lives and excretion patterns.
Metabolic issues play a key role in treatment planning
for individuals with diabetics. The most common medical
emergency that occurs in diabetics is hypoglycemia ( Pickett
& Gurenlian, 20 1 0 ) . B e cause of the daily schedule for
meals and insulin, morning appointments are usually best
in order to avoid hypoglycemia. Questioning should always
include a determination of whether or not a meal has been
eaten and whether or not insulin has been taken as a pre­
caution against hypoglycemic emergency. It is important
to remind patients to eat and maintain their nutritional
schedule following their appointments as well ( Malamed,
20 13). This is especially important when epinephrine is be­
ing considered in cardiac-compromised, poorly controlled
diabetes ( ASA III & IV ) . B ecause of epinephrine's phar­
macologic effect opposing insulin, blood glucose may in­
crease when epinephrine is used ( Little et a!. , 20 13).
Diabetes predisposes individuals to hypertension. If
hypertension, myocardial infarction, cardiac arrhythmia,
or comorbidity is present, caution with epinephrine is indi­
cated ( Little et a!. , 20 13).
H Y P E RT H YROI D I S M Patients with hyperthyroidism have
an increased risk of developing thyrotoxicosis, which can
result in what is known as thyrotoxic crisis or, more com­
monly, thyroid storm. Epinephrine is known to increase the
risk of this life-threatening medical emergency in poorly
controlled thyroid disease. The nature of the relationship
between hyperthyroidism and epinephrine is not entirely
CHAPTER 1 0 PATI E NT ASSESSMENT FOR LOCAL ANESTHESI A
• 177
Yes/N o
Yes/N o
Yes/N o
Yes/N o
Yes/N o
Yes/N o
Yes/N o
Yes/N o
Yes/N o
Yes/N o
clear ( Herman et a!., 1989; Little e t a!., 20 1 3 ) . Although a
higher-than-normal secretion rate of epinephrine has been
suspected in thyrotoxicosis, studies have suggested that
the signs and symptoms encountered in hyperthyroidism
are not secondary to high secretion rates of epinephrine
( Herman et a!. , 1989).
Epinephrine is absolutely contraindicated in patients
with poorly controlled or uncontrolled hyperthyroidism. It
is important to note that it may not be possible to safely
treat these individuals even with non-epinephrine for­
mulations until their conditions are controlled. The well­
managed euthyroid patient, however, requires no special
consideration and may receive normal concentrations of
vasoconstrictor ( Little et a!. , 20 13).
H Y POT HYROI D I SM Patients with untreated hypothyroid­
ism can generally receive dental treatment including local
anesthesia. Unless the condition is severe, dental treat­
ment does not have to be deferred. Even in severe cases,
the condition usually responds to treatment and patients
are able to tolerate dental treatment once the disease is
controlled. Reponses to local anesthetics, however, can be
exaggerated because of CNS depression and doses of local
drugs should be kept to a minimum even in more mild
cases ( Budenz, 2000).
P H E O C H R O M OCYT O M A Another less common meta­
bolic consideration is pheochromocytoma. This rare tumor
of the adrenal medulla results in increased secretions of
endogenous epinephrine. Hypertension is typical and dys­
rhythmias are not uncommon. Local anesthetics with epi­
nephrine are contraindicated. ( Findler et a!. , 1993; Peruse,
Goulet, & Turcotte, 1992) .
Examples of health history questions that focus on
metabolic systems are presented in Box 10-1 1 •·
178 SECTI O N I N JECTI O N FUNDAMENTALS
Ill •
Do you now h ave, or h ave you ever had, any of the fo l lowi ng?
1 . Dia betes - Type 1 or Type 2
2. Liver condition (hepatitis, ci rrhosis, j a u n d ice)
Excretory System
The kidneys are the primary excretory organs for local an­
esthetics. Suspected diminished function or kidney failure
should be closely evaluated. As a result of inadequate ex­
cretion, local anesthetics and their metabolic by-products
may accumulate to toxic levels as dosing increases. Exam­
ples of health history questions that focus on the excretory
system are presented in Box 10-12 •·
Contra i n d ications to Loca l Anesthesia
When patient assessment has determined that standard
local anesthetic procedures are contraindicated, an appro­
priate course of care must be defined. Assessment results
guide clinicians when determining the extent of the con­
traindications, which may be classified as either relative or
absolute.
Some contraindications are permanent, such as hered­
itary medical conditions. Others may be temporary, such
as recent cardiovascular events or pregnancies, which typi­
cally delay, rather than prevent, planned treatment.
Absolute and Relative Contraindications
Situations in which local anesthetic or vasoconstrictor drugs
may not be administered safely are known as absolute con­
traindications. There are few absolute contraindications to
the administration of local anesthetic agents. Relative con­
traindications for local anesthesia procedures are those in
which local anesthetics may be given with caution.
There are a number of medical conditions that can
be considered relative or absolute contraindications de­
pending upon the degree of compromise. For example, if
Do you now h ave, or h ave you ever had, any of the fo l lowi ng?
1 . Kidney fa i l u re
2. Kidney d i a lysis treatment
3. Kidney transplant proce d u re
Yes/N o
Yes/N o
a patient has had a cerebrovascular accident (CVA), h e or
she is classified as having an ASA IV risk (absolute con­
traindication) for a minimum of 30-180 days post-CVA
(Skaar et al., 20 12). Consultation with the patient's phy­
sician and a detailed risk assessment are recommended
when d etermining when ele ctive dental treatment is
indicated (relative contraindication) .
Relevant medical, pharmacological, and psychological
conditions are discussed next. Refer to Appendices 10-3 ,
1 0-4, 10-5 , and 1 0-6 for specific modifications related to
medical and pharmacological factors.
Examples of Medical Compromise
Atypical plasma
AT Y P I CA L P L A S M A C H O L I N E ST E RA S E
cholinesterase impairs a patient's ability to effectively me­
tabolize ester-type local anesthetics in any form, injectable
or topical. This condition is genetic (autosomal recessive)
and has a frequency of approximately 1 in 3,000 patients
(Malamed, 20 1 3 ) . Signs and symptoms of an ester local
anesthetic overdose are more likely to occur when normal
doses are administered. B ecause this condition is only a
relative contraindication, esters may be administered with
caution; however, the availability of excellent amide sub­
stitutes renders the point moot. Unless there is an absolute
contraindication to amides or there are no amide inj ect­
abies or topicals available, it is seldom necessary to use es­
ters in these individuals.
M E T H E M OGLOBI N E M IA Methemoglobinemia is a genetic
or acquired condition that reduces the oxygen-carrying ca­
pacity of blood. Acquired methemoglobinemia has been
reported following the administrations of benzocaine
and prilocaine topical agents and inj ectable prilocaine
Yes/N o
Yes/N o
Yes/N o

(B arclay & Vega, 2004; S achdeva et a!., 2003 ) . Clinical
anoxia may result from methemoglobin levels above
10% demonstrated by signs of reduced oxygenation and
cyanosis (Knobeloch et a!., 1994; Wilburn-Goo & Lloyd,
1999) (see Box 1 0-13 • and Box 1 0-14 •) . Administering
doses that exceed 4 mg/lb or 600 mg absolute maximum
of prilocaine has b e e n linked to the development of
methemoglobinemia in adults (Knobeloch et a!. , 1994) .
This risk is increased in patients with known medical condi­
tions involving enzyme deficiencies and for patients taking
oxidant drugs such as sulfonamide, anti-malarial, acet­
aminophen, or nitrite-containing medications (Knobeloch
et a!. , 1994) (see Box 10-15 • and Box 10-16 •) . An FDA
Advisory, released April 2006, states that ': . . patients with
underlying breathing problems, such as asthma or emphy­
sema, patients with heart disease, and those who smoke
may be more susceptible" (FDA, 2006) .
Prilocaine and benzocaine should be administered
with caution when any predisposing condition is reported
on the health history. For further discussions see Chapter 5,
"Dental Local Anesthetic Drugs," Chapter 8, "Topical An­
esthetics," and Chapter 17, "Local Anesthesia Complica­
tions and Management."
This condition has been reported with the use of benzo­
ca i n e and pri l oca i n e i n particu l a r. If a patient's serum oxy­
gen satu ration is red u ced, a n d other signs a n d sym pto ms
of m eth e m o g l o b i n e m i a a re detected, the patient s h o u l d
be tra nsported t o a hospita l . If the b l ood m eth e m o g l o b i n
con centration exceeds 30%, the patient w i l l need a n i ntra­
venous i nfusion of m ethylene b l u e to reverse this poten-
: . � � : � �� � ���� �� . (•H•e?���s. � . . :� · . ?�:) ·
ta l e a i n He 2
• : . � �:��� �� : :�
........
I n itial:
S l i g ht g reyish color (cya nosis) of the skin, buccal m u cous
m e m b ra n es, l i ps, a n d nail beds
Severe:
Centra l cya nosis H eadache
CNS depression Leth argy
Dizzi n ess Seizures
Dyspnea Shock
Dysrhyt h m i a Syncope
Fatig u e
Source: "Si g ns Symptoms o Methemogl o binemia" from
, Oraqix® productandinsert. Copyrightf © by Dentspl y Pharmaceutical. ,
: Used by permi s si o n o f Dentspl y Pharmaceutical.
..... .............. ......... .........•
. . . without vasoconstrictors may be selected .
CHAPTER 1 0 PATI E NT ASSESSMENT FOR LOCAL ANESTHESI A
• 179
In a ddition to b e nzoca in e a n d priloca in e, th e following
drugs m ay induce m eth e m oglobin emia:
Aceta m i n ophen; aceta n i l ide; a n i l i n e dyes; c h l o ro­
qu ine, dapsone; sulfo n a m i d es; naphth a l e ne; n itrates a n d
n itrites; n itrofu ranto i n ; n itrog lycerin; n itroprusside; p a m a ­
qu ine; para-a m i nosa l i cy l i c a c i d ; phenaceti n; phenobarbita l ;
phenytoi n ; pri m a q u i ne; a n d q u i n i n e .
Source: "Drug-Induced Methemogl o binemia" from Oraqix®
, product insert. Copyright © by Dentspl y Pharmaceutical. Used by ,
: •p•e :� i � s:o.n .o� �� n.t:p� y• P•h � r�.a �:u � i �a� • • • • • • • • • • • • • • • •
Aceta m i n ophen is a widely consumed, over-the-cou nter
drug that is used a l o n e or in com b i n ation with oth er
drugs. It has a known tendency to i n d uce a potentia l ly
l ife-th reate n i n g a n e m i a (meth e m o g l o b i n e m ia) i n a n i m a ls
(American H e a rt Association [AHA], 2007) . Altho u g h not
reported to have been observed i n h u m a ns, l iteratu re
from m a n ufactu rers cauti ons a g a i nst the use of priloca i n e
when a ceta m inophen has b e e n i n g ested (Oraq ix, Dentsply
P h a rmaceuticals; EMLA Cream and Anesthetic D isc,
Astra P h a rm a ceutica ls) (Am e rican Academy of Pediatric
Dentistry, 2009) . Because there a re s u ita b l e su bstitutes
for aceta m i nophen, i n d ividuals may wish to avoid its use
before, du r i n g, and after appointments.
In keep ing with princip les of in form ed consent, patients
, should be warn ed of th ese potentia / risks in order to m a k e ,
i f cs ns be
. • • :� � •� : �� • � ��: : �: :: • • • • •
r , u i · an a
. .
h a ·
Liver or Kidney Dysfunction
Significant liver or kidney dysfunction in category ASA
III is a relative contraindication for local anesthesia. Ester
and amide local anesthetics can be used for these patients
with caution. Articaine, particularly, in significant liver dis­
ease, may have an advantage over other drugs because it
is packaged in dental cartridges (unlike the esters) and
largely avoids liver metabolic pathways when used for oral
inj ections (unlike the other amides) . See the Chapter 5
section on articaine (Jastak, Yagiela, & Donaldson, 1995).
Cardiovascular Disease and Hyperthyroidism
Patients in category ASA III with cardiovascular disease
and controlled hyperthyroidism may present as relative
contraindications for high doses of vasoconstrictors. Vaso­
constrictors may be used in these individuals but at very
low doses (no more than 0.04 mg of epinephrine or 0.2 mg
of levonordefrin per appointment) or plain anesthetics
180 SECTI O N I N JECTI O N FUNDAMENTALS
Ill •
I n the past there was a preca ution to avoid a l l treatment
with i n 6 months of a n Ml (an absol ute contra i n d ication).
Recent l iteratu re, however, suggests that 1 month is an
evidence-based absol ute contra i n d i cation (Fleisher, 2007,
Little et a l . , 201 3) . Consu ltati on with the patient' s physici a n
a n d a deta i l e d r i s k assessment t o ensure 4 M ET l evel of
functi o n a l capacity a re reco m m ended in m a ki n g such a
: determination for elective dental care.
:. . . . . . . . . . . . . . . . .
Myocardial Infarction
Individuals with a history of myocardial infarction (heart at­
tack) within a very recent past (one month) may be at high
risk for reinfarction and dental treatment should be delayed,
if possible. During the first month following MI an increased
risk for reinfarction, arrhythmia, and heart failure exists (Little
et al. , 20 13). The ACC/AHA guidelines to determine risks
in noncardiac procedures suggests if a patient cannot climb
a flight of stairs without chest pain or shortness of breath, an
increased risk exists and a consultation with the physician
should be completed before dental procedures are attempted.
This 4 MET risk stratification applies to other conditions,
such as angina pectoris. However if angina is relieved by rest­
ing for 5 to 15 minutes, the cardiac risk may be intermediate
(Little et al., 20 13). When questioning reveals angina occurs
at rest or during sleep this has a high risk and is placed in an
ASA IV category; no dental procedures should be attempted.
Local anesthesia (and treatment) should be postponed until
medical evaluation determines that the individual's risk has
returned to acceptable levels. When treatment does occur
stress reduction and pain control are important during the
procedures (see Box 10-17 •) ( Little et al., 2013).
Cerebrovascular Events
At least three significant events occur because of ce­
rebral ischemia and infarction that impact the use of
vasoconstrictors.
C E R E B ROVASCU LAR ACCI D E NT A stroke or cerebrovascu­
lar accident (CVA) is caused by a rapid loss of brain func­
tion due to a disruption of the blood supply that results in
permanent impairment due to blockage or rupture of an
artery to the brain.
A transient ischemic at­
T RANSI E NT I S C H E M I C AT TACK
tack (TIA) that lasts only minutes to 24 hours has the
same underlying causes and symptoms as a stroke; how­
ever, the symptoms resolve within a day despite the fact
that brain inj ury may have occurred. TIAs are frequently
referred to as mini-strokes.
R E V E R SI B L E I SC H E M I C N E U ROLOGIC D E FICIT A reversible
ischemic neurologic deficit (RIND) refers to an infarct
that lasts from 24 to 72 hours, differentiating it from a TIA.
Individuals with a history of a recent CVA, TIA, or
RIND are at significant risk for recurrence. Following cere­
brovascular events, risk remains elevated for a period of at
least 6 months. A 20 1 0 evaluation to determine whether
"invasive dental treatment transiently increases the risk for
vascular events" found that "the rate of vascular events sig­
nificantly increased in the first 4 weeks after invasive den­
tal treatment," (Minassian et a!. , 20 10). Risk of recurrence
continues to remain somewhat elevated after the expira­
tion of the initial 6-month period and is estimated to be
14 % , 12 months after the initial stroke (Little et a!., 20 13).
Little et a!. recommend that elective dental treatment
•
be deferred during the initial 6-month period after which,
. •
. . . . . . . . . . . . . . . . . . . . .
if a patient is deemed to be stable, invasive dental treat­
ment is indicated with caution (Little et al., 20 13).
Similar to post MI recommendations, evidence is
mounting that waiting periods for elective dental treat­
ment following CVAs may be reduced. Skaar et a!. suggest
that waiting periods of 30 -180 days post-CVA may not in­
crease the risk of subsequent strokes (Skaar et al. , 20 12).
Additionally, serious doubts have been raised that dental­
related bacteremias are risk factors for subsequent strokes
(Skaar et al. , 20 12). Consultation with a patient's physician
and a detailed risk assessment are recommended in mak­
ing such a determination for elective dental care.
Vasoconstrictors should be avoided if possible but
may be administered if comfortable treatment requires
their use. Epinephrine's use is a relative contraindication
in these individuals and when administered, cardiac dose
maximums should be observed. Short, mid-morning ap­
pointments are recommended (Little et al. , 20 13).
Hypertension
High blood pressure increases the risk of medical complica­
tions following the administration of local anesthesia. Many
patients are unaware that they have hypertension or are un­
aware of its consequences to their overall health. If a patient is
not medically managed and their hypertension is uncontrolled
(:::: 180/110 mm Hg), elective treatment should be deferred un­
til control has been established. The decision to perform elec­
tive dental treatment when significant hypertension exists
must be based on several factors including consultation with
the patient's physician, physiological status including past
medical and dental history, and psychological status.
A reasonable course of action can be found in the
recommendations of Little, Falace, Miller, and Rhodus
(Little et a l . , 20 1 3 ) . For p atients with ASA II b l o o d
pressure values, there is no contraindication for dental
treatment; however, patients are encouraged to see a phy­
sician. When blood pressure values are at described ASA
III levels, recommended dental treatment may be initiated.
Intraoperative monitoring of blood pressure for upper
levels should be considered and patients are referred to
physicians promptly (within 1 month). For blood pressure
values :::: 1 80/1 10, all elective treatment should be deferred
and patients should be referred to a physician as soon as
possible, or immediately, if symptomatic. For a summary of
these guidelines see Table 10-1 • and Appendix 10-1.

Table 1 0-1 Guidelines for local Anesthesia M anagement in H ypertension
Blood Pressure Values Treatment and Referral Actions
> 120/80 but < 1601100 No contraindications for treatment, suggest medical referral
160/100 Treatment may be initiated with monitoring, prompt medical referral
� 180/1 10 Defer treatment, immediate medical referral
Source: Little et a!., 2013.
Considerations for Premedication
AHA GU I D E LI N E S According to the most recent American
Heart Association guidelines (2007 ) , very few individu­
als require antibiotic prophylaxis before dental treatment
compared with previous recommendations. In the current
guidelines there are no indications for antibiotic prophylaxis
(AP) before receiving a local anesthetic injection in order to
prevent infective endocarditis (IE). Individuals with artificial
heart valves, a heart transplant in which valve disease devel­
oped, unrepaired congenital heart disease, and those with a
previous history of IE should be considered for antibiotic
prophylaxis before some oral procedures (ADA, 2007).
AAOS GU I D E LINES A joint committee of the American As­
sociation of Orthopedic Surgeons (AAOS) and the Ameri­
can D ental Association (ADA) released evidence-based
guidelines for antibiotic prophylaxis for individuals with
prosthetic joints in December of 20 12. The full guideline can
be accessed at the AAOS website, www.aaos.org/guidelines
and provides guidance when treating patients with prosthetic
joints, including for local anesthesia. The need for premedica­
tion will be directed by the comprehensive treatment plan.
Allergies
Allergies to specific local anesthetic drugs or to bisulfite
preservatives are absolute contraindications to their use.
When considering alternative local anesthetic selections,
a clear knowledge of the specific allergen is necessary. If
a patient has a documented allergy to an ester, an amide
may be substituted. If a patient is allergic to any esters, all
esters must be avoided. If there is an allergy to one amide,
other amides may be used, but only after appropriate al­
lergy testing to confirm their safety.
These conditions apply regardless of whether or not
these drugs are injected or topically applied. If a patient is al­
lergic to esters, topical products containing esters may not be
used but amides such as lidocaine and prilocaine can be used.
All local anesthetics drugs with vasoconstrictors con­
tain bisulfite preservatives. These agents are also used
as preservatives in foods and drinks (such as lettuce in
salad bars and most wines). When there is a documented
allergy to bisulfites, all drugs containing vasoconstric­
tors are absolutely contraindicated. Bisulfite sensitivity is
more common in patients with asthma. Asthmatics should
be questioned specifically about their tolerance to bisul­
fites in food products before the use of local anesthetics
CHAPTER 1 0 PATI E NT ASSESSMENT FOR LOCAL ANESTHESI A
• 181
containing vasoconstrictors. If patients report any sensi­
tivity to bisulfites, vasoconstrictors should not be used. In
these patients, 3% mepivacaine is a suggested alternative.
Some patients report an allergy to epinephrine. Because
synthetic (exogenous) epinephrine is identical to endogenous
epinephrine, true allergies are highly unlikely. If they have
occurred, they are probably related to the hydrochloride
or bitartrate component introduced during manufacturing.
Reactions to the administration of epinephrine instead are
typically classified as nonallergic adverse drug events (ADR),
such as heart palpitations, tachycardia, hypertension, anxiety,
and general agitation. Vasoconstrictors should be avoided.
Pregnancy
Healthy pregnant patients are classified as health status ASA
II (see Appendix 10-1) . Pregnancy poses a temporary and
relative contraindication to local anesthetics that may require
treatment modifications. Clinical judgment should be exer­
cised before local anesthesia administration that includes the
results of medical consultation. During the first trimester, the
embryo is at greatest risk of injury from exposure to medica­
tions. The second trimester is considered to be the safest pe­
riod for both the fetus and the mother. Toward the end of the
third trimester, some mothers may have difficulty metaboliz­
ing drugs. For specific information on the safe selection of lo­
cal anesthetics during pregnancy, clinicians should consult the
Food and Drug Administration list of Pregnancy Categories
for local anesthetic agents (see Chapter 5, Table 5-4) .
Dementia-Related Diseases
Dementia-related diseases such as Alzheimer's are con­
sidered to be conditions of medical compromise; however,
concerns for the use of local anesthetic agents are not of
a medical origin. According to Eldor in a 200 1 post to the
CSEN Regional Anesthesia Newsletter, "Patients with
middle to later stage dementia are not good candidates for
local or regional anesthesia because they have difficulty
cooperating, understanding directions and keeping still."
Patients presenting with symptoms of dementia should
be evaluated to determine the safety and appropriateness
of local anesthesia. If patients are unable to provide ad­
equate assessment information or there is any question as
to the patient's ability to provide informed consent, a legal
guardian must be available. Some patients with symptoms
of dementia may tolerate short procedures with local an­
esthesia whereas others may require an oral sedative in
182 SECTI O N I N JECTI O N FUNDAMENTALS
Ill •
addition to a local anesthetic. Consultation with the pa­
tient's physician is recommended when oral sedatives are
being considered. Extensive oral procedures may require
hospitalization under general anesthesia.
Examples of Pharmacological Compromise
Many prescribed drugs and other substances can affect
the pharmacology of local anesthetics. Local anesthetics,
in turn, can alter the actions and metabolism of a num­
ber of medications and other substances. Some effects are
relatively mild when typical doses of local anesthetics are
administered, such as the slightly increased toxicity of lido­
caine when it is given on top of cimetidine, which competes
with lidocaine for sites of metabolism (Malamed, 20 1 3 ) .
Others can be dramatic and potentially life-threatening,
such as those that can occur when vasoconstrictors are ad­
ministered to an individual who is on methamphetamines.
When these compromises are present, they are re­
ferred to as interactions or considerations. A more exten­
sive list may be found in Appendix 10-5.
Beta-Blockers
Individuals taking nonselective beta-blocking agents for
hypertension or other conditions such as migraines should
be given epinephrine with caution. Epinephrine may in­
crease blood pressure through inhibition of the vasodila­
tory action of epinephrine through blocking {3-2 receptors
(Little et al. , 20 13).
When local anesthetic drugs containing vasoconstrictors
are administered in the presence of these drugs, there can be
an increased risk of a serious hypertensive episode along with
reflexive bradycardia because of their unopposed a-adren­
ergic stimulation. Clinical experience has demonstrated that
when low concentrations of epinephrine are used, untoward
events are very unlikely; however, serious reactions may occur
and actually have occurred despite the very low risk for any
particular individual. Most to nearly all patients on nonselec­
tive beta-blockers following epinephrine administration expe­
rience either no reaction or minor discomfort or headaches.
Importantly, a very few patients, with undiagnosed vascular
abnormalities in their brains are at risk of suffering strokes.
The caution to avoid epinephrine in all individuals taking
nonselective beta-blockers has been characterized as "pru­
dent" because it is impossible to identify which individuals
are at risk of suffering strokes (Horn & Hansten, 2009). Horn
and Hansten have identified three significant issues involv­
ing epinephrine and patients taking nonselective {3-blockers:
1) the potential stroke risk for a very few individuals, 2) the
greater likelihood of experiencing anaphylaxis (beta-blockers
increase the frequency of anaphylaxis), and 3) the decreased
effectiveness of epinephrine in the management of anaphy­
laxis (epinephrine is often ineffective for anaphylaxis rever­
sal in patients on beta-blockers) (Horn & Hansten, 2009) .
Goddet and colleagues describe {3-blocker use as potentially
"life-threatening" during anaphylactic episodes (Goddet et
al., 2006). There is evidence that anaphylactic risks extend to
cardioselective {3-blockers, as well (Horn & Hansten, 2009).
N o nselective
Levo b u n o l o l (Betaga n®)
M etipra n o l o l (Opti Pra n o l o l®)
N ad o l o l (Corga rd®)
Propra n o l o l (lndera l®, l n deral LA®, l n n o Pran XL®)
Sota l o l (Beta pace®, Sarin e®)
T i m o l o l (Beti mo l®, B l ocadren®, lsta lol®, Timoptic®)
Card ioselective
Acebuto l o l (Sectra l®)
Ate n o l o l (Tenormin®)
B etaxo l o l (Kerlone®, B etoptic®)
B isopro l o l (Zebeta®)
Esm o l o l (Brevib l o c®)
N e b ivo l o l (Systo l ic®)
: ��t��:o.l � l .( :�p.r� s.s ��®; ;�� r� l: ::®: · . .............•
•
In addition to these risks, propranolol may interfere
with lidocaine metabolism. This represents an additional
relative contraindication for lidocaine use with proprano­
lol. With the availability of excellent substitutes, it is easy
to avoid concurrent lidocaine and propranolol administra­
tion. Examples of commonly prescribed beta-blockers can
be found in Box 10-18 •·
" S treet Drugs"
Although this discussion is not inclusive of all street drugs,
two of great concern with the use of local anesthetic and
vasoconstrictor drugs, cocaine and methamphetamines, will
be highlighted. Methamphetamines and cocaine have sym­
pathomimetic effects and can interact with vasoconstrictors
in local anesthetics. A local anesthetic with epinephrine
can have an additive effect with methamphetamine and co­
caine resulting in tachycardia, myocardial infarction, stroke,
and hypertension (Pickett & Terezhalmy, 20 10). When drug
abuse is suspected, patients should be asked about recent
substances consumed and should be required to sign a
statement indicating that drugs have not been used within
the previous 24 hours (Pickett & Terezhalmy, 20 10) . Ratio­
nale and guidelines are provided here in order to enhance
safety when patients are users of the following drugs:
COCA I N E As an ester, cocaine is quickly biodegraded.
Peak blood levels of cocaine are typically reached within 30
minutes of consumption and are dissipated within 2 hours
because of cocaine's rapid cholinesterase metabolism (Lit­
tle et al., 20 13). Unlike most local anesthetic drugs, cocaine
is a potent vasoconstrictor and exhibits significant indirect­
acting adrenergic stimulating effects. Vasoconstrictors in
combination with cocaine significantly increase the risk of
hypertensive crisis, stroke, and myocardial infarction.

As an anesthetic drug, cocaine is a CNS depressant. The
addition of another local anesthetic such as lidocaine can in­
crease any existing CNS depression due to cocaine overdose.
Although cocaine is rapidly metabolized, it is recom­
mended that vasoconstrictors be avoided for a minimum
of 24 hours after cocaine use and patients be monitored for
local anesthetic drug overdose ( Malamed, 20 13).
Any clinical decision regarding when to treat an indi­
vidual who has consumed cocaine should take into account
the reliability of the information the patient is providing.
In discussing the need for accuracy regarding the time of
the most recent use of cocaine, it is important to empha­
size the potential catastrophic nature of the consequences
of providing false information.
M E T H A M P H E TA M I N E S B oth methamphetamine and
epinephrine are potent vasoconstrictors. In combination,
they significantly increase the risk of hypertensive crisis,
stroke, and myocardial infarction. Do not administer local
CAS E MA N A G EME N T
Carlos Martinez
S e v e r a l fa c t o rs s u g g e st c a u t i o n w h e n t r e a t i n g
M r. M a rtinez. These i n c l u d e sel ecti o n o f a loca l a n es­
thetic drug, the use of a vasoconstrictor, and observed
m axi m u m dose per appointment. When there a re m u l ­
t i p l e re l ative contra i n d i cations t o the u s e o f a d r u g , it
may be considered an absol ute contra i n d i cation o r, in
some instances, a strong re l ative contra i n d icatio n .
Ach ievi n g a d e q u ate l e v e l s a n d d u ra t i o n of p a i n
control is i m p o rtant i n determ i n i n g t h e n e e d fo r va­
soconstrictors. Using at least m i n i m a l vo l u m es of loca l
a nesthetic d rugs fo r effective n e rve b l ock a n d i nfi ltra­
tion a n esthesia is a lso i m p o rtant.
Drug d oses and a p p o i ntme nts s h o u l d be l i m ited
for M r. M a rtinez in order to avoid vasoconstrictor inter­
actions a n d local a n esthetic d ru g toxicity. Some drugs
wi l l have l ess effect on a reas of compro m ise, whereas
others wi l l have greater effects. This does not mean that
only those with the least effect may be used, but it does
means that th ose with g reatest effect s h o u l d be used
ca utious ly. For exa m p l e , 2% l i d o c a i n e with 1 : 1 00,000
epinephrine is not as safe as 4% articaine with 1 :200,000
e p i n e p h r i n e fo r this patient. In lower d oses a n d with
s h o rter appoi ntments, h owever, it is perfectly accept­
a b l e . O n ly 5% to 1 0% of a rticaine is metabol ized in the
l iver, whereas l idoca i n e is entirely meta b o l ized in the
l iver. Alth o u g h a rtica i n e provides a somewhat g reater
margin of safety when considering sign ificant l iver dam­
age, lidocaine is safe to use, particula rly in the vol u m es
used in de ntistry. Appointments s h o u l d be l i m ited re­
gard l ess of the drug in order to l i m it the tota l doses of
local a n esthetic a n d vasoco nstrictor d r u g s . Alth o u g h
there is twice t h e d r u g a m o u nt i n a rticai n e cartri dges,
CHAPTER 1 0 PATI E NT ASSESSMENT FOR LOCAL ANESTHESI A
• 183
anesthetics with vasoconstrictors for a minimum of 24 hours
after methamphetamine use. Resistance to local anesthesia
may increase with concomitant methamphetamines.
For a summary of restrictions to these and other con­
comitant drugs of concern see Appendix 10-6.
Examples of Psychological Compromise
Anxiety and fear can produce both psychological and physi­
ological changes in the body that can affect the ability to ad­
minister local anesthesia and the effectiveness of the local
anesthetic ( Bourassa & Baylard, 1994; Gutmann et al., 1997;
Newton et al., 2006; Peretz & Mann, 2000; Simon et al., 1994).
Stress reduction protocols may be used for anxious pa­
tients and can be effective at preventing psychogenically
generated adverse events during treatment ( see Appendix
1 0-2) . Achieving and maintaining good pain control will
reduce stress. Specific strategies for the management of the
psychological factors of anxiety and fear can be found in
Chapter 18.
a rticaine is ava i l a b l e in a m uch more d i l uted concentra­
tion of epinephrine, which wi l l l i m it the effects on blood
sugar elevation.
Epinephrine and levonordefrin a re re lative ly contra­
ind icated in this patient beca use of the potential for se­
rious hypertensive episodes and refl exive bradyca rd ia
in the presence of Corgard; therefore , low conce ntra­
tions a re i n d icated ( 1 : 200,000 e p i n e p h rine). Priloca i n e
a n d benzoca i n e a re re l ative contra i n d ications as we l l ,
beca use o f t h e fa m i ly h isto ry o f m eth e m o g l o b i n e m i a
a n d M r. M a rtin ez's s m o k i n g h a b it. Alth o u g h t h e i r use
is not absol ute ly contra i n d icated, both prilocaine a n d
benzoca i n e a re easily avoided . Exce l lent su bstitutions
a re read i l y ava i l a b l e a n d include l idoca i n e topica l and
2% lidocaine with 1 : 1 00,000 epinephrine, 4% a rtica i n e
with 1 :200,000 epinephrine, and 3% mepivacaine p l a i n .
O f these three, none is ideal but a l l w i l l w o r k wel l with
cauti o n . Arti caine with 1 : 200,000 e p i n e p h ri n e , fo r ex­
a m p l e , is s u perior from the sta n d po i nt of l i m iting he­
patic i nteracti o n (co m p a red with both l i d o c a i n e and
m e pivaca i n e ) , e l evati o n s i n b l oo d s u g a r (co m p a red
with l i doca i n e o n ly), a n d i nteracti o n s with the n o nse­
lective beta-blocker, n a d o l o l (co m p a red with l idoca i n e
o n ly) . Li d o ca i n e h a s m o re e p i n e p h r i n e a n d h e p atic
pathways of m eta b o l is m a n d can be used as long as
q u a ntities are l i m ited . Mepivacaine plain has no interac­
tions with beta-blockers or b l ood sugar levels but has a
slower meta b o l i c pathway thro u g h the l iver compared
with lidocaine. Because of its shorter d u rations and the
lack of epinephrine, it is genera l ly the least effective in
i nfi ltratio n p roce d u res at provi d i n g profo u n d a nesthe­
sia compared with l idocaine and a rticaine.
184 SECTI O N I N JECTI O N FUNDAMENTALS
Ill •
O n o c ca s i o n , w h e n l o n g d u ra t i o n s a re n e ce s ­
sa ry, 0 . 5 % b u p ivaca i n e with 1 : 200, 000 e p i n e p h ri n e
m a y a lso be used . It p rovides a vasoco nstrictor c h a l ­
l e n g e i d e ntica l t o a rtica i n e 's ( 1 : 200,000 e p i n e p h ri n e)
a n d l ess cha l l e n g e to the l ive r's d etoxificatio n syste m
co m p a red with l i d o c a i n e a n d m e p ivaca i n e , because
of the d e c re a s e d q u a n t i ty of d r u g (0 . 5 % s o l u t i o n
com p a red with 2% a n d 3% sol utions).
Patie nts with d i a betes a re best treated i n s h o rt
m o r n i n g a p p o i n t m e nts w h e n b l o o d s u g a r l eve l s a re
m o re l i kely to be sta b l e . If i n s u l i n is used, M r. M a rtinez
s h o u l d b e asked if h e has eaten b rea kfast to avo i d
hypog lyce m i a .
Case Discussion: M r. M a rt i n ez prese nts with sev­
e r a l c h a l l e n g e s w h e n c o n s i d e r i n g d e n t a l treatm e nt,
b u t treat m e n t is i n d icated to e l i m i n ate d isease a n d
i m p rove h i s o r a l h e a l t h , e s p e ci a l l y a s it contrib utes
to d i a betes contro l . The l i n ks between d i a b etes a n d
p e r i o d o n t a l d isease h ave b e e n c l e a r l y esta b l i s h e d .
P e r i o d o n t a l treat m e n t m a y h e l p i m p rove d i a betes
contro l . An i m p rove m e nt i n p e r i o d o nta l h e a lth a n d
e l i m i n ation o f dental d isease a re necessa ry for h i m to
achieve o pti m a l ora l health.
B l o o d p ress u re va l u es l ess t h a n 1 60/1 00 d o n ot
p re s e n t c o n t ra i n d i c a t i o n s to t re a t m e n t . B e c a u s e
M r. M a rtinez i s a l ready being treated for hypertension,
there is no need for referra l , which wou l d be suggested
if medical management were not cu rrent.
.�.h. c:t. P.t.E! �. 9.l1.E! ��.i.�.� � ........................................... .
1. The delivery of local anesthesia requires both medical
and technical skills. Which one of the following is not one
of the six elements of the ASA Medical Components of
Care associated with regional anesthesia?
a. Pre-anesthetic evaluation of the patient
b. Comprehensive tooth charting
c. Remain present during the course of the anesthesia
d. Providing indicated post-anesthesia care
2. The ASA ( American Society of Anesthesiologists )
Physical Status Classification System categorizes
patients based on their overall health. Classification
P3 describes which one of the following?
a. Normal Healthy Patient
b. Severe Systemic Disease
c. Moribund Patient
d. Severe Systemic Disease ( constant threat to life )
3. Which of the following is not considered a main
tool for patient assessment when planning for local
anesthesia?
a. The medical/dental questionnaire
b. The clinical examination
c. Drug MRDs
d. Medical consultation
S i g n ifi cant l iver d a m a g e from hepatitis C, which is
a c h ro n i c d isease, w o u l d s u g g est caution w h e n u s i n g
l o c a l a n esthetic d ru g s m eta b o l ized i n t h e l iver. Liver
d a m a g e of this nature can i n crease the toxicity of lo­
ca l a n esthetics by p ro l o n g i n g their biodegra d ati o n .
S m o k i n g is a m i l d contra i n d ication t o ce rta i n d rugs
that may impair oxyg e n ation, such as prilocaine, ben­
zoca i n e , a n d aceta m i n o p h e n . The ha bit i n creases the
risk and worse ns t h e p r o g n osis fo r p e r i o d o n ta l a n d
cardiovascu l a r d isease. I f M r. M a rtinez i s w i l l i n g , smok­
i n g cessation prog ra ms s h o u l d be reco m m e n d e d .
I n s u l i n - resistant, n o n re s p o n sive d i a betes p l a ces
M r. M a rt i n ez at r i s k of exp e ri e n c i n g e p i n e p h r i n e ­
e l evated b l o o d s u g a r l eve l s . E p i n e p h r i n e u s e s h o u l d
be m i n i m ized .
C o rg a rd , o r n a d o l o l , i s a n o n s e l e ct i v e b e t a ­
b l o c k e r. W h e n v a s o c o n st r i ct o rs a re a d m i n i s t e r e d
c o n c o m itantly, s p i kes i n b l o o d p ressu re a n d w h a t is
known as refl exive b radycard i a ca n res u lt. I n l i g ht of
p rev i o u s p reca u t i o n s a l ready d iscussed with t h e use
of vasoconstrictors, t h ey s h o u l d be used only i n low
c o n ce n trat i o n s a n d low d os e s a n d m o n it o r i n g of
blood press u re is advise d .
F i n a l ly, t h i s c a s e i l l ustrates t h a t p roce d u r a l m o d i ­
f i c a t i o n s (s h o rt a p p o i n t m e nts w i t h m o re l i m it e d
treat m e n t a reas p e r a p p o i n t m e nt) c a n b e as i m p o r­
t a n t a s t h e s e l e ct i o n of d r u g s w h e n p l a n n i n g safe
treat m e n t .
4. Which one of the following drugs is an absolute
contraindication for patients with poorly controlled
or uncontrolled hyperthyroidism?
a. Lidocaine
b. Bupivacaine
c. Epinephrine
d. Felypressin
5. Your patient has identified or you suspect that your
patient has used methamphetamines approximately
20 hours ago. Which of the following would be the
most appropriate action when considering the use of
local anesthetics?
a. Continue with procedures, as it has been more than
12 hours since the use.
b. Restrict the dose of vasoconstrictors to 20 % of
standard dose.
c. Consider postponing care for a full 24 hours.
d. Use only bupivacaine as the local anesthetic agent.
6. For which one of the following medical conditions is
it unnecessary to obtain a medical consultation from
the patient's physician before dental treatment?
a. Significant liver disease
b. Myocardial infarction within 3 weeks
c. Kidney dialysis patients
d. Organ transplant patients

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can Dental Association, I43(11), 1 190-1 198.
Wilburn-Goo, D., & Lloyd, L. M. (1999). When patients become
cyanotic: Acquired methemoglobinemia. Journal of the
American Dental Association, 130(6) , 826-831.
Wilkins, E. (20 12). Vital signs. In Clinical practice of the dental
hygienist ( 1 1 th ed., pp. 128-136). Baltimore: Lippincott
Williams & Wilkins.
ASA Physical Status Classification: Examples
of Diseases and Cond itions

(ASA Classifications may also be noted as P1 -P6)

ASA
Classification H ealth Status

ASA I ADA - Normal and healthy patient

Healthy: • Well balanced whole body health, physiological systems not compromised, main
organs healthy

Lifestyle Conditions: • Nonsmoker, minimal to nondrinker

Treatment Guidelines

• Routine dental treatment

• Recheck blood pressure in 6 months
• Implement Stress Reduction Protocol if patient is anxious

ASA II Mild systemic disease or condition (well-controlled)

Healthy with: • Allergies, Pregnancy, Age 60+ years

Psychological: • D ental anxiety

Cardiovascular • High blood pressure (140-- 1 59 mm Hg systolic 90--9 4 mm Hg diastolic)

Respiratory System: • Asthma

• Short-term upper respiratory tract infection ( cold)

Nervous System: • Epilepsy, seizure disorders

Metabolic System: • Diabetes - type 2 ( non-insulin dependent )

• Hyperthyroid or hypothyroid disorders

Lifestyle Conditions: • More than minimal drinker

• Recheck BP during three consecutive appointments

• Advise patient to monitor blood pressure at home or at the pharmacy
• Medical consult recommended if three consecutive blood measurements are in this range
• D ental treatment with careful patient observation - measure BP after local anesthesia administration
• Implement SRP as needed

187
188 SECTI O N I N JECTI O N FUNDAMENTALS
Ill •

ASA
Classification H ealth Status

ASA III Severe systemic disease or condition (uncontrolled)

Unhealthy: • Significant limits to activity but not incapacitated

Cardiovascular: • History of myocardial infarction, cerebral vascular accident, transient ischemic

attacks more than 6 months before the dental appointment with no residual signs
and symptoms
• Congestive heart failure - orthopnea and ankle edema
• Angina pectoris ( stable )
• High blood pressure (160-199 mm Hg systolic and/or 95-1 14 mm Hg diastolic)

Respiratory: • Emphysema, chronic bronchitis, chronic obstructive pulmonary disease

• Asthma- exercise induced

Nervous System: • Epilepsy (less well-controlled )

Metabolic System: • Diabetes - type 1 ( insulin dependent, well-controlled)

• Hyperthyroid or hypothyroid (patient is symptomatic )

Lifestyle Conditions: • Smoker w/one or more of above, > minimal drinker

• Recheck in five minutes

• Medical consult before dental treatment if blood pressure still elevated
• Implement SRP as needed

ASA IV Severe systemic disease or condition that is a constant threat to life uncontrolled

Cardiovascular: • Heart attack ( myocardial infarction ) less than 6 months before the dental
appointment
• Brain attack ( stroke ) within the past 6 months
• Severe heart failure or COPD ( requiring 02 supplementation or confinement in
a wheelchair)
• Angina pectoris - unstable
• High blood pressure - greater than 200 mm Hg systolic or 1 15 mm Hg diastolic

Respiratory: • Severe COPD ( requiring 02 supplementation or confinement in a wheelchair)

Nervous System: • Epilepsy - uncontrolled

Metabolic: • Diabetes - type 1 ( uncontrolled, hx of hospitalization )

• Recheck in five minutes

• Medical consult before dental treatment if blood pressure still elevated
• Implement SRP as needed

ASA V Moribund patient not expected to survive without an operation terminal systemic diseases or conditions

Moribund: • All end-stage diseases

• Recheck in five minutes

• Medical checkup immediately
• D o Not deliver dental treatment until BP corrected
• Consider arranging transportation for the patient

ASA VI Clinically dead patients being maintained for harvesting of organs

Adapted from: AS A ( American Society of Anesthesiologists) Physical Status Classification System, 2006, www.asahq.org/clinical/physicalstatus.htm,
and Malamed S. F.: Medical Emergencies in the Dental Office, 6th edition, 2007. pp. 50-53.
S R P : Stress Reduction Protocols for Anxious
Patients

*
ASA Classification Strategies for Stress Reduction

ASA I Communication: Establish trust, using empathy and effective communication skills
Healthy w/Anxiety Recognize the patient's level of anxiety
D etermine the cause of the patient's anxiety

Anxiety Reduction: Premedicate the evening before the dental appointment, as

needed
Premedicate immediately before the dental appointment, as
needed

Scheduling: Schedule the appointment early in the day (patient will be well
rested and will not worry all day about the appointment )
Minimize the patient's waiting time
Short appointments

Suggestions to Patient: Try to avoid additional stress by getting enough sleep, eating a
well-balanced meal before the appointment, and allowing
enough travel time to get to the appointment

Anxiety and Pain Control Consider sedation during therapy ( nitrous oxide )
during the Appointment: Administer adequate pain control during therapy
Obtain frequent feedback, giving the patient a sense of control and
caring

Postoperative Care: • Follow up with postoperative pain and anxiety control

• Telephone the highly anxious or fearful patient later that same
day that treatment was delivered

ASA II, ASA III Apply strategies for ASA 1 patient

Medical Compromise with the following additional procedures:
w/Anxiety

Pre-Appointment • Recognize the patient's level of medical risk

Procedures: • Complete medical consultation, as needed

Procedures during the • Monitor and record preoperative and postoperative vital signs
Appointment:

Scheduling: • Arrange the appointment for the highly anxious or fearful,

moderate-to-high risk patient during the first few days of
the week when the office is open for emergency care and the
treating doctor is available.

"Chapters 2 and 18 provide additional stress reduction strategies.

189
M odifications to Local Anesthesia for Co m m on
M edical Conditi ons

Local Anesthetic Vasoconstrictor

Condition Considerations Considerations M odifications

Diabetes None of Significance Epinephrine opposes the action
of insulin
Minute amounts used in dentistry
do not raise blood levels
significantly
Use epinephrine with caution when
there is significant cardiovascular
disease and/or uncontrolled
diabetes.

Glaucoma None of Significance Vasoconstrictors cause increased Avoid vasoconstrictors

ocular pressure

Hypertension None of Significance Vasoconstrictors can increase
the risk of hypertensive
episodes however the lack
of profound anesthesia can
increase levels of endogenous
epinephrine Controversial
topic
Clinical j udgment and medical consult
advised
Note : Uncontrolled hypertensives either
should not be treated or treated with
caution, depending upon severity
See Table 10-lASA Physical Status
Classification Blood Pressure
Guidelines for Adults

Hyperthyroidism None of Significance Hyperthyroidism appears to When there is obvious evidence of

A - Controlled increase tissue sensitivity to hyperthyroidism avoid epinephrine
epinephrine

Hyperthyroidism None of Significance Risk of seriously increased tissue Avoid all treatment until condition is
B - Uncontrolled sensitivity to epinephrine under control

Hypothyroidism Generally Safe Generally Safe Hypothyroid patients tend to be

A - Controlled sensitive to CNS depressants
Local anesthetic doses should be kept
to a minimum

Hypothyroidism Generally Safe Generally Safe Hypothyroid patients tend to be

B - Poorly Controlled sensitive to CNS depressants
with mild symptoms Caution with LA drug dosing.
Hypothermia, bradycardia, severe
hypotension and seizures are possible.

Hypothyroidism Avoid all treatment until condition is under control

C- Severe or Untreated

Myasthenia Gravis Esters and articaine None of Significance Avoid esters and articaine
compete for
diminished
supplies of acetyl
choline

190
M edical Pred ispositions That M ay Require
M odifications

Local Anesthetic Vasoconstrictor

Condition Considerations Considerations M odifications

Significant Hepatic Amides are primarily Cholinesterase is primarily Caution with use of amides
Disease metabolized in the manufactured in the liver Articaine is the preferred amide but
liver although there are extra-hepatic appointments should be shorter with
sources reduced dosages administered
If other amides are used, limit even
further

Atypical Amides are not None of Significance Avoid esters & articaine
Cholinesterase affected

Significant Renal All drugs cleared All drugs cleared more slowly, Medical consult advised
Dysfunction more slowly, with with increased risk of overdose Limitdoses of all drugs depending
increased risk of upon severity
overdose

Methemoglobinemia Increased risk with None of Significance Substitute other amides for prilocaine
prilocaine and and other topicals for benzocaine
benzocaine Avoid prilocaine or benzocaine when
excessive doses of acetaminophen are
used

Malignant local anesthetic None of Significance Medical consult is recommended

Hyperthermia agents safe for MH When treating these patients follow the
patients: articaine MHAUS' guidelines
bupivacaine lidocaine
mepivacaine
prilocaine

'MHAUS: Malignant Hyperthermia Association of the United States

191
M odifications to Local Anesthesia
for Co m m on Conco m itant Drug Therapy

Medications
Examples: Proprieta ry Loca l Anesthetic Vasoconstrictor
(gene ric) Considerations Considerations M odifications

Anticonvulsants Anxiety reduction requires None of Significance Avoid higher doses of local
Klonopin ( clonazepam) effective local anesthesia. anesthetic drugs
Dilantin (phenytoin) Sensitive to CNS depressants
D epakote (valproic acid)
Topamax ( topirama te)

Antipsychotics Increased sensitivity to CNS None of Significance Avoid higher doses of local
Zyprexa ( olanzapine) depressants anesthetic drugs
Seroquel ( quetiapine)
Risperdal ( risperidone)

Antidepressants None of Significance Increases risk of Limit doses of epinephrine

Tricyclic hypertensive episode by (observe cardiac dose
Elavil (amitriptyline) opposing the reuptake of limits)
Tofranil (imipramine) norepinephrine Avoid levonordefrin

Antidepressants None of Significance Oppose the reuptake of Suggest caution

Serotonin/Norepinephrine norepinephrine
Reuptake Inhibitor
Effexor ( venlafaxine)
Savella (milnacipran)

Antidepressants None of Significance Increases release of Suggest caution

Central A /pha-2 Antagonist norepinephrine
Remeron (mirtazapine)

Antidepressants None of Significance Oppose the reuptake of Suggest caution

Dopamine Reuptake Inhibitor norepinephrine
Wellbutrin (Bupropion)
Zyban (Bupropion)

Antidepressants None of Significance Oppose the reuptake of Suggest caution

Other norepinephrine
Cym balta ( duloxetine)

Anxiolytics CNS depressant effect of None of Significance Limit dosages

Valium (diazepam) local anesthetics may be
additive

Glucocorticoids Stress associated with local Stress associated with local Consider supplemental stress
Nasonex (mometasone) anesthesia is considered anesthesia is considered reduction such as nitrous
Entocort (budesonide) to be low to be low oxide or IV sedation
Advair (fluticasone)
Aristocort (triamcinolone)

192
 CHAPTER 1 0 PATI E NT ASSESSMENT FOR LOCAL ANESTHESI A
• 193

M ed ications
Examples: Proprieta ry Local Anesthetic Vasoconstrictor
(generic) Considerations Considerations M odifications

,8-blockers With propranolol, minimal Increased risk of Unless vasoconstriction is

Nonselective doses of lidocaine are hypertensive episode and necessary, limit or avoid
Inderal (propranolol ) recommended reflexive bradycardia vasoconstrictors
Corgard (nadolol ) and in a few individuals,
Blocadren (timolol ) strokes

Histamine Hz Receptor Tagamet competes with None of Significance Use caution with large doses
Blockers lidocaine for liver of lidocaine particularly in
Tagamet ( cimetidine ) Zantac isoenzymes the presence of significant
(ranitidine ) Slows lidocaine metabolism congestive heart failure
increasing the risk of
overdose
Zantac and others do not
have this effect

Monoamine Oxidase None of Significance None of Significance None

Inhibitors
Nardi! (phenelzine ) Parnate
(tranylcypromine )
Marplan (isocarboxazid )

Phenothiazines None of Significance Hypotension, possibly severe, Observe cardiac limit of

antipsychotic/antiemetic/ is the primary effect of vasoconstrictors (0.04 mg ) .
neuroleptics epinephrine with these Do not use 1:50,000
Thorazine (chlorpromazine ) drugs epinephrine
Mellaril ( thioridazine )

Limited examples are provided in each category; numerous drugs may be included in these categories. Current drug indexes should be consulted for the
most up-to-date information.
I lleg al (" Recreational") Drug U se*

Local Anesthetic Vasoconstrictor

D rug Considerations Considerations M odifications

Methamphetamine None of Significance Administration of Do not administer

vasoconstrictors may result local anesthetics with
in hypertensive crisis, stroke, vasoconstrictors for a
or myocardial infarction minimum of 24 hours after
methamphetamine use

Cocaine Cocaine is a strong CNS Administration of Do not administer

depressant; local anesthetics vasoconstrictors significantly local anesthetics with
compound CNS depression increases the risk of vasoconstrictors for a
and administration should be hypertensive crisis, stroke, or minimum of 24 hours after
avoided myocardial infarction cocaine use

Alcohol May decrease the None of Significance Use caution to avoid

effectiveness of local overdose
anesthetics

'If a patient is under the influence of a drug or alcohol, any informed consent taken may be invalid as the patient may not be
"competent" to give consent. For all drugs not on this list, it is prudent to consult a drug index before administering all local
anesthetic drugs.

194

�P.P..� ��- i )(_ . � i � l _i_()_9. _r c:l.P.�.Y. . . . . . . . . . . . . . . . . .
Aldrete, J. A., & Narang, R. ( 1975 ) . Deaths due to local analgesia
in dentistry. Anaesthesia, 30, 685-686.
Aldrete, J. A., Narang, R., Liem, S., et a!. ( 1975 ) . Untoward
reaction to local anaesthetics via reverse intracarotid flow.
Journal of Dental Research, 54, 145-148.
Budenz, A. W. ( 2000, August ) . Local anesthetics and medically
complex patients. Journal of the California Dental Association,
28 ( 8 ) , 61 1-619.
D ental Lexi-Drugs Online. (20 14) . Vasoconstrictor interactions
with antidepressants. Retrieved February 1, 2014, from
http:/Ionline.lexi.com/lco/ action/ doc/retrieve/docid/
dental_f/389495
Felpel, L. P. ( 1998 ) . Psychopharmacology: Antipsychotics and
antidepressants. In J. A. Yagiela, E. A. Neidle, & F. J. Dowd et a!.
( Eds. ) , Pharmacology and therapeutics for dentistry ( 4th ed.,
p. 162 ) . St. Louis, Missouri: Year B ook, Inc.
Glick, M., & Pinto, A. D. ( 2002 ) . Management of patients with
thyroid disease, oral health considerations. Journal of the
American Dental Association, 133(7), 849-858.
Hansten, P. D., & Horn, J. R. ( 2009 ) . Drug interactions: The
dangers of beta-blockers and epinephrine. Pharmacy
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pharmacytimes.com/publications/issue/2009/2009-05/
DruginteractionsBetaBlockers-0509
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• 195
Little, J. W., Falace, D. A., Miller, C. S., & Rhodus, N. L. ( 20 13 ) .
Dental management of the medically compromised patient
( 8th ed. ) . St. Louis: Mosby.
Malamed, S. F. ( 20 13 ) . Handbook of local anesthesia ( 6th ed. ) .
St. Louis: Mosby.
Naftalin, L. W., & Yagiela, J. A. ( 2002 ) . Vasoconstrictors:
Indications and precautions. Dental Clinics of North America,
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 OBJECTIVES KEY TERMS

• Defi n e a n d d iscuss the key terms in this cha pte r. aspiration test 203
cu m u l ative tra u m a
• I d entify a n d d i scuss the g e n e ra l p ri n c i p l es a n d e l e m ents of
d isorders 207
i nformed consent. de position site 1 98
• I d e ntify and d i scuss key factors that i m pact the su ccessfu l de­ fa lse neg ative
l ivery of l oca l a n esth etic agents. aspirations 204
fie l d block 1 97
• I d e ntify and d i scuss stress and a nxiety factors that i m pact
i nformed consent 1 99
both patie nts a n d c l i n i ci a n s d u ri n g the d e l ivery of l oca l a n es­
i nfi ltration 1 97
thetic i njections.
need l e pathway 1 98
• D iscuss the i m pact of c l i n i ci a n/patient com m u n ications neg ative aspiration 204
before, d u ri n g , a n d after the d e l ivery of l oca l a n esth etic n e rve b l ock 1 98
i njections. penetratio n site 1 98
positive aspirati o n 204
• D ifferenti ate between the th ree basic types of i njections.
s u p p o rtive
• List, d escri be, a n d a p p l y the basic ste ps i nvolved i n the d e l iv­ com m u n i cation 200
ery of l oca l a n esthetic i njections. s u praperiosteal 1 97
• l d ntify, d e m o n strate, a n d a p p l y the g e n e ra l p ri n c i p l es of er­
d u ri n g the Jl e l i ve rj of l oca l a n esth etic i njecti ons.

196
 CHAPTER 1 1 FUNDAMENTALS FOR ADMINISTRATI O N OF LOCAL ANESTHETIC AGENTS
• 197

I nject i on Term i n ology

CAS E S TUDY
Hector Melendez
H e ctor M e l e n d ez, a 45-year- o l d , re l ated that d u r­
i n g h i s m ost re c e n t d e nta l visit, t h e " s h ots t o o k
what s e e m e d l i ke seco n d s a n d t h ey h u rt . " H e h a d
been i n structed to r a i s e h i s h a n d if h e " n e e d e d a
bre a k " a n d he h a d d o n e so after the p a i n beca m e
i ntense b u t w a s t o l d that i t w a s a l m ost ove r.
Alth o u g h the a ct u a l treatment h a d been co m ­
forta b l e , h e h a d d e c i d e d to try o u t a n ew offi ce
and asked if t h e re w e re a way to h ave h is d e nta l
treatment acco m p l ished with out novoca i n e .
I ntrod uction
Basic skills necessary for safe and comfortable delivery of
local anesthetic inj ections will be discussed in this chap­
ter. In addition to technical and procedural skills, informed
consent, ergonomic awareness, and patient and clinician
perspectives will be discussed.
Few will argue that inj ections represent one of the
most, if not the most stressful, aspect of dental appoint­
ments (Dionne et al. , 1998; Rizzolati et al., 1996). In order
to reduce stress and provide both safe and comfortable
environments for inj ections, the development of specific
strategies and clinical skills is necessary. Local anesthetic
procedures should take into account the need for success­
ful pain control when all components of the process have
been considered. Box 1 1-1 • provides a historical perspec­
tive on the history of inj ection techniques in dentistry.
There a r e three basic types of intraoral inj e ctions fre ­
quently u s e d in dentistry: local infiltrations, field blocks,
and nerve blocks (Evers & Haegerstam, 198 1 ; Lipp, 1993 ;
Malamed, 20 1 3 ) . Infiltration and field block inj ections
are among the simplest and safest local anesthesia tech­
niques to learn. They are relatively easy to execute, have
a high rate of success, and have wide margins of safety.
A simple comparison of these techniques is illustrated in
Figure 1 1-1 •·
Infiltration Injections
Infiltration inj ections involve the deposition of local an­
esthetic drug directly at or near small terminal nerve end­
ings in the immediate area of treatment as illustrated in
Figure 1 1-1A.
Field Block Injections
Field block inj ections involve deposition of anesthetic
drugs near larger terminal nerve branches near or a small
distance from the site of the inj ection and areas of treat­
ment as illustrated in Figure 1 1-1B. They are indicated
when procedures are confined to one or two teeth and
are commonly referred to as infiltrations and by some as
supraperiosteal inj ections.
Some suggest that the terms infiltration and field block
are entirely distinct and that local infiltrations anesthetize
soft tissue only. The difficulty in making clear distinctions
between the definitions of infiltration inj ections versus
field block inj ections is confounded by the nearly uni­
versal use of the term infiltration in the dental literature

Despite advances i n armamentari u m a n d drugs, the fu n­

d a m e ntals of local a n esth esia, i n c l u d i n g re levant a n atomy
and basic i njection tech n i q u es, have not changed sign ifi­
cantly over the past centu ry. When comparing tech n i q u es
developed i n the early 1 800s to i nstru ctio n a l m ateri als pub­
l ished m o re than 60 yea rs ago a n d to those in circu lation
today, close s i m i l a rities can be observed.
Many scientists, including a n u m be r of de nta l expe rts,
h ave p l ayed key ro les in the advancement of local a n es­
thesia. Their contributions inc lude i m p rovem ents in both
the practice and science of dental local a n esthesia. M o re
recent pioneers h ave developed i m p roved del ivery opti ons
a n d tech n i q u e gu idel i n es. In the 1 940s, for exa m p l e , with
the lead of D r. H a rvey Cook, Cook-Wa ite La boratories pub­
l ished the " M a n u a l of Local Anesthesia. " FIGURE 11-1 Types of Inj ections Defined. A- Infiltrations
William Ha lsted, an early pioneer, developed nerve block involve deposition directly at or near small terminal nerve end­
anesthesia techn iques, including the inferior a lveolar nerve
ings in the immediate area of treatment. B - Field block inj ec­
block. Additional techniques have been introduced in the
twentieth centu ry, including the Gow-Gates (1 973), Vazirani­ tions involve depositions near larger terminal nerve branches.
Akinosi (1 977), P-ASA, and AMSA nerve blocks ( Friedman & C - Nerve block inj ections involve depositions near maj or nerve

�� �c
. � ��� .
·1
�. :
::� : � ;� �� � �� �� �� :::
; st k g l ,
• &
•
na
. s .
·1
•
)·
• • • • IIi trunks at a greater distance from the area of treatment, which
provide wider areas of anesthesia.
198 SECTI O N I N JECTI O N FUNDAMENTALS
Ill •
to describe two other procedures that routinely provide
pulpal anesthesia. Although specific modifiers are usually
added to these infiltration techniques, mandibular infiltra­
tions and b uccal infiltrations with articaine, they are not
described in the literature as either field or nerve block in­
j ections, yet both provide pulpal anesthesia (Kanaa et al. ,
2006; Kanaa et al. , 2009; Robertson, 2007) . For further
discussion of infiltration versus field block inj ections, see
Box 1 1 -2 •: Discussion of Infiltration versus Field B lock
Inj ections.
Nerve Block Injections
Nerve block inj ections are generally characterized as de­
positions near primary nerve trunks at greater distances
from the areas of treatment, which provide wider areas
of anesthesia. These inj ections are identified by the nerve
branches they anesthetize; for example, the inferior alveo­
lar nerve block will anesthetize the inferior alveolar nerve
as illustrated in Figure 1 1-1C.
In dentistry, field block and nerve block inj ections are
administered most frequently to provide pulpal as well as
soft tissue anesthesia. Box 1 1-2 discusses common usage
of the terms infiltration and nerve block injection.
Key terms relevant to the basic inj ection steps for local
anesthesia include penetration site, needle pathway, and
Alth o u g h the terms infiltra tion, field block, or n erve b lock
apply to a l l loca l a n esth etic tech n i q u es in this cha pter,
com m o n usage describes de nta l loca l a n esth etic injections
as either nerve b l ocks or i nfi ltrations. When used i n this
m a n n e r, the term n erve block genera l ly refers to injections
that i nvolve deposition of a n esth etic sol utions near major
tru n ks of nerves, usu a l ly at a sign ificant d ista nce from the
treatment a rea, a n d to i njections that p rovide a n esthesia
to m u ltiple teeth a n d/or other tissues via a single deposi­
tion site reg a rd l ess of the d ista n ce to the nerve. The term
infiltration is genera l ly used to describe oth er i njections
reg a rd l ess of whether they a n esthetize soft, h a rd, or p u l p a l
tissue, a n d there is occasion a l ly overlap i n the u s a g e o f t h e
terms.
These term i n o l ogy variations can create confusion.
Discussions in the peer-reviewed l iteratu re at times add
to this confusion . For exa m p le, seve ral p rom in ent i nvesti­
gators and authors h ave reported that the use of a m a n ­
d i b u l a r tech n i q u e ( m a n dib u lar or b u cca/ infiltration with
artica in e) m ay provide p u l p a l a n esth esia of m a n d i b u l a r
m o l a rs (Haase e t a l . , 2008; Ka n a a e t a l . , 2006; Ka naa e t a l . ,
2009; M a l amed, 201 3; Robertson e t a l . , 2007) . The reported
success of these infiltra tion s i n p rovi d i n g p u l p a l a n esth esia
for m a n d i b u l a r m o l a rs has been demonstrated i n a n u m b e r
o f c l i n i ca l stud ies (Haase e t a l . , 2008; Ka naa e t a l . , 2006;
Ka n a a et a l . , 2009; Robertson et a l . , 2007). All of these
i nvestigators and authors describe the tech n i q u e as an
•
i nfiltratio n .
: . . . . . . . . . . . . . . . . . . . . .
The g reater the d ista nce need l es trave l from penetration
to deposition site, the g reater the potentia l fo r deviation
of the need l e tip. For exa m p le, the d ista n ce from the site
of penetration to the deposition site in most i nfi ltrations is
usu a l ly o n ly a few m i l l i meters, whereas the penetration site
for a nerve b l ock i njection may be as m u ch as 1 6-27 m m
or more fro m its deposition site. C l ose atte ntion t o proper
•
l a n d m a rks a n d m a i nta i n i n g appropriate ba rrel a n g l es d u r- •
i n g i njections w i l l red uce these deviations.
•
•
: . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
deposition site. The penetration site is the specific location
where a needle first enters the mucosa. Locating this site
for each technique requires inspection of the oral cavity
and visual identification of key landmarks. Needle path­
way refers to the route a needle travels as it advances to a
target site. Box 1 1-3 •, "Needle Pathway Considerations,"
provides a discussion of the impact of penetration depths
on the pathway.
The deposition site may be defined as the anatomical
location at which a drug is deposited. Establishing these
locations for each technique requires an understanding of
head and neck anatomy (see Box 1 1-3) .
With all inj ection types, i t is necessary to consider
each step in the process before delivery, similar to a pilot's
"pre-flight" check. Proper functioning of the plane and its
equipment helps ensure the safety of the flight. Ten basic
steps for the administration of local anesthesia are dis­
cussed in "Basic Inj ection Guidelines." These pre-injection
checks are intended to ensure proper functioning of arma­
mentarium, appropriate drug selection, optimal access, and
ultimately safe inj ections.
A summary of key elements for each basic inj ec­
tion discussed in the following chapters is provided in
Appendices 12-1 , 1 3-1 , and 14-1. Target structures, nee­
dle gauges, penetration sites, inj ection angles, depths of
insertion, and suggested drug doses are available for quick
reference. Suggested drug volumes are provided for both
soft tissue and pulpal anesthesia.
Basic I njection G u idel i nes
Successful development o f strategies and skills necessary for
the administration of local anesthetics involves following a
framework of fundamental steps (Evers & Haegerstam, 1981;
Lipp, 1993 ; Malamed, 20 13; Robinson, Ford, & McDonald,
2000). A sequence of basic steps that incorporates various
schools of thought will be discussed in this section.
Steps in the Administration of Local Anesthesia
Ten basic steps serve as standard operating procedures
(SOPs) for monitoring safe inj ection technique, patient
. . . . . . . . . . . . . . . . . . • comfort, documentation, and follow-up. These ten steps
 CHAPTER 1 1 FUNDAMENTALS FOR ADMINISTRATI O N OF LOCAL ANESTHETIC AGENTS
• 199

are individually discussed in the following section and

summarized in Appendix 1 1-1.

ST E P 1 : P R E - I NJ E CT I O N PAT I E NT ASSESSM E NT Thorough

p atient evaluation determines individual local anes­
thetic needs based on the factors discussed in Chapter 10,
"Patient Assessment for Local Anesthesia." After consid­
eration of all precautions, contraindications, and necessary
modifications, appropriate inj ection techniques and anes­
thetic drugs are selected.

ST E P 2 : I NFOR M E D CONSE NT D iscussions with p atients

to obtain informed consent should include the nature
of and n e e d for any intended treatment and spe cific
discussions regarding the use of local anesthesia, when
anticipated (American Cancer S ociety, 2012; Malamed,
20 1 3 ; University of Washington [UW] School of Medi­
cine, 2008) . This discussion should include an explana­
tion that local anesthesia involves the delivery of an
inj ection ("shot") that results in the temporary numbing
of an area from the effects of the local anesthetic drug.
Patients must be advised of the specific risks associated
with the delivery of inj ectable local anesthetic drugs. See
Box 1 1-4 • for a summary of the elements of informed
consent and some specific risks.
Before
ST E P 3 : ASSE M BLE APPROPRIAT E ARMAM E NTAR I U M
the delivery of an inj ection, assembly of the appropriate
Obta i n i n g informed consent req u i res com m u n i cation
before p rocee d i n g with any treatment.
This com m u n i cation shou l d :
1 . Be d iscussed in a l a n g u a g e patients ca n u n dersta n d
2. Provide patients with opportun ities t o a s k q u estions
3. Exp l a i n the p rocedu res that have been recommended
a n d exp l a i n the need for each
4. Cla rify the risks a n d rewa rds of the reco m m e nded
treatment, i n c l u d i n g the risks of fa i l i n g to treat
5. Provide accepta b l e a lternatives to the recommended
treatment
Patients s h o u l d u n d e rsta nd that the topical p l acement
a n d i njecti on of local a n esthetic agents i n d uce temporary
n u m b n ess of specific a reas of the mouth a n d , although
rarely encou ntered, there a re sign ificant risks associated
with their use . These risks may inc lude but a re not l i m ited
to swe l l i ng, bruising, te m porary m uscle tighte n i n g , pro­
longed te mpora ry or permanent ti n g l i n g or n u m b n ess,
local ized pain and soren ess, a l lerg i c and overdose reac­
tions, a n d short-term raci n g of the heart.
FIGURE 11-2 Syringe Cartridge View. Keep the large window
in full view to accurately monitor the outcome of aspiration
tests, delivery rate, and the dose of drug deposited.
armamentarium and confirmation of the proper function of
local anesthetic delivery devices are required. The cartridge
is properly loaded when the harpoon is fully engaged into
the rubber stopper. This will allow the piston to be retracted
when performing aspiration tests. The cartridge should re­
main fully visible throughout the injection in order to recon­
firm that the correct drug has been loaded into the syringe,
to confirm the results of aspiration tests, and to monitor the
drug dose and rate at which it is delivered (see Figure 1 1-2 •) .
Window orientation d o e s n o t apply when using plastic
syringes with clear barrels.
Once the syringe has been properly loaded, the needle
is attached and the bevel orientation is checked (if bevel
orientation adjustment is appropriate for the particular in­
j ection) . To adjust the bevel, recap and rotate the needle
in the desired direction until the bevel is properly aligned
(see Box 1 1-5 •) .
Alth o u g h s o m e c l i n i cians consider i t u n i mportant, oth ers
b e l i eve that the needle bevel s h o u l d be oriented towa rd
bone when bony l a n d m a rks may be e n cou ntered d u r-
i n g i njection . Orienting the bevel of the need l e towa rd
bone lessens the l i ke l i h ood of d isco mfort a n d tra u m a to
the perioste u m when or if bone is contacted . In the event
of i n advertent contact, need l es ten d to g l a n ce off bone
rath er than pierce perioste u m when beve ls a re oriented to
face the bone . Withd rawi ng need l es from tissue i n order to
reposition them is not recom mended, because it can res u lt
i n u n necessary tissue tra u m a . Bevel orientation does not
� a ff t s u e s a t s '
• • �� . . �� . : . � .
� :����� � �·. �0.1 : . )
• • • • • • • • • • • • . IIi
200 SECTI O N I N JECTI O N FUNDAMENTALS
Ill •
The final step in armamentarium prep aration is to
confirm that all safety controls are in place. These controls
must include appropriate personal protective equipment
(PPE) for both clinician and patient, and must focus spe­
cial attention on the safe handling of needles. It is the clini­
cian's responsibility to comply with all Centers for Disease
Control and Prevention (CDC) and Occupational Safety
and Health Administration (OSHA) guidelines for dental
healthcare providers related to the handling of needles and
other sharps. This is required in order to assure not only
clinician safety but the safety of patients and co-workers.
Appropriate procedures and devices for recapping nee­
dles must be available and functioning properly. S e e
Appendices 9-1 and 9-2 for C D C guidelines. Needle re­
capping will be discussed in Step 9 - Completion of Inj ec­
tion, and various techniques are shown in Appendix 9-4,
"Needle Recapping."
ST E P 4 : P R E - I NJ E CT I O N P R E PARAT I ON Ideally, a patient's
head should be positioned for the clinician's direct vision
of the penetration site. Placing a patient in a position in
which the head is at the same level as the heart is recom­
mended. This position is preferred over one in which the
head is lower than the heart out of concern that respiration
might be compromised when managing medical emergen­
cies in dental settings (Malamed, 2007 ) . Attention to the
principles of proper ergonomics should be applied for all
inj ections. Further discussion of proper ergonomics is pre­
sented at the end of this chapter (see Box 1 1-8) .
S U P P O RT I V E C O M M U N I CAT I O N A N D P R E P Supportive
communication begins during the pre-inj e ction period.
Efforts to reduce stress from the beginning to the end
(A)
FIGURE 11-3 Pre-insertion Soft Tissue Retraction. A - The first step of a safe inj ection is to establish a firm but gentle grasp of the
soft tissue. B - Then fully retract the lip for vision and control during the injection.
Source: Courtesy of Megan Gibbons.
of inj ections are enhanced by maintaining positive, sup­
portive communication as a central focus. Providing reas­
surance and gaining trust can allay anxiety and fears. As
discussed in Chapter 2, "Fundamentals of Pain Manage­
ment," the PREP strategy and steps (Prepare, Rehearse,
Empower, and Praise), along with a debriefing session, can
further build trust and reassurance. To review these steps,
see Chapter 2, Box 2-2, "PREP to Minimize Patient Anxi­
ety and Fear."
It is helpful to establish strategies for patients to safely
communicate their anxiety levels or discomfort during in­
jections. This protects both patients and clinicians from sur­
prise movements while at the same time allows patients to
have a sense of control. As discussed in Chapter 2, patients
may raise a hand when they are unable to cope or need to
pause from procedures. It is important to designate which
hand a patient may raise to avoid interference with inj ec­
tions. For the highly anxious patient, planning to take a mo­
ment to pause during the procedure can give them time to
regain control and allow them to proceed.
In most cases, keeping syringes out of sight is a valu­
able patient stress reduction strategy. Impulses stimulated
from the image of the syringe travel to the brain and can
trigger a number of possible responses, including unantici­
pated anxiety, withdrawal, and autonomic recoil. For anx­
ious or fearful patients, the " show-tell-do" strategy can be
valuable when preparing them for what is actually going to
happen (Milgrom, Weinstein, & Getz, 1995).
Once specific inj ections have been determined, es­
tablish effective soft tissue retraction (see Figure 1 1-3 •) .
Palpating the areas adj acent t o the penetration site (see
Figure 1 1-4 •) will identify anatomical variations that are
(B)
 C HAPT E R 11 • FUN DAM E NTALS FOR A D M I N I STRAT I O N OF LOCAL A N E STHETI C AGENTS 201

(A) (B)
FIGURE 11-4 Injection Step: View & P alpate. A-Once stable retraction has been accomplished, establish a clear view of the selected pen­
etration site by positioning the patient ergonomically. B-Gently palpate the site for any anomalies that could interfere with the injection.
Source: Courtesy of Megan Gibbons.

(A) (B)
F I G U R E 11-5Injection P enetration Site Retraction. A-The use of gauze aids in the control of "slippery " tissues to remove gross
debris from the site and to dry the penetration site before placing topical anesthetic. B-Retraction can also be established with a
mouth mirror or metal retractor.
Source: Courtesy of Megan Gibbons.

not readily visible. Anatomical variations can interfere
with basic inj ection techniques and may require adj ust­
ment. To proceed, reestablish retraction. This will provide
clear visibility of the penetration site (see Figure 1 1-5 •)
and allow the clinician to view the needle throughout the
inj ection as demonstrated in Figure 1 1-6 •·
S T E P 5: P R E PA R E I N JE CTI O N S I T E With adequate soft tis­
sue retraction established, gently dry the mucosa with
gauze before the placement of topical . D rying tissue
with gauze will reduce dilution and inadvertent spread of
topical agents, and improve its uptake into the mucosal
tissue. It also serves as a debridement step by removing
gross and microscopic debris from the site. Using a cot­
ton-tipped or manufacturer-supplied applicator, apply a
small amount of an appropriate topical anesthetic agent
at the site of penetration (see Figure 1 1-7 •). Consult
the manufacturer's directions for the appropriate onset
time. Most agents will reach peak effectiveness in about
1 minute.
202 S E C T I O N Ill • I N J ECTION F U N D A M E NTALS

(A) (B)
F I G U R E 11-6 Soft Tissue Retraction during Injections. A - Retraction is provided manually. B - Retraction is provided by a retrac­
tion device.
Source: Courtesy of Megan Gibbons.

(A) (B)
F I G U R E 11-7Injection Step: Rehearse & Topical. A-Begin by visualizing the angle of the injection and rehearse the approach
with a cotton swab. B-Maintaining this angle, place topical anesthetic at the penetration site.
Source: Courtesy of Megan Gibbons.

Pre-inj ection preparation time can also be viewed as a
"rehearsal" time for an inj ection (see Figure 8-7 •). This is
an ideal time for clinicians to mentally review the injection
technique and reevaluate the patient for any factors that
may require adjustments to planned techniques.
Before proceeding with inj ections, test penetration sites
for effective onset of topical anesthesia (Figure 1 1-8 •).
The tip of a cotton swab, periodontal probe, or other in­
strument works well for testing topical effectiveness. If a
patient expresses that a site is not numb, allow more time
for the topical to be effective. This step may reduce patient
anxiety surrounding initial needle penetration.
ST E P 6: I N I T I AT E I N JE C T I O N Maintain supportive com­
munication with patients while keeping syringes out of
the p atient 's view as much as possible. With adequate
retraction established, gently pull the mucosa "taut" (see
Figure 1 1-9 •), which will ease penetration of the needle
and then establish a point of stability for syringes. Avoid
using the patient's body for stability. Establishing syringe
stability on patient's shoulders or chests increases the risk
of trauma if the patient moves unexpectedly. The most
stable position for a syringe is a "palm up" grasp. Stabil­
ity can be increased with the index finger extended onto
the barrel for support (see Figure 1 1-10 •, Box 1 1-6 •,
and Appendix 1 1-2) . In order to accurately evaluate the
outcome of aspiration tests and to monitor the amount of
drug delivered, the large window of the syringe should re­
main visible throughout the procedure.
Once clear vision and a stable fulcrum have been es­
tablished, penetrate the mucosa to a depth of 1-2 mm (ap­
proximately the length of the bevel) with the bevel oriented
 C HAPT E R
F I G U R E 11-8 Testing for Effective Topical Anesthesia.
Source: Courtesy of Megan Gibbons.
toward bone (see Figure 1 1-11 •). A few drops of solution
are usually deposited as needles are advanced because
even gentle contact with the thumb on the front inner sur­
face of the thumb ring will cause a few drops of anesthetic
to be deposited ahead of the needle. Note that this does
not require visibly advancing the stopper and no separate
action is required other than to proceed slowly. The total
volume administered in this manner should be less than 0.2
mL (the volume displaced by 1 stopper length).
Slowly advance the needle to the desired depth and
angle for delivery at the deposition site (see Figure 1 1-12 •).
Throughout the inj ection, observe and communicate with
the patient, monitoring for signs of discomfort, distress, and
adverse reactions.
F I G U R E 11-9 Establish Retraction. Retract and gently pull the
mucosa "taut."
Source: Courtesy of Megan Gibbons.
11 • FUN DAM E NTALS FOR A D M I N I STRAT I O N OF LOCAL A N E STHETI C AGENTS 203
FIGURE 11-10 Injection Technique: Initial Approach. Key
elements of a safe injection: A-Stable retraction; B-"P alm-up"
grasp; C-Thumb positioned for effective aspiration; D ­
Confirm cartridge drug color ID; E-Clear vision of large
window and rubber stopper (showing "1/2 cartridge").
STEP 7: ASPI RAT I O N One of the two most important safety
steps in the delivery of local anesthetic agents is the aspira­
tion test (slow delivery is the other) . This test reduces the
risk of inadvertent deposition of a drug directly into the
bloodstream.
Once the needle is advanced to the appropriate depo­
sition site for a specific injection, and before depositing so­
lution, perform an aspiration test by applying gentle, brief
back pressure on the upper inside surface of the thumb
ring. This action changes the pressure inside the cartridge
from positive to negative (see Figure 1 1- 1 3 •). If the
needle has entered a vessel, blood will be drawn into the
cartridge, referred to as a "positive aspiration." Do not
Safe d e l ivery of i nj e ctions req u i res c l i n i ci a n s to h ave c o n ­
sta nt control of the syri n g e . A s w i t h oth e r de nta l i nstru­
m e ntati o n , this can be accomp l is h e d with we l l -p l aced,
extra-ora l fi n g e r fu l cru ms. Those with s m a l l hands may not
be able to a c h i eve sta b l e fu l c r u m s using o n ly the fi n g e rs on
the hand that is h o l d i n g the syri n g e . W h e n this is the case,
a vari ety of m ethods may be used, some of w h i ch i n c l u d e
two-h a nded fu l c r u m s . Oth e rs d o not use fu l c r u m s at a l l
b u t nevert h e l ess a l low fo r stability d u r i n g i njecti o n s . For
exa mp l e, sta b i l ity can be a c h i eved t h ro u g h a rm-to-body, re­
tract i o n fi n g e r-to-ba rre l , seco n d a ry fi n g e r-to-fi n g e r, e l b ow­
sta b i l ized- o n - l e g , a n d m a ny oth e r m ethods, each of w h i c h
may be as u n i q u e as the c l i n i c i a n . T h e g o a l of sta b i l ity is t o
m a i nta i n b o t h consta nt contro l of the syri n g e a n d a position
that supp orts m uscu l oskeleta l h e a lth . App e n d ix 1 1 -2 s h ows
a n u m b e r of usefu l strateg i es fo r creati n g sta b i l ity d u r i n g •
� a
: �� � ��� : : � : !� : ��� •
s he i n c i
. . • • • • • • • • • • • • • • • • • • • • •
204 S E C T I O N Ill • I N J ECTION F U N D A M E NTALS
FIGURE 11-11 Initiate P enetration. P enetration is made slowly ,
at the height of the mucobuccal fold. Deliver a few drops of anes­
thetic solution after penetration and ahead of needle pathway.
under any circumstances deposit drug in the specific loca­
tion of a positive aspiration.
Responding to the outcomes of aspiration tests is a
primary safety factor for local anesthetic inj ections. Fail­
ure to aspirate or appropriately respond can result in toxic
overdose or injury.
(A)
F I G U R E 11-12P enetration Site: Correct/Incorrect. A - CORRECT: angle and height of penetration at the mucobuccal fold. B ­
INCORRECT: the angle i s somewhat steep and the height of penetration i s too low. This injection i s likely to encounter premature
contact with alveolar bone below the apex of the tooth.
Source: Courtesy of Megan Gibbons.
A negative aspiration, one in which no blood is drawn
into the cartridge, requires no corrective action. A clinician
may continue with the inj ection and deposit the indicated
volume of drug.
D espite performing this step correctly, it is still pos­
sible to have false negative aspirations at times. This can
occur when a bevel is in contact with a vessel wall. Dur­
ing an aspiration test, negative pressure can retract the
vessel wall into the lumen of the needle blocking the flow
of blood through the needle into the cartridge. To check
for false negative responses, rotate the syringe slightly; this
will reposition bevels away from vessel walls. This step is
encouraged for all injections in which there are greater
risks of positive aspiration.
Addition ally, improper assembly of syringes can
lead to false negative aspirations. Figure 1 1-14 • shows
a problem when harpoons are not seated in stoppers.
This occurred when the previous cartridge was n o t
properly removed a n d t h e stoppers are n o w stacked i n
t h e barrel.
A positive aspiration in which blood is visible in the
cartridge requires an immediate response (see Figure ll-
15A, Figure ll-15B, and Figure ll-15C •). If the aspira­
tion test results in a small trickle or "worm like" thread
of blood into the cartridge and does not obstruct clear
vision of a subsequent aspiration, the needle can be re­
positioned slightly and aspiration can be repeated. After
a second test that is negative, the clinician may continue
with the inj ection and deposit the drug. If the aspiration
test results in a burst of blood, creating a " cloudy and
(B)
 C HAPT E R 11
(A)
F I G U RE 11-13 Aspiration Best P ractice: Thumb P osition. A-Ideal position of the thumb ring. This position during aspiration
tests allows for a full range of backward motion (thumb flexion). B-Restricted position of the thumb ring. This position may create
difficulty for small hands and limits the range of backward motion (flexion).
F I G U RE 11-14 Improperly Loaded Syringe. False negative
aspiration can result when syringes are improperly loaded. In this
example, the are two stoppers stacked in the barrel. Although it
would feel like the harpoon seated, an aspiration test would be
impossible.
reddened" solution in the cartridge (see Figure 1 1 -lSB
and Figure 1 1-lSC) , or if the clinician for any reason
is concerned about the ability to see aspiration results
clearly, the needle should be withdrawn, the cartridge re­
placed, and the needle flushed or replaced before reiniti­
ating the inj ection.
Re-aspiration is also necessary whenever needle tip
locations change at any time during deposition. It may be
performed any time a clinician determines another "safety
check" is warranted. It may also be used to pace the rate
• FUN DAM E NTALS FOR A D M I N I STRAT I O N OF LOCAL A N E STHETI C AGENTS 205
(B)
of deposition of a drug solution. The best practice is to
perform an aspiration in two planes, rotating the syringe
slightly to reorient the bevel to a new position.
Following any positive aspiration, the inj ection site
should be evaluated immediately after completion. Ob­
serve for signs of local complications, such as swelling, and
remain alert to signs and symptoms of possible intravas­
cular inj ection. If there are no immediate complications, it
is acceptable to continue with the planned treatment. Pa­
tients should be advised according to the significance of
the situation and monitored following treatment as indi­
cated. Follow-up for a positive aspiration includes the po­
tential management of hematomas and will be discussed
in Chapter 17, " Local Anesthesia Complications and
Management."
If there are repeated positive aspirations at the same
inj ection site, rescheduling treatment should be consid­
ered. Bleeding following positive aspirations at deposition
sites may result in an inability to determine subsequent
positive aspirations. Repeated penetrations and the de­
velopment of an inflammatory response may diminish the
effectiveness of the local anesthetic agent. Clinicians may
also have other concerns such as the development of he­
matomas and postoperative pain or trismus.
It is important to maintain supportive communication
at all times during the inj ection process, especially during
aspiration tests to educate patients that these simple tests
and the responses to them are necessary in order to prac­
tice safely.
S T E P 8: D E P O S I T I O N A N D RAT E Avoid delivering too
much solution en route to the deposition site. Once at the
optimum deposition site, the most important step in the
administration of a safe inj ection is the rate of delivery.
206 S E C T I O N Ill • I N J ECTION F U N D A M E NTALS

Slow delivery of the drug reduces the risk of overdose

and complications even if inadvertently inj ected into the
bloodstream after a false negative aspiration.
Slow deposition of solution also increases the likeli­
hood of a comfortable experience by reducing the potential
for tissue trauma due to the pressure of the solution be­
ing injected. This recommendation is not always followed
by clinicians. In some cases, rapid inj ection is suspected to
be the cause of unwanted complications following local
anesthesia inj ections. A safe and more comfortable rate
of deposition allows for the delivery of 1 mL of solution
per minute, which means it requires about 2 minutes to de­
posit a 1.8-mL cartridge of anesthetic drug. Malamed states
that "a more realistic time span in a clinical situation how­
ever is 60 seconds for a full 1.8-mL cartridge" (Malamed,
(A) 20 1 3 ) . Specific exceptions to this guideline are discussed
in Chapter 13, "Inj ections for Maxillary Pain Control II­
Palatal Approach."
Time-consuming inj ections are more likely to stimu­
late anxiety in patients. A useful strategy to relieve this
anxiety is to report the progress of the inj ection such as
"V4 done, 1/z done,% done, complete." For others, distrac­
tions may be more useful.
STEP 9: C O M PLETI O N OF I N JE CTI O NUpon completion of
an inj ection, withdraw the syringe slowly. The final safety
step is to properly manage and recap the needle. It is saf­
est if the person performing the injection recaps the needle.
This reduces the number of individuals who come into con­
tact with the syringe and needle and reduces the potential
for accidental injury. After needles have been protected,
communicate with patients to observe and monitor for any
adverse effects. Once it is confirmed that patients tolerated
(B) procedures well, begin to evaluate for onset and effective­
ness of anesthesia before beginning treatment. Onset of an­
esthesia will usually occur within 3 to 10 minutes depending
on the drug administered, the injection technique, and the
accuracy of the location of the deposition site.

S T E P 10: D O C U M E N TATI O N O F L O C A L A N E ST H E T I C S As
part of a patient's medico-legal record, key elements of an
inj ection procedure should be properly documented.
The patient's record must include:
1. Date of administration
2. Typ e of drug ( s ) administered (both topical and
inj ectable)
3. Injection(s) administered (or area of delivery when
topical alone is used)
4. Total volume of drug(s) administered
(C) 5. Results of aspiration, recorded as "positive" ( +) or
P ositive Aspiration. A-A positive (+)
F I G U R E 1 1 -1 5
negative ( ) -

aspiration results in blood visible in the cartridge . B-A The volume of drug administered can be noted in
positive (+) aspiration is evident during a P SA injection. terms of the total number of cartridges, the total milliliters
C-A positive (+) aspiration is evident during an IA of solution, and/or the total milligrams of a specified drug
injection. and concentration. If a vasoconstrictor was delivered, the
 C HAPT E R 11 • FUN DAM E NTALS FOR A D M I N I STRAT I O N OF LOCAL A N E STHETI C AGENTS 207

Date Procedures

02/1 4/1 5 20% benzoca i n e top ica l , R-PSA, M SA, A S A 2 cart (3.6 m L) 2% l idoca i n e , S i g n atu re = I d e ntifi a b l e N a m e
1 : 1 00,000 ( 7 2 m g LA)' (0.036 m g ep i) (-) asp r., n o comp l i cati o n s .
03/1 7/15 5 % l i doca i n e top i c a l , R-IA, LB 1 cart (1 .8 m L) 2% m ep ivaca i n e , 1 :20,000 S i g n atu re = I d e ntifi a b l e N a m e
(36 mg LA) (0.09 mg l eva) ( +) asp r. , vis i b l e h e m ato m a , p ressu re/ice 1 5
m i n utes, m o n itor 30 m i n utes, n o fu rt h e r swe l l i n g . Treatment comp l ete
w/o comp l i catio n. Patient to ca l l if any further p ro b l e m.
03/1 8/15 T/W P a t i e n t no fu rth e r c o mp l i c a t i o n s fro m h e m a t o m a , wi l l ca l l if S i g n at u re = I d e ntifi a b l e N a m e
c h a n g es .
09/06/1 5 Vib raject, R-PSA, A M SA 2 cart (3.6 m L), 4 % a rti c a i n e 1 : 200,000 (1 44 m g S i g n at u re = I d e ntifi a b l e N a m e
LA) (0.0 1 8 m g ep i) (-) asp i rs . , n o comp l icatio n s .
1 0/22/1 5 20% b e nzoca i n e top i c a l , R-PSA, A M SA 2 cart ( 3 . 6 m L) 2% l i d o ca i n e , S i g n at u re = I d e ntifi a b l e N a m e
1 : 1 00,000 ( 7 2 m g LA)* (0.036 m g ep i) (-) asp r. , n o comp l i cati o n s .

type and dilution should also b e recorded. The specific for­

mat of the record is based on professional judgment and
workplace policy. If it is the policy of the workplace, in­
clude the gauge of any needles used. In addition to record­
ing positive aspirations, if they occur, adverse reactions
must be recorded along with the details of the responses to
them (their management) (see Box 11-7 •). The U.S. Dep a rtment of L a b o r defi n es m uscu l oske l eta l dis­
orders ( M S Ds) as inju ries or d isorders of the n e rves, tendons,
m uscles, joi nts, carti l a ge, a n d sp i n a l d iscs. The U . S . B u reau
Erg o n o m ics fo r Injection
of La bor Statistics rep orted that i nj u ries a n d i l l n esses from
Ad m i n i stration MSDs accou nted for 33% of the days a bsent from work.
Safe practice for the administration o f local anesthetics in­ M uscu l os ke l eta l d i s o rd e rs co m m o n to d e n t a l p ro­
fess i o n a l s i n c l u d e cu m u l ative tra u m a d i s o rd e rs (CTDs),
volves ergonomics in addition to drug factors and patient
w h i c h a re defi n e d as d isord e rs involvi n g t e n d o n s , m uscles,
issues. A discussion of the basic steps for administration of
n e rves, co n n ective tiss u e , b o n es, j o i nts, sp i n a l d i s cs, and
inj ectable local anesthetics is not complete without com­ even vascu l a r tissues d u e to cu m u l ative tra u m a .
menting on ergonomics. To date, very little attention has
been placed on ergonomics during local anesthetic deliv­
ery. Attention was focused on hand and body positions for
syringe stability and visibility as well as access to the site
of inj ection . The effects of non-ergonomic positions on
the development of cumulative trauma disorders (CTDs)
during procedures, including anesthetic procedures, can be
significant over a period of years and are all too common
among dental professionals (Andrews &Vigoren, 2002;
Stabbe, 2006; U. S. Department of Labor, 20 1 3 ; Wann & To m a i nt a i n g o o d e rg o n o m i c position a n d b a l a n c e :
Canull, 2003) (see Box 1 1-8 •).
Basic principles of ergonomics (see Box 1 1-9 •) suggest 1. Do n ot twist fro m t h e tru n k .
that clinicians at least consider non-traditional approaches 2. B e n d fro m t h e h ips.
3. Keep wrists at a n e utra l a n g l e .
to the delivery of inj ections that otherwise require twisting
4. Do n ot raise a r m s > 3 0 d e g rees.
the trunk, hyperextending the neck, angling the wrist in
5. Do n ot exte n d t h e n e c k > 30 d e g rees fo rwa rd.
an awkward manner, and reaching over the patient. All of
these are demonstrated in Figure 1 1-16A, Figure 1 1-16B,
Figure 1 1-16C •, and Figure 1 1-17 •).
208 S E C T I O N Ill • I N J ECTION F U N D A M E NTALS
(A)
(B)
(C)
FIGURE 11-1 6 Ergonomics: P ositioning of Armamentar­
ium. P oor ergonomics can begin with basic operatory set-up.
P ositioning of equipment and armamentarium for optimal ac­
cess is an important aspect of safe ergonomics. A-Requires
clinician to reach some distance forward away from their
torso and across the patient's face and torso. B-Although
armamentarium is in a proper location, the clinician is twisting
and reaching back behind her torso. C-In this good example,
the clinician turns her entire torso and hips on the stool in the
same direction maintaining both balance and alignment.
Source: Courtesy of Samatha Shira.
Non-traditional approaches include repositioning the
clinician and/or the patient, as well as non-dominant hand
syringe grasps to facilitate proper ergonomic positions of the
back, neck, shoulders, arms, wrists, and hands. Although these
approaches may be challenging at first, especially for nov­
ices, non-dominant hand techniques can provide ergonomi­
cally correct positions during local anesthetic administration.
Applying updated ergonomic approaches to the administra­
tion of local anesthetics can reduce musculoskeletal trauma
linked to the development of MSDs and CTDs, and possibly
reduce the impact of this trauma on existing disorders.
Operatory design can significantly impact the ability to
apply alternative ergonomic positions to the administration
of local anesthetics. Having the ability to approach patients
from either side of a chair greatly improves ergonomic posi­
tioning; however, the close physical design of some operato­
ries can make this difficult. Taking time to determine if chairs
are able to swivel can improve non-dominant side access.
A New Look at Ergonomics for Local Anesthetic
Administration
The posterior superior alveolar, middle superior alveolar,
anterior superior alveolar, inferior alveolar, Gow-Gates,
buccal, and mental/incisive inj ections when delivered with
the clinician's arms extending across patient's body forces
clinicians into awkward arm, neck, and wrist positions to
access inj ection sites (see Figure 1 1-17), while maintaining
limited vision. It is easy for clinicians to assume that they
will be in awkward positions for only brief periods, yet
F I G U R E 11-17 Ergonomics: Body Mechanics during
Injection. As with all other aspects of clinical work, the
administration of injections requires ergonomic attention.
Key ergonomic principles compromised in this example
include: A-Wrist is not in neutral position, creating undo
compression of the carpal tunnel region. B-P lacement of
armamentarium requires clinician to reach some distance
forward away from their torso and across the patient's face
and torso. C-Arms & elbows are above 30 degree angle
creating undue stress on shoulder and neck muscles.
Source: Courtesy of Samatha Shira.
 C HAPT E R 11 • FUN DAM E NTALS FOR A D M I N I STRAT I O N OF LOCAL A N E STHETI C AGENTS 209

(A) (B) (C)

F I G U RE 11-18 Ergonomics Alternatives: Left P osterior Superior Alveolar Nerve Blocks. A-This approach provides a good ergo­
nomic position during a left P SA. This position is appropriate for either right- or left-handed clinicians when seated on the left side
of the patient. Key positive ergonomic principles are wrist neutral, elbows below 30 degrees, and use of an "arm-to-body " fulcrum.
B-The palm-up position also provides for control of the syringe during aspirations. This demonstration is by a right-handed clinician
administering with the left hand. C-Good ergonomic balance is demonstrated here as a right-handed clinician, seated on the left, ad­
ministers a P SA with her right hand. Note the fulcrum strategy.
Source: Courtesy of Samatha Shira.

over the course of careers these brief periods can produce

significant "trauma." This long-term trauma is referred to
as a cumulative effect (Stab be, 2006; U.S. Department of
Labor, 2005 ; Wann &Canull, 2003).
The following are examples of corrective actions that
will improve clinician ergonomics and reduce traumas that
can lead to MSDs and CTDs for the inferior alveolar and
posterior superior alveolar inj ections. Note that each sug­
gestion places the clinician in a "neutral" working position,
minimizing stress and trauma to the wrists, shoulders, and
neck. Clinicians are encouraged to consider basic ergo­
nomic principles during the administration of inj ections
(see Box 1 1-9) that include alternative body positions and
non-dominant hand techniques (see Figure 1 1-18A •).
Posterior superior alveolar (PSA) injections may be ad­
ministered with either the dominant or non-dominant hand
from the side of the injection (see Figures 1 1-18B • and 11- FIGURE 11-19 Ergonomics Alternatives: Right Inferior

18C •). For example, a right-handed clinician can give this
injection with his or her dominant hand while seated at the pa­
tient's right side for a right PSA. Left PSA injections can also
be given with the left hand while seated on the patient's left
side. Many clinicians find it surprisingly easy to use their non­
dominant hand, appreciate the improved view and angle, and
feel more stable and comfortable throughout the injection.
The inferior alveolar and Gow-Gates blocks can be
administered with clinicians s e ated opposite the side
where the inj ection is being given. Either the dominant
or non-dominant hand may be used (see Figure 1 1-19 •).
This modified clinical position offers ergonomic position­
ing that reduces twisting of the trunk, lowers the arm,
enables the elbows to stay within 30 degrees from the
Alveolar Nerve Block. This approach provides a good ergonomic
position during a right IA. This position is appropriate for either
right- or left-handed clinicians when seated on the left side of
the patient. Key positive ergonomic principles are wrist neutral,
elbows below 30 degrees, and use of an "arm-to-body " fulcrum.
The palm-up position also provides for control of the syringe
during aspirations. This demonstration is by a right-handed
clinician, seated on the left, administering with the right hand.
Source: Courtesy of Samatha Shira.
clinician's body, and keeps the wrist in a neutral position.
Standing during administration of these blocks can also
facilitate good ergonomic balance when the patient can­
not be positioned easily (see Figure 1 1-20 •).
210 S E C T I O N Ill • I N J ECTION F U N D A M E NTALS

CASE MANAGEMENT
Hector Melendez
It w a s exp l a i n e d to M r. M e l e n d e z t h a t t h e treat­
m e n t he n e e d e d c o u l d n o t be a c c o m p l i s h e d
c o m fo rta b l y w i t h o u t l o ca l a n esth es i a . W h i l e M r.
Me l e n d e z w a s w a i t i n g fo r t h e to p i c a l a n esth etic
to ta ke effe ct, t h e a n esthetic p roced u re w a s ex­
p l a i n e d to h i m, as we l l as t h e reason why it wo u l d
b e a s l ow e r exp e r i e n ce co m p a re d with h i s p revi­
o u s one. After a bo u t 2 m i n utes, a n i nfi ltratio n ove r
#5 was a d m i n istered s l owly with a co u p l e of d rops
of s o l u t i o n a d m i n istered a h e a d of the v e ry s l ow
a d va n ce of t h e n e e d l e . O n c e t h e t a rg et site was
re a c h e d and n e g ative a s p i ra t i o n confi r m e d, s o l u ­
t i o n w a s d e posited at a rate o f 6 t o 7 seco n d s p e r
sto p p e r (0 .2 ml), w h i c h is e q u a l t o 1 m i n ute w h e n
a n entire ca rtr i d g e is a d m i n iste red .
Case Discussion: F o l l o w i n g b a s i c ste ps p ro ­
m ot e s s a fety a n d c o m fo rt . R e a ss u ra n ce d u r i n g
p re l i m i n a ry ste ps before a d m i n iste r i n g l o c a l a n es­
t h e s i a is usefu l . Rati o n a l e fo r ta k i n g t h o s e steps
F I G U R E 11-20 Ergonomics Alternatives: Standing. For any
ca n h e l p ease p a t i e n t fe a rs a n d p rov i d e s o m e
injection that requires reaching across patients, standing may sense that t h e cu rrent exp e r i e n ce w i l l n o t b e a re­
provide improved vision and balance. Key positive ergonomic peat of p revious experiences.
principles are the same as for seated delivery, wrist neutral, el­ M r. M e l e n d ez w a s a p p re h e n s ive b e c a u s e h i s
bows below 30 degrees, and use of an "arm-to-body " fulcrum. expectat i o n s fo r a satisfacto ry exp e r i e n ce, o n e i n
The palm-up position also provides for adequate control of the w h i c h t h e re w a s m i n i m a l t o n o p a i n, h a d n o t b e e n
syringe during aspirations. This demonstration is by a right­ m e t o n a p rev i o u s occa s i o n . I m p o rt a n t l y, h e h a d
handed clinician administering with the right hand. n o re a s o n fo r a lte r i n g h i s expectat i o n s i n t h e c u r­
Source: Courtesy of Samatha Shira. rent s i t u a ti o n u n t i l it w a s p rov i d e d to h i m . Loca l
a n esth e s i a p ro ce d u res d o n ot h ave to b e g i n with
A View from "Outside the Box"
"raise yo u r h a n d" state m e nts that a re m e a n i n g­
The dental opera tory provides a classic "box" for practice. l ess w h e n t h e y a re s u bseq u e n t l y i g n o re d b u t c a n
It is easy for dental professionals to become comfortable b e g i n i n st e a d wi th s o o t h i n g wo rds, fo l l ow e d by
with the uncomfortable and to believe and even accept that b r i ef exp l a n at i o n s a n d ass u ra n ces t h a t c o n t r a cts
work practices will fit only one approach in the workspace, (to res p o n d to h a n d s i g n a l s, fo r exa m p l e ) wi l l n ot
becoming complacent with sometimes physically harmful be b ro ke n .
work practices. Clinicians are encouraged to "think outside
the box" and develop ways to improve the ergonomics of
work spaces and work practices for all chairside procedures.

Ch a. . pte
.
r Questi
....
ons ..............................
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3. The first step i n the administration o f local anesthetic
1 . A technique that deposits anesthetic solution near solutions is to:
larger terminal nerve branches for treatment near the a. Assemble the armamentarium.
site of an inj ection is called: b. Obtain informed consent.
a. An infiltration injection. c. Assess the patient before proceeding.
b. A ligamenta! injection. d. Make sure that solution is able to exit the needle.
c. A field block injection. 4. A primary benefit of orienting needle bevels toward
d. A nerve block inj ection. bone during injections is that it:
2. Which one of the following describes the target site a. Reduces trauma to the periosteum when bone is
for local anesthetic solutions? contacted.
a. Needle pathway b. Deflects the needle away from the bone during
b. Deposition site penetration.
c. Penetration site c. Prevents false negative aspirations within a vessel.
d. Aspiration site d. Reduces discomfort from the advancing needle.
 C HAPT E R 11
5. Which one of the following is the most appropriate
local anesthesia patient record entry?
a. 10/2112015: Review Health History. BP 120/80. 2 car­
tridges 2% lidocaine, 1 :100,000 epi, no complications
b. Review He alth History. B P 1 20/80. 2 cartridges
2 % lidocaine, 1:100,000 epi, Rt lA, LB , (+) aspiration
c. Review Health History. BP 120/80. 72 mg of 2% li­
docaine, 0.036 mg 1 : 1 00,000 epi, lA, LB
d. 1 0/2 11201 5 : Review He alth History. BP 1 20/80.
2 cartrid g e s ( 3 . 6 m L ) 2% lidocaine ( 7 2 m g ) ,
1 : 1 00,000 epi (0.036 mg) , Rt lA, LB , (-) aspiration.
No adverse reactions.
6. When is it safe to deposit local anesthetic solution?
a. After a negative aspiration, where no blood is
drawn into the cartridge.
b. After a negative aspiration, following a positive aspi­
ration where blood was visible in the cartridge only
as a small trickle of blood or "worm like" thread.
c. Following a positive aspiration that obscures the
results of subsequent aspirations.
d. A&B .
7. The most important safety step(s) during a local anes­
thetic inj ection is/are:
a. To aspirate before depositing.
b. To administer local anesthetics slowly.
c. To direct the bevel away from bone.
d. To aspirate before depositing and to administer
drugs slowly.
8. Upon completion of an injection, the most important
subsequent step is to:
a. Rinse the patient's mouth.
b. Calculate the volume of drug delivered.
c. Make the needle safe with a one-handed technique.
d. Determine if the patient experienced discomfort.
Refe re n ces
American Cancer Society. (2012). Informed consent. Retrieved
January 31, 2014, from http://www.cancer.org/acs/groups/cid/
documents/webcontent/003014-pdf.pdf
Andrews, N., & Vigoren, G., (2002,March). Ergonomics:Muscle
fatigue, posture, magnification, and illumination. Compen­
dium,23(3),261-264,266,268,270,272,274.
Dionne, R. A., Gordon, S.M.,McCullagh, L.M., & P hero, J. C.
(1998, February). Assessing the need for anesthesia and seda­
tion in the general population. Journal of the American Dental
Association, 167-173.
Visit www.pearsonhighered.com/healthprofessionsresources to access the student resources that accompany
this book. Simply select Dental Hygiene from the choice of disciplines. Find this book and you will find the
complimentary study tools created for this specific title.
• FUN DAM E NTALS FOR A D M I N I STRAT I O N OF LOCAL A N E STHETI C AGENTS 211
Evers, H., & Haegerstam, G. (1981). Handbook of dental local
anaesthesia. Copenhagen: Schultz.
Friedman,M. J., & Hochman,M. N. (1997). A 21st century com­
puterized injection system for local pain control. Compen­
dium, 18(10), 995-1003.
Haase, A., Reader, A., Nusstein, J., Beck,M., & Drum,M. (2008).
Comparing anesthetic efficacy of articaine versus lidocaine
as a supplemental buccal infiltration of the mandibular first
molar after an inferior alveolar nerve block. Journal of the
American Dental Association, 139(9),1228-1235.
Jastak, J. T., Yagiela, J. A., & Donaldson,D. (1995). Local
anesthesia of the oral cavity. P hiladelphia: Saunders.
Kanaa,M.D., Whitworth, J.M., Corbett, I. P., & Meechan, J. G.
(2006). Articaine and lidocaine mandibular buccal infiltration
anesthesia: A prospective randomized double-blind cross-over
study. Journal of Endodontics, 32(4), 296-298.
Kanaa,M.D., Whitworth, J.M., Corbett, I. P., & Meechan, J. G.
(2009). Articaine buccal infiltration enhances the effectiveness
of lidocaine inferior alveolar nerve block. International
Endodontic Journal, 42(3), 238-246.
Lipp,M.D. W. (1993). Local anesthesia in dentistry. Carol Stream,
IL: Quintessence.
Malamed, S. F. (2007). Medical emergencies in the dental office
(6th ed.). St. Louis:Mosby.
Malamed, S. F. (2013). Handbook of local anesthesia (6th ed.).
St. Louis,Mosby.
Milgrom, P., Weinstein, P., & Heaton, L. (2009). Treating fearful
dental patients: A patient management handbook (3rd ed.).
Seattle:Dental Behavioral Resources.
Rizzolati, G., Fadiga, L., Gallese, V., & Fagassi, L. (1996). P remo­
tor cortex and the recognition of motor actions. Cognitive
Brain Research, 3, 131-141.
Robertson,D., Nusstein, J., Reader, A., Beck,M., &McCartney,M.
(2007). The anesthetic efficacy of articaine in buccal infiltra­
tion of mandibular posterior teeth. Journal of the American
Dental Association, 138(8),1104-1112.
Robinson, P.D., Ford, T. R. P., & McDonald, F. (2000). Local
anesthesia in dentistry. London: Wright.
Stabbe, K. A. (2006, March).Maintaining ergonomic positioning
during local anesthetic administration. Journal of Practical
Hygiene, 15(2), 8.
U niversity of Washington School of Medicine. (2008). Ethics
in medicine, informed consent. Retrieved January 31, 2014,
from http://depts.washington.edu/bioethx/topics/consent.
html
U.S.Department of Labor-Bureau of Labor Statistics. (2005).
Lost-working injuries and illnesses: Characteristics and result­
ing days away from work. Retrieved January 31, 2014, from
http://www.bls.gov/news.release/osh2.nrO.htm
Wann, 0., & Canull, B. (2003, May). Ergonomics and dental
hygienists. Contemporary Oral Hygiene,16-22.
10 Basic Steps in the Administration
of Local Anesthesia
Step l:Patient Assessment
• Assess the patient's medical history, treatment plan,
and individual pain control needs
• Identify alterations, precautions, or contraindications
to care
• Implement appropriate inj ection(s) and anesthetic
drug(s) to be delivered
Step 2: Obtain Informed Consent
• Review the intended treatment plan, including the
delivery of any anesthetic agents, with the patient and
obtain proper informed consent as indicated for care
Step 3: Assemble Armamentarium
• Assemble appropriate armamentarium and confirm
proper function of delivery devices
• Harpoon engaged and device able to aspirate
• Cartridge is fully visible and the correct drug is
loaded
• The needle bevel is oriented toward the bone dur­
ing injection
• Safe needle recapping controls are in place and
functioning properly
Step 4: Pre-Injection Preparation
• Position patient supine for visibility and support
during stress
• Position patient's head for good visibility
• Assume an ergonomic position to support
musculoskeletal health
• Employ positive, supportive communication
• Establish effective retraction for visibility and needle
penetration
• Palpate site for anatomical anomalies
Step 5: Prepare Injection Site
• Gently dry mucosa with gauze
• Apply controlled amount of topical agent to dry
tissue at inj ection site
• Ideally no less than 1 minute to assure effectiveness
• Visualize best inj ection angle
• Evaluate for effective onset of topical agent at
penetration site
212
Step 6: Initiate Injection
• Keep the syringe out of the patient's sight as much as
possible throughout
• Maintain positive, supportive communication with the
patient
• Retract the soft tissues for good visibility of
penetration site
• Gently make mucosa "taut" to ease needle penetration
• Establish a fulcrum or point of stability for the
syringe during the inj ection
• Penetrate the mucosa 1-2 mm, deposit a few drops of
anesthetic
• Gently advance the needle to the desired depth and
angle for deposition
Step 7: Aspiration
• Aspirate at deposition site BEFORE depositing solution
• Aspirate in two planes for highly vascular areas
• Re-aspirate if depth changes during inj ection
• Re-aspirating can help pace inj ection if needed
• NEGATIVE aspiration: continue with inj ection
• POSITIVE aspiration:
• Employ positive, supportive communication to
explain situation to patient
• Assess signs of positive aspiration
• Small trickle of blood in cartridge-reposition the needle
tip and re-aspirate, if negative continue with deposition
• Cartridge clouded with blood-withdraw the needle
and replace cartridge, replace or flush needle, and
reinitiate inj ection
• Evaluate post-inj ection for complications and advise
patient as indicated
Step 8: Deposition and Rate
• SLOWLY deposit the specified anesthetic dose (1.8 mL
over 1 to 2 minutes)
Step 9: Completion
• Completion: CAREFULLY withdraw the needle
• Make the needle safe with an accepted recapping
technique
• Observe and evaluate patient for adverse reactions
Step 10: Documentation
• Document injection specifics and complications in
patient record
Suggested Fulcrum Positions

Each clinician should determine ergonomic positions that best establish stability during inj ection procedures.
The following figures suggest a variety of fulcrums and supplemental supports for balance.

A. Rest the back of the dominant hand (with syringe) A. Keep the arm low and close to the body.
gently against the patient's shoulder. To use this rest B. A "palm-up" grasp provides stability.
safely, the clinician must be alert to the possibility
C. The third finger of the dominant hand is placed
of sudden patient movements and must be able to
against the barrel of the syringe to enhance stability.
respond to them quickly.
Along with a "palm-up" grasp, this increases stability.
B. A "palm-up" grasp provides stability.
C. The thumb of the non-dominant (retraction) hand
is placed on the barrel of the syringe.

213
214 S E C T I O N Ill • I N J ECTION F U N D A M E NTALS

A. Place a finger of the dominant hand on the patient's
chin , along with a " p alm-up " grasp p osition to
provide stability.
A. Keep the arm low and close to the body and rest
the back of the dominant hand gently against the
patient's shoulder.
B. Place a finger of the dominant hand on the patient's
chin , along with a " p alm-up " grasp p osition to
provide stability.

A. Keep the arm close to the body, along with a "palm-up" grasp position to provide stability.
B. The thumb of the non-dominant ( retraction ) hand is placed against a finger of the dominant hand to create a
"bridge" of stability.
 C HAPT E R 11
A. M aintaining a " p alm-up " grasp provides added
stability when reaching across the patient. This
also stabilizes the wrist in neutral position and
e asily aligns syringe angulations approximating
45 degrees to midsagittal ("cap on" for demonstra­
tion purposes) .
A. Similar to the previous example, the fingers can
rest on the back of the retraction hand creating a
"bridge" of stability. Note the p alm-up p osition
provides additional stability during aspiration. In
this example, a right-handed clinician administers a
left PSA, seated on the left, using her left hand, the
same position would be appropriate for left-handed
clinicians.
• FUN DAM E NTALS FOR A D M I N I STRAT I O N OF LOCAL A N E STHETI C AGENTS 215
B. When difficult to reach across a patient's torso to
achieve optimal angulations, clinicians may choose
to approach from their non-dominant side. Inj ec­
tions can then be performed with either dominant
or non-dominant hand. Note the use of the thumb of
the right hand to create a "bridge" of stability. In this
example, a right-handed clinician administers a left
PSA, seated on the left, using her left hand.
B. The back of the fingers can rest on the back of the
retraction hand to create a "bridge" of stability. In
this example, a left-handed clinician administers a
right PSA, seated on the right, using her left hand.
•
The same position would be appropriate for left-
handed clinicians using their non-dominant hand.
216 S E C T I O N Ill • I N J ECTION F U N D A M E NTALS
A. When difficult to achieve a " p al m - u p " grasp
position, "stacking" the hands provides stability. In
this example, a right-handed clinician, seated on the
left, administers a left PSA right-handed.
B. A solid bridge of stability is created by fulcruming
on the retraction finger/hand. In this example, a
right-handed clinician, seated on the right, admin­
isters a right PSA right-handed. The same position
would be appropriate for left-handed clinicians
using their right hand. Note that the palm is up
providing additional stability to the grasp during
aspiration.
Chapter 12 Injections for Maxillary Pain Control I

Chapter 13 Injections for Maxillary Pain Control 11-Palatal Approach

Chapter 14 Injections for Mandibular Pain Control

Chapter 15 Supplemental Techniques and Adjunctive Strategies

Chapter 16 Troubleshooting Inadequate Anesthesia

Chapter 17 Local Anesthesia Complications and Management

C h a pters 1 1, 1 2, 13, a n d 1 4 i n c l u d e d iscussions of a n ato m i c a l fa ctors re l evant to

each i nj e cti o n tech n i q u e a n d ass u m e c l i n i c i a n s h ave at l east a basic know l e d g e
of h e a d a n d n e c k a n ato my. A p pe n d ix 1 : A n a to m ica l review p rovi d e s a g e n e r a l
d i scuss i o n of h e a d a n d n e c k a n ato m y a n d h a s b e e n d e s i g n e d to assist i n t h e
i d e ntificati o n a n d review of loca l a n esth etic l a n d m a rks a n d t h e a n ato m i c struc­
tu res i n o r n e a r the pathways of i ntraora l i njections.
··························································· @ ··························································

Injections for Maxillary Pain Control I

OBJECTIVES KEY TERMS

• Defi n e a n d d i sc u ss the key ter m s in t h i s c h a pter. anterior s u perior a lveo l a r

(ASA) n e rve b l ock 223
• Descri be a n d discuss the in d i ca t i o n s , releva n t a n atomy, a n d
cross-i n n e rvation 225
tech n i q ue featu res o f t h e i njecti o n s discu ssed i n t h i s c h a pter.
d e nta l p l exus 219
• Descri be the b a sic tec h n i q ue steps fo r safe a n d effective d e position site 219
a d m i n i strat i o n fo r the fo l l owi n g i njectio n s : fie l d b l ock 219
• I nfi ltrati o n s h e m ato m a 223
• Field b l ocks i nfi ltration 219
• Anterio r s u peri o r a lveo l a r nerve b l ock i nfraorbita l (10) n e rve
b l ock 228
• M i d d l e s u pe ri o r a lveo l a r nerve b l oc k
maxi l l a ry n e rve b l ock 236
• I nfra o rbita l n e rve b l ock
m i d d l e su perior a lveo l a r
• Posteri o r s u peri o r a l veo l a r nerve b l ock
(MSA) n e rve b l ock 225
• M axil l a ry nerve b l oc k (seco n d d iv i s i o n o r V2 b l oc k)
need l e pathway 219
p e n etratio n site 219
poste rior s u perior a lveo l a r
(PSA) n e rve b l ock 232
rescue i njectio n 242
second d ivision n e rve
b l ock 236
V2 n e rve b l ock 236

218

CASE ST U DY
Elena Gagarin
E l e n a G a g a r i n n e e d e d resto rative t re a t m e n t o n
h e r r i g h t m a xi l l a ry a nt e r i o r teeth . D e s p ite a n ASA
n e rve b l o c k, s h e was u n co m fo rta b l e w h e n cavity
p re p a rat i o n was c o m m e n ce d w i t h a h i g h -s p e e d
h a n d p iece o n # 8 . Desp ite a repeat ASA i nj e ct i o n,
#8 re m a i n ed u n comfo rta b l e .
I ntrod u cti o n
Local infiltrations, field blocks, and nerve blocks are the
three basic types of intraoral inj ections frequently used in
dentistry and were defined in Chapter 1 1 , "Fundamentals
for A d m i n i s t r a t i o n of L o c a l A n e s th e t i c A g e n t s . "
Additional relevant terminology includes anatomic land­
marks and considerations for e ach maxillary inj ection
technique discussed in this chapter and will be presented
in reference to a penetration site , needle pathway, and
deposition site as described in Chapter 1 1. The penetration
site will be related to hard and soft tissue landmarks. The
needle pathway will be described in terms of the types of
tissue that will be penetrated by or located in the vicinity
of the needle, including mucosa, superficial fascia, muscle,
vessels, nerves, and bone. The deposition site will be de­
scribed in terms of the tissues at or near the target and in
relation to specific landmarks.
Note that inj ection techniques in this and the follow­
ing chapters may describe nerve blocks in several ways.
Full descriptive phrases may be used, such as posterior
superior alveolar nerve blocks. Acronyms followed by
descriptive phrases may also be used, such as PSA nerve
block. Full or partial acronyms may be used, such as PSA
and PSANB. Regardless of the description, all are equiva­
lent in meaning.
M axi l l a ry I njection Tech n i q ues
This chapter will discuss nonpalatal maxillary inj ection
techniques commonly used in dentistry. Even though they
are also maxillary techniques, palatal inj ections will be dis­
cussed separately in Chapter 1 3 , " Inj ections for Maxillary
Pain Control II - Palatal Approach," because of common
modifications specific to the sensitive and low to moderate
compliant tissues in the palate. The exception to this orga­
nization is the maxillary or second division nerve block that
can be administered from both palatal and nonpalatal ap­
proaches. The palatal approach to the maxillary nerve block
will be discussed in this chapter along with the nonpalatal
approach for ease of reference. Key factors for each maxil­
lary inj ection discussed in this chapter are summarized in
Appendix 1 2-1. Common variations and precautions will
be discussed where applicable (B lanton & Jeske, 2003 ;
C HAPT E R 1 2 • I N J E C T I O N S F O R MAXI LLARY PAI N C O NTROL I 219
Jastak, Yagiela,&Donaldson, 1995; Malamed, 20 13; Wong,
200 1 ) .
I nfi ltration ( F i e l d B lock) I njecti o n
Field block inj ections, commonly referred t o a s infiltration
inj ections, are indicated when procedures are confined to
one or two teeth or to tissues in a limited area. Infiltration
injections are among the simplest and safest local anesthe­
sia techniques to learn. They are relatively easy to execute,
have a high rate of success, and have wide margins of
safety.
Field of Anesthesia
Inj ections characterized as field blocks will be referred to
in this text as infiltrations and include the dental plexus of
the injected site (the pulp of the tooth and facial areas of
the gingiva, periodontal ligament, and alveolus) . Addition­
ally, because of the diffusion of anesthetic solution, some
terminal branches of the facial nerve (VII) are frequently
affected. All or a portion of the upper lip, cheek, and lower
nose are anesthetized with many maxillary infiltration in­
jections (see Figure 12-1 • and Appendix 12-2).
Anatomical Factors
Small terminal nerve endings of the posterior superior,
middle superior, and anterior superior alveolar nerve
branches form the maxillary dental neural plexus. This
plexus innervates the pulps of the teeth and facial peri­
odontium as previously described. The facial and palatal
bone of the maxilla is relatively thin and permeable. Local
anesthetic solutions diffuse easily through this bone anes­
thetizing the nerves of the dental plexus. This allows for
high success rates when administering infiltrations on the
maxillary arch.
Technique Factors
The following information describes key factors for suc­
cessful infiltration inj ections.
P E N ETRAT I O N SITE The optimum site of penetration for
infiltration inj ections is at the height of the mucobuccal
fold closest to the apex of the tooth to be anesthetized.
A bony ridge, or eminence, can usually be palpated in the
mucosa overlying the facial root of most maxillary teeth.
This eminence serves as a landmark for visualizing the
long axis of the tooth and locating the apex of the tooth
for the penetration site (see Figure 12-2 •).
Examining radiographs for root lengths and inclina­
tions, as well as assessing crown-root ratios can be helpful
when determining optimum penetration and deposition
sites for infiltration inj ections (see Figure 12-3 •).
N E E D LE PATH WAY The needle generally parallels the long
axis of the tooth and the slope of the alveolus in maxil­
lary infiltrations. The needle passes through thin mucosal
tissues to superficial fascia containing loose connective
220 S E C T I O N IV • C LI N I C AL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A

I nfi ltration
Teeth anesthetized:

at injection site

Periodontium/Soft tissues:

at injection site

F I G U RE 12-1 Field of Anesthesia for Infiltration Injections.

Anesthesia will occur in a small, confined area close to the site
of deposition.
Source: Courtesy of LED Dental.

F I G U R E 12-2 P enetration Site for Infiltration Injections. The F I G U R E 12-3 Height of P enetration for Infiltration Injections.
penetration site for infiltration injections will be near the apex Average crown-to-root ratios can be used to select the height of
of a single tooth or in a small, confined area of tissue. penetration near the apex of a tooth for infiltration injections.
Source: Courtesy of Megan Gibbons.

tissue, and avoids small vessels and microvasculature, as
well as nerve endings.
D E PO S I T I O N SITE The deposition site is slightly above the
apex of the root of the tooth being anesthetized. Contact
needles out of concern for comfort, although increased
discomfort with larger diameter needles has not been dem­
onstrated (Diggle et al., 2006; Flanagan et al., 2007).
I N JE CT I O N P R O C E D U R E Gain access to the penetration

with bone is unnecessary and should be avoided for com­
fort (see Figure 12-4 •).
Technique Steps
Apply the basic inj ection steps outlined in Chapter 11 and
summarized in Appendix 1 1-1.
N E E D L E S E L E CT I O N The selection of needle gauge for
infiltrations is made based upon clinical judgment. Either 27-
or 25-gauge short needles are appropriate for infiltrations.
Based on the low risk of positive aspiration (1 % or less) and
the shallow depths of penetration, many clinicians choose
to use 27-gauge short needles. Some prefer to use 30-gauge
site by retracting the lip, pulling the tissue taut with the
thumb and index finger (see Figure 1 2-5 •). Locate the
appropriate penetration site. In order to achieve proper
angulations, align the barrel of the syringe parallel to the
long axis of the tooth, following the contour of the maxilla
(see Figure 12-6 •). The depth of penetration (to the site
of deposition) is based on the location of the apex of the
tooth and is usually achieved within 3 to 6 mm.
Following negative aspiration, deposit an adequate
volume of an appropriately selected local anesthetic drug
to achieve anesthesia. When performing maxillary infiltra­
tions, a generally accepted minimum volume of anesthetic
is 0.6 mL (1/3 of a cartridge) . Adequate volumes will vary
 C HAPT E R 1 2 • I N J E C T I O N S F O R MAXI LLARY PAI N C O NTROL I 221

F I G U RE 12-6 Syringe Angulations for Infiltration of a Single

Tooth. Align the syringe barrel parallel to the long axis of the
tooth, along a plane parallel to the slope of the maxilla.
Source: Courtesy of Megan Gibbons.

F I G U RE 12-4 Deposition Site for Infiltration of a Single

pain during the procedure at the site of injection. For a gen­
Tooth. Deposition for an infiltration will be near the apex of a
eral discussion on confirming anesthesia, see Box 12-1 •.
single tooth or in a small, confined area of tissue.

Common Causes of Injection Failure

The most common causes of failure after infiltrations in­
clude deposition of solution too far from the apex of a tooth
and inadequate volumes of solution. Other causes of fail­
ure include inflammation or infection in the area of deposi­
tion, inadequate diffusion of solution to the palatal roots of
molars because of dense bone, and accessory innervations.

Troubleshooting
When infiltrations are unsuccessful, it is helpful to re­
evaluate by visualizing, palpating, checking radiographs,
reassessing syringe angulations and depths of penetration,
and reconsidering volumes of solution deposited. Failure
of infiltration anesthesia occurs most commonly when
solution is deposited too far from the apex of a tooth (see
Box 12-2 •). In some instances, adequate diffusion of so­
F I G U R E 12-5 Tissue Retraction. Make the tissue taut to im­
lution is impossible because of anatomic obstructions. In
prove ease of insertion and increase the visibility of the penetra­
these instances, nerve blocks (discussed later in this chap­
tion site.
ter) or supplemental techniques, such as periodontal liga­
Source: Courtesy of Megan Gibbons.
ment inj ections, may be indicated (discussed in Chapter 15,
"Supplemental Techniques and Adjunctive Strategies").
regardless of the technique, depending on a variety of
patient and pharmacological factors as well as the length
of planned procedures. For example, procedures with lon­
ger durations will require a greater pool of anesthetic in
the deposition area to provide a longer-term supply of
base molecules. Some patients will require greater vol­ B efo re p e rfo r m i n g a n y p roced u res, it is i mp o rtant to assess
umes even for relatively short procedures. fo r effe ctive a n esth esia (n u m b n ess) i n the a re a of i nj e cti o n .
T h i s c a n be confi rm e d o bj e ctive ly u s i n g a n e l ectro n i c p u lp
Confirming Anesthesia test i n g device (E PT) (see F i g u re 1 2-7 •l or t h e app l icati o n
of c o l d (see F i g u res 1 2-8 • a n d 1 2-9 •l o n the teeth i n
Subj ective signs of anesthesia for infiltration inj ections in­
q u esti o n . W i t h a l l i nj e cti o n tech n i q u es, a d e q u ate a n es­
clude a sense of numbness of the gingival and labial tissues
t h e s i a is confi r m e d w h e n t h e re is n o p a i n rep o rted d u r i n g
at the site of inj ection. Obj ective signs include a lack of
response to gentle stimulation with an instrument and no
: p roced u res.
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . •
222 S E C T I O N IV • C LI N I C AL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A

F I G U R E 12-7 Electric P ulp Tester (EP T) to Confirm Anes­

thesia. An EP T can provide objective feedback to determine
whether or not patients are profoundly anesthetized.
F I G U RE 12-9 Cold Stimulation to Confirm Anesthesia ­
"Icicles" Method. In addition to EP T devices and cryo-anesthet­
ics, pain stimuli can be initiated with the use of small "icicles" to
test for anesthesia.
Source: Courtesy of Albert "Ace" Goerig D D S, MS.

Fa i l u re to c o n s i d e r n e ed l e a n g u l at i o n s a n d p e n etrat i o n
depths c a n res u lt i n deposition of s o l u t i o n that is too fa r
away fro m t h e ap ex of a tooth or ta rget site. T h i s c a n occu r
w h e n d eposition is too fa r fro m targ ets in o n e or m o re of
F I G U RE 12-8 Cold Stimulation to Confirm Anesthesia ­ t h e fo l l ow i n g o ri e ntati o n s :
"Freeze" Method. P ain stimuli can be initiated with the use of s up e r i o r a nterior l atera l •
••
• • •
a cryo-anesthetic ("cold spray ") to test for anesthesia similar to : • i nfe r i o r • p oste rior • medial
the use of an EP T. : . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Occasionally, medially displaced branches of the PSA
nerve and/or branches of the greater palatine nerve pro­
vide sensory innervation to the palatal roots of maxillary
molars and premolars. In these instances, solution may
not diffuse far enough palatally through the bone to reach
these branches. To anesthetize these branches, a supple­
mental greater palatine nerve block can be administered
(Blanton &Jeske, 2003).
Technique Modifications and Alternatives
In some situations, it is apparent during initial patient
evaluation that standard inj ection techniques will not be
successful. In these instances, technique modifications
or alternate approaches will be necessary. This is often
related to anatomical variations that may include hard
and soft tissue obstructions and accessory or aberrant
innervations.
Large facial bony eminences, exostoses, and skel­
etal variations can interfere with syringe angulations,
requiring modifications or alternate techniques to infil­
tration inj ections. A modification appropriate for these
situations is to position the syringe at an angle that will
bypass the bony obstruction and still allow access to the
deposition site. When adaptive angulations are not pos­
sible or are ineffective, an alternate inj ection technique(s)
may be indicated.
When infiltrations are unsuccessful, alternative injec­
tions may be considered. To anesthetize incisors, canines,
and premolars, alternatives include:
1. anterior superior alveolar (ASA) nerve blocks
2. infraorbital (10) nerve blocks
3. anterior middle superior alve olar (AMSA) nerve
blocks
4. p alatal anterior superior alveolar (P-ASA) nerve
blocks
For molars, alternatives include:
1. posterior superior alveolar (PSA) nerve blocks

Supplemental greater palatine (GP) nerve blocks may
be indicated if anesthesia is not profound (see Chapter 13,
" Inj e c t i o n s for M axillary Pain C o n t r o l I I - Pal a t a l
Approach").
Pe riodontal ligament (PDL) inj ections are also
appropriate alternatives to all of the infiltration inj ections
described previously (see Chapter 1 5 , " S upplemental
Techniques and Adjunctive Strategies").
Complications
The risk of complications following infiltration inj ection
techniques is minimal. These may include postoperative
pain at the site of inj ection , postoperative edema, and
rarely, hematoma (bleeding in tissue spaces surrounding
inj ured vessels ) . For further discussion see Chapter 17,
"Local Anesthesia Complications and Management."
Ante r i o r S u pe r i o r Alveo l a r
N e rve B l ock
The anterior superior alveolar (ASA) nerve block is a
common technique, similar to the basic anterior infiltration
technique. Unlike infiltrations, the ASA avoids multiple
needle penetrations when anesthesia is needed for more
than one maxillary anterior tooth in the same quadrant.
Field of Anesthesia
The ASA nerve block will anesthetize structures inner­
vated by the anterior segment of the ASA nerve (Jastak,
Yagiela, &D onaldson, 1995 ) . They include the pulps of
the maxillary central incisor through the canine on the in­
jected side and their facial periodontium. Because of diffu­
sion of anesthetic solution, some terminal branches of the
facial nerve are affected, as well. All or a portion of the
upper lip, cheek, and lower nose may be anesthetized (see
Figure 12-10 • and Appendix 12-2).
ASA
Teeth anesthetized:
canine, lateral, central
Periodontium/Soft tissues:
facial to affected teeth
F I G U RE 12-10 Field of Anesthesia for ASA Nerve Blocks. The
field of anesthesia for ASA nerve blocks is indicated by the shaded
area.
C HAPT E R 1 2 • I N J E C T I O N S FOR MAXI LLARY PAI N C O NTROL I 223
Anatomical Factors
The ASA nerve is the internal terminal branch of the max­
illary division of the trigeminal nerve. It branches from the
infraorbital nerve within the infraorbital canal 6 to 10 mm
before the infraorbital foramen.
The ASA nerve descends through the anterior wall of
the maxillary sinus to supply sensation to the dental plexus
of the canine and lateral and central incisors. As previously
discussed, the facial bone of the maxilla is relatively thin
and permeable. Local anesthetic solution diffuses easily
through the bone anesthetizing the ASA nerve.
Technique Factors
The following information describes key factors for suc­
cessful ASA nerve block injections.
P E N ETRAT I O N S I T E The optimal site of penetration for
an ASA inj ection is at the height of the mucobuccal fold
anterior to the canine eminence. This area is called the ca­
nine fossa (see Figure 12-1 1 •) .
N E E D LE PATHWAY The needle pathway parallels the long
axis of the canine, passing through thin mucosal tissues to su­
perficial fascia containing loose connective tissue, and avoids
small vessels and microvasculature, as well as nerve endings.
D E PO S I T I O N S I T E The deposition site is above the apical
area of the canine at the height of the canine fossa (see
Figure 12-12 •) . Contact with bone is unnecessary and
should be avoided for comfort.
Technique Steps
Apply the basic injection steps outlined in Chapter 11 and
summarized in Appendix 1 1-1.
N E E D L E S E L E CT I O N A 27- or 25-gauge needle is rec­
ommended for this technique. Similar to infiltrations, a
224 S E C T I O N IV • C LI N I C AL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A
F I G U R E 12-11 P enetration Site for ASA Nerve Blocks. The
penetration site for ASA Nerve Blocks is indicated by the
needle.
F I G U R E 12-12 Deposition Site for ASA Nerve Blocks. The
deposition site for ASA nerve blocks is indicated in the spot­
lighted area.
27-gauge short needle is most commonly used and is con­
sistent with the shallow depth of penetration and the low
rate of positive aspiration ( 1 % ), although some clinicians
prefer a 25- or 30-gauge needle.
I N JE CTI O N P R O C E D U R E Gain access to the penetration
site by retracting the lip, pulling the tissue taut with the
thumb and index finger (see Figure 12-5 ) . Locate the ap­
propriate penetration site. In order to achieve proper
angulations, align the barrel of the syringe parallel to the
long axis of the canine, following the contour of the max­
illa (see Figures 12-1 1 and 12-13 •). The depth of penetra­
tion to the site of deposition is based on the location of
the apex of the tooth and is usually achieved within 3 to
6 mm. Following negative aspiration, deposit an adequate
volume of an appropriately selected local anesthetic drug
to achieve anesthesia. A generally accepted minimum vol­
ume of anesthetic to accomplish this is 0.9 mL ( 1 12 of a
cartridge). Adequate volumes will vary regardless of the
technique depending on a variety of patient and pharma­
cological factors as well as planned procedures.
Confirming Anesthesia
Subjective signs of anesthesia for ASA inj ections include
a sense of numbness of the gingival and labial tissues from
the distal of the canine through the mesial of the central
incisor. Obj ective signs include a lack of response to gentle
stimulation with an instrument and no pain during proce­
dures in the expected field of anesthesia (see Box 12-1) .
Common Causes of Injection Failure
As with infiltration techniques, the most common causes
of anesthetic failure in the ASA technique include depo­
sition of solution too far from the target (see Box 1 2-2)
and inadequate volumes of solution. Other causes include
inflammation or infection in the area of deposition and in­
adequate diffusion of solution.
Troubleshooting
Similar to infiltrations, when ASA nerve blocks are unsuc­
cessful, it is helpful to reevaluate by visualizing, palpating,
checking radiographs, reassessing syringe angulations and
the depths of penetration, and the volumes of solution de­
posited. In some instances, adequate diffusion of solution
is impossible because of anatomic obstructions.
F I G U RE 12-13 Syringe Angulations for ASA Nerve Blocks.
Correct syringe barrel angulations for ASA nerve blocks parallel
the long axes of the canines, following the contour of the maxilla.
Source: Courtesy of Megan Gibbons.

Incomplete anesthesia with ASA nerve blocks can
also be attributed to what is known as cross-innervation or
overlap of terminal fibers of the contralateral ASA nerve
at the midline of the maxilla. When this is the case, teeth
in one anterior segment of the maxilla will receive sensory
innervation from the contralateral ASA nerve. To achieve
adequate anesthesia in these instances, an infiltration over
the same side central incisor is necessary.
Technique Modifications and Alternatives
Large facial bony eminences, exostoses, and other skeletal
variations can interfere with syringe angulations, requir­
ing modifications or alternate techniques. Positioning the
syringe at an angle that bypasses bony obstructions may
allow access to the deposition site. When adaptive angula­
tions are not possible, alternate inj ection techniques may
be indicated.
Nerve blocks that may be effective when ASA nerve
blocks are unsuccessful include the infraorbital (IO ) ,
anterior middle superior alveolar (AMSA ) , and palatal
anterior superior alveolar (PASA) . PDL inj ections may
also be used (see Chapter 15, "Supplemental Techniques
and Adjunctive Strategies") .
Complications
The risk of complications following ASA nerve block
inj ections is minimal. These may include postoperative
pain at the site of inj ection and, rarely, hematoma and
postoperative edema.
M id d le S u perior Alveo l a r N e rve B lock
Middle superior alveolar (MSA) nerve blocks are often
used in combination with other maxillary nerve blocks.
The MSA injection is indicated for pain management of
both premolars in one quadrant.
MSA
Teeth anesthetized:
maxillary premolars and
mesiobuccal root of first molar*
• For most people
Peri odontium/Soft tissues:
facial to affected teeth
FIGURE 12-14 Field of Anesthesia forMSA Nerve Blocks. The field
of anesthesia forMSA nerve blocks is indicated by the shaded area.
C HAPT E R 1 2 • I N J E C T I O N S F O R MAXI LLARY PAI N C O NTROL I 225
Field of Anesthesia
The MSA nerve block will anesthetize structures innervated
by the MSA nerve, when present, and its terminal branches,
to include the pulps of the maxillary first and second premo­
lars and their facial gingiva, periodontal ligament, and alveo­
lar bone. In some individuals, the MSA nerve also innervates
the mesiobuccal root of the first molar. Because of diffusion
of anesthetic solutions, some terminal branches of the maxil­
lary and facial nerves that innervate the cheek and upper lip
may be affected (see Figure 12-14 • and Appendix 12-2).
Anatomical Factors
The MSA nerve separates at varying points from the
infraorbital branch of the maxillary nerve within the in­
fraorbital canal. It supplies sensation to the dental plexus
of the first and second premolars and, in some individuals,
the mesiobuccal root of the maxillary first molar.
Studies have reported the absence of an MSA nerve
branch in somewhere between 50% and 72 % of individuals.
In the absence of an MSA nerve, branches of the anterior
superior alveolar and/or the posterior superior alveolar
nerve innervate the first and second premolars and the
mesiobuccal root of the first molar (Jastak, Yagiela, &
Donaldson, 1995; Loestscher &Walton, 1988).
An anatomical variation that can complicate MSA
nerve blocks is the presence of a large zygomaticoalveolar
crest. These excessive bony processes may obstruct access
to the apices of the maxillary second premolars (Blanton
&Jeske, 2003; Jastak, Yagiela,&Donaldson, 1995).
In general, the presence or absence of MSA nerves
in an individual is unknown. Despite uncertainties over
innervation, profound anesthesia of the maxillary first
molars can nevertheless be determined using electric pulp
testers. When these devices are not readily available, it is
common practice to administer local anesthetics with the
presumption that MSA innervation exists in order to avoid
unnecessary pain (see Box 12-3 •).
226 S E C T I O N IV • C LI N I C AL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A

Anato m ica l ly, n e rves te n d to fo l l ow what a re termed

patterns of in n e rvation . T h e right p oste rior s up e r i o r
a lveo l a r n e rve, fo r exa mp l e , c a n be exp e cted to p rovi d e
i n n e rvat i o n to the m axi l l a ry right m o l a rs, a n d the r i g h t
m i d d l e s up e r i o r a l veo l a r n e rve c a n be exp e cted to p rovide
i n n e rvat i o n to both right p re m o l a rs. Becaus e t h e m i d d l e
s up e r i o r a lveo l a r n e rve is absent m o re often t h a n it is p res­
ent, in a nywh e re fro m 50% to 72% of i n d iv i d u a ls, t h e re is a
known deviati o n i n these p atte rns. Even w h e n p resent, t h e
M SA n e rve may o r m ay not p rovi d e i n n e rvati o n to t h e m e ­
s i o b u cc a l root of the m axi l l a ry fi rst m o l a r. It is poss i b l e that
F I G U RE 12-15 P enetration Site for MSA Nerve Blocks.
fi b e rs fro m o n e o r a ny co m b i n at i o n of the M SA, ASA, G P,
The penetration site for MSA nerve blocks is indicated by the
a n d PSA n e rves m ay p rovide i n n e rvati o n to t h e m e s i o b u c­
needle.
c a l root of t h e m axi l l a ry fi rst m o l a r.
From a p r a cti c a l sta n dp o i nt, the iss u e of w h i c h fi b e rs
i n n e rvate t h e m es i o b u cca l root of m axi l l a ry m o l a rs is i r­
re l evant. To ove rco m e u n certa i nty reg a rd i n g t h e s o u rce of
its i n n e rvati o n , c l i n i c i a n s routi n e l y a d m i n ister a n i nfi ltrati o n
ove r t h e m es i o b u cc a l root of the m a xi l l a ry fi rst m o l a r i n a d ­
d i t i o n to a P S A n e rve b l ock. If i nfi ltrati o n tech n i q ues a l o n e
a re p l a n n e d fo r t h e m a xi l l a ry fi rst m o l a r, a n i nfi ltrati o n over
each fa c i a l root is reco m m e n d e d because of the d ista nce
betwee n t h e roots, t h e u n ce rta inties of d i ffu s i o n , a n d t h e

� � � �� � � �:� � � � � �� �� �
ex e n
. . .
S
. :
· an
. . .
S i
.
r t on
. :
• • • • • • • • • • IIi
Technique Factors
The following information describ e s key factors for
successful MSA nerve block inj ections.

P E N ETRAT I O N SITE The optimum site of penetration is at

the height of the mucobuccal fold over the maxillary sec­
ond premolar (see Figure 12-15 •) .

N E E D L E PAT H WAY The needle advances parallel t o the

long axis of the second premolar through thin mucosal
tissue to superficial fascia consisting of loose connective F I G U RE 12-16 Deposition Site for MSA Nerve Blocks. The
tissue, microvasculature, and nerve endings. deposition site for MSA nerve blocks is indicated in the spot­
D E PO S I T I O N S I T E The deposition site is well above the
lighted area.
apex of the second premolar. In order to be certain that
both first and second premolars are anesthetized, solution
Technique Steps
must be deposited superior to the branching of the nerve
to the first premolar. A deposition site inferior to the Apply the basic injection steps outlined in Chapter 11 and
branching would anesthetize only the second premolar; summarized in Appendix 1 1-1.
therefore, solution must be deposited well above the apex N E E D LE S E L E CT I O N A 27- or 25-gauge short needle is rec­
of the second premolar. Some clinicians prefer to split the ommended for this technique. A 27-gauge short needle is
difference between the first and second premolars, essen­ used most commonly for the MSA nerve block, which is
tially depositing solution between the apices of both teeth. consistent with the shallow depths of penetration and the
Although this highly successful approach also involves low rate of positive aspiration (1 % ) A 25-gauge needle is
.

only one penetration and is often easier to perform from also frequently used for this injection.
the standpoint of access, it should be pointed out that it is
not a true MSA nerve block. Contact with bone should be I N JE CT I O N P R O C E D U R E Gain access to the penetration
avoided for comfort (see Figure 12-16 •). site by retracting the lip, pulling the tissue taut with the

F I G U RE 12-17 Tissue Retraction for the MSA Nerve Block.
Maintain gentle but taut lateral retraction.
Source: Courtesy of Megan Gibbons.
F I G U RE 12-18 Syringe Angulations for MSA Nerve Blocks.
Align the syringe barrel along the contour of the maxilla.
Source: Courtesy of Megan Gibbons.
thumb and index finger (see Figure 1 2-17 •) . Locate the
appropriate penetration site. In order to achieve proper
angulations, follow the contour of the maxilla (see Figure
1 2-18 •) . The depth of penetration to the site of deposi­
tion is based on the location of the apex of the tooth and
is usually achieved within 5 to 8 mm. Following negative
aspiration, deposit an adequate volume of an appropri­
ately selected local anesthetic drug to achieve anesthesia.
A generally accepted minimum volume of anesthetic to
accomplish this is 0.9 to 1.2 mL (1/2 to 2/3 of a cartridge) .
Adequate volumes will vary regardless of the technique
depending on a variety of patient and pharmacological
factors, and procedures that are planned.
Confirming Anesthesia
Subj ective signs of anesthesia for MSA inj ections include
a sense of numbness of the gingival and labial tissues from
the distal of the second premolar through the mesial of the
first premolar. Objective signs include a lack of response
C HAPT E R 1 2 • I N J E C T I O N S F O R MAXI LLARY PAI N C O NTROL I 227
to gentle stimulation with an instrument and no pain dur­
ing the procedure in the expected field of anesthesia (see
Box 12-1) .
Common Causes of Injection Failure
Similar to both infiltration techniques and anterior su­
perior alveolar nerve blocks, the most common causes of
anesthesia failure for the MSA technique include deposi­
tion of solution too far from the target (see Box 12-2) and
inadequate volumes. Other causes include inflammation
or infection in the areas of deposition and inadequate dif­
fusion of solutions, because of anatomic (fascial plane)
deflection of solution away from target sites.
Troubleshooting
As is true for most other inj ections, when MSA nerve
blocks are unsuccessful it is helpful to reevaluate by
visualizing, palpating, checking radiographs, reassessing
syringe angulations, and depths of penetration as well as
to reconsider volumes of solution deposited. As previously
noted, when adequate diffusion of solution is impossible
because of anatomic obstructions, such as the presence of
a large zygomaticoalveolar crest, alternate nerve blocks or
supplemental techniques are indicated. These include PDL
inj ections (see Chapter 15, "Supplemental Techniques and
Adjunctive Strategies").
Occasion ally, medially displaced branches of the
PSA nerve and sometimes branches of the greater pala­
tine nerve provide pulpal innervation to the palatal roots
of maxillary molars and accessory innervation to the pre­
molars. Solution deposited for infiltrations and blocks of
premolars and molars may not diffuse far enough lingually
to reach these branches. In this situation, a supplemen­
tal greater palatine nerve block will anesthetize palatal
branches (Blanton &Jeske, 2003).
Technique Modifications and Alternatives
As with infiltration inj ections and anterior superior alveo­
lar nerve blocks, large facial bony eminences, exostoses,
and skeletal variations can interfere with syringe angula­
tions, requiring modifications or alternate techniques to
MSA inj ections. Positioning the syringe at an angle that
will bypass the bony ob struction will allow access to
the deposition site. When adaptive angulations are not
possible, an alternative inj ection technique(s) may be
indicated.
Alternate inj ection techniques for MSA inj ections in­
clude the anterior superior alveolar (ASA), the infraorbital
(IO), the anterior middle superior alveolar (AMSA), infil­
trations of each premolar and the palatal anterior superior
alveolar (P-ASA) nerve block. Infiltrations of both premo­
lars or between the apices of the premolars (field blocks)
and PDL inj ections are also appropriate alternatives.
Complications
The risk of complications following MSA nerve block
inj ections is minimal. These may include postoperative
228 S E C T I O N IV • C LI N I C AL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A
pain at the site of inj ection and, rarely, hematoma and
postoperative edema.
I nfraorb ita l N e rve B l ock
The infraorbital (10) nerve i s a continuation o f the maxil­
lary nerve within the infraorbital groove and canal located
in the portion of the inferior orbit formed by the maxilla.
It branches into the middle superior and anterior superior
alveolar nerves within the maxilla. The terminal branches
of the infraorbital nerve enter the maxilla at the infraor­
bital foramen and provide sensory innervation to the up­
per lip, lateral portion of the nose, and the lower eyelid
on one side. The discussion of the 10 nerve block can be
confusing because, like the ASA nerve block, it also anes­
thetizes the ASA nerve. The discussion of the ASA and 10
nerve blocks as distinctly different techniques is explained
in Box 1 2-4 •· A maj or distinction is that, in addition to
the area of anesthesia provided by the ASA nerve block,
the 1 0 nerve block typically provides numbness over a
large portion of the face, the premolars on the same side as
the inj ection, and some percentage of the time, the mesio­
buccal root of the maxillary first molar on the same side.
The 10 nerve block is indicated for pain management
of anterior and premolar teeth in one quadrant. A benefit
of the 10 nerve block is that smaller volumes of local anes­
thetics are needed to accomplish the same field of anesthe­
sia compared with administering both an anterior superior
alveolar and a middle superior alveolar nerve block, or
multiple infiltrations. This inj ection technique also avoids
multiple needle penetrations required when separate ante­
rior and middle superior alveolar nerve blocks or infiltra­
tions are administered.
Field of Anesthesia
The 10 nerve block will affect structures innervated by
the anterior and middle superior alveolar and 10 nerves.
Areas anesthetized include the pulps of the maxillary
10
Teeth anesthetized:
premolars, canine,
lateral, central
PerlodontlumiSoft tl88uee:
facial to affected teeth
FIGURE 12-19 Field of Anesthesia for IO Nerve Blocks. The field
of anesthesia for IO nerve blocks is indicated by the shaded area.
T h e i nfra orb ita l n e rve b l ock tech n i q u e a n d the a nterior
s up e r i o r a lveo l a r n e rve b l o c k tech n i q u e a re d isti n ct l y d iffe r­
ent i n t h e fo l l ow i n g ways:
1 . Penetratio n site: T h e p e n etrat i o n s ite fo r a n 10 n e rve
b l o c k is l o cated ove r the fi rst p re m o l a r, w h e reas the
p e n etrat i o n site fo r t h e ASA n e rve b l o ck is l o cated
over t h e ca n i n e .
2. Dep osition site: T h e d epos iti o n site fo r a n 1 0 n e rve
b l o c k is l o cated at the i n fra o rbita l fo ra m e n , w h e reas
t h e d eposition site fo r t h e ASA n e rve b l ock is l ocated
at the ap ex of the ca n i n e in the ca n i n e fossa .
3. Nerves an esth etized: T h e 10 n e rve b l o c k a n esth etizes
the ASA, M SA, and 1 0 n e rves, w h e reas the ASA n e rve
b l o c k typ i ca l ly a n esthetizes o n l y the ASA n e rve.
4. Effect by diffusion through bone: Only t h e ASA n e rve
b l o c k re q u i res d iffu s i o n t h ro u g h b o n e .
5. Effect b y direct con tact with n e rve: T h e 1 0 n e rve b l ock
d i rectly bathes t h e n e rve with a n esth et i c s o l ution at
the 10 fo ra m e n a n d in the 1 0 ca n a l . It does not req u i re
diffu s i o n t h ro u g h b o n e .
6. Su ccess rates: T h e A S A n e rve b l ock d e m o n strates a
m u ch h i g h e r rate of s u ccess, w h i c h m ay be because of
��� ? � ��
• •
: • • • .
c i i ia
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.
ex ri n c
. . . . · · . .
it h l n e e � ks
�� . •. �• • • • • •
central incisors through the canine, and premolars, and
their facial periodontium, the lower eyelid, lateral aspect
of the nose, and the upper lip. In some individuals, the me­
siobuccal root of the maxillary first molar is also anesthe­
tized (see Figure 12-19 • and Appendix 12-2).
Some authors describe 10 nerve blocks as ASA nerve
blocks and others describe two separate techniques similar
to the descriptions in this text (Jastak, Yagiela,&Donaldson,
1995; Malamed, 20 1 3 ) . It is important to remember that
most dental nerve blocks do not block the entire extents
 C HAPT E R 1 2 • I N J E C T I O N S F O R MAXI LLARY PAI N C O NTROL I 229

(A) (B)
F I G U RE 12-20 Comparison of Adult and Child IO Foramen. A-In a typical adult, the IO foramen is located approximately 8 to
10 mm below the IO ridge. B-Because of incomplete vertical growth of the facial skeleton in children and adolescents, this distance
is shorter.

of the nerves whose names they bear. As such, they should

be viewed as techniques that block impulses from specific
branches or segments of branches of the nerves that are
identified in the technique name.

Anatomical Factors
As previously discussed, the maxillary nerve segment
within the IO groove and canal is called the infraorbital
nerve. The anterior and middle superior alveolar nerves
branch from the IO nerve within the infraorbital canal.
The IO nerve then exits the infraorbital foramen and fur­
ther divides to provide innervation to areas of the upper
lip, cheek, nose, and lower eyelid ( Blanton &Jeske, 2003).
The height of the mucobuccal fold and the position of
the IO foramen vary, based on facial size, vestibular depth,
and age. In a typical adult, for example, the IO foramen is
located approximately 8 to 10 mm below the IO ridge. This
is a safe distance from the orbit. In children and adoles­
cents, however, the vertical growth of the facial skeleton F I G U R E 12-21 P enetration Site for I O Nerve Blocks. The pen­

is incomplete. Incomplete growth results in a shorter dis­ etration site for IO nerve blocks is indicated by the needle.
tance between the IO foramen and the IO ridge compared Source: Courtesy of Megan Gibbons.

with adults. These differences warrant caution in these

individuals ( see Figure 12-20 •).
Technique Factors
The following information describes key factors for suc­
cessful 10 nerve block inj ections.
P E N ETRAT I O N S IT E The typical penetration site is at the
height of the mucobuccal fold directly over the first pre­
molar ( see Figure 12-21 •).
N E E D L E PAT H WAY The n e e d l e a d v a n c e s t h r o u g h
thin mucosal tissue to sup erficial fascia consisting o f
connective tissue, microvasculature, and nerve endings to
the infraorbital foramen.
D E PO S I T I O N S I T E The deposition site is anterior to or
superficial to the infraorbital foramen at a depth adequate
to reach the foramen ( see Figure 1 2-22 •). The foramen
is located inferior and slightly medial to the infraorbital
notch.
Although contact with bone is not necessary for suc­
cess, some sources recommend contact with bone at the
height of the infraorbital foramen to assure adequate
depth of penetration ( Malamed, 20 13).
230 S E C T I O N IV • C LI N I C AL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A

(A)

F I G U RE 12-22 Deposition Site for IO Nerve Blocks.

The deposition site for IO nerve blocks is indicated in the
spotlighted area.

Technique Steps
Apply the basic inj ection steps outlined in Chapter 11 and
summarized in Appendix 1 1-1.

N E E D L E S E L E CT I O N A 27-or 25 -gauge needle is recom­

mended for this technique. A 27-gauge short needle is
used most commonly for the I O nerve block , which is
consistent with the shallow-to-moderate depths of pen­
etration and the low rate of positive aspiration (less than
3 %) (Malamed, 20 13). In some cases, a 27-gauge long or a
25-gauge short or long needle may be preferred.
I N J E CT I O N P R O C E D U R E To gain access to the site of pen­
etration, lift the lip, pulling the tissue taut with the thumb
and index finger (see Figures 1 2-23A • and 1 2-23B •) .
After locating the foramen (see Box 12-5 •) , the angle of
insertion is oriented toward the foramen along a line par­
allel to the pupil of the eye on the side of inj ection (see
Figures 12-24 • and 1 2-25 •) . Following a negative aspi­
ration, deposit a minimum of 0.9 mL (112 of a cartridge)
of an appropriately selected local anesthetic drug. An
important step after deposition is to apply finger pres­
sure over the deposition site for 1 to 2 minutes to enhance
diffusion of the anesthetic solution into the infraorbital
canal. It is customary to maintain a finger position on
the infraorbital notch throughout the inj ection to avoid
overinsertion of the needle as shown in Figure 1 2-23B.
Following the administration of the anesthetic, pressure is
applied at this same spot, over the deposition site as shown
in Figures 12-23B and 12-26 •·
(B)
F I G U R E 12-23 Retraction. A-To gain access to the site
of penetration, retract the lip, pulling the tissue taut with the
thumb and index finger, lifting the tissues away from the max­
illa. B-The thumb or forefinger is located over the IO foramen
to assist in establishing tissue retraction and is maintained at
that site during the injection.
Source: Courtesy of Megan Gibbons.
Confirming Anesthesia
Subjective signs of anesthesia for IO inj ections include a
sense of numbness of the gingival and labial tissues from
the distal of the second premolar through the mesial of the
central incisor. In addition, numbness occurs in the facial
tissues from the lip to the lower eyelid, including the side
of the nose. Obj ective signs include a lack of response to
gentle stimulation with an instrument and no pain during
procedures.
 C HAPT E R 1 2 • I N J E C T I O N S F O R MAXI LLARY PAI N C O NTROL I 231

T h e s u ccess of 10 i nj e cti o n s is i m p roved w h e n the

i nfrao rbita l fo ra m e n is correctly l ocate d . T h i s l a n d m a rk is
e a s i l y i d e ntifi ed i nfe rior to t h e i nfra orb ita l r i d g e by p a l p at­
i n g the i nfra o rb ita l rim on the s i d e of i nj e cti o n a n d l o c a t i n g
the 1 0 n otch . From t h e n otch, m ove t h e fi n g e r i nfe riorly
a l o n g a l i n e p a ra l l e l to t h e p u p i l of t h e eye a p p roxi mately
10 mm. Typ i c a l ly, t h e rim of t h e fo ra m e n c a n be p a l pated

: � � � : ��
•

. . � ;�
a t i i e ( e i re 1 2 6 ·
. �}
· · · � • • • • • • • • • • • • • • • • • • • .

FIGURE 12-2 5 Syringe Angulations for IO Nerve Blocks. Align

the syringe barrel toward the foramen along a line parallel to the
pupil of the eye on the side of injection. Note the stable fulcrum
on the chin (A) and the palm-up grasp (B) to aid stability.
Source: Courtesy of Megan Gibbons.

F I G U R E 12-26 Locating the Infraorbital Foramen. The infra­

orbital foramen is easily located inferior to the infraorbital ridge
by palpating the infraorbital rim and locating the IO notch.
Source: Courtesy of Megan Gibbons.

Other causes may include inflammation or infection

in the area of deposition, inadequate diffusion of solution
into the foramen because of anatomical factors such as
an unusually small foramen and technical factors such as
insufficient duration, or incorrect application of pressure
F I G U RE 12-24 Cues for Syringe Angulations for IO Nerve
following the injection.
Blocks. To establish syringe angulations, visualize a line parallel
to the midsagittal plane and to the pupil of the eye on the side of Troubleshooting
injection.
When 10 nerve blocks are unsuccessful, it is helpful to
Source: Courtesy of Megan Gibbons.
reevaluate by visualizing and palpating the location of
the foramen, reassessing syringe angulations and depths
Common Causes of Injection Failure of penetration, and to reconsider volumes of solution de­
The most common causes of anesthetic failure include posited. When necessary, repeat the injection, paying close
deposition of solution too inferior to the infraorbital fo­ attention to these factors.
ramen or too superficial to the foramen and inadequate In some instances, the post-inj ection pressure applied
volumes of solution. is adequate ; however, the location of the foramen is
232 S E C T I O N IV • C LI N I C AL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A

at the site of inj ection, hematoma, and transient numbness

of peripheral nerve fibers of the facial nerve.

To red u ce re petitive stresses o n c l i n i c i a n s ' h a n d s , it is h e l p­

Posterior S u perior Alveo l a r
fu l to ask patie nts to a p p l y extra o ra l p ress u re over t h e N e rve B lock
fo ra m e n fo l l ow i n g d e p ositi o n of s o l ut i o n a n d n e ed l e w i t h ­
Posterior superior alveolar (PSA) nerve blocks are indi­
d rawa l . Patie nts s h o u l d be re m i n d e d , i f they a g ree to t h i s
t a s k , that p ress u re m u st be a p p l i e d i n a spe cified d i rec-
cated for pain management of multiple molar teeth in one
tion and in a ste ady, constant m a n n e r over the e n t i re 1 - to quadrant. Alternate names for PSA nerve blocks include

� � � �� �� �
•

2- n u r od tuberosity or zygomatic blocks. Some clinicians refer to

. . . . : . • • • • • • • •
incorrectly assessed. In others, the foramen is correctly
located but the depth of penetration is inadequate, the
needle direction is incorrect, or pressure is applied for too
short a period of time or ineffectively (see Box 12-6 •) .
Some foramina are quite small and do n o t accept solu­
tions readily. Whenever IO inj ections prove to be ineffec­
tive repeatedly, choose an alternate technique.
Technique Modifications and Alternatives
In some instances, an ideal pathway is not possible be­
cause of anatomical factors such as restrictive musculature
and tissue inflexibility. In these cases, a more anterior pen­
etration and pathway may be necessary or an alternative
technique selected.
Alternative inj ections can include anterior superior
alveolar nerve blocks, along with middle superior alveo­
lar, anterior middle superior alveolar, and palatal anterior
superior alveolar nerve blocks, multiple infiltrations, max­
illary nerve blocks, and PDL inj ections (see Chapter 15,
"Supplemental Techniques and Adjunctive Strategies").
Complications
The risk of complications following IO nerve block tech­
niques is minimal. These may include postoperative pain
• • • • • • • • • • • • • • • • • • • the PSA as a "maxillary block," which is not entirely ac­
curate because a true maxillary, or division 2, block is a
specific and different technique that anesthetizes an entire
hemi-maxilla (maxillary blocks are discussed later in this
chapter) .
Field of Anesthesia
Anesthesia will affect the structures innervated by the
PSA nerve, including pulps of the maxillary first, sec­
ond, and third molars, and the facial periodontium on
the inj e cted side ( s e e Figure 1 2-27 • and Appendix
1 2-2 ) . In some individuals, the mesiobuccal root of the
maxillary first molar will not receive its entire innerva­
tion, or any innervation, from the PSA nerve, and a PSA
block would not provide profound anesthesia for the
entire tooth.
Anatomical Factors
The PSA nerve branches from the maxillary nerve in
the pterygopalatine fossa before the maxillary nerve's
entrance into the infraorbital canal. The PSA nerve then
enters the maxillary tuberosity on its infratemporal sur­
face. Generally, there are two or more posterior superior
alveolar branches. One branch traverses downward along
the external surface of the posterior maxilla and innervates
the facial gingiva and mucosa of the molars. One or more
internal branches typically divide further and the nerve

PSA
Teeth anesthetized:

maxillary molars except

mesiobuccal root of first molar

Periodontium/Soft tlaauea:

buccal to affected teeth

FIGURE 1 2-27 Field of Anesthesia for P SA Nerve Blocks. The field

of anesthesia for P SA nerve blocks is indicated by the shaded area.
 C HAPT E R 1 2 • I N J E C T I O N S FOR MAXI LLARY PAI N C O NTROL I 233

fibers enter the maxilla through small foramina located

on the posterior surface of the tuberosity of the maxilla.
These nerve fibers serve the dental plexuses of the molar
teeth with the common exception of the mesiobuccal root
of the first molar. The innervation of the mesiobuccal root
is further discussed in Box 12-3 .
The area posterior to the infratemporal surface of the
maxilla contains the infratemporal and pterygopalatine
fossae. The infratemporal fossa contains the maxillary ar­
tery and its branches, the pterygoid plexus of veins, and
branches of the mandibular nerve. The maxillary nerve
traverses the superior area of the fossa. Branches of the
maxillary artery and the maxillary nerve continue into the
pterygopalatine fossa, which is located medial to the infra­
temporal fossa.

Technique Factors
The following information describes key factors for suc­
cessful PSA nerve block inj ections.

P E N ETRAT I O N S I T E The penetration site is at the height (A)

of the mucobuccal fold, posterior to the zygomatic process
of the maxilla and generally superior to the distobuccal
root of the maxillary second molar (see Figure 12-28 •) .
When 3rd molars are present, the penetration site can be
adj usted posteriorly to the distobuccal root of the maxil­
lary 3rd molar.

N E E D L E PAT H WAY The needle advances through thin

mucosal tissue, superficial fascia consisting of loose con­
nective tissue, avoiding vessels, and nerve endings to a
location close to the PSA nerve(s) on the posterior surface
of the maxilla.

D E PO S IT I O N S I T E The deposition site is adj acent to the

foramina for the PSA nerve branches on the posterior sur­
face of the maxilla (see Figure 12-29 •) .
(B)
F I G U R E 12-29Deposition Site for P SA Nerve Blocks.
A - The deposition site for P SA nerve blocks is indicated in
the spotlighted area. B - At optimum "depth and angle" only
approximately 9 mm of the needle shaft will be visible beyond
the needle hub.
Source: Courtesy of Megan Gibbons (B).

Technique Steps
Apply the basic injection steps outlined in Chapter 11 and
summarized in Appendix 1 1-1.

N E E D L E S E L E CTI O N A 25- or 27-gauge needle is recom­

F I G U RE 12-28 P enetration Site for P SA Nerve Blocks. The
penetration site for P SA nerve blocks is indicated by the needle.
At "minimum penetration" nearly the entire length of the nee­
dle shaft is visible.
Source: Courtesy of Megan Gibbons.
mended for this technique. A 27-gauge short is most
commonly used, which is consistent with the low rate of
positive aspiration (slightly greater than 3 %) (Malamed,
20 1 3 ) . Some clinicians prefer to use a long needle for a
PSA nerve block. Others prefer 25-gauge short or long
needles because of the moderate penetration depths nec­
essary in this technique.
234 S E C T I O N IV • C LI N I C AL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A

I N JE CT I O N P R O C E D U R E To gain access to the site of

penetration, retract the lip upward and outward , lift­
ing the buccal mucosa laterally as demonstrated in Fig­
ures 1 2-30 • and 1 2-3 1 •· The angle of needle insertion
is up ward (at a 45-degree angle to the occlusal plane of
the maxillary teeth), inward behind the maxillary tuber­
osity (at a 45-degree angle to the midsagittal plane) , and
then must be advanced backward behind the posterior
aspect of the maxilla. To achieve this, the barrel of the
syringe must b e angled downward from the occlusal
table and outward from the patient's midsagittal plane

(A)

(A)

(B)
F I G U RE 12-31 Retraction for P SA Nerve Blocks. A-To
establish access, first retract the lip downward to reduce
pressure on the barrel from the lower lip. B-Retract 45 degrees
to occlusal table.

(B) ( s e e B ox 1 2-7 •) . The optimum depth of insertion is

16 mm (9 mm from the hub of an average 25-mm short
needle) (see Figure 1 2-29B ) ; however, clinicians should
allow for anatomical variances c o n tributing t o the
depth of insertion, which can range from 1 0 to 16 mm.
At depths greater than 16 mm the risk of hematoma in­
cre ases. D eposit anywhere from 0 . 9 mL to 1 . 8 mL (112
t o 1 cartridge) after negative aspiration. For further dis­
cussion on depth, see B ox 1 2-8 •·
Aspirations in more than one plane are recommended
when administering PSA inj ections because of the pres­
ence of the pterygoid plexus of vessels.

(C) Confirming Anesthesia

F I G U RE 12-30 Retraction for P SA Nerve Blocks. Retracting Subj ective signs of anesthesia for PSA inj ections include
the soft tissues both upward and outward provides for direct a sense of numbness of the gingiva and, in some cases, ex­
access to the penetration site and allows for the "upward" and tending into the buccal mucosa from the distal of the third
"inward" pathway. A - Retraction can be provided manually or molar through the first molar. It is not uncommon for
B-with the use of a mirror or C-tissue retractor. patients to report no sensations of numbness. Objective
Source: Courtesy of Megan Gibbons. signs include a lack of response to gentle stimulation with

The pathway of t h e n e e d l e fo r the PSA n e rve b l ock has
fre q u ently been descri bed as a n up ward, inward, a n d back­
ward moveme nt. This can be confu s i n g to vis u a l ize a n d u n ­
dersta n d . It m a y be e a s i e r to co n s i d e r t h i s pathway i n terms
of the m otion of the h a n d and syri n g e d u r i n g the i njectio n .
T h e upward n e ed l e pathway is a c h i eved w h e n t h e c l i ­
n i c i a n a n g l e s t h e syri n g e ba rre l down ward a t a 45- d e g ree
a n g l e , away fro m t h e o cc l u s a l plane of t h e m a xi l l a ry teeth
(see F i g u re 1 2-3 1 ) . T h e in ward n e e d l e p athway is a c h i eved
when t h e c l i n i c i a n a n g l es t h e syri n g e b a rre l o utward l ater­
a l ly at a 45- d e g ree a n g l e , away fro m t h e patie nt's m i d s a g it­
tal p l a n e (see F i g u re 1 2-32 •). The backward m ove m e n t
s i m p ly refe rs to the advancem e n t of t h e n e e d l e to t h e
d e p ositi o n s i t e . I n s h o rt, the syri n g e w i l l be m oved " d own
and out" befo re adva n c i n g to d e p t h .
It c a n be h e l pfu l to ask patie nts to close t h e i r m o uths
h a lf way a n d s h ift their m a n d i b l es to t h e s i d e of i nj e cti o n .
T h i s i m p roves visi b i l ity a n d a ccess for syri n g e a n g u l at i o n s
i n order to a c h i eve u pward, i nward, a n d ba ckward m ove­
m e nts. U s i n g the t h u m b o n the retra ct i o n h a n d can a d d
sta b i l ity to m a n a g e a n y p ress u re fro m t h e l ower l i p; t h i s is
d e m o n strated i n F i g u re 1 2-33 •·
Additi o n a l vis u a l cues fo r a c h i ev i n g opti m a l a n g u l a ­
t i o n s fo r PSA n e rve b l o cks a re p rovi d e d i n F i g u re 1 2-34
F i g u re 1 2-35 • d e m o n strates i d e a l , a ccepta b l e , a n d
: i n co rrect a n g u l at i o n s .
. . . . . . . . . . . . . . . . . . . . . . . .
an instrument and no pain during the procedure in the
expected field of anesthesia.
Com mon Causes of Injection Failure
The most common causes of anesthetic failure include de­
position of solution too far from the PSA foramina (too
(A)
F I G U R E 12-32Angulation for P SA Nerve Blocks. A-The "upward" needle pathway is achieved when the clinician angles the sy­
ringe barrel down and away from the occlusal plane. The "inward" needle pathway is achieved when the clinician angles the syringe
barrel outward laterally away from the patient's midsagittal plane. B-P lacing the thumb on the barrel can add stability.
Source: Courtesy of Megan Gibbons.
C HAPT E R 1 2 • I N J E C T I O N S F O R MAXI LLARY PAI N C O NTROL I 235
inferior, posterior, or lateral) and inadequate volumes of
solution.
Other causes may include inflammation or infection
in the area of deposition.
Troubleshooting
Occasionally, displaced branches of the PSA nerve and the
greater palatine nerve may provide innervation to the pal­
atal roots of maxillary molars and accessory innervation
to the premolars. In this situation, a supplemental greater
palatine nerve block will anesthetize these nerve branches
(Blanton &Jeske, 2003).
Contact with bone is not expected. If contact occurs,
the needle is touching the periosteum of the tuberosity.
Withdrawing the n e e dle and repenetrating at a more
lateral site will avoid this obstruction. If an initial pen­
etration site is too anterior to the ideal site, it is possible
to contact the posterior surface of the zygomatic process,
resisting further progress to the target site posterior to
the tuberosity and causing discomfort. Withdrawing the
needle and reassessing the posterior extent of the zygo­
matic process helps establish a new penetration site that
is posterior and/or lateral to the previous site.
Technique Modifications and Alternatives
The depth of penetration is reduced to prevent overinsertion
•· in children and small adults. When skeletal anatomy prevents
clinicians from establishing an initial insertion angle at 45
degrees to the midsagittal plane, it may be helpful to begin
. . . . . . . . . . . . . . . . • the injection with the syringe oriented parallel to the maxilla
before establishing ideal angles as the needle is advanced.
Alternatives include multiple infiltrations and PDL or
intraosseous inj ections (see Chapter 15).
Com plications
B ecause of its proximity to the pterygoid plexus of veins
and maxillary arteries, the PSA inj ection has the highest
(B)
236 S E C T I O N IV • C LI N I C AL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A

(A) (B)
F I G U RE 12-33 Fulcrum and Access for P SA Nerve Blocks. Using the thumb on the retraction hand can add stability and manage
pressure from the lower lip.
Source: Courtesy of Megan Gibbons.

(A) (B)
F I G U R E 12-34P SA Nerve Blocks-Visualizing the "Inward" Needle P athway. Following an imaginary line that marks an "X"
across the patient's face can provide a visual cue for the inward needle pathway that is achieved when the syringe barrel is angled out­
ward 45 degrees laterally away from the patient's midsagittal plane.
Source: Courtesy of Megan Gibbons.

risk of hematoma of all other intraoral techniques in this
text with the exception of the tuberosity approach to the
maxillary or second division nerve block. The risk of he­
matoma is more likely if needles are overinserted into the
pterygopalatine fossa. This risk also increases when needle
penetrations are located too posterior to deposition sites
on the posterior surface of the maxilla. B ecause of the
higher risk of hematoma associated with PSA inj ections,
the technique may be contraindicated in patients with
clotting disorders or on anticoagulant therapy. Alternate
techniques, such as multiple infiltrations, may be safer in
these instances (see Chapter 17, "Local Anesthesia Com­
plications and Management").
M axi l l a ry N e rve B l ock
A maxillary nerve block, a l s o referred to as a second
division nerve block or a V2 nerve block, is indicated for
hemimaxillary pain management. The benefit of maxillary
nerve blocks is that a single injection can replace multiple
inj ections when providing anesthesia for an entire half of
the maxilla. Maxillary nerve blocks are also useful when
 C HAPT E R 1 2 • I N J E C T I O N S F O R MAXI LLARY PAI N C O NTROL I 237

(A) (B)

F I G U R E 12-3 5 Evaluating Optimal Syringe Angulations.

A-The ideal angulations for P SA nerve blocks create a needle
pathway at a 45-degree angle to the midsagittal plane. B-In
some situations it may be difficult or impossible to achieve this
angle and a lesser angle, approximately 20 degrees, may be ac­
ceptable. Angulations less than 20 degrees (parallel to the mid­
sagittal plane ) are unacceptable. C-Angulations greater than
45 degrees outward are incorrect.
(C)

Routine use of maxillary nerve blocks in most situations

is discouraged, and they are perhaps best learned and
practiced when an individual who has administered many
maxillary blocks is mentoring.
There are three well-recognized techniques for anesthe­
As with oth e r proce d u res, t h e re a re a ccepted re g i o n a l a n d
tizing the maxillary nerve. The first involves a facial approach
p rofessi o n a l p h i l o s o p h i e s o f care. T h i s a lso a p p l ies t o varia­
t i o n s i n l o c a l a n esthetic tech n i q ues. A n u m be r of va riati o n s
and has been referred to as a high-tuberosity, tuberosity, or
fo r PSA a n esth esia a re t a u g ht, fo r exa m p l e . O n e variati o n facial- or buccal-approach maxillary nerve block. The second
a d m i n isters the P S A i nj e cti o n as a s h a l low i nfi ltrat i o n , w h i c h involves a palatal approach and is referred to as a greater
is re l ative ly s u ccessfu l fo r soft t i s s u e p ro ce d u res; h owever, palatine, pterygopalatine canal, or simply palatal approach
it m a y be i n a d e q u ate fo r p u l p a l a n esth es i a . Oth e r terms maxillary nerve block. Even though the greater palatine
used to describe PSA i nj e cti o n tech n i q u es i n c l u d e deep maxillary nerve block fits the description of a palatal tech­
infiltration a n d shallow block. nique in this text, it will be discussed in this chapter rather
It is i m p o rtant to n ote that in states w h e re d e n t a l hy­ than in Chapter 13, "Inj ections for Maxillary Pain Control
g i e n ists a d m i n ister loca l a n esth e s i a , a few states a l l ow o n ly • II - Palatal Approach," in order to create a single reference
� : : � :� �� � :��
i fl r t nt ni s
. . •� • • • • • • • • • • • • • • • • • • • • • • • point for readers. The third technique uses an extraoral ap­
proach and is not discussed in this text.

other penetration sites or pathways on the same side of Field of Anesthesia

the maxilla are infected and needle penetrations for local Anesthesia will affect the structures innervated by the
anesthesia risk deeper spread of the infections or do not maxillary nerve, including the pulps and periodontium of
effectively anesthetize the target tissues or both. Despite all teeth, and palatal tissues to the midline on the inj ected
these benefits, there are significant risks and challenges in­ side. Other unilateral facial tissues such as the upper lip
volved when opting to administer maxillary nerve blocks. and cheek, lower eyelid, and lateral aspect of the nose are
They can be difficult to master from palatal aspects and also affected. Hemostasis of the tissues to be treated is not
risk significant complications from facial approaches. provided by either of the approaches. All fields represented
238 S E C T I O N IV • C LI N I C AL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A

by the ASA, MSA, IO, GP, and NP nerve blocks previously Palatal Approach to Maxillary Nerve Blocks
discussed are included in the maxillary nerve block. See This is also referred to as the palatal approach, greater
Appendix 1 2-2, "Field of Anesthesia - Maxillary Inj ec­ palatine or pterygopalatine canal maxillary nerve block.
tions," and Appendix 13-2, "Field of Anesthesia - Palatal
Inj ections," for anatomical representations of the hemi­ P E N ETRAT I O N S ITE The penetration site for a greater pala­
maxillary field of anesthesia. tine maxillary nerve block is in the mucosa that lies directly
over the greater palatine foramen (see Figure 12-36 •) .
Anatomical Factors
N E E D L E PAT H WAY The needle advances through thin
Branches of the maxillary nerve arise in the cranium, pterygo­
mucosal tissue, superficial fascia consisting of loose con­
palatine fossa, infraorbital canal, and facial tissues of the max­
nective tissue, avoiding vessels, and nerve endings through
illa. The latter three pass through various foramina and canals
the greater palatine foramen and pterygopalatine canal to
to join posterior branches of the maxillary nerve in the ptery­
a location within the pterygopalatine fossa. To reach this
gopalatine fossa before the maxillary nerve's entrance into
location the syringe (or needle) must be angled upward
the cranium by means of the foramen rotundum. The trunk
(see Figure 12-37 •) and advanced to a depth of 30 mm or
of the maxillary nerve formed in the pterygopalatine fossa
2 mm from the hub of 32-mm needles (1 mm from the hub
by the convergence of its branches is then joined by menin­
in 3 1-mm needles) . There should be no resistance to the
geal branches from the dura mater just before the maxillary
needle's movement at any point along its pathway to the
nerve trunk's entrance into the trigeminal ganglion. Together,
deposition site.
the right and left maxillary nerves innervate the maxillae and
their overlying skin, the nasal cavity, palate, maxillary sinuses, D E PO S I T I O N SITE The deposition site is in proximity to
nasopharynx, and a portion of the dura mater. the maxillary nerve trunk within the pterygopalatine fossa
The maxillary artery is protected from the pressures of (see Figure 12-38 •) .
mastication by the pterygoid plexus of veins, which emp­
ties in response to compression in order to allow an un­ Technique Steps
interrupted flow of blood through the artery (Fehrenbach Apply the basic inj ection steps outlined in Chapter 11 and
&Herring, 20 12). The maxillary artery is situated within summarized in Appendix 1 1-1.
the plexus and lies in the direct pathway of high-tuberos­ Use the two-step topical pre- anesthesia technique,
ity maxillary nerve block inj ections. Inadvertent nicking described in Chapter 13 under injection procedure, before
of the artery can result in rapid and vigorous hematoma providing infiltration pre-anesthesia. Additional pre­
formation and has been characterized as involving a rela­ anesthesia by infiltration is strongly suggested here for the
tively high degree of risk when high-tuberosity maxillary benefit of both patient and clinician. This is accomplished
blocks are administered (Hawkins &Isen, 1998). This is in
addition to the technique's characterization as being less
predictable, more arbitrary, and prone to more complica­
tions (Hawkins &Isen, 1998; Malamed, 20 1 3 ) compared
with the pterygopalatine canal or palatal approach.
The palatal approach is most successful when the pter­
ygopalatine canal is relatively straight and unobstructed.
This has been estimated to be the case anywhere from 85 %
to 95 % of the time (Hawkins & Is en, 1998; Malamed &
Trieger, 1983). Although far less likely to occur, hematomas
are also possible with this approach. The positive aspiration
risk is estimated to be less than 1 % , an indication of the in­
frequency of encounter. Penetration of the orbit is possible
in greater palatine maxillary nerve block overpenetrations.
Ocular complications include periorbital swelling and pro­
ptosis (exophthalmos) , diplopia, transient loss of vision,
mydriasis, retrobulbar hemorrhage, and corneal anesthesia.
The needle may also penetrate the thin medial wall of the
nasal cavity, noted by a lack of fluid during aspiration and
a bubble of air in the cartridge. Patients may complain of
liquid running down their throats (Malamed, 20 13). FIGURE 12-36 P enetration Site-P alatal Approach-Maxillary
Nerve Blocks. The penetration site for maxillary nerve blocks is
Technique Factors into the greater palatine foramen as indicated by the needle. At
The following information describes key factors for suc­ "minimum penetration" nearly the entire length of the needle
cessful maxillary nerve block inj ections. Two sets of factors shaft is visible. The penetration site and needle modification are
will be described, one set for each approach. demonstrated.

FIGURE 12-37 Syringe Angulation-Palatal Approach-Maxillary
Nerve Blocks. The demonstrated syringe angulation is necessary to
navigate the greater palatine canal with both modified and straight
needle techniques.
by locating the anterior depression of the greater palatine
foramen, moving a few millimeters posterior to that loca­
tion, then following the steps for infiltration inj ections.
N E E D L E S E L E CT I O N A 25-gauge needle is preferred for
this technique. Considering the limited space available in
the posterior areas of the oral cavity, some clinicians find
it useful to bend needles when performing this technique.
B ending needles is discussed in Chapter 1 5 , B ox 15-3 ,
which provides a discussion of safe practices if clinicians
elect to bend needles.
I N JE CT I O N P R O C E D U R E It cannot be overemphasized
that pre-anesthesia is helpful and recommended before
(A)
F I G U RE 12-38 Deposition Site-Palatal Approach-for Maxillary Nerve Blocks. A-The deposition site for-palatal approach ­
maxillary nerve blocks is indicated in the spotlighted area. B-At optimum "depth and angle" only approximately -2 mm of the
needle shaft will be visible beyond the needle hub.
C HAPT E R 1 2 • I N J E C T I O N S F O R MAXI LLARY PAI N C O NTROL I 239
performing this technique (Hawkins &Isen, 1998 ) . This
promotes a more comfortable procedure, allows clinicians
to concentrate on the technique itself, and helps patients
tolerate deep needle insertions in posterior areas of their
palates. Although not always necessary, it may be helpful
to bend needles to a 45-degree angle (see Figure 12-37),
which can help negotiate greater palatine canals and may
be critical to success when there is very limited access.
When supporting their recommendation for bending nee­
dles, Hawkins and Isen point to the wide variation in the
slope of the greater palatine canal (from 20 to 70 degrees),
which can be better accommodated with bent needles.
Regardless of whether or not clinicians choose to bend
needles, care should be taken to avoid medial deviation
of needles and subsequent nasal cavity penetrations dur­
ing insertions to depth. No resistance should be felt dur­
ing penetration to the deposition site, although the lateral
walls of the canal can be used to help guide the needle to
its optimal depth of 30 mm.
Once the deposition site is reached, aspiration is re­
quired. Multiple aspirations in more than one plane are
recommended when administering all maxillary nerve
block inj ections. It is important to note, if the needle, at
any time, is unable to move beyond an obstruction, it
should be withdrawn and the procedure terminated.
Facial Approach to Maxillary Nerve Blocks
This is also referred to as a high tuberosity, tuberosity, or
facial- or buccal-approach maxillary nerve block.
P E N ETRAT I O N SITE The penetration site is at the height
of the mucobuccal fold over the dis to buccal aspect of the
maxillary second molar (see Figure 12-39 •) .
N E E D L E PAT H WAY The needle advances through thin
mucosal tissue and superficial fascia consisting of loose
(B)
240 S E C T I O N IV • C LI N I C AL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A
F I G U RE 12-39 P enetration Site for-High-Tuberosity
Approach-Maxillary Nerve Blocks. The penetration site for
maxillary nerve blocks is indicated by the needle. Both the
penetration site and syringe angulation are similar to P SA
injections.
connective tissue, avoiding vessels and nerve endings to a
location within the pterygopalatine fossa to a depth of 30
mm or 2mm from the hub of a 32-mm needle and 1 mm
from the hub of a 3 1-mm needle as j udged by the por­
tions of needles that are protruding from the tissues after
optimal insertions. There should be no resistance to the
needle's movement at any point along its pathway to the
deposition site.
D E PO S I T I O N S I T E The deposition site is in proximity to
the maxillary nerve trunk within the pterygopalatine fossa
(see Figure 12-40 •) .
Technique Steps
Apply the basic inj ection steps outlined in Chapter 11 and
summarized in Appendix 1 1-1.
N E E D L E S E L E CT I O N A 25-gauge needle is preferred for
this technique considering the vascularity of the deposi­
tion site as well as the depth of insertion.
Injection Procedure
This technique shares many elements with the PSA nerve
block. An upward needle pathway is achieved when the
clinician angles the syringe barrel downward at a 45-de­
gree angle, away from the occlusal plane of the maxillary
teeth (see Figure 1 2-28) . An inward needle pathway is
achieved when the clinician angles the syringe barrel out­
ward laterally at a 45-degree angle, away from the patient's
midsagittal plane (see Figure 12-34A). A backward move­
ment simply refers to the advancement of the needle to the
deposition site. In short, the syringe will be moved "down
and out" before advancing to depth.
F I G U R E 12-40 Deposition Site for High-Tuberosity
Approach-Maxillary Nerve Blocks. The deposition site for
maxillary nerve blocks is in close proximity to the maxillary
nerve trunk within the pterygopalatine fossa. At optimum
"depth and angle" only approximately -2 mm of a 32-mm
needle shaft will be visible beyond the needle hub. This
will be 30 mm compared with 16 mm for a P SA.
The needle should be inserted to 30 mm and at least
two aspirations should occur in at least two planes and be
confirmed as negative before depositing any solution. A
full cartridge (1.8 mL) is recommended.
It can be helpful to ask patients to close their mouths
half way and shift their mandibles to the side of inj ection.
This improves visibility and access for syringe angulations
in order to achieve upward, inward, and backward move­
ments. Using the retraction hand thumb can add stability
to manage any pressure from the lower lip similar to PSA
nerve blocks; this is demonstrated in Figure 12-33.
Additional visual cues for achieving optimal angula­
tions for maxillary nerve blocks are provided in Figure
12-34. Figure 1 2-35 demonstrates ideal, acceptable, and
incorrect angulations that are similar to the PSA nerve
blocks.
Confirming Anesthesia
Subj ective signs of anesthesia for maxillary nerve block in­
jections include a sense of numbness in the gingiva overly­
ing all of the maxillary teeth on one side, the pulps of the
teeth, the rest of the periodontium, and palatal tissue to
the midline. The upper lip, lateral aspect of the nose, and
inferior eyelid are also numb.
Common Causes of Injection Failure
Common causes of anesthetic failure include deposition
of solution too far from the maxillary nerve and inad­
equate volumes of solution . Impassable obstructions and
penetration of the nasal cavity or orbit and intravascular

deposition are also sources of failure in greater palatine
maxillary blocks. Hematoma formation during high­
tuberosity maxillary blocks and positive aspirations are
common sources of failure. Other causes may include in­
flammation or infection in the area of deposition.
Troubleshooting
Occasionally, obstruction or an inability to open wide
enough makes it impossible to reach adequate depth in
greater palatine maxillary nerve blocks. There is no rem­
edy when either of these occurs other than to use alternate
techniques.
Contact with bone is not expected in tuberosity ap­
proaches. If contact occurs, the pathway should be altered
after fully withdrawing the needle and reassessing the lo­
cation of the maxillary tuberosity and zygoma.
Greater p alatine maxillary nerve blocks generally
have fewer complications compared with high-tuberosity
maxillary nerve blocks. They are, however, potentially
more traumatic (Malamed, 20 13).
B ecause there are numerous alternatives to either of
these inj ections and because almost all of them are more
familiar to clinicians than maxillary nerve blocks, clini­
cians usually have no trouble finding suitable alternatives.
Technique Modifications and Alternatives
The depth of penetration is reduced to prevent over­
insertion in smaller adults. When skeletal anatomy pre­
vents clinicians from establishing an initial insertion angle
at 45 degrees to the midsagittal plane in high-tuberosity
blocks, it may be helpful to begin the inj ection with the
syringe oriented parallel to the maxilla before establishing
ideal angles as the needle is advanced, similar to the PSA
technique.
Alternatives include every other technique listed in
this text for achieving maxillary anesthesia, including PSA,
MSA, ASA, IO, NP, GP, AMSA, infiltration, PDL, intrasep­
tal, intraosseous, and intrapulpal injections when indicated.
Complications
B ecause of its proximity to the pterygoid plexus of veins
and maxillary arteries, the maxillary nerve block injection
has the highest risk of peri-inj ection hematoma formation.
The technique is contraindicated in patients with clotting
disorders or on anticoagulant therapy. Alternate tech­
niques should be used in these instances.
The following are possible risks with the tuberosity
approach (Malamed, 20 13):
Hematoma (vigorous hematoma if the maxillary
artery is nicked)
Infection
The following are p o ssible risks with the greater
palatine foramen approach
Displacement of orbital structures
Diplopia (anesthesia of the sixth cranial nerve)
C HAPT E R 1 2 • I N J E C T I O N S FOR MAXI LLARY PAI N C O NTROL I 241
Retrobulbar block (mydriasis, anesthesia of the
cornea, ophthalmoplegia)
Optic nerve block (transient loss of vision in that
eye is possible)
Infection
Penetration into the nasal cavity
F utu re Perspectives
Intranasal Anesthesia
Nasal delivery of drugs also referred to as intranasal
administration can provide local or systemic effects (see
Figure 12-4 1 ) . Examples of administrations for local effect
include decongestant and allergy medications and nar­
cotics for pain relief following surgery (Shelley &Peach,
2008 ) . Administrations for systemic effect include drugs
for relief of migraine headaches (especially when nausea
precludes oral administration) and, more recently, intrana­
sal flu vaccines (Veldhorst-Janssen, et al. , 2009) . A num­
ber of physicians and dentists use intranasal delivery to
avoid inj ections in children when sedating them (Shelley
&Peach, 2008; Wolfe &Braude, 20 10).
As with other delivery methods, the intranasal route
is not always appropriate; for example, when administer­
ing through nasal mucosa, rapid enzymatic degradation
can result in the deactivation of certain drugs and the rich
vascular supply of the nasal mucosa can lead to undesired
systemic effects for others (Ttirker, Onur, &Ozer, 2004) .
At times, circulatory levels of intranasally administered
drugs have been reported to approach levels seen after
intravenous administration (Ttirker, Onur,&Ozer, 2004).
Undesired effects can also occur when a portion of the
delivered dose is swallowed or bypasses the nasal mucosa
leading to increased uptake via the lower respiratory tract.
To increase retention of drugs on mucosa, specific bioad­
hesive polymers known as mucoadhesives are sometimes
incorporated. These polymers temporarily adhere medi­
cations to mucosa enhancing drug uptake and efficacy
(Shaikh, et al. , 20 1 1 ) . Vasoconstrictors have been added to
prolong drug actions and decrease systemic uptake.
Kovacaine Mist™
A product currently under development for intranasal
anesthesia of a portion of the maxilla, Kovacaine Mist™ ,
is a formulation of an ester local anesthetic and a vaso­
constrictor. The aqueous formulation of Kovacaine Mist™
includes 3% tetracaine (a potent ester anesthetic and early
replacement for the more toxic drug, cocaine), 0.05 % oxy­
metazoline (a vasoconstrictor currently used in some OTC
sprays to relieve nasal congestion) , and mucoadhesives.
The concentration of tetracaine in the formula is predicted
to provide profound anesthesia of the maxillary teeth and
their associated structures including palatal tissues. For
comparison, ophthalmic preparations are typically formu­
lated as 0.5 % , spinal inj ections as 1 % , and popular topical
preparations in dentistry as 2 % .
242 S E C T I O N IV • C LI N I C AL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A

Published Phase 2 clinical trials reported an 83.3 % lidocaine were administered during the study in attempts
success rate with Kovacaine Mist™ intranasal adminis­ to provide profound anesthesia whenever intranasal ad­
trations compared with lidocaine inj ections (93 .3 % ) dur­ ministrations of Kovacaine Mist™ or initial inj ections of li­
ing procedures in which no rescue injection of lidocaine docaine failed to provide profound anesthesia. There were
was required ( Ciancio, et al. , 20 10). Rescue inj ections of five failures of Kovacaine Mist™ to provide profound
anesthesia. However, in one of the five failed attempts,
the subsequent rescue inj ection of lidocaine also failed
to provide profound anesthesia. Success of premolar-to­
premolar (#4-# 1 3 ) anesthesia was demonstrated to be
90 % via intranasal anesthesia (Ciancio, et al. , 20 10).

Kovacaine Mist™ Press Release

In a press release dated February 2 1 , 20 14, St. Renatus,
LLC announced the completion of Phase 3 multisite clini­
cal studies in which they tested the safety and efficacy of
their nasal mist technology in adult and pediatric subj ects
(St. Renatus, 20 14) .
Results of the Phase 3 trials were not available when
this text went to publication.

CASE MANAGEMENT
Elena Gagarin
An i nfiltratio n was a d m i n istered ove r #8 to s u p p l e ­
m e n t t h e ASA b l ock a n d treatment w a s fi n i s h e d i n
comfo rt.
Case Discuss i o n : C ross- i n n e rvati o n fro m t h e
o p pos ite s i d e ASA n e rve p revented a n oth e rwise
effe ctive ASA b l o c k fro m p rovi d i n g co m p l ete a n ­
est h e s i a of # 8 . T h i s v e ry co m m o n p a tte rn of a c ­
cessory i n n e rvation i n t h e maxi l l a ry a nterior a rea i s
easily re m e d i e d with a n i nfi ltration a bove t h e a p ex
of the centra l i n cisor on the s i d e on w h i c h a n esthe­
F I G U R E 12-41 Example of intranasal delivery device. sia is desire d .
Source: Courtesy of St. Renatus, LLC.

.�.h. Ia.P..t.E! r. . 9.l1.� �� .i.e>.fl � . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . d. The needle i s perpendicular t o the long axis o f the
tooth, passing through thick mucosal tissue, dense
1 . Which one of the following statements best describes connective tissues, muscle , and vessels, and past
the needle pathway for an infiltration inj ection microvasculature and nerve endings.
technique? 2. When infiltration inj ections are unsuccessful, it may
a. The needle is parallel to the long axis of the tooth, be helpful to:
passing through thin mucosal tissues to superficial fas­ a. Change the length of the needle and repeat the
cia containing loose connective tissue, and past small injection.
vessels and microvasculature, and nerve endings. b. Visualize, palpate, check radiographs, and reassess
b. The needle is distal to the long access of the tooth, the technique.
passing through thin mucosal tissue to deep fascia c. Establish contact with bone before administering
of connective tissues, and past small vessels, alveo­ one cartridge of anesthetic solution.
lar bone, and nerve endings. d. R e p e a t the s a m e inj ection and d e p o s i t m o r e
c. The needle is parallel to the long axis of the tooth, solution.
passing through thin mucosal tissues to superficial
tissue, and past small vessels, nerves, and bone.

3. The middle superior alveolar nerve is absent in
approximately 28% - 50% of individuals.
a. True
b. False
4. In a typical adult patient, the infraorbital foramen
is approximately 8 to 10 mm below the infraorbital
ridge.
a. True
b. False
5. Which one of the following provides the most accurate
description of the field of anesthesia in a PSA injection?
a. Pulps of the maxillary premolars and molars, and
their facial gingiv a , periodontal ligament, and
alveolar bone on the side inj ected
b. Pulps of the maxillary and mandibular molars on
the side injected
c. Pulps of the maxillary teeth to the midline , and
their facial gingiv a , periodontal ligament, and
alveolar bone on the side injected
d. Pulps of the maxillary molars, except sometimes
the mesiobuccal root of the first molar, and their
facial gingiva, periodontal ligament, and alveolar
bone on the inj ected side
6. Which one of the following is most likely to increase
the risk of hematoma following a PSA nerve block?
a. The needle is inserted too deep or too posterior to
the deposition site on the posterior surface of the
maxilla.
b. The needle is inserted too inferior to the posterior
surface of the maxilla.
c. The porous bony surface of the maxilla allows the nee­
dle to penetrate the maxilla-piercing blood vessels.
d. A long needle is inserted, contacting the bony peri­
osteum on the surface of the maxilla.
Refe re n ces
Blanton, P., & Jeske, A. (2003, June). The key t o profound local
anesthesia-neuroanatomy. Journal of the American Dental
Association, 134, 755-756.
Ciancio, S. G., Hutcheson,M. C., Ayoub, F. , P antera, E. A.,
Jr., P antera, C. T., Galrapo, D. A., et al. (2010). Safety and
Visit www.pearsonhighered.com/healthprofessionsresources to access the student resources that accompany
this book. Simply select Dental Hygiene from the choice of disciplines. Find this book and you will find the
complimentary study tools created for this specific title.
C HAPT E R 1 2 • I N J E C T I O N S FOR MAXI LLARY PAI N C O NTROL I 243
efficacy of a novel nasal spray for maxillary dental anesthe­
sia. Journal of Dental Research, 92(7, Suppl.), S43-S48.
Diggle, L.,Deeks, J. J., P ollard, A. J. (2006). Effect of needle
size on immunogenicity and reactogenicity of vaccines in in­
fants: Randomized controlled trial, British Medical Journal,
333(7568), 571-578.
Fehrenbach, M. J., & Herring, S. W. (2012). Illustrated anatomy
of the head and neck (4th ed. ). St. Louis: Saunders Elsevier.
Flanagan T., Wahl M. J., Schmitt M. M, Wahl J. A (2007). Size
doesn't matter: Needle gauge and injection pain, General
Dentistry, 55(3), 216-217.
Hawkins, J. M., & Isen, D. (1998). Maxillary nerve block: The
pterygopalatine canal approach. Journal of the California
Dental Association, 26 (9), 658-664.
Jastak, J. T., Yagiela, J. A., & Donaldson, D. (1995). Local anes­
thesia of the oral cavity. P hiladelphia: Saunders.
Loestscher, C. A., & Walton, R. E. (1988). P atterns of innerva­
tion of the maxillary first molar: A dissection study. Oral
Surgery Oral Medicine Oral Pathology, 65, 86-90.
Malamed, S. F. (2013). Handbook of local anesthesia (6th ed.).
St. Louis: Elsevier Mosby.
Malamed, S. F., & Trieger, N. (1983). Intraoral maxillary nerve
block: An anatomical and clinical study. Anesthesia Progress,
30, 44--4 8.
Shaikh, R., Raghu, T., Singh, R., G arland, M. J., Woolfson, A.
D., & D onnelly, R. F. (2011). Mucoadhesive drug delivery
systems. Journal of Pharmacy and Bioallied Sciences, 3(1),
89-100.
Shelley, K., & P each, M. J. (2008). The clinical applications of
intranasal opioids. Current Drug Delivery, 5(1), 55-58.
St. Renatus. (2014, February 21). St. Renatus, LLC. , has
completed all planned FDA clinical studies of a nasal
anesthetic for dentistry. P ress Release. Fort Collins, CO:
Author.
Tiirker, S., Onur, E., & Ozer, Y. (2004). Nasal route and
drug delivery systems. Pharmacy World & Science, 26 (3),
137-142.
Veldhorst-Janssen, N. M., Fiddelers, A. A., van der Kuy, P. H.,
Neef, C., & Marcus,M. A. (2009). A review of the clinical
pharmacokinetics of opioids, benzodiazepines, and antimi­
graine drugs delivered intranasally. Clinical Therapeutics,
31 (12), 2954-2981
Wolfe, T. R., & Braude,D. A. (2010). Intranasal medication
delivery for children: A brief review and update. Pediatrics,
126, 532-531
Wong, J. A. (2001). Adjuncts to local anesthesia: Separating fact
from fiction. Journal of the Canadian Dental Association, 67,
391-391
....
t Nerve Block Needle Penetration Site Deposition Site Dose•
Field of Anesthesia (f)
See Appendix 1 2-2 c
Local
infiltration
Extra-short
or short
Height of
mucobuccal fold
Depth of Insertion Antle of lnHrtion 0.6 m l Teeth anesthetized: 3
in jections 25/27/30 buccal to tooth
Needle tip i nserted
to a depth of 3-6 mm
Approximately
20 degrees to long
At i njection site
3
gauge Fig. 1 2-2 OJ
to apex axis of tooth, di rected
toward apex of tooth
bevel toward bone
--<
Target Peridontium/Saft tissues: 0
�
Selected soft tissue, At injection site
g i ngival or apex of tooth
Fig. 1 2-4
�
OJ
Anterior Short Height of Depth of Insertion Aftt le of Insertion 0 . 9- 1 . 2 ml Teeth anesthetized: ><
superior 25/27 gauge mucobuccal fold
Va riable, needle tip Need le di rected Canine, lateral, centra l
alveolar (ASA) above canine
i nserted to a point 25 deg rees medially
Fig. 1 2- 1 1
above apex of canine. bevel toward bone
Target Peridontium/Soft tissues:
Above apex of canine Facial to affected teeth ::::J
'-- ·
Fig. 1 2- 1 2 (J)
Middle
superior
Short
25/27 gauge
Height of
mucobuccal fold
Depth of Insertion
Variable, needle tip
Aftt le of Insertion
Needle di rected
0 . 9- 1 .2 ml Teeth anesthetized:
r
Maxillary emolars
Q.
alveolar (MSA) above the second inserted to a point well 20 degrees medially and mesic uccal root 0
premolar above apex of second bevel toward bone of first molar* ::::J
Fig. 1 2- 1 5 premolar (f)
•For most people
Target Peridontium/Saft tissues:
Well above apex of second premolar. Facial to affected teeth
Fig. 1 2- 1 6
Infraorbital Short or long Height of Depth of Insertion Angle of '-'lion 0.9-1 .2 ml Teeth anesthetized:
(10) 25/27 gauge mucobuccal folder
Va riable, needle tip Needle P.Orallel to long Premolars, cani ne, lateral,
above first
premolar inserted to a �oint axis of tooth bevel central
Fig. 1 2-2 1 lateral to t e toward bone
infraorbital foramen
Target Peridontium/Solt tissues:

Infraorbital foramen Facial to affected teeth

Fig. 1 2-22

* Dose volumes provided are minimum recommendations for pulpal anesthesia. (Continued)
 Field of Anesthesia
Nerve Block Needle Penetration Site Deposition Site Dose•
See Appendix 1 2-2

Posterior Short Height of Depth af I nsertion Angle of Insertion 0.9-1 . 8 mL Teeth anesthetized:
superior 25/27 gouge mucobuccol fold
Needle tip inserted to a Need le advanced Maxillary molars except
alveolar (PSA) above second
depth of 1 6 mm along a path mesiobuccal root of first molar
molar
45 degrees medially
Fig. 1 2-28
to m idsaggital plane,
k
45 degrees su erior
to occlusal p one

Target Peridontium/Soft tissues:

Slightly above and dista l to distobuccal root of Buccal to affected teeth
last molar, second or third if present
Fig. 1 2-29A

Maxillary Long GP foramen Depth af Insertion Angle of Insertion 1 . 8 mL Teeth anesthetized:

nerve block 25 gauge Fig. 1 2-36 Needle tip inserted After pre-anesthesia, Entire hemi-maxi lla
palatal to a depth of 30 mm negotiate the
tuberosity pterygopalatine (GP)
approach canal (if obstructed,
(MxNB) withdraw and use
alternate techn ique)
Target Peridontium/Soft tissues:
Close proximity to the maxillary Entire hemi-maxi lla
nerve trun k with i n the pterygopalatine fossa
Fig. 1 2-37
Maxillary Long Height of Depth af I nsertion Angle of Insertion 1 .8 ml Teeth anesthetized:
nerve block 25 gouge mucobuccal fold
Needle tip inserted Needle advanced Entire hemi-maxilla
high tuberosity opposite the
to a depth ol 30 mm along a path
approach DB cusp of the
45 deg rees medially
maxi llary 2nd
to midsaggital plane,
molar
45 degrees superior to
Fig. 1 2-28
occlusal plane
Target Peridontium/Soft tissues:
Close proxi mity to the maxillary nerve trunk Entire hemi - maxilla
withi n the pterygopalatine fossa
Fig. 1 2-39
• Dose volumes provided are minimum recommendations for pulpal anesthesia.

"'
"'
Ul
Field of Anesthesia
ASA 10

Teeth an esthetized: Teeth an esthetized:

ca n i n e , l atera l , central Maxillary I njections p remolars, canine,

l ate ra l , central

Peridonti um/Soft tissues:

faci a l to affected teeth Peridontl um/Soft tissues:

faci a l to affected teeth

MSA
I nfi ltrati o n
Teeth a nesthetized:

max i l l a ry premolars and Teeth an esthetized :

mesiobuccal root of first molar* at inj ection s ite

* For most people

Pe ridonti um/Soft tissues:

Peridonti um/Soft tissues: at i nj ection s ite

faci a l to affected teeth

PSA

Teeth ane sth e tized :

maxi l l a ry molars except

mesiobuccal root of first molar

Peridonti um/Soft ti ssues: Courtnyof:

b u ccal to affected teeth

Source: Courtesy of LED Dental.

246
OBJECTIVES KEY TERMS

• Define a n d d i sc u ss the key terms in t h i s c h a pter. anterior m i d d l e s u perior

a lveo l a r (A MSA) n e rve
• Descri be a n d d i sc u ss the in d i ca t i o n s , re leva n t a n atomy, a n d
b l ock 254
tech n i q ue featu res o f t h e inject i o n s d i scu ssed i n t h i s c h a pter.
d e ntal p l exus 256
• Descri be the b a s i c tec h n i q ue steps fo r safe a n d effective a d ­ d e p osition site 248
m i n istra t i o n of the fo l l owin g i njecti o n s : G ate Control Theory 250
• N a sopa l at i n e nerve b l ock g reater p a l ati n e (G Ps) n e rve
• P a l ata l (a p p ro a c h ) a n terio r s u peri o r a l veo l a r nerve b l o ck b l ock 260
• Anteri o r m i d d l e su perio r a l veo l a r nerve b l o ck nasopalati n e ( N P) n e rve
b l ock 248
• G reater pa l at i n e nerve b l o ck
need l e pathway 248
p a l ata l anterior s u perior
a lveo l a r (P-ASA) n e rve
b l ock 252
p e n etratio n site 248
p re-a nesthesia 249
p ress u re a n esth esia 250

247
248 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A
CASE ST U DY
Elena Gagarin
E l e n a G a g a r i n was a p p o i nted fo r two-a n d - o n e - h a l f
h o u rs to treat t h e m ax i l l a ry r i g h t q u a d ra n t . S h e
n e e d e d a co m b i n a t i o n o f restorative a n d d e nta l
h yg i e n e t h e ra py a n d o pted to h ave it co m p l eted
i n one a p p o i n t m e n t because of d iffi cu l ty a rra n g ­
i n g h e r a p p o i n t m e nts. A n e st h e s i a w a s n e cessa ry
fo r the entire q u a d rant, i n c l u d i n g the p a l ate. T he re
were n otes of h e r p revi o u s req u ests that p a l ata l i n­
j e ct i o n s be m i n i m ized o r avo i d e d a n d th at, w h e n
necessa ry, s h e wo u l d req u i re n itro u s oxi d e .
S h e s t a t e d t h a t s h e h a d r e q u i re d s o m a n y
sh ots t h e l ast t i m e s h e was in s h e a l m ost ca n ce l e d
t o d a y 's a p p o i n t m e n t . S h e a l s o h a d a g re e d to
s p e a k to h e r d a u g hte r's c l a ss i m m e d iately fo l l ow­
i n g h e r a p p o i nt m e n t a n d was c o n c e r n e d that h e r
l i ps wo u l d be n u m b . S h e re m i n d e d t h e offi ce staff
on a rriva l that s h e wanted fewer s h ots a n d h o p e d
t h e n u m b i n g wo u l d work b ette r t h i s t i m e . T h e of­
fice staff c h ecked t h e record a n d verifi e d that five
i n fi ltrati o n s on t h e l e ft m a xi l l a, i n c l u d i n g two o n
t h e p a l ate, h a d b e e n a d m i n istered d u ri n g h e r l ast
a p p o i nt m e nt.
I ntrod u cti o n
A s discussed i n Chapter 1 1 , "Fundamentals for Adminis­
tration of Local Anesthetic Agents," and Chapter 12, "In­
j ections for Maxillary Pain Control 1," local infiltrations,
field blocks, and nerve blocks are the three basic types of
intraoral inj ections frequently used in dentistry. Additional
relevant terminology introduced in Chapter 12 includes
anatomic landmarks. This chapter will discuss consider­
ations for each palatal inj ection technique and will be pre­
sented in reference to the penetration site, needle pathway,
and deposition site as described in Chapter 1 1 , "Funda­
mentals for Administration of Local Anesthetic Agents."
The penetration site will be related to hard and soft tissue
landmarks. The needle pathway will be described in terms
of the types of tissue that will be penetrated by or located
in the vicinity of the needle, including mucosa, superficial
fascia, muscle, vessels, nerves, and bone. The deposition
site will be described in terms of the tissues at or near the
target and in relation to specific landmarks.
Pa l ata l Injecti o n Tech n i q ues
This chapter will discuss palatal injection techniques. Pala­
tal inj ections are true maxillary injections, usually discussed
with other maxillary techniques. They are separated in this
text because there are common technique considerations
that apply to all palatal procedures that do not apply to
non palatal maxillary techniques. Some of these consid­
erations address the pain that is often associated with
administering palatal anesthesia. Others address unique
challenges presented by palatal anatomy. These consid­
erations and challenges have direct impacts on the safety
and success of palatal techniques. Key elements for each
inj ection discussed are summarized in Appendix 1 3-1.
Common variations and precautions will be discussed
where applicable.
N asopa l ati n e N e rve Block
Nasopalatine (NP) nerve blocks are indicated for pain
management of palatal soft and osseous tissue in the an­
terior third of the palate, approximately from canine to
canine. The NP nerve occasionally provides pulpal anes­
thesia to the central incisors, and the NP block is some­
times needed when traditional methods of anesthetizing
the central incisors fail to provide profound anesthesia
(Blanton&Jeske, 2003). The NP nerve block is also known
as an incisive or sphenopalatine nerve block.
Field of Anesthesia
Anesthesia will affect the structures innervated by the
nasopalatine nerves bilaterally. This field includes struc­
tures located in the anterior one-third of the palate (see
Figure 13-1 • and Appendix 13-2) .
Anatomical Factors
The nasopalatine nerve is the longest branch of the poste­
rior superior nasal branch of the maxillary nerve. It passes
along the nasal septum and descends to the anterior por­
tion of the maxilla. B oth the right and left nasopalatine
nerves exit the maxilla through the incisive foramen. The
fibers innervate the mucosa and osseous tissue of the an­
terior hard palate and palatal gingiva to the mesial aspects
of the first premolars or slightly posterior to that location
because of some degree of overlap with fibers of the right
and left greater palatine nerves. The nasopalatine nerves
occasionally provide pulpal innervation to central incisors,
NP
Teeth eneethetlza d :
none
PerlodonU u m :
palatal t o incisors and canines
F I G U R E 13-1 Field of Anesthesia for N P Nerve Blocks. The
field of anesthesia for NP nerve blocks is indicated by the
shaded area.
 C H APT E R 1 3
as well. When this pattern is present, it is frequently nec­
essary to anesthetize the nasopalatine nerves in order
to provide profound anesthesia of the central incisors
(Blanton &Jeske, 2003).
Technique Factors
The following information describes key factors for suc­
cessful NP nerve block inj ections.
P E N ETRAT I O N S I T E The optimum site of penetration for
the NP nerve block is the palatal mucosa lateral to the
widest anteroposterior dimension of the incisive papilla
(see Figure 13-2 •) .
N E E D L E PAT HWAY The needle advances under the inci­
sive papilla through dense mucosal tissues to contact the
opposite wall of the incisive canal near its entrance.
D E PO S I T I O N SITE The deposition site is near the center of
the incisive canal (see Figure 13-3 •) .
F I G U RE 13-2 P enetration Site for NP Nerve Blocks. The pen­
etration site for NP nerve blocks is indicated by the needle.
FIGURE 13-3 Deposition Site for NP Nerve Blocks. The deposi­
tion site for NP nerve blocks is indicated in the spotlighted area.
• I N J E C T I O N S F O R M AXI LLARY PAI N C O NTROL I I-PALATAL A P P ROAC H 249
Technique Steps
Apply the basic injection steps outlined in Chapter 11 and
summarized in Appendix 1 1-1.
N E E D L E S E L E CT I O N A 27-gauge short needle is recom­
mended and consistent with the minimal penetration
depths required and the low rate of positive aspiration
(less than 1 % ). Some clinicians prefer to use a 30-gauge
short or x-short needle in the palate.
I N JE CT I O N P R O C E D U R E Palatal injections have a repu­
tation for causing discomfort. They can be administered
more comfortably if a technique alteration known as pre­
inj ection anesthesia, also referred to as pre-anesthesia, is
used. Pre-anesthesia may be defined as anesthesia that is
already in effect from previous injections in the area (see
Figure 13-4 •) or a two-step topical method that includes
an initial 1-minute application of topical followed by firm
pressure for a subsequent minute (see Figure 13-5 •) .
(A)
(B)
F I G U R E 13-4 P re-anesthesia Infiltration. A-Step 1, Infiltrate
labial mucosa. B-Step 2, Infiltrate "through" the interdental
papilla tissue. These steps are followed by the penetration under
the incisive papilla (demonstrated in Figure 13-2.)
250 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A
FIGURE 13-5 P re-anesthesia-Topical Anesthetic and P ressure.
The pres sure can b e applied to the tissue with a
cotton-tipped applicator (used to place the topical) or with
a smooth, blunt-ended instrument handle, until blanching
is observed at the penetration site. Pressure anesthesia to
deeper tissues will develop, enhancing patient comfort dur­
ing needle penetration. It is important to apply constant
pressure to the site for a full minute in order to achieve pro­
found pressure anesthesia of deeper tissues. After 1 minute,
continue to maintain constant pressure during the initial
needle penetration, avoiding contact with the applicator.
This two-step method reduces the potential for pain
when penetrating sensitive palatal tissues. A number of
other strategies for decreasing or eliminating discomfort
during palatal inj ections may also be quite useful. Most of
these rely on what is known as the Gate C ontrol Theory
The G ate Co ntro l T h e o ry of P a i n Percepti o n s u g gests that
t h e re a re n e u ro l o g i c a l g ates that c a n b l ock s i g n a l s to t h e
b ra i n . T h e t h e o ry asserts t h a t :
1 . T h e p e rcept i o n of p hys i c a l p a i n is n ot based s o l e l y o n
t h e a ctivati o n of n o c i cepti o n .
2 . The experience o f p a i n is a m o d u l ation between a cti­
vation of l a rg e n o n-pa i n tra nsm itti n g ( n o n - n o ciceptive)
n e rve fi bers a n d s m a l l p a i n tra nsm itti n g (noci ceptive)
n e rve fi b e rs.
3 . T h e a ctivat i o n of l a rg e n o n - n o c i ce ptive fi b e rs can i n ­
te rfe re with s i g n a l s fro m s m a l l n o c i ce ptive fi b e rs .
4. If the sti m u l ation of non-nociceptive fibers is greater t h a n
the sti m u l ation of nociceptive fibers, p a i n w i l l be i n h ib­
ited or b l ocked.
Press u re a n est h e s i a a d m i n istered by p ress i n g fi rm l y
u s i n g a cotto n -t i p p e d a p p l i c a t o r o r s m o o t h i n st r u -
m e n t h a n d l e a g a i nst t h e g i n g iv a l t i s s u e s ca n re d u ce o r
: e l i m i n ate p a i n fro m n e e d l e p u n ct u re s . In a d d it i o n to
: �� � �
pr i ng a
� � � �� � ��� : � : � � : � �:
r se i s i i i y e o te p o r r
• • • • • • • . . . . . • • • • • • • • • • • • .
of Pain Perception, which states that there are certain lo­
cations or gates within the spinal nervous system. When
flooded with impulses from less painful stimuli, impulses
generated from more painful and subsequent stimuli, such
as needle penetrations, can be blocked (Deardorff, 2007).
Box 1 3-1 • provides a more in depth discussion of the
Gate Control theory of pain perception.
Topical anesthetic patches can also be useful for injec­
tion site preparation in palatal techniques. Some may pro­
vide a 4 to 6 mm depth of penetration compared with 2 to
4 mm for standard topical agents.
To gain access to the site of penetration, ask the pa­
tient to tip his or her head up and slightly away, with the
mouth wide open. Penetrate lateral to and at the base of
the broadest anteroposterior aspect of the incisive papilla
(see Figure 13-2 ) . Continue penetrating at a 45-degree
angle under the papilla as demonstrated in Figure 13-7 •·
Advance slowly until the opposite wall of the incisive canal
is contacted. Once bone is contacted, withdraw the needle
-1 mm. The depth of insertion ranges from 4 to 7 mm.
Following neg ative aspirati o n , deposit a minimum of
0.4 mL (a little less than 114 of a cartridge) of an appropri­
ately selected local anesthetic drug (the tissue will usually
blanch to a region extending to the lingual aspects of the
anterior teeth) (see Figure 13-8 •).
In order to avoid discomfort, the rate of deposition
should be reduced to 0.4 mL over 40 seconds. This rate is
significantly slower than the previously mentioned stan­
dard inj ection rate of approximately 1.8 mL over 1 minute
(0.4 mL over about 13 to 14 seconds) and may be thought
of as a palatal rate (3 minutes per cartridge). Very slow rates
for NP blocks and other palatal injections may seem tedious,
a n ox i a , d u l l p ress u res g e n e ra t e d fl o o d n e u r a l g a t e s w i t h
l ess p a i n fu l st i m u l i co m p a re d w i t h n e e d l e p e n etrati o n s .
Two devices d e s i g n e d to g e n e rate G ate C o n t r o l
d e s e n s itizati o n a re t h e V i b raJ e ct® ( M i ltex, I n c, PA)
(se e F i g u res 1 3-6A • and 1 3-6 B •l a n d t h e DentaiVibe
(De nta iVi b e , F L) (see F i g u re 1 3-6C •) . DentaiVibe p ro d u ct
l iterature states that it " . . . sti m u l ate[s] t h e sensory recep­
to rs at the i nj e ct i o n s ite " and V i b raJ ect (see F i g u res 1 3-6A
a n d 1 3-6 B) l iteratu re states that it " . . . b l o ck[s] p a i n fro m
i nj e cti o n s based on the G ate Contro l T h e o ry. " T h e V i b ra ­
J e ct re l i es o n a m otor atta c h e d to a conventi o n a l syri n g e ,
w h i c h g e n e rates ra p i d v i b rations at t h e n e e d l e t i p . Ac­
cord i n g to the p ro d u ct i n s e rt " . . . the h i g h v i b ration of t h e
n e e d l e sti m u l ates n e rve e n d i n gs a n d b l o cks t h e tra n s m is­
sion of p a i n fe e l i n g s to t h e b ra i n . "
Sources: C h u d l e r, C. H . (2007). P a i n a n d w h y i t h u rts. Neuroscien ce
for Kids. http://fa c u lty.wa s h i n gt o n . e d u/ch u d l e r/pa i n . ht m l . (Accessed
Febru a ry 1 , 201 4); V i b r a J e ct LLC, http ://www. v i b raj ect. com/
patients. h t m l . (Acce s s e d F e b r u a ry 1 , 201 4); D e n t a i V i b e . c o m , •
�� ���� � � � : � �� �� : �� �� : � ? ��1�):
ht � e n a v be c ( ce s b a 1
. . . . . ; •
• • • •
 C H APT E R
(A)
(B)
(C)
F I G U RE 13-6 Gate Control Desensitization. A-VibraJect
device attached near needle adaptor. B-VibraJect device at­
tached near finger grip and obscured from view in larger hand.
C - Retraction established with the DentalVibe device.
but the dense tissues of the palate resist deposition and do
not accommodate solution easily. In addition to providing
increased comfort, slow rates also avoid unnecessary tissue
trauma.
13 • I N J E C T I O N S F O R M AXI LLARY PAI N C O NTROL I I-PALATAL A P P ROAC H 251
F I G U R E 13-7 Syringe Angulations. Align the syringe barrel at
a 45-degree angle to the palate.
F I G U R E 13-8 Blanching from the NP Nerve Block. As solu­
tion is deposited, blanching will occur, extending laterally and
lingually to the anterior teeth.
Confirming Anesthesia
Subj ective signs of anesthesia for NP injections include a
sense of numbness of the gingiva on the anterior palate.
Objective signs include a lack of response to gentle stimu­
lation with an instrument and no pain during the proce­
dure in the expected field of anesthesia.
Common Causes of Injection Failure
The most common causes of anesthetic failure include in­
adequate depth of penetration and inadequate volumes of
solution deposited.
Other causes include inflammation or infection in the
area of deposition, inadequate diffusion of solution, and
overlapping innervation by the greater palatine nerve.
Troubleshooting
When NP inj ections are unsuccessful, it is helpful to re­
evaluate by visualizing and reassessing syringe angulations
and depths of penetration as well as volumes of solution
deposited.
252 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A
The NP block may result in unilateral anesthesia if the
opposite wall of the canal is not contacted. This may be
the desired outcome if teeth in only one half of the ante­
rior maxilla are being treated. When the NP nerve block
inj ection technique is followed, bilateral anesthesia will
develop. If this is desired but fails to occur, repeat the pro­
cedure, making sure to meet resistance on the opposite
side of the incisive canal.
Technique Modifications and Alternatives
An alternate method for administering the NP inj ection
uses a multiple inj ection technique. This is sometimes
helpful in children and whenever patients are afraid of
palatal inj ection pain. It is first necessary to infiltrate and
deposit about 0.3 mL of anesthetic near the facial midline
(see Figure 1 3-4A ) . After the midline tissues have been
anesthetized, slow penetration can begin, from the facial
aspect proceeding to the lingual aspect of the interdental
papilla, administering a few drops of solution ahead of the
needle until the palatal tissues have been initially numbed.
This is known as an interpapillary injection (see Figure
13-4B) . After an appropriate pause for soft tissue anesthe­
sia to be effective (30 seconds) , a standard NP inj ection is
administered.
Computer-controlled local anesthetic devices
( CCLADs) are ideal for this type o f inj ection because they
provide electronically regulated, slow rates of inj ection
recommended for all palatal techniques and accomplish
this without causing hand fatigue (Loomer &Perry, 2004;
Sculean, et a!. , 2004) .
When administering 4 % solutions, the total volume
delivered can be reduced by half. This does not affect the
rate of deposition, for example 0.9 mL of a 4% solution
should take the same amount of time to deliver as 1.8 mL
of a 2% solution. For further discussion of CCLADs, see
Chapter 9, "Local Anesthetic Delivery Devices."
PASA
Teeth anHthetlzecl :
central, latera l , canine
ParlodonUum:
t o affected teeth
F I G U RE 13-9 Field of Anesthesia for P -ASA Nerve Blocks.
The field of anesthesia for P -ASA nerve blocks is indicated by
the shaded area.
Complications
The risk of complications following NP injections is minimal.
Complications may include postoperative pain at the site of
injection, hematomas, and postoperative edema. If 1 :50,000
concentrations of epinephrine are used, there is an increased
risk of necrosis due to the vigorous vasoconstriction it pro­
vides, depriving the tissues of oxygen for extended periods.
Pa l ata l Anterior S u perior Alveo l a r
N e rve B l ock
Palatal anterior superior alveolar (P-ASA) nerve blocks
were define d by Friedman and Hochman in the 1990s
as "palatal approach - anterior superior alveolar nerve
blocks" and will be discussed as palatal anterior superior
alveolar nerve blocks (PASANB or P-ASANB ) . They are
indicated for pain management of maxillary anterior sex­
tants and are especially useful in cosmetic procedures that
involve perioperative assessment of "smile lines" and when
public speaking is anticipated after appointments because
they do not usually result in labial numbness or motor dis­
turbances (Friedman &Hochman, 1999; Malamed, 20 13).
Field o f Anesthesia
Anesthesia will affect the structures innervated by the right
and left nasopalatine nerves and the anterior branches of
the ASA nerves, to include the facial and palatal soft and
hard tissues associated with the teeth and the pulps of the
teeth in the sextant (see Figure 13-9 • and Appendix 13-2) ,
although pulpal anesthesia of the canines is more question­
able (Malamed, 20 1 3 ) . Results of one study published in
2004 determined that the success rate of the P-ASA when
using 2% lidocaine with 1:100,000 epinephrine for any of the
anterior teeth resulted in a disappointing 32 % to 58 % . Even
more disappointing results were achieved with 3% mepiva­
caine at 22 % to 38% (Burns et a!., 2004) . As is true of other
 C H APT E R
techniques with low published success rates, such as the 10
nerve block, clinicians who are more familiar with this tech­
nique often experience much higher rates of success.
Anatomical Factors
The right and left nasopalatine nerves and vessels travel
together through the nasopalatine canal. The canal pro ­
vides a pathway for nerves and vessels that supply the entire
anterior palate. Access to the superior portion of the canal
is through the incisive foramen.
Technique Factors
The following information describes key factors for suc­
cessful P-ASA nerve block inj ections.
This inj ection is performed similar to the NP technique,
with an important exception. Rather than deposit solution
shortly after meeting resistance on the opposite wall of the
canal, the barrel is adjusted to a steep angle relative to the
wall once contact has been confirmed (see Figure 13-6).
The needle is then advanced up the canal approximately 6
to 10 mm, parallel to the inclination of the roots of the cen­
tral incisors using the opposite wall as a guide.
PEN ETRATION SITE The optimum site of penetration for the
P-ASA is the palatal mucosa lateral to the widest antero­
posterior dimension of the incisive papilla (see Figure 13-2).
N E E D L E PAT HWAY The needle advances under the inci­
sive papilla through dense mucosal tissue, to contact the
opposite wall of the incisive canal just below the foramen.
From this point, the needle advances superiorly into the
canal until penetrated to depth (see Figure 13-10 •) .
D E PO S IT I O N S ITE The deposition site i s within the incisive
canal at a penetration depth of approximately 6 to 10 mm
(Malamed, 20 13) (see Figure 13-1 1 •) .
Technique Steps
Apply the basic injection steps outlined in Chapter 11 and
summarized in Appendix 1 1-1.
FIGURE 13-10 Needle P athway for P -ASA Nerve Blocks. The
needle pathway for P -ASA nerve blocks is indicated by the needle.
13 • I N J E C T I O N S F O R M AXI LLARY PAI N C O NTROL I I-PALATAL A P P ROAC H 253
F I G U R E 13-11 Deposition Site for P -ASA Nerve Blocks. The
deposition site for P -ASA nerve blocks is indicated in the spot­
lighted area.
N E E D L E S E L E CT I O N A 27-gauge short needle is recom­
mended. This is consistent with the moderate penetration
depths required and the low rate of positive aspiration
(assumed to be less than 1 % ) in P-ASA nerve blocks
( M alame d , 20 1 3 ) . Some clinicians prefer a 3 0 - gauge
x-short needle, although extra-short needles may lack suf­
ficient length to reach the target area.
I N JE CT I O N P R O C E D U R E D iscomfort a s s o ciated with
palatal inj ections can be significantly reduced when pre­
anesthesia is used. This can be achieved by applying a topi­
cal drug followed by physical pressure. Follow the two-step
method, beginning with a 1-minute application of topical
anesthetic. Topical patches may have added benefit when
used with P-ASA nerve blocks because of the significant
sensitivity often experienced in this area of the mouth.
To gain access to the site of penetration, ask patients to
tip the head up and slightly away, opening the mouth wide.
The penetration site is lateral to the incisive papilla. The an­
gle of penetration should be adjusted to one that is parallel
to the roots of the central incisors after initial bony contact
on the opposite wall of the canal. The angle of insertion is
approximately 45 degrees to the palate on a line that will
enter the nasopalatine canal (see Figure 13-12A •) . Admin­
ister a few drops of solution ahead of the needle. Advance
the needle slowly, 1 to 2 mm every 4 to 6 seconds, to an inser­
tion depth of 6 to 10 mm (see Figure 13-12B •) . Following a
negative aspiration at the deposition site, deposit a minimum
of 1.4 mL (a little over 2/3 of a cartridge) of an appropriately
selected local anesthetic drug.
D E PO S I T I O N RATE M O D I FI CATI O N The rate of deposition
is modified for this inj ection to 0.5 mL over 60 seconds
(Malamed, 20 1 3 ) . Note that this rate is even slower than
the previously described palatal inj ection rate of approxi­
mately 1.8 mL over 3 minutes.
2 54 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A
(A)
(B)
F I G U R E 13-12 A-Syringe Angulations. Align the syringe
barrel approximately 45 degrees to the palate. B-Insertion
into the Incisive Foramen. Before deposition for P -ASA nerve
blocks, the needle is advanced into the incisive foramen.
Confirming Anesthesia
Subj ective signs of anesthesia for P-ASA inj ections in­
clude an immediate sense of tightness and numbness of
the gingiva on the anterior palate following inj ection. Ob­
jective signs include a lack of response to gentle stimula­
tion with an instrument and no pain during the procedure
in the expected field of anesthesia.
Common Causes of Injection Failure
In addition to a lack of familiarity with the technique, the
most common causes of failure include inadequate depths
of penetration and inadequate volumes of solution de­
posited. In one study of the efficacy of this technique, the
results were quite disappointing, approaching 5 8 % at best
(Burns et al., 2004) . Although this procedure failed to pro­
vide profound anesthesia more frequently than any other
technique described in this text, those more familiar with
it have experienced greater rates of success.
Other causes of failure include inflammation or infection
in the area of deposition, inadequate diffusion of solution,
and overlapping innervation by the greater palatine nerve.
Troubleshooting
When P-ASA inj ections are unsuccessful, it is helpful to
reevaluate by visualizing and reassessing syringe angula­
tions and depths of penetration, and by reconsidering vol­
umes of solution deposited.
Technique Modifications and Alternatives
The use of a CCLAD is ideal for this type of injection be­
cause it provides a controlled, continuous, and slow rate of
deposition.
When administering 4% solutions in the palate, the
maximum volume delivered should be reduced to half of
what is normally deposited with other drugs, because each
cartridge of any 4 % drug has the same amount of drug as
one full cartridge of any 2% drug. The rate of deposition
is also important. A 4% solution should be administered
no faster than half the rate of any 2 % or 3 % solution
(note that this represents the total milligrams of drug ad­
ministered per minute, compared with 2 % solutions). This
means that a maximum of one-half of a cartridge of 4 %
articaine, compared with one cartridge o f 2 % lidocaine,
should be administered no faster than over a full 3 minutes
in the palate, regardless of the technique.
Alternatives to the P-ASA include bilateral ASA
blocks, bilateral IO blocks with an NP injection, and bilat­
eral AMSA blocks (Malamed, 20 13).
Complications
The risk of complications following P-ASA inj ections is
minimal. These may include postoperative pain at the site of
injection, hematoma, infection, and edema. When high con­
centrations of vasoconstrictors are used, necrosis is possible.
Anterior M i d d l e S u perior Alveo l a r
N e rve B l ock
Anterior middle superior alveolar (AMSA) nerve blocks
are indicated for pain management of the incisors, canine,
and premolars on the side anesthetized as well as palatal
tissue from the midline through the molars and the buccal
periodontium of the pulpally affected teeth (Friedman &
Hochman, 1998; Malamed, 20 13). A significant benefit of
this technique is that it reduces the number of injections and
therefore the total volumes of solution necessary to achieve
the same field of anesthesia as traditional ASA/IO, MSA,
NP, and GP approaches. In addition, the typical lack of labial
anesthesia in AMSA blocks allows for normal patterns of
speech and facial expression (Friedman&Hochman, 200 1).
Although e arly literature raised doubts about the
AMSA's efficacy, both its subsequent adoption by clini­
cians around the world and recent research provide strong
evidence that the AMSA not only works as described but
that it does so with the promised efficiency of one inj ec­
tion replacing multiple inj ections ( Corbett et al. , 20 1 0 ;
Patel, et al. , 2 0 1 2 ; Yenisey, 2009). A recent study compar­
ing the AMSA to the infraorbital (IO) nerve block found
 C H APT E R 13 • I N J E C T I O N S F O R M AXI LLARY PAI N C O NTROL I I-PALATAL A P P ROAC H 255

Table 1 3-1 Benefits of the A M SA Tec h n i q u e

Traditional Approach A M SA Approach

Requires 4 to 5 injections Requires 2 injections

Option 1: ASA,MSA, P SA, N P, G P P SA, AMSA
5 penetrations 2 penetrations
Option 2: IO, P SA, N P, G P
4 penetrations

Anesthesia to associated labial tissues Typically no anesthesia to associated labial tissues

Useful for cosmetic dental procedures (does not interfere with "smile line")

Total drug dose varies 2 to 3 cartridges Total drug dose varies 121.3 to 2 cartridges
Reduce total local anesthetic and vasoconstrictor drugs administered

Significant post-op labial anesthesia Minimal to no residual post-op labial anesthesia Important to
patients in public speaking roles

that success rates for AMSA nerve blocks were signifi­

cantly higher than for 10 blocks. At 75 % to 85.7 % , they
were found to approach accepted success rates for inferior
alveolar nerve blocks (Corbett et a!. , 20 10). The benefits
of AMSA nerve blocks over other techniques are summa­
N e it h e r t h e ASA n o r M SA n e rve p rovides l a b i a l soft t i s s u e
rized in Table 13-1 •· i n n e rvati o n . S e n s o ry i n n e rvat i o n of t h e m axi l l a ry l a b i a l
tissues is p rovided b y term i n a l b r a n c h es o f t h e i nfra o r­
Field of Anesthesia b i t a l ( u p p e r l i p) a n d zyg o m ati cofa c i a l n e rves (s k i n of t h e
Anesthesia will affect the structures innervated by the ASA c h e e k) . T h e s e a re a l so b r a n c h es of t h e m axi l l a ry (V2) d iv i ­
nerve, the MSA nerve, the nasopalatine nerve, and terminal s i o n of t h e tri g e m i n a l (V) n e rve a n d a re u s u a l ly a n esthe­
branches to include the pulps of the central and lateral inci­ tized when oth e r i nj e ct i o n tech n i q u es, s u c h as i nfi ltrat i o n s
sors, canine, and premolars on the anesthetized side. It is im­ a n d A S A o r M SA n e rve b l o c ks, a re u s e d to a n esthetize
portant to note that the AMSA injection does not typically
provide labial anesthesia (Friedman &Hochman, 20 0 1 )
� � � � :� � � ���h
.
t
.
a �� y t
. • :
• • • • • • • • • • • • • • • • • • • • • • • • Ji
(see Figure 13-13 •, Appendix 13-2, and Box 13-2 •) .

AMSA
Teeth anesthetized:

centra l , canine,

lateral, premolars

Periodonti u m :

t o incisors and premolars,

palatal to molars

F I G U RE 1 3-1 3 Field of Anesthesia for AMSA Nerve Blocks.

The field of anesthesia for AMSA nerve blocks is indicated by the
shaded area.
256 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A

Anatomical Factors
The median palatine suture and its overlying raphe appear
to inhibit the diffusion of solution to the opposite side of
the palate. Palatal bone is porous and has multiple nutrient
canals through which solution easily diffuses to the dental
plexus of the ASA and MSA nerves (Malamed, 20 13). The
region of the maxillary plexus is demonstrated in Figure
13-14 •· Diffusion through porous palatal bone is enhanced
by gentle hydraulic pressure that develops when solution is
deposited within tightly bound palatal tissues (Baker, 2010;
Pansky&Gest, 20 14) .

Technique Factors
The following information describes key factors for suc­
cessful AMSA nerve block inj ections.

P E N ETRAT I O N S IT E The optimum site of penetration for

AMSA injections is located between the premolars approxi-
mately halfway along an imaginary line drawn from the me- (A)
dian palatine raphe to the gingival margin on the side to be
anesthetized. This can also be described as the junction be-
tween the vertical and horizontal aspects of the palate di-
rectly above the free gingival margin between the maxillary
premolars on the side to be anesthetized (see Figure 13-15 •).

N E E D L E PAT H WAY The needle p athway is very short,

through dense palatal tissue directly to bone.

D E PO S I T I O N SITE The deposition site is near the junction

of the vertical alveolar process and the horizontal palatal
process (see Figures 13-15 and 13-16 •) . Note that if the
ideal site does not have enough tissue thickness to accom­
modate solution, a nearby site with greater thickness may
be chosen. This can be determined by probing the chosen
area with a cotton-tipped applicator (see Figure 13-17 • ) .
(B)
F I G U R E 13-15 P enetration Site for AMSA Nerve Blocks. The
penetration site for AMSA nerve blocks is at the junction of the
horizontal and vertical aspects of the palate (A) and is indicated
by the needle (B).

Technique Steps
Apply the basic injection steps outlined in Chapter 11 and
summarized in Appendix 1 1-1.

A 27-gauge needle is recommended

N E E D L E S E L E CT I O N
(Malamed, 20 1 3 ) . A 27-gauge short needle is most com­
monly used, although some clinicians prefer a 30-gauge
x-short. Considering the limited depths of penetration
required as well as the low risk of intravascular inj ection
(positive aspiration less than 1 % ) , 30-gauge x-short needles
are appropriate.

I N JE CTI O N P R O C E D U R E As previously discussed with the

NP and P-ASA nerve blocks, discomfort associated with
palatal injections can be reduced significantly with the use
F I G U R E 13-14 Maxillary Dental P lexus. The maxillary dental of pre-anesthesia. This can be achieved by applying the
plexus is highlighted along the apices of the maxillary teeth. two-step method of topical anesthesia already discussed.
 C H APT E R 13 • I N J E C T I O N S F O R M AXI LLARY PAI N C O NTROL I I-PALATAL A P P ROAC H 257

(A)
F I G U R E 13-16 Deposition Site for AMSA Nerve Blocks.
The deposition site for AMSA nerve blocks is indicated in the
spotlighted area.

Some clinicians prefer topical patches for inj ection site

preparation for AMSA inj ections.
Ask the patient to tip the head up and slightly away,
opening the mouth wide. The angle of insertion is approx­
imately 45 degrees to the palate with the syringe barrel
positioned over the opposite side of the mouth and the
bevel facing bone. This is demonstrated in Figure 13-18 •·
Advance slowly until resistance is met (contact with
bone). The insertion depth is variable, often no more than
enough penetration to bury the bevel of the needle in tis-
sue. After a negative aspiration, deposit a minimum of 0.9 (B)
to 1.2 mL (112 to 2/3 of a cartridge) of an appropriate 2 % ....-----=--..,
or 3 % local anesthetic drug at a rate not to exceed 0.6 mL
per minute. When administering a 4 % drug, it was men­
tioned in the previous edition of this text that no more

F I G U RE 13-17 Determining Tissue Thickness at AMSA
Deposition Site. Adequate tissue thickness to accommodate
solution can be determined by probing the chosen area with a
cotton-tipped applicator.
(C)
F I G U R E 13-18 Insertion Angulations for AMSA Nerve
Blocks. The angle of insertion is approximately 45 degrees to
the palate with the syringe barrel over the opposite side of the
mouth. A-P enetration with a standard, manual syringe. B ­
P enetration with a Wand CCLAD handpiece. C-For access,
ask the patient to tip the head up and slightly away, opening the
mouth wide.
258 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A

It is n ot u n co m m o n to m o d ify deposition rates fo r the a d m i n - return t o n o rm a l co l o rati o n fro m a sta rk wh ite a p pe a ra n ce

istrati o n of local a nesthetics in some situ ati ons. I n the A M SA
n e rve b l o ck, for exa m p l e , a l a rge vo l u m e of s o l ution m ust be
deposited i nto tig htly b o u n d , fibrous p a l atal tissues. These
tissues resist the vo l u m es sometimes necessary to a c h i eve
profo u n d a n esth es i a . Altho u g h the m i n i m u m deposition rate
of 1 .8 m l in m ost l ocations has been descri bed as 1 m i n ute
(60 secon ds), i n the A M SA tech n i q u e this rate is slowed to ;o,3
m i n utes (see F i g u re 1 3-1 9 •l. When 4% sol utions a re a d m i n -
istered, the time fo r e q u a l vo l u m es o f s o l ution t o be depos-
ited s h o u l d be d o u b l ed; fo r exa m p l e , depositi n g 0.9 m l of
a rtica i n e s h o u l d take a m i n i m u m of 3 m i n utes.
T h e p revi o u s l y described rate s h o u l d be re g a rd e d a s
a sta rt i n g p o i n t i n determ i n i n g t h e i d e a l rate of deposition
fo r each i n d ivi d u a l A M SA b l ock. To determ i n e t h e a ctu a l
rate fo r a n i n d ivid u a l patient i n a spe cific a rea of the pal-
a t e , it is n e cessary to determ i n e w h eth e r o r n ot s o l ut i o n is
b e i n g deposited too q u ickly by observi n g fo r tiss u e b u l g -
ing and excess ive b l a n c h i n g . If either occu rs, conti n u e with
•
t h e depositi o n o n ly a ft e r p a u s i n g to a l l ow fo r d iffu s i o n a n d
w h e n t h e re is excessive b l a n c h i n g . T h i s re d u ces tiss u e i n -
j u ry fro m stretc h i n g and a l l ows n o rm a l blood flow to retu rn
to the a r e a . In e i t h e r i nsta nce, w h e n deposition res u m es,
the rate s h o u l d be s l owed fro m the p revi o u s rate (l ess t h a n
1 .8 m l per 3 m i n utes fo r 2% or 3% d ru gs) .
Alth o u g h excessive b l a n c h i n g s h o u l d be avo i d e d , it
is i m p o rtant to observe l i g ht b l a n c h i n g i n t h e p a l ate be-
c a u s e it confi rms that t h e resist i n g tissues a re n e a r i n g t h e i r
l i m it fo r acco m m o dati n g s o l u t i o n (see F i g u re 1 3-20A •l.
T h i s g e ntly forces the s o l ution in m e d i a l , l atera l , a nterior,
and poste r i o r d i recti o n s , a n d , i m p o rtantly, i nto the p a l a -
ta l b o n e . D e p os ited s o l u t i o n t h e reafter wi l l be d i ffu s i n g
t h ro u g h b o n e at the de positi o n site, i nto t h e m a xi l l a ry
d e n t a l p l exus, a n d progress i n g t h ro u g h out t h e soft tissues
of the e n t i re h a lf o f t h e p a l ate ove rlyi n g the affected s i d e
o f the m a xi l l a ry b o n e . As the s o l u t i o n d iffuses t h ro u g h the
m a xi l l a ry d e n t a l p l exus t o t h e b u cca l aspect o f t h e a lveo-
lar p rocess, b l a n c h i n g c a n be observed f rom the p a l at a l ,
o cc l u sa l , a n d b u cc a l vi ews (see F i g u res 1 3-20A, 1 3-20 8 •. •

� �� �: �� �� � � : �� � �� :� : ��� � �� ��� � � �:
a r i th s l u i r a as o l i a n 1 3 oc
: . . . . . . . • • • • • • • • • . . . �);
. . • • • • • • • • • • • • • • • • • • • • • • • • • • • • •
than 0.7 to 0.9 mL of solution should be deposited to lessen
the risk of toxicity to the nerves. In light of a review by the
Pharmacovigilance Working Party of the European Union
that investigated the incidence of dental-related paresthe­
sia in 57 countries where it is estimated that 100 million pa­
tients receive articaine annually, it is not at all clear that this
modification is necessary (Malamed, 20 13; Stenver, 20 1 1 ) .
The report conclude d that t h e " o ccurrence of sensory
impairment is apparently slightly more frequent follow­
ing the use of articaine and prilocaine. However, consider­
ing the number of patients treated, sensory impairments
rarely occur." Slow deposition of all 4% solutions in the
palate, no more than 0.3 mL per minute continues to be
recommended by the authors of this text. This translates to
0.9 mL over 3 minutes. Note that this rate is much slower
than the standard inj ection rate of 1.8 mL over 3 minutes
for 2% and 3 % drugs. CCLADs are especially safe and
effective for palatal administrations of local anesthetics
and are strongly recommended for AMSA nerve blocks.
If the tissues swell or excessive blanching is noticed (a
stark white appearance) , slow deposition rates even more
until no swelling and only pale blanching are seen (see
Box 13-3 •).

Confirming Anesthesia
Subj ective signs of anesthesia for AMSA inj ections include
an immediate sense of tightness and numbness of the palatal
tissues and periodontium from the central incisors through
the second molar on the side of injection and a numb sensa­
tion in the teeth from the central incisor to the second pre­
molar on the same side. Obj ective signs include a lack of
F I G U RE 13-19 Deposition Rate for AMSA Nerve Blocks.
Although the standard deposition rate has been described previ­
ously as 1.8 mL over a period of 1 minute (60 seconds), in the
AMSA technique this rate is increased to 3 minutes (approxi­
mately the time lapsed on a standard egg timer).
 C H APT E R
F I G U R E 13-20A P alatal blanching with AMSA nerve
blocks may develop between the anterior midline and the
first molars.
F I G U RE 13-20C As solution continues to diffuse through the
maxillary plexus, blanching with AMSA nerve blocks may be
visible from the buccal aspect of the teeth.
response to gentle stimulation with an instrument and no
pain during procedures in the expected field of anesthesia.
Com mon Causes of Injection Failure
The most common causes of failure include inadequate
depths of penetration and inadequate volumes of solution
deposited. Inexperience with the technique also decreases
success rates, initially.
Other causes include inflammation or infection in the
area of deposition and inadequate diffusion of solution. In­
adequate anesthesia of the incisors may occur because of
overlapping innervation by the contralateral ASA nerve.
Troubleshooting
When AMSA inj ections are unsuccessful, it is helpful to re­
evaluate by visualizing and reassessing syringe angulations
13 • I N J E C T I O N S F O R M AXI LLARY PAI N C O NTROL I I-PALATAL A P P ROAC H 259
F I G U R E 13-208 As solution diffuses into theMaxillary P lexus,
blanching with AMSA nerve blocks may be visible from the
occlusal aspect of the teeth.
F I G U RE 13-200 Blanching with AMSA nerve blocks. This
pattern of blanching followed the delivery of 1 .2 mL of a 2%
local anesthetic solution for an AMSA nerve block. Note the lim­
ited anterior blanching. Re-penetration more distal is indicated.
and depths of penetration, as well as volumes of solution
deposited. Penetration site selection is slightly more vari­
able compared with most other techniques. Understanding
this variability can be crucial to success. Sites that provide
adequate tissue thickness, for example, can accommodate
solution much more readily than supposedly ideal sites. If
an ideal site appears to lack adequate thickness, an adj acent
site that is thicker is not only acceptable but preferable.
Inadequate anesthesia of incisors may occur because
of overlapping fibers of the contralateral ASA nerve. An
infiltration over the same side central incisor will anesthe­
tize these overlapping fibers.
If solution is flowing in only one direction from the
penetration site, posteriorly for example, it may be neces­
sary to allow the diffusion to reach the molars in that case
(see Figure 1 3-20D •) (follow the blanching to confirm)
260 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A
and then withdraw and choose a slightly more anterior
penetration site. Once negative aspiration has been con­
firmed, blanching should be seen progressing anteriorly.
Technique Modifications and Alternatives
Computer-controlled local anesthetic delivery (CCLAD)
devices are ideal for this type of inj ection because they
provide controlled, continuous, and slow rates of deposi­
tion. At least one study has indicated higher success rates
when these devices are used compared with conventional
syringes (Lee et al. , 2004) .
A previous edition of this text suggested that when
administering 4% solutions the total volume delivered
should be reduced to no more than 0.9 mL because of the
potential for paresthesia. Although the evidence is unclear
at this time, this modification may not be necessary. This
does not affect the rate of deposition (no less than 3 full
minutes for 1/2 cartridge of any 4% drug).
Excessive blanching, more commonly seen when
administering higher concentrations of epinephrine
( 1 :50,0 0 0 ) , should be avoided. Failure to notice and re­
spond to the color of the tissue as it lightens can result in
postoperative pain and possible necrosis.
The AMSA may be used as an alternative to the ASA,
IO, MSA, GP, and NP nerve blocks, as well as multiple
infiltrations.
C O M P L I CAT I O N S The risk of complications following
AMSA inj e ctions is minimal. These may include post­
operative p ain at the site of inj ection , hematoma, and
postoperative edema. When high concentrations of va­
soconstrictors are used, necrosis is possible. Some indi­
viduals experience an intense burning sensation during
deposition of AMSA blocks, regardless of the drug used.
This reaction contraindicates the use of AMSA nerve
blocks in these individuals.
GP
Teeth anesthetized:
none
Periodonti u m :
palatal tissues of
posterior teeth
FIGURE 13-21 Field of Anesthesia for GP Nerve Blocks. The field
of anesthesia for GP nerve blocks is indicated by the shaded area.
G reate r Pa lati n e N e rve B l ock
Greater palatine (GPs) nerve blocks, also referred to as
anterior palatine nerve blocks, are indicated for pain man­
agement of palatal soft and osseous tissues distal to the ca­
nine in one quadrant.
Field of Anesthesia
Anesthesia will affect the structures innervated by the
greater palatine nerve and its terminal branches to include
the posterior portion of the hard palate and its overlying
soft tissues, anteriorly as far as the first premolar and me­
dially to the midline (Malamed, 20 13) (see Figure 13-22 •
and Appendix 13-2) .
Anatomical Factors
The greater palatine nerve branches from the maxillary nerve
within the pterygopalatine fossa before traveling inferiorly
through the pterygopalatine canal. It exits the canal through
the greater palatine foramen on the hard palate of the max­
illa. The foramen is located at the junction of the alveolar
process of the maxilla and the palatine bone. The greater pal­
atine nerve innervates one side of the posterior portion of the
hard palate and its overlying soft tissues. It travels anteriorly
as far as the first premolar and medially to the midline. Ter­
minal fibers overlap the nasopalatine nerve anteriorly.
The location of the greater palatine foramen is variable
but can usually be noted palatal to the apices of the second
and third maxillary molars, depending on the size and age of
the patient. The position may be more posterior than com­
monly expected. In children, it is often found anterior to
typical adult locations, close to the second primary molar.
Anesthesia of the soft palate is not uncommon because
the lesser palatine nerve and foramen are located immedi­
ately posterior to the greater palatine foramen and may be
anesthetized inadvertently when the GP nerve is anesthetized.
 C H APT E R
FIGURE 13-22 P enetration Site for G P Nerve Blocks. The
penetration site for G P nerve blocks is indicated by the needle.
Technique Factors
The following information describes key factors for suc­
cessful GP nerve block inj ections.
P E N ETRAT I O N S I T E The optimal penetration site for GP
nerve blocks is in the p alatal soft tissue slightly ante­
rior to the greater palatine foramen, at the anterior bor­
der of the depression formed by the foramen. The angle
of insertion is perpendicular to the palatal bone at the
foramen, with the syringe barrel near the lower lip (see
Figure 1 3-22 •) .
N E E D LE PATHWAY The needle advances slowly for 4-10 mm
through dense mucosal tissue to make gentle contact with
bone. Small vessels and capillaries are present in the tissue.
D E POSITION SITE The deposition site is anterior to the open­
ing of the anterior palatine foramen (see Figure 13-23 •).
F I G U R E 13-23 Deposition Site for GP Nerve Blocks. The depo­
sition site for GP nerve blocks is indicated in the spotlighted area.
13 • I N J E C T I O N S F O R M AXI LLARY PAI N C O NTROL I I-PALATAL A P P ROAC H 261
FIGURE 13-24 Locate the Optimum GP Nerve Block P enetra­
tion Site. Use a cotton-tipped applicator to gently palpate the pos­
terior palate near the apices of the second molar. This site will be a
soft spongy depression over the greater palatine foramen.
Technique Steps
Apply the basic injection steps outlined in Chapter 11 and
summarized in Appendix 1 1-1.
A 27-gauge short needle is recom­
N E E D L E S E L E CT I O N
mended for this inj ection, consistent with the minimal
penetration depths required and a low positive aspiration
rate (less than 1 % ) (Malamed, 20 13). A 27-gauge short or
a 30-gauge short or x-short needle is commonly used.
I N J E CT I O N P R O C E D U R E As previously discussed with all
palatal inj ections, discomfort associated with palatal in­
jections can be significantly reduced with the use of pre­
anesthesia. Apply the two-step method of topical anesthesia.
To gain access to the site of penetration, ask the pa­
tient to tip the head up and slightly away, opening the
mouth wide. To locate the penetration site (a soft spongy
depression over the greater palatine foramen) use a cot­
ton-tipped applicator to gently palpate the posterior palate
near the apices of the second molar (see Figure 13-24 •) .
The penetration site i s located a t the anterior aspect o f the
depression. Advance slowly until bone is contacted. Once
resistance has been met, withdraw the needle 1 mm. The
depth of insertion ranges from 4 to 6 mm and sometimes
up to 10 mm. Following a negative aspiration, deposit
a minimum of 0.45 mL ( 1 14 of a cartridge) of an appro­
priately selected local anesthetic drug (blanching and
palatal "sweating" around the needle are common during
deposition) .
D E PO S I TI O N RATE The rate of deposition for this in­
jection is 0.4 mL over 30 seconds or approximately 1.8 mL
over 2 minutes.
Confirming Anesthesia
Subj ective signs of anesthesia for GP nerve block inj ections
include an immediate sense of tightness and numbness of
the gingiva on the same side posterior palate following
262 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A

inj ection. Obj ective signs include a lack of response to Technique Modifications and Alternatives
gentle stimulation with an instrument and no pain during Although rarely administered in young children, when a
the procedure in the expected field of anesthesia. decision is made to perform the GP in children, the fora­
men will be located posterior to all the erupted teeth if
Common Causes of Injection Failure only primary teeth are present.
The most common causes of inadequate anesthesia include Alternatives include the AMSA, palatal infiltrations,
deposition of solution that is too shallow, too lateral, or too PDL inj ections around the teeth to be treated, and maxil­
medial to the foramen as well as inadequate volumes of lary blocks.
solution.
Other causes include inflammation or infection in the Complications
area of deposition. The risk of complications is minimal with this technique.
Post-procedural lesions such as herpes ulcerations are not
Troubleshooting uncommon in the palate but more frequent in anterior
When adequate anesthesia is not achieved, reevaluation is areas. Hematomas are possible, although infrequent, and
indicated. Start by visualizing, palpating, and reassessing sy­ tend to be minimal when they occur. Although infrequent,
ringe angulations and depths of penetration, as well as vol­ ischemia and necrosis occur with greater frequency in the
umes of solution deposited. Repeating the injection is almost palate than elsewhere in the mouth. They usually require
always sufficient if profound anesthesia is not established. no more than palliative therapy.

CASE MANAGEMENT
Elena Gagarin
Because of h e r prior experien ce, a PSA b l ock was a d ­
m i n iste red a l o n g with a n A MSA n e rve b l o c k d u ri n g
n itro u s oxi d e a d m i n istrati o n . 2 . 8 m l o f 2% l i d o ca i n e
w i t h 1 :100, 0 0 0 e p i n e p h r i n e w e re a d m i n istered fo r
both (56 m g of l i d o ca i n e or a b o u t o n e - a n d - o n e - h a l f
ca rtr i d g es a n d 0 . 02 8 m g o f e p i n e p h ri n e ) .
Case Discussion: Diffusion o f a n esth etic s o l uti o n s
t h ro u g h m a xi l l a ry b o n e is u s u a l ly q u ite effe ctive b ut
is n o t as effi c i e n t i n s o m e i n d iv i d u a l s . T h i s was t h e
case fo r M s . G a g a r i n . PSA n e rve b l ocks, because they
d i rect l y expose t h e n e rve m e m b r a n es to a n esth et i c
s o l utions, a re exce l l e n t a ltern atives to i nfi ltrati ons fo r
a n esthesia of m a xi l l a ry m o l a rs . The A MSA b l o c k p ro­
vides p u l pa l and periodonta l a n esthesia of the rest of
the teeth i n the q u a d ra n t as we l l as n e a r l y a l l p a l a ­
ta l tiss u e s i n t h e q u a d ra n t . T h e n u m b e r o f i nj e cti o n s
i s re d u ce d i n t h i s p l a n b e c a u s e o n l y t w o a re n e ces­
s a ry to p rovi d e e q u iv a l e n t a n esth e s i a to oth e r co m ­
b i n at i o n s of i nfiltrati o n s o r b l ocks of a h e m i - m axi l l a .
M s . G a g a r i n was p l eased afte rwa rd th a t h e r s p e e c h
w a s u n a lte red b e c a u s e n e i t h e r t h e P S A n o r A MSA
n e rve b l ocks typ i ca l ly a n esthetize t h e l a b i a l tissues .

.�.h. c:l. P..t.� r. 9.lJ.��� .i.C>.rl �

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0
3. The AMSA technique can provide anesthesia for
areas traditionally anesthetized by which one of the
1 . Which one of the following statements best describes following groups of inj ections?
the deposition site for a nasopalatine nerve block? a. ASA, MSA, PSA, NP, and GP
a. The deposition site is within the nasopalatine canal. b. ASA, MSA, NP, and GP
b. The deposition site is near the wall of the incisive canal. c. PSA and GP
c. The deposition site is anterior to the opening of the d. NP and MSA
anterior palatine foramen. 4. Which one of the following statements is true of NP
d. The deposition site is near the junction between the nerve blocks?
vertical alveolar process and the horizontal palatal a. They have the highest rate of positive aspiration in
process. the palate.
2. The most common cause of failure for palatal injec­ b. They have the second-highest rate of positive aspi­
tion techniques is: ration in the palate.
a. Solution is deposited too far from the associated c. They provide more durable anesthesia compared
bone or foramen. with other palatal techniques.
b. Inadequate volumes of solution are deposited. d. They provide bilateral anesthesia.
c. B only.
d. Both A and B .
 C H APT E R
5. Which one of the following is an important consider­
ation in all palatal LA procedures?
a. Always apply topical anesthetic for 1 to 2 minutes.
b. Always administer solutions slowly.
c. Always use patch anesthetics.
6. AMSA nerve blocks provide bilateral anesthesia of
palatal tissues at least 20 % of the time.
a. True
b. False
Refe re n ces
Baker, E. W. (2010). Head and neck anatomy for dental medicine.
New York: Thieme.
Blanton, P. , & Jeske, A. (2003, June). The key to profound local
anesthesia-neuroanatomy. Journal of the American Dental
Association, 134, 755-756.
Burns, Y., Reader, A. , Nusstein, J. , Beck,M. , & Weaver, J. (2004).
Anesthetic efficacy of the palatal-anterior superior alveolar
injection. Journal of the American Dental Association, 135(9),
1269-1276.
Chudler, C. H. (2007). Pain and why it hurts. Neuroscience for
Kids. Accessed February 1, 2014. http://faculty.washington.
edu/chudler/pain.html.
Corbett, P. , Jaber, A. A. , Whitworth, J.M. , & Meechan, J. G.
(2010). A comparison of the anterior middle superior alveolar
nerve block and infraorbital nerve block for anesthesia of
maxillary anterior teeth. Journal of the American Dental As­
sociation, 141(12), 1442-1448.
Deardorff, W. W. (2007). Modern ideas: The gate con­
trol theory of chronic pain. Retrieved from http://
www.spine-health.com/conditions/chronic-pain/
modern-ideas-gate-control-theory-chronic-pain
Friedman, M. J., & Hochman,M. N. (1998). The AMSA injection:
A new concept for local anesthesia of maxillary teeth using a
computer-controlled injection system. Quintessence Interna­
tional, 29(5), 297-303.
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complimentary study tools created for this specific title.
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Friedman,M. J. , & Hochman,M. N. (1999). P -ASA block injec­
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Friedman,M. J. , & Hochman, M. N. (2001). Using AMSA and
P -ASA nerve blocks for esthetic restorative dentistry. General
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Anesthetic efficacy of the anterior middle superior alveolar
(AMSA) injection. Journal of the American Dental Society of
Anesthesia, 51 (3), 80-89.
Loomer, P.M., & Perry,D. A. (2004). Computer-controlled de­
livery versus syringe delivery of local anesthetic injections for
therapeutic scaling and root planing. Journal of the American
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Malamed, S. F. (2013). Handbook of local anesthesia (5th ed.).
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Pansky, B., & Gest, T. R. (2014). Lippincott's concise illustrated
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dk/en/news/20 11/n urn ber -of -suspected -adverse-reactions­
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414-420.
 gauge

Palatial anterior Extra-short Infiltration: just lateral

superior alveo­ or short
lar ( PASA) 30/27 gauge
Block: center of papilla
on midline
see Figure 1 3- 1 0
Beneath incisive papilla, slightly To affected teeth
into incisive foramen
see Figure 1 3- 1 1

Anterior
middle superior
alveolar
(AMSA)

MUST have adequate

Above apex, between premolars To incisors and premo­
tissue thickness on the palatal side lars, palatal to molars
see Figure 1 3- 1 5
see Figure 1 3- 1 6

' Dose volumes provided are minimum recommendations for pulpal anesthesia.
Modified from: l ) Melamed SF, Handbook of local anesthesia, ed 5, St Louis, 2004, Mosby; 2) Jastak JT, Yagiela JA, Donaldson D. Local anesthesia of the oral
cavity. Philadelphia, 1 995.
(Continued)
 Field of Aniesthesia
Nerve Block Needle Penetration Site Deposition Site Dose* See Appendix 1 3-2

Greater palatine Extra-short In the anterior depression
(GP) or short of the GP foramen at
30/27 gauge junction of flOiatine b one
and alveolar process
above and l i n � ual to
second mo or.
see Figure 1 3-2 1
Depth of Insertion Al9e of "--ion 0.4-D.6 ml Teeth anesthetized:
Need le inserted to From opposite side None
4-6 mm ( < 1 0 mm) of mouth at right an � le
(to boney resistance) to target area beve
toward palate
Target Periodontium:
Greater palatine foramen Palatal tissues of
see Figure 1 3-22 posterior teeth

Local i nfi ltration Extra-short In palatal mucosa lingual Depth of Insertion Al9e of "--ion 0.2-D.4 ml Teeth anesthetized:
in jections or short to tooth
Needle tip inserted Di reeled toward apex None
30/27 gauge
to boney resistance of tooth bevel toward
bone

Target Periodontium:
Selected soft tissue, gingiva l or apex of tooth At injection site

"'Dose volumes provided are minimum recommendations for pulpal anesthesia.

Modified from: 1 ) Malamed SF, Handbook of local anesthesia, ed 5, St louis, 2004, Mosby; 2) Jastak JT, Yagiela JA, Donaldson D. local anesthesia of the oral
cavity. Philadelphia, 1 995.
Field of Anesthesia
Palatal I njections

NP GP
Teeth an esthetized : Teeth an esthetized :

none none

Periodonti u m : Period onti u m :

pal atal to i ncisors and ca n i n e s pa l atal tissues of

posterior teeth

PASA
AMSA
Teeth an•thetlzed:
Teeth a n estheti zed :
central , latera l , canine
centra l , canine,

Periodontiu m : l atera l , prem olars

Upper/Lower Arch
t o affected teeth
Periodonti u m :

I nfi ltratio n to i ncisors a n d premolars,

Teeth anesthetize d: pal atal to molars

at injection site

Period ontiu m :

a t injection site

266
··························································· @ ···························································

Injections for M an d i b u lar Pain Control

OBJECTIVES KEY TERMS

• D efi n e a n d d i scuss t h e key terms in t h i s c h a pte r. b u cca l n e rve b l ocks 282

coro n o i d notch 269
• Descri be a n d d i scuss t h e i n d icati o n s , re l eva nt a n atomy, a n d
d e position site 268
tech n i q u e fe atu res o f t h e i nj e cti o n s d i sc u ssed i n t h i s c h a pte r.
G ow-G ates (G G ) n e rve
• Descri be t h e b a s i c tech n i q u e ste ps fo r safe a n d effective b l ock 288
a d m i n i strati o n fo r the fo l l owi n g injecti o n s : i n cisive n e rve b l ock 286
i nfe rior a lveo l a r (lA) n e rve
• I nfe ri o r a l veo l a r n e rve b l oc k
b l ock 268
• Li n g u a l n e rve b l o c k
i ntern a l o b l i q u e ridge 270
• B u cca l n e rve b l o ck
l i n g u a l n e rve b l ock 280
• M e n ta l n e rve b l o ck
m a n d i b u l a r i nfi ltrations with
• I n c isive n e rve b l o ck a rtica i n e 276
• G ow-G ates n e rve b l o ck m e nta l n e rve b l ock 283
• Va z i ra n i -Aki n os i (Ak i n osi) n e rve b l ock mylo hyoid n e rve b l ock 275
need l e pathway 268
pa resthesia 278
penetration site 268
p re m atu re contact 275
pte ryg o m a n d i b u l a r
ra p h e 269
tris m u s 278
Vazira n i -Akinosi (Aki nosi)
n e rve b l ock 292

267
268 S E C T I O N IV • C LI N I C AL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A

or located in the vicinity of the needle, including mu­

CASE ST U DY
Lee Chung
Lee C h u n g is a hea lthy m ot he r of five w h o wa nted
both s i d e s of h e r l ow e r jaw treated at the s a m e
a p p o i n t m e n t b e c a u s e of h e r h e c t ic s c h e d u l e . I t
h a d b e e n exp l a i n e d to h e r t h a t t h i s m i g h t c a u s e
co n s i d e ra b l e a l t e r a t i o n of fu n cti o n , b u t s h e h a d
i n sisted that s h e d i d n o t h ave t i m e t o retu rn t o the
office fo r a n oth er a p p o i ntment. A l l other treatment
had been co m p l eted o n p rev i o u s vis its. The fi rst
p re m o l a r a n d a nt e r i o r teeth on t h e r i g h t m a n d i ­
b l e , w h i c h h a d b e e n treated p revi o u s l y, re q u i re d
fo l l ow- u p w i t h l o c a l a n esth esi a . T h e l eft m a n d i b l e
w a s t h e o n l y u n t re a t e d q u a d ra n t a n d i t a l s o re­
q u i red local a n esth esi a .
cosa, superficial fascia, muscle, vessels, nerves, and bone.
The depo sition site will b e describ e d in terms of the
tissues at or near the target and in relation to specific
landmarks.
M a n d i b u l a r I njecti o n Tech n iq u es
This chapter will discuss mandibular inj ection techniques
commonly u s e d in dentistry. Key elements for e ach
mandibular inj ection discussed are summarized in Appen­
dix 14-1. Common variations and precautions will be dis­
cussed where applicable.
I nfe rior Alveo l a r N e rve B lock
Inferior alveolar (lA) nerve blocks, also referred to as man­
dibular or lower blocks, are indicated for pain management
of mandibular teeth in one quadrant.

I ntrod u ction
Anatomic landmarks a n d considerations for each man­
dibular inj ection technique discussed will be presented
in reference to the penetration site, needle pathway, and
deposition site as described in Chapter 1 1 , "Fundamen­
tals for Administration of Local Anesthetic Agents."
The p e netration site will b e related to hard and soft
tissue landmarks. Needle pathway will be described in
terms of the types of tissue that will be penetrated by
Field of Anesthesia
lA nerve blocks anesthetize the structures innervated by
the lA nerve and typically the lingual nerve on the in­
j ected side, to include the mandibular teeth to the mid­
line, soft tissues of the inferior portion of the ramus and
body of the mandible, the lower lip and buccal periodon­
tium of the premolars and incisors, the lingual soft tis­
sues and periodontium, the floor of the mouth, and the
anterior two-thirds of the tongue (see Figure 14-1 •) .
B ox 14-1 • provides further discussion o n lingual nerve
anesthesia.

lA
(w/ llngual)

Teeth anesthetized:

all teeth in quadrant

Periodontium/Soft tlaauea:

all peri odonti um. buccal muoosa

premolars to midline,

floor of mouth and

11. tongue in quadrant

FIGURE 1 4-1 Field of Anesthesia for Inferior Alveolar Nerve

Blocks. Anesthesia will occur in hard and soft structures of half
the mandible with the exception of the buccal tissues in the
molar region.
 C HAPT E R 14 • I N J E CT I O N S FOR M AN D I B U LA R PAI N C O NTROL 269

is made. In other words, penetration must be made slightly

lateral to the raphe. Penetration that is medial to the raphe
is likely to result in an inj ection that places the needle tip
too far posterior to the ideal site for depositing solution .
W h e n lA n e rve b l ocks a re a d m i n istered, t h e l i n g u a l n e rve is The appearance of t h e raphe (observed under t h e fold)
us u a l ly a n esth etized a l o n g with the i nfe rior a lveo l a r n e rve . will vary significantly among patients. It can appear quite
T h i s occurs because t h e l i n g u a l n e rve is typ i c a l l y l o cated distinct in some individuals and ne arly nonexistent in
m e d i a l and anterior to the i nfe rior a lveo l a r n e rve a l o n g t h e others. It can appear to be nondistinct but can then become
p e n etrat i o n pathway. Suffi c i e n t a n esthetic s o l ut i o n is often
more obvious when patients open their mouths wide. The
d e p osited near t h e site of t h e l i n g u a l n e rve (wh e re d rops
raphe is easier to visualize when individuals open their
of a n esth etic s o l u t i o n h ave b e e n deposited ahead of the
n e e d l e) and fro m t h e d iffu s i o n of s o l ut i o n fro m t h e s ite of
mouths, although in some individuals the raphe is barely
l A d e p ositi o n to a c h i eve l i n g u a l n e rve a n esth e s i a . The fi e l d detectable, regardless (see Figure 14-2 •) . The architecture
o f a n esth e s i a fo r lA n e rve b l o cks is ro uti n e l y e n h a n ced i n of the raphe and the thickness of the mucosa overlying it
t h i s w a y to i n c l u d e a n esth e s i a of stru ctu res i n n e rvated b y are primarily responsible for obscuring the raphe when it

� � � � �� � �� ��
.
t i ua
.
r -
• . • • • • • • • • • • • • • • • • • • • • • • • • • .li is not clearly visible.
The second key intraoral fe ature is the coronoid
notch of the mandible. The significance of the notch is
that it defines the height of the injection. The ideal height
Anatomical Factors is slightly higher than the deepest concavity of the notch.
The inferior alveolar nerve is the largest branch of the In other words, penetrations that are below this point are
mandibular division of the trigeminal nerve. It branches likely to place the tips of needles too far inferior to the
from the posterior division of the mandibular nerve in
the infratemporal space, then travels medial to the lateral
pterygoid muscle and passes through the pterygomandibu­
lar space between the sphenomandibular ligament and the
medial surface of the ramus of the mandible. It then enters
the mandibular foramen and canal.
The infratemporal and pterygomandibular spaces also
contain arteries and veins. The maxillary artery, a termi­
nal branch of the external carotid artery, traverses the in­
fratemporal space either superficial or deep to the lateral
pterygoid muscle and divides into several branches, includ­
ing the inferior alveolar artery. The inferior alveolar artery
descends through the pterygomandibular space anterior
to the nerve and enters the mandibular foramen along
with the inferior alveolar nerve. The inferior alveolar vein (A)
travels within the mandibular canal with the inferior al­
veolar artery and inferior alveolar nerve. It exits through
the mandibular foramen, and travels medioanteriorly to
the inferior alveolar artery, through the pterygomandibu­
lar and infratemporal spaces and drains into the pterygoid
plexus of veins located in the infratemporal space.
There are three key intraoral landmarks for successful
lA inj ections: the pterygomandibular raphe, the coronoid
notch on the anterior border of the ramus of the mandible,
and the internal oblique ridge on the medial surface of the
mandible close to the molars and continuing posteriorly.
The purpose of locating these landmarks is to limit the
areas into which penetrations are made. This allows the
tips of needles to end up as close to inferior alveolar
nerves as possible, once solution is deposited. (B)
The mucosa of the pterygomandibular fold overlies F I G U RE 1 4-2 The P terygomandibular Raphe. A-The
the pterygomandibular raphe , which is the attachment of arrow identifies the pterygomandibular raphe (observed
the buccinator muscle to the superior constrictor muscle of under the fold ) . B-The pterygomandibular raphe
the pharynx. The significance of the raphe is that it repre­ represents the medial extent of the penetration site and
sents the medial extent of the area into which penetration the pterygomandibular triangle.
270 S E C T I O N IV • C LI N I C AL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A

FIGURE 1 4-4 P remature Contact Near the Internal

The Coronoid Notch. Slightly above the
F I G U RE 1 4-3
Oblique Ridge. P remature contact of the tip of the needle
deepest concavity of the notch on the anterior border
with the bone of the mandible, slightly superior and poste­
of the mandible identifies the approximate height of the
rior to the internal oblique ridge. The needle needs to be
mandibular foramen.
relocated in order to penetrate to the mandibular foramen.

ideal site for depositing solution. This landmark is used area into which penetration is made. By penetrating well
to identify a minimum height of penetration that allows medial to this landmark, premature contact of the tip
for advancement of the needle to a site directly above of the needle with the bone of the mandible is avoided
the mandibular foramen (Baker, 20 10; Jastak, Yagiela, & (see Figure 14-4 •) . Not only can premature contact be
Donaldson, 1995; Malamed, 2006; Pansky&Gest, 20 14) . It uncomfortable but it prevents further penetration to the
should be noted that deposition of solution below this site ideal site for depositing solution. It also risks barbing the
results in more failures compared with deposition above needle. The internal oblique ridge is a posterior and su­
the site. perior extension of the mylohyoid line, forming the me­
The term coronoid notch is used in dentistry to define dial border of the retromolar triangle (see Figure 14-5 •) .
the concavity on the anterior border of the ramus of the It represents the most medial surface o f the mandible at
mandible (see Figure 14-3 •) . It extends inferiorly from the inferior aspect of the pterygomandibular sulcus (see
the external oblique ridge to the superior aspect of the Figure 14-6 •) . Penetrating too far lateral can result in
coronoid process. The greatest concavity of the coronoid premature contact with bone. Figures 14-7 • and 14-8 •
notch is located approximately 6 to 10 mm superior to the contrast an ideal penetration and a penetration too far
mandibular occlusal plane. See Box 14-2 • for further dis­ lateral.
cussion on the term coronoid notch. The location of the mandibular foramen is variable. It
The third key intraoral landmark for lA nerve block may be located at, below, or above the mandibular molar
inj ections is the internal oblique ridge. The significance occlusal plane. Panoramic radiographs can be helpful
of the ridge is that it represents the lateral extent of the when locating the mandibular foramen (Blanton &Jeske,
2003 ; Malamed, 2006).

Technique Factors
The following information describes key factors for suc­
cessful lA nerve blocks.

P E N ETRAT I O N SITE The penetration site for an lA nerve

The o ri g i n of the word coron oid re l ates to its G re e k root, block can be described as slightly lateral to the pterygo­
m e a n i n g crown o r crown shaped, w h i c h describes t h i s mandibular raphe (see Figure 14-7) at a height 2-3 mm
b o n y featu re of t h e m a n d i b l e .
superior to the greatest concavity of the coronoid notch,
I n d e ntistry, refe re n ce t o the coron oid n o tch i s
and well medial to the internal oblique ridge.
fre q u e ntly m a d e i n re l a t i o n t o l A i nj e cti o n s . I nteresti n g ly,
t h e term coron oid n otch is used p ri m a ri l y in de ntistry.
M e d i c a l references defi n e the reg i o n conta i n i n g the N E E D LE PATH WAY The needle advances along the lateral
n otch as t h e a nterior border of t h e ra m u s of the m a n d i b l e aspect of the pterygomandibular raphe through thin mu­

� � : �� � �� � �� � �� � : � � :
.
i ho
.
e r e t it s n c h f t e
. • • . . . • • • • • • • • • • • • . IIi
cosal tissue and fibers of the buccinator muscle into the
pterygomandibular space. It then passes lateral to the

F I G U RE 1 4-5 Bony Landmarks: Internal and External
Oblique Ridges. P alpating these structures provides guidance
to the location of the correct penetration site. A-The external
oblique ridge. B-The internal oblique ridge.
medial pterygoid muscle, lingual nerve, and sphenoman­
dibular ligament, and superior to the lingula and mandibu­
lar foramen (see Figure 14-9 •) .
D E PO S I T I O N S I T E The deposition site i s 1 m m lateral to
the medial aspect of the ramus and above the mandibular
foramen (see Figures 14-10 • and 14-11 •) .
C HAPT E R 1 4 • I N J E CT I O N S FOR M AN D I B U LA R PAI N C O NTROL 271
(A)
(B)
F I G U RE 1 4-6 Soft Tissue Landmarks: External and
Internal Oblique Ridges. A-P alpation of the external
oblique ridge. B-P alpation of the internal oblique ridge.
Technique Steps
Apply the basic inj ection steps outlined in Chapter 1 1 ,
"Fundamentals for Administration o f Local Anesthetic
Agents," and summarized in Appendix 1 1-1.
A 25 -gauge long needle is recom­
N E E D L E S E L E CTI O N
mended, consistent with the significant depths of pen­
etration required and the high rate of positive aspiration
( 1 0 % -15 % ) in lA nerve blocks. A 27-gauge long needle is
acceptable and is used most commonly for this inj ection
(see Box 14-3 •) .
INJ ECTIO N PROCE D U R E Gain access to the site o f penetration
by retracting the cheek laterally, avoiding overly aggressive
retraction that can displace soft tissue landmarks, particu­
larly the penetration site. Hold the mucosa taut by keeping
the index finger or thumb on the anterior border of the ra­
mus at the depth of the coronoid notch (see Figure 14-12 •)
or on the internal oblique ridge. If the internal oblique ridge
is selected as the location of the finger or thumb, it is impor­
tant to avoid needle contamination and needlestick injury,
which are more likely to occur whenever fingers remain in
proximity to penetration sites (see Box 14-4 •).
272 S E C T I O N IV • C LI N I C AL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A

F I G U RE 1 4-7 P enetration Site for IA Nerve Blocks. FIGURE 14-8 P enetration Site Too Far Lateral.
The optimal penetration site for IANB is slightly lateral P enetration sites too far lateral to the pterygomandibular
to the pterygomandibular raphe, at the depth of the raphe can result in premature contact on the medial
pterygomandibular sulcus. surface of the ramus.

(A) (B)
F I G U RE 1 4-9 Needle P athway for IA Nerve Blocks. A-Demonstrates premature bony contact. B-Demonstrates an optimal
needle pathway. Key: A-parotid gland, B-masseter muscle, C-ramus of mandible, D-medial pterygoid muscle, E-buccinator
muscle, F-pterygomandibular raphe, G-superior constrictor muscle, H-sphenomandibular ligament, I-lingual nerve, J-inferior
alveolar nerve, K-inferior alveolar artery/vein.

F I G U RE 1 4-1 1 Deposition Site for IA Nerve Blocks ­

Superior View. The deposition site for IA nerve blocks
Deposition Site for IA Nerve Blocks -Medial
F I G U RE 1 4-1 0 is superior to the mandibular foramen as indicated by
View. The deposition site for IA nerve blocks is indicated by the the needle. Note the barrel of the syringe is over the
spotlight. contralateral premolars.

N ee d l es i n d e ntistry a re f l exi b l e . T h e h i g h e r t h e g a u g e
o f a n e e d l e , the g reater its f l exi b i l ity a n d d e f l ecti o n i n
tissues (J astak, Ya g i e l a , & D o n a l ds o n , 1 995) . I n a reas w h e re
tissues a re m o re f i b ro u s or i n w h i c h g reater d e pths m u st be
p e n etrated i n o rd e r to p l ace s o l ut i o n c l ose to n e rves, t h e
risk o f n e e d l e de f l ecti o n i n creases. A 25-ga u g e n e e d l e wi l l
de f l e ct l ess co m p a red with a 27-g a u g e n e e d l e , w h i c h wi l l
de f l e ct l ess t h a n a 30-g a u g e n e e d l e .
Desp ite i n creased d e f l e ct i o n , a m aj o rity o f c l i n i c i a n s
s e l ect 27 - g a u g e n e e d l es out o f c o n cern fo r p a t i e n t comfo rt
even t h o u g h i n creased discom fo rt with l a rg e r d i a m eter
n e e d l es h a s n ot b e e n d e m o nstrated ( H a m b u rg , 1 972;
M a l a m e d , 201 3). N evert h e l ess, 27 -gauge need l es a re
p e rfectly a ccepta b l e as evi d e n ced by t h e l o n g-term safety
record o f d e n t a l l o c a l a n esth e s i a , i n c l u d i n g a m aj o rity o f
i n fe r i o r a l veo l a r b l ocks h a vi n g been a d m i n istered with
27- g a u g e n e e d l es . T h e p ro b a b i l ity o f d e f l e ct i o n is an
even g reater issue i n G ow-G ates m a n d i b u l a r n e rve b l ocks
(descri bed l ater i n th is c h a pter), w h e re typ i c a l p e n etrati o n
a ve a
. .
���� � ���' �� :)�
d e pths a re e q u a l to o r g reater t h a n t h e d e pths fo r i n f e r i o r
: � � � : �� � � � ��
•
rv b c
. . .
2
• • • • • • • •
The syringe barrel is positioned at the labial commis­
sure over the premolars on the contralateral side of the
mouth. The barrel remains parallel to and above the oc­
clusal plane of the mandibular molars as the syringe is ad­
)
vanced (see Figure 14-12 • . After resistance from bone is
encountered, which confirms that the needle is at a depo­
sition site near the medial aspect of the ramus, withdraw
F I G U RE 1 4-1 2 Retraction and Syringe Angulations for
IA Nerve Block. To establish firm retraction, hold the
mucosa taut by keeping the index finger or thumb on the
anterior border of the ramus at the depth of the coro­
noid notch. The syringe barrel is positioned at the labial
commissure over the premolars on the contralateral side
of the mouth. The barrel remains parallel to and above
the occlusal plane of the mandibular molars throughout
the injection.
C HAPT E R 14 • I N J E CT I O N S FOR M AN D I B U LA R PAI N C O NTROL 273
T h e risk o f n e e d l esti c k i nj u ry is g reater w h e n ever the f i n g e r
is h e l d o n t h e i ntern a l o b l i q u e r i d g e . S e l ecti n g a s ite at t h e
d e pth of t h e coro n o i d n otch o n t h e ra m u s c a n d e crease
this risk by p rovi d i n g m o re c l e a r a n ce d u r i n g i n it i a l n e ed l e
a p p roach . Altern ative retract i o n tech n i q u es m ay b e
a p p l i e d o n ce a n opti m u m p e n etrati o n site is d eterm i n e d .
•
See C h a pter 1 2, " I nj e cti o n s fo r M axi l l a ry P a i n Contro l ! , "
: :� � �
F i r 1 30 f r xa
• • • � � �_P� � :
�•• . .
s
• • • • • • • • • • • • • • • • • • • •
.li
1 mm. Following negative aspiration, slowly deposit a
minimum of about 1.5 mL (3/4 of a cartridge of any ap­ )
propriately selected local anesthetic drug over no less than
1 minute. Avoid depositing too much solution before the
needle reaches the deposition site. After depositing the so­
lution, slowly withdraw the needle parallel to the pathway
of insertion to avoid soft tissue trauma. See B ox 14-5 •
• • • •
.li
T h e i n fe r i o r a l veo l a r n e rve is the l a rgest d i v i s i o n o f the
tri g e m i n a l n e rve. As a l a rg e , h e a v i l y mye l i n ated n e rve,
g reater vo l u m es o f s o l ut i o n a re req u i red to f l o o d e n o u g h
l e n gth o f its m e m b ra n e i n order t o t e m p o r a r i l y d i s a b l e
sa ltatory co n d u cti o n . I n o t h e r words, i f a n i n s u ffi cient
l e n gth o f t h e lA n e rve is fl o o d e d with s o l ut i o n , i m p u lses
wi l l h ave e n o u g h e n e rgy to pass t h ro u g h seve r a l nodes
(eve n i f those p a rti cu l a r n o d es a re effectively a n esthetized)
to the f i rst n o d a l a rea o f t h e lA n e rve that is n ot affected by
the a n esthetic s o l uti o n . D r u g vo l u m e s in lA n e rve b l o cks
a re g reater co m p a red with m a n y oth e r tech n i q u es . T h e
fo l l o w i n g fa ctors a re h e l p f u l to co n s i d e r w h e n d eterm i n i n g
vo l u m es t o a d m i n ister:
Factor 1 : N e rve Anatomy
T h e l a rg e d i a m eter o f the lA n e rve at the site o f deposition
req u i res a m i n i m u m o f 1 . 5 ml o f s o l ut i o n to p rovide
a d e q u ate d i ffus i o n t h ro u g h t h e n e rve and p rofo u n d
a n esth esia fo r t h e typ ica l patient.
Factor 2 : " B u d g eti n g " for the B u cca l N e rve B l ock
Fol l owi n g the a d m i n istrat i o n s o f reco m m e n d e d doses o f
a n esth etic d r u g fo r an lA n e rve b l ock, 1 . 5 m l, a b o u t 0 . 3 m l
o f s o l u t i o n re m a i n s i n t h e ca rtri d g e . T h i s i s a n a d e q u ate
vo l u m e to co m p l ete a b u cc a l n e rve b l ock w h e n n e e d e d .
Factor 3 : M u lt i p l e Cartri d g es as I n it i a l Dose
Lo n g p ro ce d u res o r past p a t i e n t exp e ri e n ce m a y
esta b l is h a n e e d fo r a d d iti o n a l i n it i a l v o l u m e s o f
a n esthetic s o l uti o n . D e s p ite t h e e ffe ctiven ess of t h i s i n it i a l
d o s e , s o m e c l i n i c i a n s a d m i n iste r m o re t h a n o n e c a rtri d g e
f o r l A n e rve b l o cks every t i m e , re g a rd l ess o f t h e l e n gt h o f
p ro ce d u re or p a st exp e r i e n c e . A l l FDA-a p p roved d e nta l
l o c a l a n est h et i c d r u g i n s e rts m a ke s i m i l a r state m e nts
t h at the s m a l l est dose t h at p rovides c l i n i ca l l y effe ctive
• •
: �� �� � � ��� � �� ���
an t i ul u
• • . .
·
•. • • • • • • • • • • • • • • • • • • •
274 S E C T I O N IV • C LI N I C AL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A
for further discussion of drug doses for the IA nerve
blocks inj ection.
Confirming Anesthesia
Subj ective signs of anesthesia for IA nerve blocks include
a sense of numbness on the inj ected side, including soft tis­
sues of the inferior portion of the ramus and body of the
mandible, the lower lip, and the buccal periodontium of
the premolars and incisors. Typically, patients will report
anesthesia of the lingual soft tissues and anterior two­
thirds of the tongue as well.
Obj ective signs include a lack of response to gentle
stimulation with an instrument and no pain during the
procedure for soft tissues or mandibular teeth.
Common Causes of Injection Failure
IA nerve blocks are considered by some to be among the
most difficult inj ections from a technical standpoint. Pub­
lished failure rates support this and vary from 1 0 % to 31 %
or more, placing the IA block among the highest failure
rates in dentistry, regardless of whether figuring from the
high or low end of the failure range (B lanton &Jeske,
2003 ; Hamburg, 1972; Jastak, Yagiela, &Donaldson, 1995 ;
Malamed, 20 13).
There are several causes of failure of IA nerve blocks.
Greater anatomical variation and the need for deeper
needle penetrations are key factors to understanding these
failures. The most common specific failures are technique­
related , such as depositing solution too far away from
the foramen (too shallow, too medial, too posterior, and,
especially, too inferior) . Shallow deposition of solution
(less than 20-25 mm for a typical adult) decreases the rate
of success. Deposition medial to soft tissue barriers, such
as the sphenomandibular ligament, can block diffusion of
solution to the IA nerve.
Most variations in anatomical form can be accommodated
with an understanding of basic technique. Figure 14-13 •
F I G U R E 1 4-1 3 Impact of Anatomical Variations.
P remature contact on the lingula requires redirection
of the needle and may have been prevented by needle
penetration more medial or by slightly deflecting the
pterygomandibular raphe medially.
demonstrates premature contact on the lingula; needle
penetration more medial or slight medial deflection of the
pterygomandibular raphe with needle insertion can help
avoid or clear this obstruction.
Other anatomic factors also contribute to failure, in­
cluding accessory, aberrant, and ectopic innervations. These
are discussed in detail in Chapter 16, "Troubleshooting In­
adequate Anesthesia." Among these, midline overlapping
of branches of incisive, mental, and mylohyoid nerves is a
common occurrence that provides additional innervation of
the incisor teeth and associated soft tissue from the side op­
posite the inj ection (Blanton &Jeske, 2003). This is an ex­
ample of what is known as accessory innervation, which is
an expected pattern of innervation that deviates from what
is considered normal. Midline overlapping of fibers in the
mandible is fairly common, so much so that it could actually
be considered less of a deviation and more of a variation.
In some individuals, the medial aspect of the penetra­
tion site for IA nerve blocks may be difficult to identify
because of an obscure pterygomandibular raphe. This can
lead to inaccurate assessments of the penetration site and
inadequate anesthesia. For further discussion on anatomi­
cal variations of consequence in IA nerve blocks, see Box
14-6 • and Chapter 16.
Troubleshooting
When IA nerve blocks are unsuccessful, it is helpful to
reevaluate by visualizing, palpating, and checking radio­
graphs and to reassess syringe angulations and depths of
Anatomical
Absence of a Pte ryg o m a n d i b u l a r Raphe
At l e ast o n e study d e m o n strates a co m p l ete a bs e n ce of
t h e pteryg o m a n d i b u l a r ra p h e i n a s i g n ificant p e rcenta g e
of i n d iv i d u a l s . I n 3 6 % of ra p h es reviewed, t h e re was a
conti n u at i o n of the b u cci n ator a n d s u p e r i o r p h a ry n g e a l
constrictor m uscles with no obvious presence of a
pteryg o m a n d i b u l a r ra p h e ( M a l a m ed, 2006; S h i m a d a &
G asser, 1 989) .
Cervical N e rve I n n e rvatio n to M a n d i b u l a r Teeth
Cervi c a l n e rves h ave b e e n described as p rovi d i n g
a ccessory i n n e rvati o n t o m a n d i b u l a r teeth i n t h e past.
A recent study d e m o n strated that a ccessory cervi ca l
i n n e rvati o n of t h e m o l a rs a n d p re m o l a rs is u n l ikely,
h owever sti l l poss i b l e . T h e controve rsy re m a i ns u n resolved
( B l a nton & J eske, 2003) .
Bifid a n d Ectopic lA N e rves
O n ly 60 of 6,000 p a n o ra m i c ra d i o g r a p h s stu d i e d i d e ntifi e d
t h e p rese n ce of b i f i d lA n e rves a n d ecto p i c m a n d i b u l a r
ca n a l s (J astak, Ya g i e l a , & D o n a l d s o n , 1 995; La n g l a is,
• B ro a d u s, & G l ass, 1 985) . This re l ative ly ra re variation was •
: � �� � : � �� � � � � � ; ��� � ; � � �
f o e t un l t a i at r
. . . • • . • • • • • • • • • • ••

penetration. Safe increases in the volume of solution ad­
ministered should also be considered.
In some instances, adequate diffusion of solution is
impossible because of anatomic obstructions. Alternate
nerve blocks (discussed later in this chapter) or supple­
mental techniques, such as the periodontal ligament inj ec­
tion, are indicated when this is the case (see Chapter 15,
"Supplemental Techniques and Adj unctive Strategies")
because their success is not restricted by these barriers.
M andibular infiltration with articaine, which has
been demonstrated to be effective as a primary technique
for anesthetizing mandibular first molars, is also quite
useful as a supplemental technique when profound an­
esthesia of mandibular teeth has not been achieved with
inferior alveolar nerve blocks. This technique is discussed
in Box 14-7 •·
If anatomical variances are encountered, document­
ing them as well as any modifications that were imple­
mented to overcome them can be helpful at subsequent
appointments.
Sensory fibers of the mylohyoid nerve, an efferent
nerve to the mylohyoid and anterior digastric muscles,
can provide a small portion of the pulpal innervation of
mandibular teeth, especially the mandibular molars (Stein,
Brueckner, &Milliner, 2007 ) . A mylohyoid nerve block
can be a useful supplement to lA blocks that appear to be
profound but prove to be inadequate (see Box 14-8 • and
Figure 14-14 •).
There are a number of approaches for anesthetizing
the inferior alveolar nerve. All are considered inferior
alveolar nerve blocks and can be clinically effective at
providing profound anesthesia of mandibular teeth. One
in particular, the Lorna Linda technique, is described in
Box 14-9 •· A technique that is mentioned but for which
specific technique details are not provided in this text, the
" short-needle block anesthesia at the mandibular fora­
men," is nevertheless referred to in the literature and is
discussed in Box 14-10 •·
F I G U R E 1 4-1 4 P enetration Site for Mylohyoid Nerve Blocks.
The penetration site for mylohyoid nerve blocks is indicated by
the needle.
C HAPT E R 14 • I N J E CT I O N S FOR M AN D I B U LA R PAI N C O NTROL 275
Technique Modifications and Alternatives
Because of variations in anatomical landmarks, slight tech­
nique adjustments are frequently necessary. One common
technique challenge occurs when premature contact is
made with bone on the medial surface of the ramus before
reaching the optimum deposition site. This is referred to as
premature contact (see Figure 14-1 3 ) . If bony resistance
is met immediately after penetration, it is probable that
penetration was too low and/or too lateral to the pterygo­
mandibular raphe. If this occurs, withdraw the needle com­
pletely, reevaluate the anatomical landmarks, and proceed
by repenetrating at the adjusted site.
If premature contact with bone occurs at less than
one-half the penetration depth, withdraw the needle to a
more superficial depth and reposition the syringe barrel
anteriorly over the contralateral canine or lateral incisor
before re-advancing the needle. If no further resistance is
encountered, reposition the syringe barrel back over the
premolars and advance the needle until contact with bone
(resistance) occurs at optimum depth.
When no contact is encountered with bone at the
target d e p t h , withdraw the n e e d l e at l e a s t h alfway
and r e p o s it i o n the syring e b a r r e l p o s t e r i o r l y o v e r
t h e molars. Advance until bone is contacte d . If b o n e
is n o t encountered after t h i s adj ustment, do n o t d e ­
posit anesthetic. Withdraw t h e needle a n d consider al­
ternate techniques to achieve inferior alveolar nerve
anesthesia.
Examples of variations in the form of the mandible
are demonstrated in Figures 14-15 •, 14-16 •, and 14-17 •·
Alternatives to lA nerve blocks include Gow-Gates
nerve blocks ( G G ) , Akinosi (Vazirani-Akinosi) nerve
blocks (VA ) , periodontal ligament (PDL) and intraos­
seous inj ections, infiltrations with articaine ( s e e B ox
14-7 ) , and incisive nerve blocks (if treatment is limited
to teeth located anterior to the mental foramen) , or
mental nerve blocks (if treatment is limited to buccal
soft tissues anterior to the mental foramen) . Infiltration
inj ections for incisors may provide pulpal anesthesia
depending on the density and thickness of the cortical
bone over each tooth. The intraosseous and periodon­
tal l i g a m e n t i nj e c t i o n t e c h n i q u e s are d i s cu s s e d in
Chapter 15, " S upplemental Techniques and Adj unctive
Strategies."
Complications
The lA injection has a 10% to 15 % positive aspiration rate.
This is the highest rate of all inj ections described because
of the presence of the inferior alveolar artery and veins
at the mandibular foramen and the frequent presence of
the maxillary artery in the lower pterygomandibular space.
When present in this location, the maxillary artery has
been demonstrated to be located immediately above the
level of the mandibular foramen (Blanton &Jeske, 2003 ) .
Some authorities have recommended avoiding higher de­
position sites for this reason, whereas others recommend
higher deposition sites because they appear to be related
276 S E C T I O N IV • C LI N I C AL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A
Ach i e v i n g m a n d i b u l a r m o l a r a n esth e s i a is a m o n g t h e m ost
ch a l l e n g i n g tasks in d e n t a l l o c a l a n esth es i a . Strate g i es that
i m p rove t h e su ccess rates of traditi o n a l i nfe rior a l veo l a r
n e rve b l ocks (80%-85% o r worse) a re s u bj e cts o f u n ivers a l
i nterest t o c l i n i c i a n s atte m pt i n g to p rovi de re l i a b l e a n d
p rofo u n d m a n d i b u l a r a n esth esia ( B l a nton & J eske, 2003;
Wo n g , 200 1 ). In response to this c h a l l e n g e , m a ny p r i m a ry
a n d s u p p l e m enta l tech n i q u es h ave b e e n i ntro d u ced that
a d d ress the i n a d e q u acies of lA n e rve b l ock a n esth e s i a .
T h e s e i n c l u d e high block a n d i ntraosseous tech n i q u es, as
we l l as and m o re than 20 variations of t h e i nfe rior a lveo l a r
n e rve b l o c k t h a t H a l lste a d a n d H a l l descri bed over a
centu ry a g o w h e n t h ey fi rst d e m o n strated that a n e rve
tru n k co u l d be b l ocked at any p o i n t a l o n g its co u rs e .
M a n y ch a l l e n g es a re e n c o u ntered i n a d u lt a n d
p e d i atric p o p u l at i o n s w h e n p rovi d i n g m a n d i b u l a r m o l a r
a n esth esia ( B l a nton & J eske, 2003; Zwa i n , 2006) . These
ch a l l e n ges h ave b e e n t h e target of m a ny re l evant stu d i es
on t h e effi cacy of bu ccal o n l y a n d bu cca / p l u s lingua/
a rt i ca i n e i nfi ltrat i o n tech n i q u es .
Mandibular infiltrations with articaine h ave
d e m onstrated superior effi cacy for m o l a r a n esthesia
co m p a red with i nfi ltrations of l i d o ca i n e . Reported su ccess
rates for fi rst m o l a rs of 87% and 88% com p a re to su ccess
rates of 57% and 7 1 % when l i d o ca i n e was used ( H a ase, et a l . ,
2008; M cEntire, e t a l . , 201 1 ; Robertso n , e t a l . , 2007). T h e
su ccess rates fo r a rtica i n e i n i nfi ltrations o f fi rst m o l a rs i s
s i m i l a r t o t h e overa l l su ccess rates o f lA b l ocks as re p o rted
i n this text (80%-85%), a lt h o u g h it h a s been s u g g ested that
su ccess rates of lA b l ocks may be m u c h l ower, at 69%, w h e n
fi rst m o l a rs a re sym ptomatic a n d e v e n l ower w h e n t h ey ex­
h i b it i rreve rs i b l e p u l p itis, 30% (Qu i n n , 1 998; Wo n g , 200 1 ) .
T h e specific tech n i q ues used t o investigate a rtica i n e i nfi l­
trations to provide m a n d i b u l a r a n esthesia a re not necessa rily
u n iform, with some using a bucca/ approach a n d oth ers us­
i n g a com b i ned bucca/ p l us lingua/ approach. Some studies
h ave selected deposition sites i n the m u cobucca l fo l d over
the apex of each root, and others h ave selected sites over
the bucca l a p i ces p l us l i n g u a l deposition sites or m i dway
between the bucca l roots of the tooth (Haase, et a l . , 2008;
Ka naa, et a l . , 2006; Ka naa, et a l . , 2009; Robertson , et a l . , 2007).
One s m a l l stu dy of the d iffe re nce i n success rates between
buccal o n l y a n d bucca/ p l us lingual approaches reported
s i m i l a r efficacy (Corbett, et a l . , 2008). G reater vo l u mes of 4%
a rtica i n e (one cartridge per site) tended to be associated
with m o re profo u n d a n esthesia and m o re d isco mfort d u r i n g
i njection (Haase, e t a l . , 2008; Ka n a a , e t a l . , 2006; Ka naa, et a l . ,
2009; M a lamed, 201 3; Robertson, e t a l . , 2007). Regard l ess of
variation i n tech n i q ue, a rtica i n e demonstrated consiste ntly
bette r efficacy com p a red to l idoca i n e .
M a n d i b u l a r i nfi ltrati o n s w i t h a rtica i n e a p p e a r t o
p rov i d e effective p ri m a ry a n d s u p p l e m e n t a l a n esth e s i a o f
m a n d i b u l a r m o l a rs . S u ccess rates a p p e a r to be s i m i l a r to lA
n e rve block s u ccess rates fo r rout i n e resto rative d e ntistry
of m a n d i b u l a r m o l a rs .
Altern ate t e r m s fo r man dibular infiltration with
articain e i n c l u d e bu cca/ infiltration with articain e,
m a n dibular buccal infiltration with articain e, bu ccal and
lingual infiltration with articain e, a n d bu cca/ infiltration of
man dibular p osterior teeth with articain e.
Field of An esthesia
Anest h e s i a typ i ca l ly is confi n e d to t h e tooth a n esthetized
and t h e b u cc a l periodonti u m if a l i n g u a l i nj e cti o n is not
given, and t h e b u cca l and l i n g u a l p e r i o d o nti u m if both
s ites a re s e l e cted fo r i nj e cti o n , a l t h o u g h wider a reas of
a n esth esia s o m et i m es d eve l o p in the m a n d i b l e .
Anato mical Factors
S o l ut i o n m ust p e n etrate the b u cca l (a n d l i n g u a l , if
s e l e cted) cort i c a l p l ates of the m a n d i b l e .
Tech n i q u e Factors
The fo l l ow i n g i nfo rmation describes key facto rs fo r
s u ccessfu l m a n d i b u l a r i nfi ltrati o n s with a rtica i n e .
Penetration Site
Penetratio n sites a re located in the m ucob u ccal tiss ues close
to the a p i ces of the tooth to be a n esthetized . When l i n g u a l
sites a re e l ected, sites a re located i n t h e m u cosa close t o the
a p i ces of the tooth . An a lternate l i n g u a l penetration site is
j u st b e l ow the attached g i n g iva of the toot h .
N e e d l e Pathway
The n e e d l e passes t h ro u g h t h i n m u cos a l tissues to
s u p e rfici a l fascia conta i n i n g l o ose c o n n e ctive tissue a n d
avo i d s s m a l l vess e l s a n d m i crovascu l atu re, as we l l as n e rve
e n d i n gs to the a p i c a l a reas of the teet h .
Deposition Site
Deposition s ites a re l o cated at b u cc a l a p i c a l a reas a n d ,
w h e n e l e cted, l i n g u a l a p i c a l a reas o r j u st b e l ow t h e l i n g u a l
atta c h e d g i n g iva of t h e tooth .
Tech n i q u e Steps
Apply the b a s i c i nj e ct i o n steps outl i n e d in C h a pter 1 1 ,
" Fu n d a m e nta ls fo r Ad m i n istrati o n of Loca l Anesthetic
Age nts, " and s u m m a rized i n Appe n d ix 1 1 -1 .
N e e d l e Sel ecti o n
A 25- o r 27-ga u g e l o n g n e e d l e is co m m o n fo l l ow i n g a n
lA i nj e cti o n . If a d m i n istered s e p a rate ly, a 27-g a u g e s h o rt
n e e d l e m a y be u s e d .
I njection Proce d u re
To g a i n a ccess to t h e s ite of p e n etrati o n , refl e ct t h e l i p to
expose t h e m u co b u cc a l fo l d o p p osite t h e b u cca l s u rfaces
of the tooth o r teeth to b e a n esth etize d . P e n etrate i nto
the m u co b u cc a l fo l d of the tooth (s i n g l e ro ot) o r m e s i a l
a n d d ista l a p i c a l a reas b u cc a l t o t h e tooth ( m u l t i p l e roots)
with o u t m a k i n g b o n y c o n t a ct. F o l l ow i n g a n e g ative a s p i ­
rati o n , s l ow l y d e p o s i t a m i n i m u m of b etwee n 0 . 6 m l (V3 o f
a c a rtr i d g e) a n d 0 . 9 m l (Vz of a c a rtri d g e) of s o l ut i o n over
each a p ex. T h e i n se rt i o n d e pth v a r i e s and is a nywh e re
fro m a b o u t 3 to 6 m m . If a l i n g u a l i nfi ltrat i o n is a l so d e ­
s i re d , a s i m i l a r p ro ce d u re ca n b e fo l l owed except t h at t h e
 C HAPT E R 1 4 • I N J E CT I O N S F O R M AN D I B U LA R PAI N C O NTROL 277

d e p o s i t i o n sites a re e i t h e r l i n g u a l to e a c h a p ex or a s i n g l e b o n e i n t h e a p i c a l a reas o f m a n d i b u l a r teeth, p a rticu l a rly

d e p o s i t i o n s ite h a s b e e n described t h a t is l o cated j u st when t h e cort i c a l p l ate i n the d epositi o n site is very d e n s e .
b e l ow t h e att a c h e d g i n g iva l i n g u a l to t h e tooth .
Tech n i q u e M o d ifications a n d Alte r n atives
Confi r m i n g Anesthesia Altern atives to m a n d i b u l a r i nfi ltrati o n s with a rti ca i n e i n ­
S u bj e ctive s i g n s of a n esth e s i a i n c l u d e a sense of n u m b n ess c l u d e b l ock tech n i q ues a n d s u p p l e m ental tech n i q u es fo r
of the teeth in q u esti o n and the affected vest i b u l a r a reas m a n d i b u l a r a n esth e s i a . These i n c l u d e the lA, G ow-G ates,
b u cc a l and l i n g u a l to t h e teet h . O bj e ctive signs i n c l u d e a Vaz i r a n i-Aki n o s i , and the i ntraosseous and PDL i nj e cti o n .
l a c k of res ponse to g e n t l e sti m u l at i o n with an i nstru m e nt
Co m p l icatio n s
a n d no p a i n d u r i n g procedu res i nvolvi n g p u l p a l tissues of
the i nvolved m a n d i b u l a r teet h . Co m p l ications fo l l ow i n g m a n d i b u l a r i nfiltratio n s w i t h a r­
tica i n e a re i nfre q u e n t a n d i n c l u d e b l e e d i n g , h e m at o m a ,
Co m m o n Ca uses o f I njection Fai l u re swe l l i n g i n t h e a reas of i nj e cti o n , a n d posto pe rative d is­
W h e n ever s o l u t i o n is n ot a b l e to p e n etrate to t h e a p i c a l comfo rt. Corbett and co l l e a g u es specu l ate that by avo i d ­
a reas o f t h e teeth fro m t h e d e p ositi o n s ites, b u cc a l i nfi ltra­ i n g typ ica l i nfe rior a l veo l a r n e rve b l ocks, fewe r p a resthesias
tions w i l l not p rov i d e p rofo u n d a n esth e s i a o r p rofo u n d m a y be expected fro m m a n d i b u l a r i nfi ltrat i o n s with a rtic­
s u p p l e m e n t a l a n esth es i a . a i n e (Co rbett et a l . , 2008) .
W h e n l a rg e r vo l u mes of a rt i ca i n e versus l i d o c a i n e
Tro u b lesh ooti n g
were a d m i n istered at e a c h s i t e , 1 . 8 m l fo r exa m p l e , t h e re
B u cca l i nfi ltratio n s with a rtica i n e m ay be u n s u ccessfu l was a noticea b l e i n crease i n rep o rted d iscomfo rt (Corbett
•
: w h e n ever s o l ut i o n is n ot a b l e to effective ly p e n etrate t h e et a l . , 2008) .
: . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . •

FIGURE 14-1 6 Anatomical Variances of the Ramus-Medial

View. When viewed from medial and superior view, the prominence
of the internal oblique ridge and the lingula are clearly evident.

F I G U R E 1 4-1 5 Anatomical Variances of the Ramus-Superior F I G U R E 1 4-1 7 Anatomical Variances-Flare of the Ramus.
View. P remature contact can be related to prominence of the Variations in the flare of the mandible can impact angulations
medial surface of the ramus at the internal oblique ridge and for IA nerve blocks. Note the differences in both the overall
variations in the flare of the lingula anterior to the deposition size of the examples and the degree of lateral flare. Insertion
site. Note the increasing flare and prominence of the lingula angulations may need to be adjusted to reach the optimum
from the bottom up. deposition site.
278 S E C T I O N IV • C LI N I C AL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A
M y l o hyoid n e rve b l o cks a re i n d i cated fo r s u p p l e m e nta l
p a i n m a n a g e m e n t d u r i n g proce d u res involvi n g m a n d i b u l a r
m o l a rs w h e n lA b l ocks fa i l t o p rov i d e p rofo u n d a n esth esia
(M a l a m ed , 201 3).
Field of An esthesia
The mylohyoid nerve is primarily an efferent nerve, a lthough it
has been recogn ized that it frequently provides sensory fibers
to mandibular teeth (Stein, B rueckner, & M i l l iner, 2007). The
sensory innervation of the mylohyoid nerve is an accessory in­
nervation, the extent of which is l i m ited to providing only a mi­
nor portion of the innervation of these teeth (Stein, Brueckner,
& M i l l iner, 2007) . The nerve is frequently blocked during inferior
a lveo l a r blocks, but anesthetic sol ution may be prevented from
reach i n g the mylohyoid nerve because of the location of its
branching from the mandibular nerve and because of anatom i c
obstructions s u c h as t h e pterygomandibu l a r fascia and sphe­
nomandibular l i gament (Stein, Brueckner, & M i l l i ner, 2007).
Anato mical Factors
T h e m y l o hyoid n e rve is a b r a n c h of the t h i rd division of t h e
tri g e m i n a l n e rve, p rov i d i n g efferent fi b e rs to t h e m y l o h y o i d
m us c l e a n d t h e a nterior b e l l y of the d i g astri c.
Tec h n i q u e Factors
The fo l l ow i n g i nfo rmation describes key facto rs fo r
s u ccessfu l m y l o h y o i d n e rve b l o c ks .
Penetration Site
T h e p e n etrati o n site is l o cated in t h e l i n g u a l m u cosa b e l ow
the a pex of t h e tooth i m m e d i ately poste r i o r to t h e tooth
re q u i r i n g s u p p l e m e n t a l a n esth e s i a (see F i g u re 1 4-1 4) .
Needle Pathway
T h e n e e d l e adva n ces t h ro u g h t h i n m u cos a l tissues to t h e
a p i c a l a rea of the t o o t h j u st poste r i o r to t h e o n e req u i ri n g
s u p p l e m e n t a l a n est h es i a .
Deposition Site
The deposition site is at the mesi o l i n g u a l a p ex of the tooth
j u st poste r i o r to the one req u i r i n g s u p p l e m e nta l a n esth es i a .
Tech n i q u e Steps
Apply t h e b a s i c i nj e cti o n steps outl i n e d i n C h a pter 1 1 ,
" Fu n d a m e nta ls fo r Ad m i n istrat i o n of Loca l Anesthetic
� � � : ·� : ��: : �� : ���� :� � �
gen s nd su rz n nd 1- · i co f t
. • • • • . . . . . • • • • •
to increased rates of success (Blanton &Jeske, 2003; Gow­
Gates &Watson, 1979; Wong, 200 1 ) .
Postinj ection muscle soreness or limitation of man­
dibular movement can occur because of localized injury to
muscle fibers at the site of inj ection. This is referred to as
trismus. The risk of trismus increases with the number of
needle penetrations.
N e e d l e Sel ecti o n
A 25- or 27-ga u g e l o n g n e e d l e is co m m o n fo l l ow i n g lA
i nj e cti o n s . I f a d m i n istered s e p a rate ly, a 27-ga u g e s h o rt
n e e d l e m ay be u s e d .
I njection Proce d u re
To g a i n a ccess to t h e s ite of p e n etrati o n , retra ct t h e
to n g u e a n d a p p ro a c h fro m t h e o p p os ite s i d e . P e n etrate
b e l ow the a p ex of the tooth i m m e d i at e l y poste r i o r to
the tooth in q u esti o n a n d a dva n ce u nt i l res i st a n ce is m et
( b o n y c o n t a ct) . T h e i n se rti o n d e pth is a nywh e re fro m
3 to 5 m m . Fo l l ow i n g a n e g ative a s p i rati o n , s l ow l y
( 2 0 secon ds) d e posit a m i n i m u m of 0 . 6 m l of s o l u t i o n
(1/3 of a ca rtri d g e) .
Confi r m i n g An esthesia
S u bj e ctive s i g n s of a n esth e s i a fo r m y l o h y o i d n e rve b l ocks
i n c l u d e a s e n s e of n u m b n ess of t h e tissues l i n g u a l to
t h e m a n d i b u l a r m o l a rs . O bj e ctive s i g n s i n c l u d e a l a c k of
resp o n s e to g e n t l e sti m u l at i o n with a n i n stru m e n t a n d
n o p a i n d u r i n g proce d u res i n v o l v i n g p u l p a l tissues of
the m a n d i b u l a r m o l a rs (wh e n p e rfo r m e d after lA n e rve
b l o cks) .
Co m m o n Ca uses of I njection Fai l u re
M y l o h y o i d n e rve b l ock fa i l u res a re ra re a n d occu r
p ri m a ri l y because of o p e rator error i n assess i n g d e pths of
p e n etrat i o n a n d de positi o n sites.
Tro u b l esh ooti n g
M y l o h y o i d n e rve b l o cks h ave l ittl e p u rpose i n de nta l
loca l a n esth esia oth e r t h a n as s u p p l e m e nts to lA b l o cks .
Alth o u g h fa i l u re is t h e refore n ot a p a rticu l a r issue,
reassess m e n t of t h e p e n etrat i o n a n d deposition s ites and
of t h e vo l u m es of s o l ut i o n used may be h e l pfu l .
Tech n i q u e M o d ifications a n d Alte r n atives
Altern atives to m y l o h y o i d n e rve b l o cks a re essenti a l ly
a ltern atives to i nfe ri o r a lveo l a r b l ocks, i n c l u d i n g
G ow-G ates n e rve b l o cks, Vazi ran i-Aki nosi b l ocks, a n d
i ntraosseous i nj e ct i o n s , i n c l u d i n g t h e P D L .
Co m p l i cati o n s
Co m p l ications fo l l ow i n g m y l o h y o i d n e rve b l ocks a re ra re
and i n c l u d e b l e e d i n g , h e m ato m a , and posto pe rative
� : � �� . IIi
.
• • • • • • • • • • • . . • • • • • • • • • • • • • • • • • • • • • • • • • • • • • •
Paresthesia (prolonged anesthesia) can occur follow­
ing lA nerve blocks, but it is usually transient. Studies of
the risks of paresthesia have suggested many etiologies but
have largely failed to identify specific cause-and-effect re­
lationships in nonsurgical procedures. The use of 4% drugs
for lA nerve blocks continues to be controversial. In 2010,
Garisto et al. reported on the occurrence of paresthesia

T h e key a n at o m i c a l l a n d m a rks fo r the Lo rn a L i n d a
tech n i q u e a re the d e e pest p o rti o n of t h e coro n o i d n otch
and t h e intern a l o b l i q u e l i n e . Visu a l iz i n g a p l a n e p a r a l -
l e l t o the o cc l u s a l ta b l e at the d e e p est conto u r o f t h e
coro n o i d n otch h e l ps esta b l ish t h e m i n i m u m h e i g ht o f
p e n etrat i o n fo r i n fe r i o r a lveo l a r n e rve b l o ck i nj e cti o n s . T h e
a nterior/poste rior p o i nt of t h i s i nj e cti o n is d eterm i n e d b y
l o cati n g the i ntern a l o b l i q u e l i n e , w h i c h is t h e i n s e rt i o n
p o i n t for the d e e p te n d o n of t h e t e m p o ra l is m us c l e . T h e
d e pth of p e n etrat i o n is esta b l i s h e d by t h e fa ct that the
d ista n ce f rom t h e i ntern a l o b l i q u e line to the l i n g u a l is
9-1 1 m m fo r m ost a d u lts and ch i l d re n . D i ffe rent f ro m other
sta n d a rd block te c h n i q ues a 25-g a u g e s h o rt n e ed l e is
reco m m e n d e d for t h i s tech n i q u e . Box 1 4-1 0 p rovides a n
a d d iti o n a l d iscuss i o n o n s h o rt- n e e d l e b l ock tech n i q u e s .
T h e fo l l ow i n g ste ps exp l a i n h ow to p e rform the Lo rn a
L i n d a tech n i q u e :
1 . Cons istent with o t h e r b l o c k tech n i q u es, (1 ) l o cate t h e
d e pth of t h e coro n o i d n otch o n the a nteri o r p o rt i o n o f
t h e ra m us, b u cca l to t h e m o l a rs; (2) l o cate t h e ptery­
g o m a n d i b u l a r ra p h e ; t h i s assists i n l o cati n g the i nter­
n a l o b l i q u e l i n e j u st l atera l to the ra p h e .
2 . Retract tissues l atera l ly u nt i l t h e f i n g e r rests at t h e
d e pth of t h e coro n o i d n otch . Retract i n g tissues taut
a i d s vis u a l izat i o n of t h e p e n etrati o n site a n d n e e d l e
i n s e rti o n . As noted e a r l i e r, rest i n g the fi n g e r in t h e
� • • • • • �� : � �� �� �� �� : ��� � � : � �: �� � � ��
co n o
.
t t ls h he gh
• • .
n e ra i -
. .
M u ch h a s b e e n written i n t h i s text a n d i n m a ny other
res o u rces reg a rd i n g the d i ffi cu lties e n c o u ntered w h e n at-
te m pt i n g to p rov i d e re l i a b l e and p rofo u n d a n esth e s i a o f
m a n d i b u l a r teet h .
Ye a rs a g o , D r. G ow-G ates descri bed h i s high block
tech n i q u e a n d b a s e d it, a m o n g o t h e r co n s i d e rations, o n
m e a s u re m e nts l e a d i n g t o re l evant a n ato m i c a l avera g e s . I n
determ i n i n g o n e of these avera g es, h e u s e d m u lt i p l e s ku l ls
t o m e a s u re t h e d ista nce f ro m t h e poste rior m a n d i b u l a r
occ l u s a l p l a n e to the l i n g u l a because it l i es a n ato m i c a l l y
s u p e r i o r a n d m e d i a l t o t h e m a n d i b u l a r fo r a m e n a n d rep-
rese nts a p re d i cta b l e l ocator of t h e i n fe r i o r a l veo l a r n e rve's
l ocati o n . H e fo u n d t h at fo r a m e n s were l o cated h i g h e r t h a n
traditio n a l b l ock ta rget s ites a b o u t 1 4% o f t h e t i m e . For
h i g h block tech n i q u es (pe n etrat i o n sites 5 m m o r h i g h e r
t h a n tra d i ti o n a l b l ocks), fo r a m e n s were h i g h e r t h a n target
s ites o n ly a b o u t 6% of the t i m e . I n descri b i n g t h e b e n efits
o f h is tech n i q u e , G ow-G ates cited h i g h f a i l u re rates o f tra-
diti o n a l i n ferior a lveo l a r n e rve b l o cks (G ow-G ates, 1 979) .
� .� � � �� � �� . · · · �� : � �� � �: � :� � :
i i · h e ex a n e t t e n r t n s i h e u p
. . . . . . • • . ;�: • •
C HAPT E R 14 • I N J E CT I O N S FOR M AN D I B U LA R PAI N C O NTROL 279
3 . With the syri n g e ba rre l over the contra l atera l p re m o ­
l a rs, i nsert t h e n e ed l e l atera l a n d s l i g htly poste r i o r t o
t h e ra p h e . A s w i t h oth e r tech n i q u es, it is advised t o
p a u s e a n d deposit a few d rops of a n esthetic befo re
p roceed i n g .
4. A t t h i s p o i n t contact is m a d e with t h e m e d i a l s u rfa ce
o f the ra m us, j u st poste rior to t h e i ntern a l o b l i q u e
l i n e-wh i l e sti l l a nteri o r t o t h e l i n g u a l . It is a n t i c i p ated
that the l i n g u l a is now a p p roxi m ately 1 0 mm f rom t h i s
p o i nt.
5 . Fro m t h i s point t h e needle is i n cre m e nta l l y adva n ced
along t h e m e d i a l s u rface o f t h e ra m u s by withd rawi n g
the n e e d l e 1 m m after contact, a dj u st i n g t h e b a rre l o f
t h e syri n g e s l i g htly towa rd t h e m i d l i n e a n d adva n c­
i n g u n t i l contact is m a d e a g a i n . T h i s is repeated u nti l
t h e n e e d l e h a s b e e n adva n ced a p p roxi m ately h a l fway
betwee n t h e i ntern a l o b l i q u e l i n e and t h e l i n g u l a to
a d e pth o f 5 m m . The l i n g u a l n e rve is a n esthetized at
this p o i nt, fo l l ow i n g a s p i rati o n , by d e p ositi n g a p p roxi­
m ately 0.5 mL of a n esth etic.
6 . T h e needle is again i n cre m e nta l ly a dvanced u nt i l the
n e e d l e n o longer m a kes contact with t h e ra m u s i n t h e
m a n d i b u l a r s u l cus ( a s t h e n e e d l e s l ides o v e r t h e l i n ­
g u a l notch). 0 . 7 5-1 m L of a n esthetic is deposited h e re .
Kra l l , B . (2008-2009) . Th e L o m a Lin da Infe rior Alve olar
Nerve B lock Te chnique, f ro m Lo rn a L i n d a U n ive rs ity S c h o o l
. • • • • • •
f en i t h e oc l
� .� . � � �� � • • � . � .� . �� �� � .� . �� :
ne h i an l
• • • • • • • • • . Ji
reg i o n s o f t h e pterygo m a n d i b u l a r space wo u l d l i ke l y de-
crease the n u m b e r o f vascu l a r e n c o u nters. This was l ater
con f i r m e d by M a l a m e d (M a l a m e d, 1 98 1 ) .
H e a l so referenced t h e w o r k o f M e n ke a n d G owg i e l
w h o p rovi d e d evi d e n ce that traditi o n a l b l ocks u s i n g l o n g
n e e d l es m i g ht n ot be i d e a l w h e n co n s i d e r i n g t h e a ctu a l
l ocat i o n s o f i n fe r i o r a l veo l a r n e rves. M e n ke a n d G owg i e l
descri bed a sh ort-needle m a n d i b u l a r b l ock based o n
t h e i r eva l u at i o n of 35 cadaver h e a d s . T h e resu lts of the
eva l u ati o n reve a l ed t h a t t h e d e pth of p e n etrati o n at t h e
n a rrowest a nteroposte rior wi dth o f t h e ra m u s and pte ry-
gote m po ra l d e p ress i o n was determ i n e d to be h a l f t h e n a r-
rowest a nteroposte rior w i d t h of t h e ra m u s p l u s o r m i n us 1
mm. T h i s d e pth was descri bed as being within the limits of
a short n e edle a n d easier t o estim ate with a sh o rt n e e dle
than a l o n g n e e d l e . It was fu rt h e r stated that a s h o rt
n e e d l e was less likely to go too deep or deviate compare d
with a l o n g n e e dle. S u c h d iscuss i o n s m ust be b a l a n ced
b y t h e risks i nvolved w h e n s h o rt n e ed l es a re u s e d i n deep
• • • • • •
ne r i s
�� : �� ��
. : • • • • • • • • • • • • • • • • • • • • • • • • • • • • . li
280 S E C T I O N IV • C LI N I C AL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A
after the administration of dental local anesthetics in the
United States from November 1997 to August 2008 and
found that 4% prilocaine and 4% articaine accounted for
a disproportionate number of paresthesias, similar to previ­
ous results in other countries. Also similar to previous re­
sults, the maj ority involved the lingual nerve. Garisto et al.
also noted that there is no convincing evidence that either
articaine or prilocaine is superior to lidocaine for IA blocks.
Clinicians should continue to weigh the risks and benefits of
4% drugs for IA blocks before deciding to use them.
If the facial nerve's pathway is anterior to its typical
location or if anesthetic solution is deposited well poste­
rior to the mandibular foramen, it is possible to anesthe­
tize branches of the facial nerve (VII ) . Drooping of the
upper lip and inability to close the eyelid on the inj ected
side are signs of facial nerve anesthesia, which usually lasts
only as long as the anesthetic effect on other tissues. In
some individuals, branches of the facial nerve lie directly
in the insertion pathway for IA nerve blocks and facial
nerve anesthesia in those instances is unavoidable (Jastak,
Yagiela,&Donaldson, 1995).
Perioperative soft tissue self-injury (lip or cheek biting)
may occur at any time while anesthesia is in effect, partic­
ularly when associated with IA nerve blocks. It is impor­
tant to remind patients, especially small children and their
caretakers, to monitor for postanesthetic lip chewing. See
Chapter 17, "Local Anesthesia Complications and Manage­
ment," for additional discussion and management protocol.
Li n g u a l N e rve B l ock
Lingual nerve blocks are indicated for pain management
during procedures that involve the anterior two-thirds of the
tongue and lingual soft tissues of the mandible on one side.
Field of Anesthesia
The lingual nerve provides anesthesia to the lingual soft
tissues, the floor of the mouth, and the anterior two-thirds
of the tongue (to the midline) (see Figure 14-18 •) .
32 31 30 2t 28 27 H 25 24 23 22 21 20 1 t 1 1 1 7
FIGURE 14-1 8 Field of Anesthesia for Lingual Nerve Blocks. The field
of anesthesia for lingual nerve blocks is indicated by the shaded area.
Anatomical Factors
The lingual nerve is located in proximity to the inferior
alveolar nerve and is usually located medial and anterior
to it.
Technique Factors
The following information describes key factors for suc­
cessful lingual nerve blocks.
A separate inj ection is usually not necessary in order
to anesthetize the lingual nerve. Because of its typical lo­
cation anterior and medial to the inferior alveolar nerve, it
is routinely anesthetized when the inferior alveolar nerve
is anesthetized.
Techniques to anesthetize the lingual nerve all have
significant similarities and include the following:
1. The process of depositing solution for IA nerve blocks
2. A supplemental inj ection after depositing solution for
IA nerve blocks
3. A single inj ection not associated with IA nerve blocks;
for lingual-only anesthesia (when there is no need to
anesthetize buccal soft tissues, buccal periodontium,
or mandibular teeth)
P E N ETRAT I O N S ITE The penetration site for lingual nerve
blocks is the same as for IA nerve blocks (see Figure 14-7)
and is slightly lateral to the pterygomandibular raphe and
medial to the internal oblique ridge at a height that ap­
proximates a few millimeters above the deepest concavity
of the coronoid notch.
N E E D LE PATHWAY The needle advances along the lateral
aspect of the pterygomandibular raphe through thin mu­
cosal tissue and fibers of the buccinator muscle into the
pterygomandibular space. The needle then passes lateral
to the medial pterygoid muscle to the lingual nerve (see
Figure 14-9).
D E PO S I T I O N S I T E The path of the lingual nerve varies.
Deposition at a point halfway between the ramus and the
RIGHT LEFT

penetration site will usually allow sufficient diffusion for
profound anesthesia (see Figure 14-19 •) .
Technique Steps
Apply the basic inj ection steps outlined in Chapter 1 1 ,
"Fundamentals for Administration o f Local Anesthetic
Agents," and summarized in Appendix 1 1-1.
N E E D LE S E L E CTI O N For lingual nerve inj ections, 25- or
27-gauge long needles are recommended when adminis­
tered in conjunction with lA nerve blocks. When adminis­
tered alone, a 25- or 27-gauge short needle may be preferred.
I N JE CTI O N PRO C E D U R E When performed in conjunction
with lA nerve blocks, the needle is withdrawn halfway af­
ter deposition for the lA block and, after negative aspira­
tion, a minimum of 0. 1-0.2 mL (one-half to one) stopper
of solution is administered. When a lingual nerve block
only is desired, 0.2 mL (119 of a cartridge or one stopper)
of solution is administered.
F I G U RE 1 4-1 9 Site for Lingual Nerve Blocks. The deposition
site for lingual nerve blocks is indicated by the spotlight.
(A)
F I G U RE 1 4-20 Depth of P enetration for Lingual Nerve Blocks. The depth of penetration for lingual nerve blocks is - 1/3-lfz
the length of a long needle ( -10-13 mm ) . A-Depth of penetration for lingual nerve blocks. B-Depth of penetration for IA
nerve blocks.
C HAPT E R 14 • I N J E CT I O N S FOR M AN D I B U LA R PAI N C O NTROL 281
When administered as a separate injection, a long nee­
dle may be used to penetrate in the same manner as for the
lA nerve block but is advanced only 10-13 mm. If a short
needle is used, the length of the shank showing after opti­
mum penetration is about 8-1 1 mm (see Figure 14-20 •) .
Confirming Anesthesia
Subj ective signs of anesthesia for lingual nerve blocks in­
clude a sense of numbness of the lingual soft tissues and
half of the anterior two-thirds of the tongue. Obj ective
signs include a lack of response to gentle stimulation with
an instrument and no pain during procedures involving
soft tissues lingual to the mandibular teeth.
Common Causes of Injection Failure
These techniques rarely fail to provide profound anesthesia of
the lingual soft tissues except perhaps in the midline where
fibers from the contralateral lingual nerve may overlap.
Troubleshooting
If lingual anesthesia is not achieved, reevaluate by visual­
izing the site and depth of penetration as well as volumes
of solution deposited.
Technique Modifications and Alternatives
The Gow-Gates nerve block is an excellent alternative
for achieving lingual anesthesia because it anesthetizes
the trunk of the lA nerve before the branching of the
lingual nerve and not only anesthetizes the lingual nerve
but avoids lingual nerve encounters and subsequent inju­
ries because the solution is deposited anywhere from 5 to
10 mm away from the inferior alveolar nerve trunk.
Complications
The lingual nerve is one of the most frequently inj ured
nerves during dental inj ections. The symptoms associ­
ated with these inj uries range from transient " electric
shocks" to permanent paresthesias. See Chapter 17, "Local
(B)
282 S E C T I O N IV • C LI N I C AL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A
Anesthesia Complications and Management," for further
discussion on nerve injuries and paresthesia.
B u cca l N e rve B l ock
Buccal nerve blocks are indicated for pain management
during procedures involving the buccal soft tissue along
the molar teeth in the mandibular region. B uccal nerve
blocks are also referred to as long buccal and buccinator
nerve blocks (Jastak, Yagiela,&Donaldson, 1995).
Field o f Anesthesia
The buccal nerve and its terminal branches provide innervation
to the soft tissue and periodontium buccal to the mandibular
posterior teeth, primarily the molars (see Figure 14-21 •).
Anatomical Factors
The buccal nerve crosses the coronoid notch of the ra­
mus at the level of the occlusal plane. It then divides into
several branches, one of which penetrates the buccinator
muscle to innervate the buccal mucosa and gingiva of the
mandibular molars and occasionally of the premolars.
Technique Factors
The following information describes key factors for
successful buccal nerve blocks.
PEN ETRATION S ITE The penetration site is located in the buc­
cal fold just distal and buccal to the most posterior molar for
which soft tissue anesthesia is required (see Figure 14-22 •).
N E E D LE PATH WAY Because of the thinness of the mucosa
in the area and the limited depths of penetration, the nee­
dle is advanced very slowly until the bevel is fully inserted,
to avoid discomfort.
D E PO S I T I O N S I T E The deposition site is at the buccal as­
pect of the ramus, lateral to the external oblique ridge as
Buccal
Teeth anesthetized:
none
Periodontium/Soft tiaauea:
buccal to molars
FIGURE 1 4-21 Field of Anesthesia for Buccal Nerve Blocks. The field
of anesthesia for buccal nerve blocks is indicated by the shaded area.
the nerve passes over the anterior border of the ramus
(see Figure 14-23 •) .
Technique Steps
Apply the basic inj ection steps outlined in Chapter 1 1 ,
"Fundamentals for Administration o f Local Anesthetic
Agents," and summarized in Appendix 1 1-1.
N E E D L E S E L E CT I O N For buccal nerve blocks, 2 5 - o r
27-gauge long needles are common following l A injections.
When administered alone, a 27-gauge short needle is rec­
ommended, consistent with the shallow depth of penetra­
tion and the low rate of positive aspiration (less than 1 % )
(Jastak, Yagiela,&Donaldson, 1995).
I N JE CT I O N P R O C E D U R E To gain access to the site of
penetration, retract the lip and cheek laterally, pulling
the tissue taut (see Figure 14-22) . The penetration site
is located in the buccal fold just distal and buccal to the
most posterior molar in the arch or j ust p o sterior to
the most posterior molar requiring treatment or rubber
dam clamp placement. The angle of insertion is parallel
to the occlusal plane on the side of inj ection as dem­
onstrated in Figure 14-22. The insertion depth is about
3-4 mm. Following a negative aspiration, begin deposit­
ing 0.2 to 0.3 mL (119-116 cartridge) of an appropriately
selected local anesthetic drug. This inj ection has a high
tendency to cause discomfort if solution is administered
too rapidly.
The bevel must be fully inserted into the tissue. If pen­
etration is initiated in an area with inadequate tissue thick­
ness, resistance may be met, preventing complete bevel
insertion. If this occurs, withdraw and penetrate more
laterally, away from the ramus. To confirm proper bevel
insertion after aspiration, observe for backflow at the pen­
etration site while depositing. If this occurs, the solution
will leak into the patient's mouth (the patient may experi­
ence a bitter taste from the solution).

F I G U R E 1 4-22 P enetration Site for Buccal
Nerve Blocks. The penetration site for buccal
nerve blocks is indicated by the needle.
Confirming Anesthesia
Subj ective signs of anesthesia for BNBs include a sense
of numbness of the buccal soft tissues of the mandibu­
lar molars. Obj ective signs include a lack of response to
gentle stimulation with an instrument and no pain during
procedures involving soft tissues buccal to the mandibular
molars.
Common Causes of Injection Failure
BNB failures are rare and occur primarily because of op­
erator error. Failure to reserve adequate volumes after lA
nerve blocks or to fully insert the bevel into the tissue can
result in the deposition of inadequate volumes of solution.
Troubleshooting
When reevaluating failed buccal anesthesia, it is useful to
consider the following factors:
1. Adequate retraction is critical. If the tissue is not held
taut during penetration, it can be difficult to achieve
full bevel penetration. Additionally, if retracted tissues
are allowed to slump over the penetration site, it may
seem that bevels are inserted when they actually are
not.
2. If the site of penetration is too medial, the tissue may
be too thin and fibrous for adequate penetration. The
needle may even contact bone on the lateral surface or
retromolar region of the ramus, preventing adequate
bevel insertion and causing sharp pain. Locating a
C HAPT E R 14 • I N J E CT I O N S FOR M AN D I B U LA R PAI N C O NTROL 283
F I G U RE 1 4-23 Deposition Site for Buccal Nerve
Blocks. The deposition site for buccal nerve blocks is
indicated by the spotlighted area.
more lateral penetration site in more loosely attached
mucosa can provide greater success and comfort.
Technique Modifications and Alternatives
Alternatives to buccal nerve blocks are rarely needed be­
cause of their high rate of success. Localized infiltrations
can be administered for site-specific anesthesia. Addition­
ally, buccal nerve anesthesia is usually achieved with the
administration of Gow-Gates nerve blocks, and PDL in­
jections are effective as well.
Complications
Complications following buccal nerve blocks are rare
and include bleeding, hematom a , and p o stop erative
discomfort.
M e nta l N e rve B l ock
Mental nerve blocks are administered for procedures re­
quiring pain management of the buccal soft tissues in the
mandible anterior to the mental foramen (Jastak, Yagiela,
&Donaldson, 1995; Malamed, 20 13).
Field o f Anesthesia
Anesthesia of the mental nerve will affect the buccal mu­
cous membrane and skin of the lower lip and chin anterior
to the mental foramen to the midline (see Figures 14-24A •
and 14-24B •) .
Anatomical Factors
The mental nerve exits the mandible on the anterolateral
surface through the mental foramen, usually between the
apices of the first and second premolars.
Technique Factors
The following information describes key factors for suc­
cessful mental nerve blocks.
P E N ETRAT I O N S I T E The penetration site varies with the
location of the mental foramen. It is helpful to locate the
foramen before selecting the penetration site. This can be
284 S E C T I O N IV • C LI N I C AL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A

RIGHT
32: 31 30 2t 28 27 28 25 24 23 22 21 20 , . 1 1 17

Mental
Teeth anesthetized:

pulpal limHed to tooth

at site of infiltration

Periodontium/Soft tissues:

premolars to midline

(A) (B)
F I G U RE 1 4-24 Field of Anesthesia for Mental Nerve Blocks. A-The field of anesthesia for mental nerve blocks is indicated by the
spotlighted area. B-Field of Anesthesia Limitations. Note that the field of anesthesia for mental nerve blocks does not include the
teeth, only the soft tissue anterior to the mental foramen.

accomplished with the aid of radiographs and by gentle
palpation in the buccal vestibule beginning with the first
molar and moving anteriorly until the foramen is located,
most typically in relationship to the apices of the first or
second premolars. The foramen may appear as a small de­
pression, a "crater," or a rough elevation or ledge. Gentle
pressure applied over the area of the foramen frequently
elicits a slight achy discomfort or tingling sensation. Pa­
tients can be asked to confirm this as the vestibular area is
palpated, by raising their hands when they feel these sensa­
tions. The site of penetration is in the depth of the muco­
buccal fold superior to the foramen (see Figure 14-25 •) .
A n alternate site i s i n the mucobuccal fold anterior t o the
foramen. This alternate penetration site will be described in
Technique Modifications and Alternatives toward the end
of this topic.
Donaldson, 1995 ) . A 27-gauge needle is most commonly
used and is also recommended.
I N J E CT I O N P R O C E D U R E To gain access to the site o f
penetration, the clinician i s seated at a posterior position.
Begin by retracting the lip and cheek laterally, pulling the
tissue taut at the mucogingival junction (see Figure 14-28 •) .
After asking the patient t o close his o r her eyes, the syringe
is aligned vertically with the patient's cheek to approach
the penetration site (see Figure 14-29 •) . Following initial
penetration, advance the needle tip at an angle directly
vertical to the foramen to a depth j ust superior to it. The
depth of insertion varies with the height of the alveolar
process and the angle of tissue retraction but is typically
about 4-6 mm.

N E E D LE PATH WAY The needle passes through thin mu­

cosal tissues to superficial fascia containing loose connec­
tive tissue, small vessels and microvasculature, and nerve
endings.

D E PO S I T I O N S I T E The deposition site is j ust superior to

the mental foramen for both techniques discussed (see
Figures 14-26 • and 14-27 •) .

Technique Steps
Apply the basic inj ection steps outlined in Chapter 1 1 ,
"Fundamentals for Administration o f Local Anesthetic
Agents," and summarized in Appendix 1 1-1.

N E E D LE S E L E CTI O N A 25-gauge needle is recommended F I G U R E 1 4-2 5 P enetration Site forMental Nerve

for this inj ection, consistent with its relatively high rate Blocks. The penetration site for mental nerve blocks is
of positive aspiration (ne arly 6 % ) (Jastak, Yagiela, & indicated by the needle.

F I G U R E 1 4-26 Deposition Site for Mental Nerve
Blocks. The deposition site for mental nerve blocks is
indicated by the spotlighted area.
F I G U R E 1 4-2 7 Deposition Site for Mental Nerve
Blocks-Superior Lateral View.
Following negative aspiration, slowly deposit a mini­
mum of 0.6 mL (1/3 of a cartridge) of an appropriately
selected local anesthetic drug. This inj ection can be quite
uncomfortable if adequate topical has not been applied, if
solution is administered too rapidly, or if bone is inadver­
tently contacted.
Confirming Anesthesia
Subj ective signs of anesthesia for mental nerve blocks in­
clude a sense of numbness on the inj ected side, including
the buccal soft tissues of the chin and lower lip, and of the
premolars and incisors.
Obj ective signs include a lack of response to gentle
stimulation with an instrument and no pain during proce­
dures involving soft tissues overlying the premolars and
incisors.
C HAPT E R 14 • I N J E CT I O N S FOR M AN D I B U LA R PAI N C O NTROL 285
F I G U R E 1 4-28 Tissue Retraction for Mental Nerve
Blocks. Establish gentle lateral retraction to make the
tissue taut for ease of penetration and accuracy of depth
of insertion.
F I G U RE 1 4-2 9 Vertical Approach to
Needle Insertion. For this technique,
align the syringe vertically to approach
the penetration site. The clinician is
seated at the 12:00 position.
Source: Courtesy of Megan Gibbons.
Common Causes of Injection Failure
This inj ection is highly successful. Failure to achieve anes­
thesia of the buccal tissues in the area of the mental nerve
block is rare. This usually involves failure to correctly
identify the location of the foramen, which results in in­
sufficient diffusion of solution or inadequate volumes of
solution deposited.
Troubleshooting
When adequate anesthesia is not achieved, reassess the
volume of solution deposited and the deposition site, as it
286 S E C T I O N IV • C LI N I C AL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A
may have been located too far superior, inferior, anterior,
posterior, or lateral to the foramen.
Incomplete anesthesia after mental nerve blocks
can frequently be attributed to what is known as cross­
innervation or overlap of terminal fibers of the nonanes­
thetized or contralateral mental nerve, at the midline of
the mandible, similar to the cross-innervation that occurs
with the anterior superior alveolar nerve as discussed in
Chapter 12, "Inj ections for Maxillary Pain Contrail."
When this is the case in the mandible, tissues of the
anterior segment of the mandible will receive sensory in­
nervation from the mental nerve on the nonanesthetized
side. To achieve adequate anesthesia in these instances, an
infiltration over the apex of the central incisor is necessary
(see Figure 14-30 •) . (Note: Other than the difference in
anatomic location, the technique for performing a man­
dibular anterior infiltration is the same as the technique
for a maxillary anterior infiltration.)
Technique Modifications and Alternatives
An alternative to the technique previously described is to
approach the penetration from an anterior position, with
the angle of insertion parallel to the occlusal plane on the
side of inj ection (see Figure 14-3 1 •) . This is considered
by many to be a less "threatening" approach because it is
easier to keep the syringe out of the patient's line of sight.
For situations in which bilateral soft tissue anesthesia
is desired but where pulpal anesthesia of one of the two
posterior segments is not needed, many clinicians adminis­
ter mental nerve blocks on the side where only soft tissue
anesthesia is needed, in conjunction with a contralateral
lA nerve block. This approach can also be useful when
there are overlapping branches of the contralateral men­
tal nerve. In these situations, the clinician will typically use
the same 25- or 27-guage long needle that was used for lA
nerve blocks.
F I G U R E 1 4-30 Infiltration to Supplement Mental­
Incisive Injections. Incomplete anesthesia due to
cross-innervation at the midline is easily managed by
infiltration injection of the cetral incisor.
Source: Courtesy of Megan Gibbons.
Complications
Complications following mental nerve blocks are infre­
quent and can include bleeding, hematoma, and postop­
erative discomfort.
I n cisive N e rve B l ock
Incisive nerve blocks are administered for procedures re­
quiring pain management in the mandible anterior to the
mental foramen. This inj ection is nearly identical to the
mental nerve block. Unlike the mental nerve block, the in­
cisive nerve block incorporates an additional step in order
to achieve pulpal anesthesia. Some clinicians refer to this
injection as a "mental incisive" nerve block because it is im­
possible to deliver an incisive nerve block without also anes­
thetizing the mental nerve. Conversely, mental nerve block
techniques alone do not reliably anesthetize incisive nerves.
Field of Anesthesia
When the incisive nerve is anesthetized, the distributions
of both the mental and incisive nerves will be affected,
including the buccal mucous membrane and skin of the
lower lip and chin, and the pulps and facial periodontium
of the teeth anterior to the mental foramen, to the midline
(see Figures 14-32 • and 14-33 •) .
Anatomical Factors
The incisive nerve travels within the mandibular canal
from the mental foramen to the midline, and terminal
fibers frequently innervate contralateral incisors.
F I G U RE 1 4-3 1 Horizontal Approach to Needle Insertion. For
this technique, align the syringe horizontally , parallel to the oc­
clusal place, to approach the penetration site. The clinician is
seated at the 8:00 position.
Source: Courtesy of Megan Gibbons.

I ncisive
Teeth MMthetlzed :
premolars ID midline
Perlo clonll umt8Gft tiHu .. :
premolars ID midline
F I G U R E 1 4-32 Field of Anesthesia for Incisive Nerve Blocks.
The field of anesthesia for incisive nerve blocks is indicated by the
shaded area.
F I G U RE 1 4-33 Field of Anesthesia Limitations. Note
that the field of anesthesia for incisive nerve blocks
includes the soft tissue anterior to the mental foramen.
Technique Factors
The following information describes key factors for suc­
cessful incisive nerve blocks.
PEN ETRATION SITE Similar to mental nerve blocks, penetra­
tion sites vary with the locations of mental foramina. It is
helpful to locate the foramen before selecting the penetration
site. As with the mental block, it can be accomplished with
the aid of radiographs and by gentle palpation in the buccal
vestibule beginning with the first molar and moving anteri­
orly until the foramen is located, most typically in relation­
ship to the apices of the first or second premolars. It may feel
like a small depression, or "crater," or a rough elevation, or
ledge. Gentle pressure applied over the area of the foramen
frequently elicits a slight discomfort or tingling sensation.
C HAPT E R 14 • I N J E CT I O N S FOR M AN D I B U LA R PAI N C O NTROL 287
RIGHT LEFT
F I G U R E 1 4-34 Deposition Site for Incisive Nerve
Blocks. The deposition site for incisive nerve blocks is
indicated by the spotlighted area.
The site of penetration is in the mucobuccal fold su­
perior to the foramen or alternately in the mucobuccal
fold anterior to the foramen (see Figure 14-25) . This al­
ternate penetration site will be further discussed in Tech­
nique Modifications and Alternatives toward the end of
this topic.
N E E D L E PAT H WAY The needle passes through thin mu­
cosal tissues to superficial fascia containing loose connec­
tive tissue, small vessels and microvasculature, and nerve
endings.
D E PO S I T I O N S I T E The deposition site is j ust superior to
the mental foramen for both techniques discussed (see
Figure 14-34 •) .
288 S E C T I O N IV • C LI N I C AL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A
Technique Steps
Apply the basic inj ection steps outlined in Chapter 1 1 ,
"Fundamentals for Administration o f Local Anesthetic
Agents," and summarized in Appendix 1 1-1.
N E E D L E S E L E CTI O N A 25-gauge needle is recommended
for incisive nerve blocks because of the high rate of posi­
tive aspiration (nearly 6 % ) (Jastak, Yagiela,&Donaldson,
1995 ) . A 27-gauge needle is more commonly used and is
also recommended.
To gain access to the site of pen­
I N J E CTI O N PROCE D U R E
etration, the clinician is seated at a posterior position and
begins by retracting the lip and cheek laterally, pulling the
tissue taut at the mucogingival junction (see Figure 14-28).
After asking the patient to close his or her eyes, the syringe
is aligned vertically near the patient's cheek to approach the
penetration site (see Figure 14-29). Following initial pene­
tration, advance the needle tip at an angle directly vertical
to the foramen to a point just superior to it. The depth of
insertion varies with the height of the alveolar process and
the angle of tissue retraction. This is typically about 4-6 mm.
Following negative aspiration, slowly deposit a minimum
of 0.6 mL (one-third of a cartridge) of an appropriately se­
lected local anesthetic drug. Once the full dose of solution is
delivered, tissue at the injection site will bulge. Unlike men­
tal nerve blocks, the incisive nerve block requires that gentle
pressure be exerted over the bulge of solution in the direc­
tion of the mental foramen, in order to force solution through
the foramen to flood the incisive nerve (see Figure 14-35 •).
Pressure can be applied either intra- or extraorally by
the clinician or patient. It is important to remind patients,
if they are applying the pressure, that it must be applied
over the foramen and maintained with consistent pressure
for at least 1 full minute for reliable success. This injection
can be uncomfortable if adequate topical has not been ap­
plied, if inadvertent contact with bone occurs, or if solution
is administered too rapidly.
F I G U R E 1 4-3 5 Key Step to Successful Incisive Nerve.
Gently apply pressure over the bulge of solution in
the direction of the mental foramen to force solution
through the foramen to flood the incisive nerve.
Source: Courtesy of Megan Gibbons.
Confirming Anesthesia
Subj ective signs of anesthesia for the incisive (mental in­
cisive) nerve block include a sense of numbness on the in­
j ected side, including the buccal mucous membrane, skin
of the lower lip and chin, and the pulps and periosteum
anterior to the mental foramen to the midline. Objective
signs include a lack of response to gentle stimulation with
an instrument and no pain during procedures involving
the premolars, canine, and incisors.
Common Causes of Injection Failure
This inj ection is highly successful. Failure to achieve anes­
thesia of the incisive and mental nerves is uncommon. This
usually involves failure to correctly identify the location of
the foramen, which results in insufficient diffusion of solu­
tion into it. This can also result from anatomical factors, such
as unusually small foramina, or technical factors, such as in­
sufficient duration or incorrect location of pressure over the
foramen following the injection. Other causes may include
inflammation or infection in the area of deposition.
Troubleshooting
When inadequate anesthesia occurs, reassess the deposi­
tion site for proximity to the foramen. It is also possible
that the direction or duration of the postinjection pressure
was inadequate or that insufficient volumes were depos­
ited preventing successful passage of solution through the
foramen.
Technique Modifications and Alternatives
As with mental nerve blocks, the deposition site may be
approached from an anterior position, with the angle of
insertion parallel to the occlusal plane on the side of inj ec­
tion. This is considered by many to be a less "threatening"
approach, as the syringe may be below the patient's line of
sight (see Figure 14-3 1 ) .
For situations i n which bilateral anesthesia i s desired, but
posterior anesthesia of one of the quadrants of the mandible
is not needed, many clinicians administer incisive nerve blocks
on the side where posterior anesthesia is not needed in con­
junction with contralateral lA nerve blocks. This approach
can also be useful when there are overlapping branches of the
contralateral incisive nerve. In these situations, the clinician
will typically use the same 25- or 27-gauge long needle that
was used for the contralateral lA nerve block.
Complications
Following incisive nerve blocks, complications are infre­
quent and can include bleeding, hematoma, and postop­
erative discomfort.
G ow-Gates N e rve B lock
Similar to lA nerve blocks, Gow-Gates (GG) nerve blocks
are indicated for pain management of multiple teeth in
one quadrant. Unlike lA blocks, GG nerve blocks are

"true" mandibular blocks because they routinely anesthe­
tize the full extent of a mandibular quadrant (Gow-Gates
&Watson, 1977; Jastak, Yagiela, &Donaldson, 1995; Mal­
amed, 20 13).
Field o f Anesthesia
GG nerve blocks routinely anesthetize structures inner­
vated by the inferior alveolar, mental, incisive, lingual,
mylohyoid , and auriculotemporal nerves to the midline.
Unlike lA nerve blocks, GG nerve blocks anesthetize the
buccal nerve 75 % of the time (see Figure 14-36 •) .
Anatomical Factors
As previously discussed, the inferior alveolar nerve is the
largest branch of the mandibular division of the trigeminal
nerve. It branches from the posterior division of the man­
dibular nerve within the infratemporal space, then travels
medial to the lateral pterygoid muscle and passes through
the pterygomandibular space between the sphenomandib­
ular ligament and the medial surface of the ramus of the
mandible. It then enters the mandibular foramen and trav­
els through the mandibular canal (B aker, 20 10; Hamburg,
1972; Jastak, Yagiela, &Donaldson, 1995 ; Pansky &Gest,
2014).
Numerous arteries and veins are also located within
infratemporal and pterygomandibular spaces. The maxil­
lary artery traverses the infratemporal space either super­
ficial or deep to the lateral pterygoid muscle. The middle
meningeal artery branches from the maxillary artery
within the space, whereas several other arteries, including
the inferior alveolar, branch off afterward.
The inferior alveolar vein travels within the mandibular
canal along with the inferior alveolar artery and nerve. It ex­
its through the mandibular foramen, travels medioanteriorly
with the inferior alveolar artery, through the pterygomandib­
ular and infratemporal spaces, and drains into the pterygoid
plexus of veins located in the infratemporal space.
GG
(G--Oat..)
Teeth an..thetlzed:
all teeth I n quadrant
Periodontium/Soft tluuea:
all periodontiu m , buccal mucosa
premolars to midline,
ftoor of mouth and
% longue in quadrant
F I G U RE 1 4-3 6 Field of Anesthesia for G G Nerve Blocks. The
field of anesthesia for GG nerve blocks is indicated by the shaded
area.
C HAPT E R 14 • I N J E CT I O N S FOR M AN D I B U LA R PAI N C O NTROL 289
Importantly, although the deposition site of local anes­
thetic solution in a GG nerve block is often at least 5-10 mm
from the inferior alveolar nerve trunk (which includes the
inferior alveolar, lingual, and 75 % of the time, the buccal
nerve) , the relatively structure-free upper portion of the
pterygomandibular space does not restrict the downward,
anterior, and medial movement of solution. In fact, the
initial volume of solution recommended (about 1.8 mL or
more) nearly fills the pterygomandibular space at that level.
Technique Factors
The following information describes key factors for suc­
cessful GG nerve blocks.
P E N ETRAT I O N SITE The penetration site is located in the
buccal mucous membrane, directly posterior to the max­
illary second molar, at the level of its mesiolingual cusp.
The precise location, however, is variable and must be
established using extraoral landmarks, in addition to the
intraoral landmarks. The existence of both intra- and
extraoral landmarks makes the G G block unique (see
Figure 14-37 •) .
N E E D L E PAT HWAY The needle passes through thin mu­
cosal tissues and limited amounts of superficial fascia that
contain loose connective tissue, small vessels and micro­
vasculature, large vessels, and nerve endings. Typically, less
resistance to forward movement is encountered in the up­
per portion of the pterygomandibular space because it is
relatively free of blocking fascia.
D E PO S I T I O N S I T E The deposition site is on the antero­
lateral surface of the neck of the condyle, j ust below the
insertion of the lateral pterygoid muscle. The deposition
site for GG nerve blocks is at the highest point in the
pterygomandibular space of all three mandibular block
techniques, lA (lowest) , Akinosi (intermediate) , and Gow­
Gates (highest) (see Figures 14-38 • and 14-45 •) .
290 S E C T I O N IV • C LI N I C AL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A
F I G U R E 1 4-37 P enetration Site for G G Nerve Blocks.
The penetration site for GG nerve blocks is indicated by
the needle.
F I G U R E 1 4-38 Deposition Site for GG Nerve Blocks.
The deposition site for G G nerve blocks is indicated by
the spotlighted areas.
Technique Steps
Apply the basic inj ection steps outlined in Chapter 1 1 ,
"Fundamentals for Administration o f Local Anesthetic
Agents," and summarized in Appendix 1 1-1.
N E E D L E S E L E C T I O N A 25-gauge long needle is recom­
mended, consistent with the depth of penetration, which
is equal to or greater than the depth of an lA block for
the same individual. The rate of positive aspiration is con­
sidered to be relatively low (2% ), but some sources have
F I G U RE 1 4-3 9 GG Nerve Blocks: Key Landmarks 1.
A line visualized from the intertragic notch to the labial
commissure is indicated by the cotton swab. This is the
angle of the needle pathway. Observing the flare of the
tragus can indicate the corresponding flare of the ramus
of the mandible.
F I G U RE 1 4-40 GG Nerve Blocks: Key Landmarks 2.
The optimum height of penetration is indicated by the
height or most occlusal aspect of the mesiolingual cusp
of the second molar.
placed this rate much higher, reinforcing the recommenda­
tion of 25-gauge needles (Watson, 1992) .
I N J E CTI O N PROCE D U R E In preparing for GG nerve blocks,
there are two key landmarks to observe:
1. a line visualized from the intertragic notch to the la­
bial commissure (Figure 14-39 •)
2. the height or most occlusal aspect of the mesiolingual
cusp of the second molar (Figure 14-40 •)
The flare of the tragus of the ear is also important be­
cause it can provide confirmation regarding the location
of the barrel of the syringe (see Figure 14-39). Although
not a critical landmark (the flare of the ramus can also
be assessed by visualization and external palpation of the
posterior mandible and condyle) , the flare of the tragus is
nevertheless useful in confirming barrel location (see Fig­
ures 14-39 and 14-41 •) . The significance of all landmarks
will be explained in the following discussion:

F I G U R E 1 4-4 1 GG Nerve Blocks: The "Wide Open"
Technique. GG nerve blocks require that the mouth re­
main wide open during the entire procedure, including a
2-minute period after completion of the injection.
F I G U R E 1 4-42 Variations of Syringe Angulations
for the G G Nerve Block. The barrel orientation to
the molars is variable with the GG nerve block. The
orientation of the barrel is dependent on the flare of the
ramus and condyle. Note the unilateral differences in the
flare of the ramus of this mandible.
GG nerve blocks require that the mouth remain wide
open during the entire procedure (see Box 14-1 1 •). This an­
terior orientation of the mandible allows the condyle to re­
main fully translated over the articular eminence and provides
needle access to the neck of the condyle (see Figure 14-41 ).
Retract the cheek laterally to gain access to the site
of penetration. While keeping the thumb on the coronoid
process, place the index finger over the intertragic notch.
The line between these two points provides the upward an­
gulation of the syringe for this injection (see Figure 14-41).
Unlike lA nerve blocks, the barrel orientation to the mo­
lars is more variable. Orientation of the barrel is dependent
on the flare of the ramus and condyle. See Figure 14-42 •
for an example of asymmetrical flare of the condyles on the
same mandible. Each side would require different angula­
tions. Dr. Gow-Gates observed that the flare of the tragus of
the ear roughly corresponded to the barrel orientation over
C HAPT E R 14 • I N J E CT I O N S FOR M AN D I B U LA R PAI N C O NTROL 291
•
Criti ca l to the s u ccess of G G n e rve b l o cks, patie nts m ust
re m a i n in wide open positi o n s t h ro u g h o u t p roced u res, a n d
a p p roxi m ately 30-60 seco nds fo l l ow i n g d e p ositi o n . If t o l e r­
ate d , it c a n be h e l pfu l to p l ace a b ite b l ock i n t h e m o uth
as soon as the n e e d l e has been with d rawn . Another key to
s u ccess is to seat the patient u p r i g h t i m m ed i ately fo l l ow i n g
t h e i nj e cti o n , to fa c i l itate d iffus i o n towa rd t h e n e rve.
C l o s u re at a n y time d u r i n g a G ow-G ates p roced u re
can p revent t h e n e e d l e fro m re a c h i n g t h e depositi o n site .
C l os u re i m m e d i ately u p o n co m p l et i o n of t h e i nj e cti o n a n d
•
fa i l u re t o u p r i g h t t h e patient c a n c a u s e d iffus i o n of s o l ut i o n •
: ; �� �
awa r th n v
: • • • . . . �� � � • • • • • • • • • • • • • • • • • • • • • • • • .
the lower dentition. A tragus that arises from the side of the
face at a right angle suggests a more posterior location of
the barrel of the syringe, over the molars. One that is flush
with the face suggests a more anterior location of the barrel,
over the canine and incisors. A tragus at a 45-degree angle to
the face suggests a barrel orientation that is initially over the
premolars. It is important to note that these are typical start­
ing points, and adjustments may be necessary.
Advance slowly until resistance is met, confirming that
the tip of the needle has reached the condylar neck (see Fig­
ure 14-38). If contact is not made and the needle is nearly fully
inserted, it is likely that medial deflection has occurred. To ad­
just for this deflection, withdraw the needle slightly, reposition
the barrel of the syringe posteriorly, and reinsert until contact.
In practical terms, the deposition site is confirmed
by gently contacting bone at the neck of the condyle. The
insertion depth is variable, although typically it is about
25 mm. It has been described as being the same to some­
what greater than the penetration depth of lA nerve
blocks for the same individual.
Once contact has been establishe d , withdraw the
needle 1 mm and, following negative aspiration, deposit a
minimum of 1.8 mL (one cartridge) of an appropriately se­
lected local anesthetic drug.
Confirming Anesthesia
Subjective signs and symptoms of anesthesia for GG nerve
blocks include a sense of numbness on the injected side, which
includes the buccal and lingual mucous membranes, the skin of
the tongue, lower lip, chin, and ramus of the mandible, and the
pulps and periodontium of the teeth as well as the distributions
of the mylohyoid, buccal (75 % of the time), lingual, and auric­
ulotemporal nerves. Objective signs include a lack of response
to gentle stimulation with an instrument and no pain during
procedures involving the molars, premolars, and incisors.
Common Causes of Injection Failure
As with any technique, failures may occur because of lack
of experience. This seems particularly true for GG nerve
blocks because of the use of both intra- and extraoral
292 S E C T I O N IV • C LI N I C AL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A
landmarks and the importance of postinj ection protocols.
In addition, Dr. Gow-Gates used cartridges that contained
greater volumes of solution (2.2 mL) compared with car­
tridges containing 1.8 mL. Volumes higher than 1.8 mL
may be necessary at times in order to provide reliable and
profound anesthesia because of the distance from depo­
sition site to target. Onset is also much slower compared
with many other techniques (estimated at anywhere from
5 to 10 minutes, although frequently closer to 10). Because
of slow onset times, less familiar clinicians may declare
failure prematurely.
As previously mentioned, failure to upright patients
after making the needle safe and to instruct them to re­
main in wide open positions both during and after the
procedure can cause solution to diffuse away from the
nerve.
Troubleshooting
When inadequate anesthesia occurs, reassess the deposi­
tion site, the flare of the tragus, the line from the intertragic
notch to the angle of the mouth, the barrel orientation, the
ability of the patient to maintain a "wide open" position
during and following the injection, prompt uprighting, and
the volumes of solution deposited.
Modifications may include the selection of more lat­
eral or more medial penetration sites, slightly higher or
lower penetration sites, and the use of more concentrated
drugs such as 4% articaine, 4% prilocaine, and 3 % mepi­
vacaine. Greater volumes of solution may also be effective,
particularly if 1.8 mL fails repeatedly to achieve profound
anesthesia in a particular patient.
Technique Modifications and Alternatives
Alternatives include IA nerve blocks, PDL injections, VA nerve
blocks, incisive nerve blocks, and intraosseous techniques.
Complications
Injury can occur from inj ection into the temporomandibu­
lar j oint capsule and otic ganglion. The most reliable way
to prevent injury to these structures is to confirm that the
needle is at the neck of the condyle by making gentle con­
tact with bone.
Although the rate of positive aspiration with G G
nerve blocks i s reportedly low, there are maj or vessels in
the pathway of this inj ection. The large and prominent
maxillary artery and a maj or branch, the middle menin­
geal artery, are located in the superior portion of the pter­
ygomandibular space.
Possible temporary paralysis of cranial nerves III ( oc­
ulomotor) , IV (trochlear) , and VI (abducens) may occur
on occasion and will resolve as soon as the anesthetic ef­
fect diminishes (Fish, Mcintire,&Johnson, 1989; Malamed,
20 13 ) . This may have occurred because of missing the tar­
get area or failure to adequately aspirate before inj ection
(Johnson &B adovinac, 2007 ) . Hematomas and trismus
of the lateral pterygoid muscle have also occurred with
typical uneventful healing (B udenz & Osterman, 1995 ;
Malamed, 2006) .
A rare postoperative complication affecting the mid­
dle ear was reported in 2001. It was concluded that the
effects were likely the result of inflammation or occult
(concealed) hematoma formation or both (Bro dsky &
Dower, 200 1 ) .
Vaz i ra n i-Aki nosi N e rve B lock
Vazirani-Akinosi nerve blocks are ideal for pain manage­
ment of the mandibular teeth in a single quadrant when
j aw opening is limited because of physiologic, pathologic,
or phobic circumstances. This inj ection is also referred
to as the Akinosi or " closed-mouth" technique (Jastak,
Yagiela,&Donaldson, 1995 ; Malamed, 20 13 ) .
Vazirani-Akinosi nerve blocks may also be of use in
initiating anesthesia in fearful patients who will not open
their mouths wide enough for IA nerve blocks. In this situ­
ation, Akinosi blocks can be used to provide profound an­
esthesia of the structures through which the needle passes
in IA nerve blocks. The IA nerve blocks can then be ad­
ministered comfortably.
Field of Anesthesia
B ecause of their location, Vazirani-Akinosi nerve blocks
can provide wider areas of anesthesia compared with IA
nerve blocks and slightly more limited areas compared
with GG nerve blocks. The inferior alveolar, mental, inci­
sive, lingual, mylohyoid, and frequently buccal nerves are
all affected (see Figures 14-1 , 14-18, and 14-21).
Anatomical Factors
Relative to IA and GG nerve blocks, Vazirani-Akinosi
nerve blocks are administered in an intermediate position
in the pterygomandibular space. Their location actually
places them closer to target nerve trunks. Tissue resistance
is minimal because of the relative lack of fascia that might
deflect needles or solutions.
Technique Factors
The following information describes key factors for suc­
cessful Vazirani-Akinosi nerve blocks.
P E N ETRAT I O N S ITE The site of penetration is in the soft
tissue medial to the ramus, directly adj acent to the maxil­
lary tuberosity at the height of the mucogingival junction
of the maxillary molars (see Figure 14-43 •) .
N E E D L E PAT H W AY The needle advances slowly
through thin mucosal tissue parallel to the mandibular
molar teeth and passes lateral to the me dial pterygoid
m u s c l e , l i n g u a l n e r v e , and s p h e n o m a n d i b u l a r l i g a ­
m e n t , w e l l s u p e r i o r t o t h e ling u l a a n d m a n d i b u l a r
foramen.
D E PO S I T I O N S I T E The deposition site is well above the
mandibular foramen on the medial surface of the ramus
in the pterygomandibular space (see Figure 14-44 •) .
Figure 14-45 • shows the deposition site in comparison to
both the IA and GG nerve blocks.

F I G U R E 1 4-43 P enetration Site for VA Nerve Blocks.
The penetration site for VA nerve blocks is indicated by
the needle.
FIGURE 1 4-44 Deposition Site for VA Nerve Blocks.
The deposition site for VA nerve blocks is indicated by the
spotlighted area.
F I G U R E 1 4-4 5 Deposition Site Differences: IANB,
G GNB, VANB. Note the differences in the deposition
site of each of these nerve blocks: A - Inferior alveolar,
B-Vazirani-Akinosi, C-Gow-Gates. The height of the
coronoid notch is indicated by the dotted line.
Technique Steps
Apply the basic inj ection steps outlined in Chapter 1 1 ,
"Fundamentals for Administration o f Local Anesthetic
Agents," and summarized in Appendix 1 1-1.
C HAPT E R 14 • I N J E CT I O N S FOR M AN D I B U LA R PAI N C O NTROL 293
N E E D L E S E L E CT I O N Both 25- and 27-gauge long needles
are recommended, consistent with penetration depths that
do not exceed 25 mm. Moderate positive aspiration rates
between 5% and 1 0 % have been observed with this tech­
nique (Malamed, 20 13; Johnson &Badovinac, 2007).
INJ ECTION PROC E D U RE With the patient's teeth in a comfort­
ably closed position (not maximum intercuspation), gain ac­
cess to the site of penetration by retracting the cheek laterally.
Penetrate in the soft tissue medial to the ramus, directly
adjacent to the maxillary tuberosity at the height of the mu­
cogingival junction of the maxillary molars (see Figure 14--43 ).
The angle of insertion is parallel to the mandibular molar teeth.
Advance slowly to the deposition site medial to the
ramus and well superior to the mandibular foramen to a
depth of 25 mm for the average adult patient (Haas, 20 1 1 ) .
This depth i s approximately one-half the anteroposterior
dimension of the ramus in the area. Contact with bone is
unusual and is not desired in this inj ection. Although mini­
mal, there is a tendency for deflection away from the nerve
with Vazirani-Akinosi nerve blocks; therefore, it is advised
that bevels be oriented medially to encourage lateral de­
flection toward the ramus. Some clinicians prefer to bend
the needle slightly toward the mandible in order to avoid
penetrating the medial pterygoid muscle (Haas, 20 1 1 ) . If a
decision is made to bend the needle, the bend should not
be made at the hub. Following negative aspiration, deposit
1.8 mL (one full cartridge) of an appropriately selected
local anesthetic drug and seat the patient upright after
withdrawal.
Confirming Anesthesia
Subjective signs and symptoms of anesthesia for Vazirani­
Akinosi nerve blocks include a sense of numbness on the
inj ected side, including the buccal and lingual mucous
membranes, the tongue, skin of the lower lip and chin, the
ramus of the mandible, and the pulps and periodontium
of the teeth on the side of inj ection as well as the distribu­
tion of the mylohyoid nerve. Obj ective signs include a lack
of response to gentle stimulation with an instrument and
no pain during procedures involving the molars, premolars,
and incisors.
Common Causes of Injection Failure
As with any inj ection, failures may occur because of lack
of experience with the technique. This seems particularly
true for Vazirani-Akinosi nerve blocks. Haas suggests a
success rate of roughly 80 % to 85 % , similar to lA nerve
blocks, whereas Akinosi claimed a success rate of 93 %
with Vazirani-Akinosi nerve blocks; however, many have
been frustrated when performing this technique (Johnson
&Badovinac, 2007; Haas, 20 1 1 ) . Whether this is because
of a lack of specific landmarks, or to a lack of comfort with
the closed position or both, is not known.
In the event of medial deflection of the needle, solu­
tion may be deposited medial to the sphenomandibular
ligament, which may prevent it from reaching the nerve.
When penetration is too low, the deposition will be at a
2 94 S E C T I O N IV • C LI N I C AL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A

further distance from the nerve because of the flare of the Complications
ramus. Over- or under-insertion may place the solution too Complications are rare and include hematomas, trismus,
far from the nerve. Because there is no confirming contact and postoperative soreness.
with bone, the location of the tip of the needle is more
speculative compared with lA and GG blocks.

Troubleshooting CASE MANAGEMENT

When Vazirani-Akinosi nerve blocks are unsuccessful, it
may be helpful to reevaluate anatomy and technique steps. Lee Chung
In some instances, anatomy differs markedly from typical A l eft l A n e rve b l o c k w a s a d m i n i s t e r e d to L e e
patterns and may make alternate nerve blocks (discussed C h u n g a l o n g w i t h a b u cca l n e rve b l ock fo l l owed by
previously in this chapter) or supplemental techniques a m e ntal i n cisal n e rve b l ock o n the right s i d e . I nter­
such as the PDL inj ection more effective (see Chapter 15, p a p i l l a ry i nj e cti o n s between #2 7, 2 8, a n d 29 were
"Supplemental Techniques and Adjunctive Strategies"). a l so a d m i n istered to p rovi d e a n esth esia of t h e l i n ­
g u a l g i n g iva o f these teeth (th ese i njections d o n ot
Technique Modifications and Alternatives a n esthetize the to n g u e on the right side).
Modifications to the technique are necessary for individu­ Case Discussion: B i l atera l m a n d i b u l a r a n est h e s i a,
als in whom the anteroposterior dimension of the ramus is a lt h o u g h n ot contra i n d i cated, s h o u l d be avo i d e d
considerably smaller than typical, including children and w h e re possi b l e because o f the co n s i d e ra b l e a ltera­
adults with smaller mandibles. Penetration depth must be tion of fu n ct i o n that fo l l ows. N u m b i n g the e n t i re
adjusted accordingly. to n g u e, i n p a rt i c u l a r, p l a ces patie nts at r i s k both
Alternatives for Vazirani-Akinosi nerve blocks in­ d u ri n g treatment a n d afterwa rd because of t h e l oss
clude G G, lA, and incisive nerve blocks, as well as in­ of n o r m a l p rotective fee d b a c k m e c h a n isms. These
filtrations and supplemental techniques, such as PDL m e c h a n i s m s m a y rem a i n o p e ra b l e u n d e r local a n ­
inj ections. est h e s i a b u t t h e y req u i re s e n s a t i o n fo r i n it i a ti o n .
The Vazirani-Akinosi block can be particularly useful in Fore i g n su bsta n ces a n d i nj u ri o u s s u bsta n ces, s u c h
children and adults who are reluctant to open and in any pa­ as hot l i q u i d s, w i l l not b e sensed a n d can res u lt i n
tients who are unable to open wide enough for other inj ec­ everyt h i n g fro m i n h a lation o f fo re i g n o bjects t o lo­
tion techniques to be performed. This can be the case when c a l tiss u e d a m a g e and a n i n a b i l ity to s p e a k co h e r­
an infection, requiring immediate treatment, makes opening ently. A u n i l atera l b l ock of t h e to n g u e wi l l p rovi d e
painful. By relieving painful symptoms, a Vazirani-Akinosi m o re reaso n a b l e feedback.
block can allow the patient to open wide to be treated.

.�.h. Cl. P..t.E! r. . 9.l1.���.i.C>.r1 � . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4. When administering a Gow-Gates mandibular nerve

block, all of the following are essential, except:
1 . The rate of positive aspiration in the inferior alveolar a. Performing one or more aspirations
nerve block is the highest of all techniques and b. Meeting bony resistance
approximates which one of the following? c. Determining the site, height, and depth of penetra­
a. 2 % -5 % tion as well as the syringe barrel orientation
b . 5 %-10% d. Having the client remove all ear j ewelry before
c. 1 0 % -15 % administering
d. 1 5 % -20 % 5. Palpating anatomy before all mandibular anesthetic
2. Which one of the following techniques is an alterna­ procedures is:
tive to nearly all mandibular anesthetic techniques? a. An unnecessary step in anesthesia techniques
a. Gow-Gates b. Helpful in some techniques and useless in others
b. Vazirani-Akinosi c. The least important aspect of anesthetic assessment
c. PDL d. Critical to the success of these techniques
d. Infiltrations 6. Which one of the following is the correct order,
3. Which one of the following result(s) in pulpal from inferior to superior location, of the mandibular
anesthesia? techniques listed in relation to the pterygomandibular
a. Buccal nerve block space?
b. Mental nerve block a. lA, Gow-Gates, Akinosi
c. A and B b. lA, Akinosi, Gow-Gates
d. Neither A nor B c. Gow-Gates, lA, Akinosi
d. Akinosi, lA, Gow-Gates

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Garisto, G. A., Gaffen, A. S. , Lawrence, H. P., Tenenbaum, H. C.,
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Gow-Gates, G. A., & Watson, J. E. (1977). The Gow-Gates
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Gow-Gates, G. (1979). Master's Thesis University of Sydney.
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Comparing anesthetic efficacy of articaine versus lidocaine
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complimentary study tools created for this specific title.
C HAPT E R 14 • I N J E CT I O N S FOR M AN D I B U LA R PAI N C O NTROL 295
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 Field of Anesthesia
Nerve Block Needle Penetration Site Deposition Site Dose'
See Appendix 1 4-2
Inferior alveolar Long Med ial to i nternal Depth of Insertion � of lnsfton 1 .5-1 . 8 m l Teeth anesthetized:
{ lA) w/ lingual 25/27 gauge oblique ridge, lateral
to pterygomandibular lei to :Y. length of lei to '/. length of All teeth in quadrant
raphe, at or above need I\ until contact needle until contact
with one bevel with bone, bevel
height of coronoid notch
toward b one toward bone
see Figure 1 4-7
Target Periodontium/Soft
tissues:
On medial su rface of ramus, slightly superior
to mandibular foramen All periodontium, buccal
see Figure 1 4- 1 0 mucosa eremolars to
midl ine, floor of mouth
and 1/2 tongue i n
quadrant ( n o t soft
tissues buccal to molars)

Buccal Short' or Mucous membrane Depth of Insertion Angle of .__ 0 . 2-0. 3 Teeth anesthetized:
long" 25/27 distal and lateral to ml'
gauge most posterior molar # 4 mm, bevel under St i n p e parallel to oc - None
see Figure 1 4-22 tissue, bevel toward c usa plane lateral to ' Width of
bone teeth , rubber
• When g iven
bevel toward bone stopper
alone
" Usually given Target Periodontium/ Soft
following lA tissues: ::J
Supraperiosteal, distal, and buccal to most '-- ·
posterior molar Buccal to molars ([)
see Figure 1 4-23

Mental (M) Short Mucobuccal fold at or just Depth of Insertion Angle of .__ 0.6 ml Teeth anesthetized:
�
Incisive {I) 25/27 gauge anterior to mental foramen
5-6 mm Approximately 20 (M) pulpal limited
0
see Figure 1 4-25
deg rees to lon r, axis of to tooth at site of ::J
premolars, evel infi ltration (f)
toward bone (I) premolars to midline
Target Periodontium/Soft
�
Slight superior to mental foramen,
Note: I) Keep pressure over foramen
tissues:
Premolars to midline
for 1 minute alter injection
see Figure 1 4-26
!Continued)
 Field af Anesthesia
Nerve Block Needle Penetration Site Deposition Site Dose•
See Appendix 1 4-2
Gow-Gates Long Distal to maxi llary second Depth af Insertion Angle af Insertion 1 .8 m L Teeth anesthetized:
(GG) 25/27 gauge molar at hei p ht of
mesiol ingua cus7 1/2 to 3/4 length of Barrel of syrin �e in All teeth in quadrant
see Figure 1 4-3 need le, MUST contact corner of mout on
bone opposite side. Proceed
on a parallel line from
corner of mouth to
tragus

Target Periodontium/Soft
tissues:
Lateral side of condylar neck
Note: Patient should keep mouth open All periodontium, buccal
for 1 -2 minutes after in jection, mouth mucosa premolars
prop recommended to midline, f loor of
see Figure 1 4-38 mouth and 1/2 tongue
in quadrant
Local i nfi ltration Extra-shor t or Mucobucca l fold buccal Depth aF Insertion At9e of I.-lion 0.6 m L Teeth anesthetized:
in jections shor t to tooth
25/27/30 see Figure 1 4-30 3-6 mm to apex Approximately 20 At injection site
gauge de rees to long axis
oJ tooth, d i reeled
toward apex of tooth,
bevel toward bone

Target Periodontium/Soft
tissues:
Selected soft tissue, gingival or apex of tooth
At i njection site
Field of Anesthesia
lA I nc isive
(w/ lingual)

Mandibular I njections
Teeth anaathetlzad :
Teeth anesthetized:
premolars to midline
all teeth i n quadrant
GG
Periodonti um/Soft Uaauaa:
Periodonti um/Soft tissues: (Gow-Gatea)
premolars to midline
all periodont i u m , buccal m u cosa Teeth anesthetized:

premolars to m i d l i n e , all teeth i n quadrant

M e ntal
floor of mouth and
Periodonti um/Soft tiaaues:
Y.. tongue i n q uadrant Teeth a nesthetized:
a l l periodontium , b u ccal mucosa
pul pal l i m ited to tooth
premolars to midline,
at site of infi ltration
B u ccal floor of mouth and

Teeth anesthetized: Y.. tongue in quadrant Periodonti u m /Soft tissues:

none

Periodonti um/Soft tissues:

I nfi ltrati o n

buccal to molars Teeth anesthetized:

at injection site

Pe riodonti um/Soft tissu es:

at injection site
Tongue - Lateral View

RIGHT LEFT
32 3 1 30 21 28 27 2S 25 2.. 23 22 21 20 11 1 8 17

Court"yof:

Upper/Lower Arch Tongue - U nderside

Source: Courtesy of LED Dental.

298
OBJECTIVES KEY TERMS

• Defi n e a n d d i sc u ss t h e key terms in t h i s c h a pte r. B a c kflow 300

b l a n c h i n g 302
• An a l yze a n d d i scuss t h e i n d i ca t i o n s , re l eva n t a n ato m y, a n d
ca n c e l l o u s b o n e 305
tech n i q u e fe atu res o f t h e i nj e cti o n s d i scu ssed i n t h i s c h a pter.
co m p uter-co n t ro l l e d l o ca l
• Describe t h e b a s i c tech n i q u e ste ps fo r safe a n d effective a n est h etic d e l ive ry (CCLAD)
a d m i n i st ra t i o n fo r the fo l l owi n g i nj e cti o n s : d evices 300
• P e r i o d o n ta l l i g a m e nt ( P D L) cortica l p l ate 305
• I ntraosse o u s d e nta l p l ex u s 305
d e p os i t i o n site 300
• l n tra se pta l
i n t ra l i g a m e n t a ry 300
• l n tra p u l p a l
i ntraoss e o u s 300
• D i scuss t h e p h a rm a c o l o g y o f b u ffe r i n g 2% l i d o ca i n e , 1 : 0 0 , 000 i n t ra p u l p a l 311
e p i n e p h ri n e so l u t i o n s . i n trasepta l 309
• I d e n tify pote n ti a l p a t i e n t b e n efits of b u ffe ri n g 2% l i d o ca i n e , n e e d l e pathway 300
1 : 00 , 000 e p i n e p h ri n e so l ut i o n s . O n set® 313
O raVe rse® 313
• Descri be t h e m o d e of a ct i o n of p h e n to l a m i n e m esylate a n d its
p e n etration site 300
i m p l icati o n in d e ntistry.
p e r i d e n t a l 300
• cribe t h e b a s i c tech rl!i q u e ste ps fo r safe a n d effective p e r i o d o n t a l l i g a m e n t ( P D L)
adm1 tion fo f t h e fo l l owi n g : i nj e ct i o n 300
• O n set s p o n g y b o n e 305

299
300 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E S T H E S I A
CASE ST U DY
John Jones
J o h n J o n e s , a 4 5 -y e a r- o l d m a l e , p re s e n t e d fo r
treatment at a u n ive rsity c l i n i c fo r a resto rative pro­
ced u re o n tooth #4. A s h e was b e i n g seate d , he
stated that h e had d re a d e d this a p p o i nt m e n t be­
cause n o one had eve r been a b l e to n u m b #4. " It's
t h e o n l y tooth t h ey ca n 't n u m b , " h e s a i d to t h e
stu dent. S i g n ificantly, h e re m e m be red the toot h 's
n u m ber.
An i nfiltrati o n u s i n g 2% l i d o ca i n e with
1 :100,000 e p i n e p h ri n e was attem pted but fa i l e d to
p rovide any signs o r sym ptoms of a n esthesia in the
a re a , n ot even i n the soft tiss u e s . The stu d e nt d e ­
c i d e d t o u s e a rtica i n e but a s e c o n d i nfi ltratio n with
4% a rtica i n e with 1 : 1 00,000 e p i n e p h ri n e y i e l d e d
n o bette r resu lts . A t h i rd i nfi ltratio n with a rtica i n e ,
w h e re the p e n etrati o n site w a s l o cated as h i g h as
poss i b l e i n t h e vesti b u l e , res u lted i n w i d e s p re a d
a n esthesia over the b u ccal su rface o f the tooth a n d
u p p e r l i p but a p u l p test q u ickly p roved t h a t p u l pa l
a n esthesia was i n a d e q u ate.
I ntrod u ction
Anatomic landmarks and considerations for each supple­
mental inj ection technique discussed will be presented
in reference to the penetration site, needle pathway, and
deposition site as described in Chapter 1 1 , "Fundamentals
for Administration of Local Anesthetic Agents." The
penetration site will be related to hard and soft-tissue
landmarks. The needle pathway will be described in terms
of the types of tissue that will be penetrated by or located
in the vicinity of the needle, including mucosa, superficial
fascia, muscle, vessels, nerves, and bone. The deposition
site will be described in terms of the tissues at or near the
target and in relation to specific landmarks.
S u p p l e m e nta l I njecti o n Tech n i q ues
This chapter will discuss supplemental inj ection techniques
that are used primarily in special situations in dentistry.
Key elements for each of these inj ections are summarized
in Appendix 15-1. Common applications, variations, and
precautions will be discussed where applicable.
Pe riodonta l L i g a m e nt I njecti o n
Perhaps the most universal o f the supplemental inj ections
is the periodontal ligament (PDL) inj e ction. This tech­
nique is indicated as a primary method of anesthesia for
single teeth, for supplemental anesthesia of individual teeth
when other techniques have failed to provide profound
anesthesia, when widespread anesthesia is contraindicated,
and when total doses need to be minimized (Blanton &
Jeske, 2003 ) . It can also be beneficial for individuals with
bleeding disorders and when needle insertions into vascu­
lar regions may be a risk and, in some very specific appli­
cations, may provide widespread anesthesia when inferior
alveolar blocks have failed to provide it. The PDL is also
referred to as an intraligamentary or peridental technique.
PDL injections are classified as intraosseous techniques be­
cause they appear to rely on diffusion of solution through
bone in order to achieve anesthesia.
A standard dental syringe can be used to administer
PDL inj ections. Specialized syringes for administering
these inj ections have been available for over a century
and provide for easier delivery of anesthetic solution.
As discussed in Chapter 9, " Local Anesthetic D elivery
D evices," these syringes require l e s s hand pressure.
Computer-controlled local anesthetic delivery (CCLAD)
devices eliminate manual pressures altogether, and regu­
late the rate of delivery of anesthetics electronically.
Field of Anesthesia
PDL inj ections anesthetize individual teeth at the sites of
inj ection and their associated periodontium. The field of
anesthesia is minimal. Individual teeth can be profoundly
anesthetized along with their lingual and buccal mucosa
without any anesthesia of the tongue or cheek.
Occasionally, more widespread anesthesia can develop
from PDL inj ections in the mandible providing anesthesia
to all of the teeth on one side (discussed in Box 15-1 • ), or
when 4% articaine is used, which has reportedly provided
wider areas of anesthesia (Quinn, 1998; Reitz et al. , 1998a)
(see Figure 15-1 •) .
Anatomical Factors
PDL inj ections deposit anesthetic solution into the peri­
odontal ligament. Anesthetic solutions diffuse through
alveolar bone to the apex of inj ected teeth. Solution does
not diffuse through dense, fibrous periodontal ligament. In
order to arrive at apical regions of teeth, solution follows
paths of least resistance, which includes thin, porous layers
of alveolar bone proper and spongy underlying bone sur­
rounding the ligaments and teeth. To better appreciate this
difference in resistance, imagine creating a pool of anes­
thetic solution over a sheet of dense, fibrous periodontal lig­
ament versus creating the same pool over porous alveolar
bone. The bone will absorb the solution much more readily.
In order to diffuse through bone, solution must be fully sur­
rounded by and enclosed between dense fibers of the peri­
odontal ligament and the teeth. If solution fails to enter the
periodontal ligament, it will flood the sulcus, following the
path of least resistance. Solutions will then backflow (leak)
into the patient's mouth rather than diffuse through bone.
Technique Factors
Key factors for successful PDL inj ections are discussed as
follows.
 C HAPTER 15 • S U PPLE M E NTAL TEC H N IQU ES A N D ADJU N CTIVE STRATEG I E S 301

Symptomatic veri f i c ation of anesthesia following l A nerve Some clinicians have observed profound inferior
blocks can be problematic. Despite confirmation that the al veolar nerve anesthesia developing after admini stering
teeth, lip, and chin "feel" numb before treatment, pain i s PDL injections around al l four aspects of the mandibular
sometimes experienced. This can occur because of what second molar (ML, DL, DB, MB). The location of the
i s referred to as accessory innervation where fibers from mandibular canal in proximity to the apices of the roots of
other sources provi d e at least some of the innervation to the mandibular second molar may provi d e insight into the
the teeth in question. See Chapter 16, "Troubl e shooting efficacy of this approach.
Inadequate Anesthesia," for a more detailed description No lingual anesthesia i s provided wi t h this series of
of accessory innervation. This can al s o occur because PDL injections (other than in the vicinity of the lingual
of incomplete l A nerve blocks that are estimated to be surface of the second molar), and the duration of the
onl y 80% to 85% successful (Malamed, 2013). Even after bl o ck i s usually no greater than 60 minutes. When using
negati v e electri c pul p tests (EPT) have confirmed pulpal a Wand STA Single Tooth Anesthesia System® lnstru-
anesthesia, pain can be experienced during treatment. ment (di s cussed in Chapter 9, "Local Anestheti c Deli v ery
When accessory innervation from afferent fibers Devi c es," and Appendi x 9-5) for PDL injections, durations
of non-primary nerves provides pulpal sensations to are typically l o nger because of the larger volumes of sol u -
teeth, techniques that address those fibers can provide tion deposi t ed (Hochman, 2007). The failed I ANB usually
profound anesthesia. For example, when afferent fibers provi d es adequate soft-tissue anesthesia in the area of
of the mylohyoid nerve provide pulpal sensation to the PDL injections. I f the soft ti s sues are not adequatel y
mandibular molars, mylohyoid nerve blocks can provide anestheti z ed, pre-anesthesia using a buccal and/or
profound anesthesia. See Box 1 4-8 "Mylohyoid Nerve lingual nerve block will allow the PDLs to be admini s tered
Blocks," i n Chapter 14, "Injections for Mandibular Pain comfortabl y. When using a Wand STA instrument, pre-
Control," for a description of the mylohyoid nerve block anesthesia may be unnecessary.
technique. Once PDL anesthesia is in effect, patients frequentl y
When the di ff i c ulty ari s es because of inadequate l A touch their chins and say, "It's reall y getting numb now."
blocks rather than accessory innervation, techniques to The increased symptoms of anesthesia in the chin are
block accessory sources of innervation will not provi d e good indications that core bundl e s of the l A nerve
profound anesthesia. Instead, indi v idual teeth can be anes- have been flooded with sufficient anesthetic to provide
theti z ed using PDL injections. PDL injections can provi d e profound anesthesia. Rapid onset is typical. Durations
profound anesthesia even when accessory sources are are relati v el y short when using standard or specialized
innervating the teeth, because PDLs are effective at the syringes, about 10 minutes (Hochman, 2007); however,
apical regions of teeth, blocking impul s e conduction in all this is frequentl y enough time to complete treatment in
•

d ire n s f o h a o t n o f t •

: . . • �� � . . � .� � . � � �� :� :
• • • • • • • • • • • • • • • • • • • • • • • • • • � .� �: � • • • • • • • • • • • • • •• • • • • • • • • • • • • • • • • • •

POL
Teeth anesthetized:

Individual tooth at
site of Injection

Periodontium/Soft tiaauea:

associated periodontium

FIGURE 1 5-1 Field of Anesthesia for Periodontal Ligament

Inj ections. The field of anesthesia for PDL inj ection is indicated by
the shaded areas.
302 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E STH E S I A
P E N ETRATION SITE The penetration site for a PDL inj ec­
tion is within the sulcus that surrounds a tooth. Multiple
sites are often necessary in order to achieve profound an­
esthesia. The easiest areas to approach are the mesial and
distal gingival aspects. In single-rooted teeth, selecting up
to two sites is usually adequate, whereas in multiple rooted
teeth, selecting three to four sites is more typical (see
Figures 15-2 • and 15-4 •) .
N E E D L E PATHWAY The needle i s inserted into the sulcus
penetrating the junctional epithelium. Following the root
surface of the tooth as a guide, it is advanced within the
periodontal ligament to a point of resistance.
The d e p o sition site for a P D L in­
D E P O S I T I O N S IT E
j e ction is any point within the p eriodontal ligament in
which the tip of the needle is inserted between the root
of a tooth and the adj acent alveolar bone (see Figure
15-3 •). This is typically no more than enough tissue to
FIGURE 1 5-2 Penetration Site for PDL Inj ections. The pen­
etration site for a PDL inj ection is indicated by the needle.
FIGURE 1 5-3 Deposition Site for PDL Injections. The deposi­
tion site for a PDL inj ection is indicated by the needle in the
spotlighted area.
cover the bevel, or 3 to 4 mm beyond the attachment.
Functionally, this means that the depth is ade quate to
prevent backflow of anesthetic solution into the sulcus
and to establish light blanching or paling of the attached
gingiva when depositing s o lutio n . If b ackflow o ccurs
or blanching is not seen, a slightly deeper penetration
within the p eriodontal ligament is indicated . If slightly
deeper penetration fails to establish blanching, select a
new site. Box 15-2 • discusses how to observe for ad­
equate blanching.
Technique Steps
As with any intraosseous technique, establishing soft­
tissue anesthesia ( " pre-anesthesia " ) is recommended
before attempting PDL inj ections with manual devices.
B ecause the rationale for performing intraosseous anes­
thesia is to control pain, anesthetizing associated soft tis­
sues before needle insertions is recommended.
FIGURE 1 5-4 Bending Needles for Access in
PDL Inj ections. Enhanced visibility and access
can be achieved using a bent needle for a PDL
inj ection. Factors related to bending needles for
PDL inj ections are discussed in B ox 15-3 .
Light blanching in the attached gingi va of teeth being
anestheti z ed confirms that solution is being retained in the
ti s sues (not exi t ing via the sulcus) and the ti s sues are near­
ing their limit for accommodating solution. The deposition
time period of 20 seconds begins onl y after there i s no ob­
served backflow and blanching is observed (t he accommo­
dation limi t is reached). Thereafter solution will be diffusing
through bone.
When evaluating for light bl a nching, attached ti s sues
should appear pal e pink wi t h visibl y less color compared
wi t h adjacent tissues. Stark, white blanching indicates sol u ­
tion i s not diffusing through the bone, and the depth of
� .�e.n ��r�t: � n. s.h�� �d. � e. i�� r��:e•d• s� i : �t� y� • • • • • • • • • • .IIi
 C HAPTER
As an adjunctive technique, the PDL inj ection is com­
fortably administered where soft-tissue anesthesia has
previously been established. In the absence of preexisting
anesthesia, an infiltration or nerve block technique (such
as a buccal nerve block) may be used to pre-anesthetize
soft tissues at penetration sites.
When using CCLAD devices pre-anesthesia may not be
required. According to the manufacturer's literature, an
" anesthesia pathway " is established maintaining com­
fort during PDL inj ections. Specific technique steps for
the Wand STA device are discussed in Chapter 9 and
Appendix 9-5.
Needles for PD L inj ections vary.
N E E D L E S E L E CT I O N
Standard syringe needles of all gauges may be used, in­
cluding ultra-short 30-gauge needles, which are designed
specifically for limited penetration inj ections such as the
PDL. Some CCLAD systems provide their own needles,
which do not fit standard syringes and are available only
in 27- and 30-gauge diameters, and manufacturers' recom­
mendations should be followed.
Successful PDL inj ections have been performed using
25- , 27- , and 30-gauge standard and specialized needles.
B ecause there is a negligible rate of positive aspiration
and the penetration depth is minimal, safety is not com­
promised with 30-gauge needles. Although these needles
may be more convenient from the standpoint of access,
many clinicians find their excessive flexibility to be prob­
lematic and prefer 27-gauge needles. It has also been noted
that the smaller diameter of 30-gauge needles creates
higher fluid pressures during deposition (Rifkind, 20 1 1 ) .
Long needles can present difficulties when positioning in
posterior areas of the mouth.
Accessing posterior sites, in general, can be challeng­
ing with standard needle angulations. Although not an ideal
practice, this restriction can be eliminated by bending the
needle to a 45-degree angle (see Figure 15-4 •) . Before
attempting to bend a needle, see Box 15-3 • for detailed in­
formation on bending needles and safety recommendations.
For optimal safety, commercially designed syringe
adaptors with 45-degree angles are available and recom­
mended (see Figure 9-3 3 ) . These attachments eliminate
the need for bending needles, and their use does not com­
promise safety. O SHA regulations relating to workplace
safety do not prohibit bending sterile needles. Bending of
contaminated needles, however, is prohibited except under
certain "compelling circumstances." These devices are dis­
cussed in Chapter 9.
I NJ E CT I O N PRO C E D U R E Once pre-anesthesia has been
established, PDL inj ections may be administered in com­
fort and with confidence. The selection of penetration sites
around a tooth is based upon ease of access, penetrating
within areas of existing anesthesia, and confirmation of
diffusion through bone (no backflow and light blanch­
ing). If any of the three conditions is absent, a different site
should be chosen (see Box 15--4 •) .
15 • S U PPLE M E NTAL TEC H N IQU ES A N D ADJU N CTIVE STRATEG I E S 303
Some experts discuss the option of bending needl es in
very speci f i c circumstances (Jastak, Yagiela, & Donaldson,
1 995; Malamed, 2013). I f a decision i s made to modify a
needle and there is minimal risk that the needl e will be
lost wi t hin tissue, the following safe practi c es shoul d be
observed: a sterile technique; the l e ast amount of torque
placed on the hub/shaft interface; the ready availabili ty of
sterile hemostats or l o cking pliers; and a bend in the nee­
dle of no greater than 45 degrees (see Figure 1 5-4). Bends
•
in needl es should never be inserted into tissue (Rifkind, •
20 )
: . . :: � •
• • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • •
FIGURE 1 5-5 Technique for B ending Needles. A one­
handed technique for bending a needle with a sterile
hemostat is illustrated, using a 90-degree bend and
allowing the needle to spring back to a 45-degree final
position relative to the shank.
B evel orientation is irrelevant to the success of PDL
inj ections. If bevels are oriented to face the roots of teeth,
however, two useful purposes can be served. Easier pen­
etration to depth is possible when the sharp tips of needles
are kept away from root surfaces, and gouging can be min­
imized while needles are advancing.
B egin by inserting through the sulcular epithelium
and the periodontal ligament attachment, until resistance
is met. At the point of resistance, start depositing solution.
Aspiration is unnecessary because there is no significant
risk of intravascular inj ection with this technique. In fact,
there are no features for aspiration on manual syringes de­
signed for PDL inj ections. Once the tissues blanch lightly
and no backflow of solution has occurred, deposit 0.2 mL,
at a rate of 0 . 2 mL ( about one stopper) over a full 20
seconds. Slow timing is critical; the solution needs adequate
time to diffuse to the apex. It may be helpful to count si­
lently while depositing (100 1 , 1002, 1003, . . . 1020) to make
sure that adequate time is allowed for diffusion of solution.
In single-rooted teeth, 0.2 mL of solution is recommended
in one or two different sites. In multiple-rooted teeth,
304 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E STH E S I A
Ease of access i s key to maintaining stability during PDL
injections. Pre-anesthesia eliminates concerns of discom­
fort during penetrations and deposi t i o n. A primary benefit
of eliminating these concerns is enhancing clinician con­
fidence when solutions are forced into ligamenta! areas
under pressure. I f patients react, cl i nicians typicall y "ease
up" on the pressure resul t ing in inadequate pressure for
diffusion through the bone. Blanching and the absence
of backflow confirm that selected sites are adequatel y
accommodating solution and will likel y result in success.
The following guidelines enhance ease of access and
success in PDL injections:
Select si t es that are easy to access; i t may be help­
ful to use a periodontal probe to evaluate tooth
•
angul a tions
Monit or for backfl o w
Observe blanching in primary si t es before penetrating
• posited for each penetration site, and when administering
subsequent sit es
• 4 % articaine, 0.45 mL is recommended. Other CCLAD
When blanching is observed circumferentially, no more
e n r t n s a ce a
•
• •
: • � . � � � :� . . :� �� . � � ?
• • • ....... •
. .
three to four sites are usually necessary, or 0.6 to 0.8 mL
(up to -112 cartridge) of total solution.
Syringes designed specifically for PDL inj ections are
discussed in Chapter 9, (see Figure 9-3 1 ) . These devices
are able to deliver controlled volumes of drug while con­
trolling doses.
Confirming Anesthesia
Subj ective signs of anesthesia for PDL inj ections are
variable. When used as a primary method of anesthesia,
patients typically report a sense of numbness of the sur­
rounding soft tissues, and when biting down, on the anes­
thetized tooth or teeth. When given as a supplemental
inj ection to standard nerve blocks, patients typically report
the rapid development of more profound numbness.
Obj ective signs include a lack of response to gentle
stimulation with an instrument, a negative response to
pulp testing, and no pain during procedures.
Common Causes of Injection Failure
Failures occur most frequently while clinicians are learn­
ing this technique. Common errors include needle posi­
tions that are not maintained securely in the PDL space,
solution that b ackflows into the sulcus, or deposition
rates that are accelerated (less than 20 seconds) . Fail­
ures also occur when penetration sites are too resistant
to allow solution to be deposited. In this case solution
will not flow out of the tip of the needle or blanching is
not observed . There should be no hesitation to select a
different site.
Troubleshooting
If anesthesia is inadequate, repeat the procedure in a
different site on the tooth, making sure there is no back­
flow and that light pink blanching develops before deposit­
ing over a 20-second interval.
Technique Modifications and Alternatives
B ecause PDL inj ections can serve as alternatives to nearly
all other techniques, alternatives to PDLs include nearly
all other techniques, depending on the location of the teeth
in question. The choice of device also provides alternatives
to the delivery of PDLs. This includes standard and spe­
cialized manual syringes, and CCLAD devices (Blanton &
Jeske, 2003).
It is important to read manufacturers ' instructions
furnished with these devices as recommended needles,
volumes of solution, and inj ection times vary significantly.
For example, when using the Wand STA device, it is rec­
ommended that 0.9 mL of any 2% or 3% solution be de­
devices in use recommend 0.2 mL per site similar to man­
ual PDL inj ections, and deposition rates vary from 20 to
• . . . • . . •
30 seconds. These devices are discussed in Chapter 9; see
Figures 9-37 and 9-38.
Complications
Patients occasionally experience slight postoperative sore­
ness or sensitivity in the areas of PDL inj ections, as may be
true with other intraosseous techniques. It may be helpful
to inform patients that they may expect some postopera­
tive soreness around teeth that were inj ected. Even though
greater tissue trauma can be expected following PDL in­
jections compared with most nonintraosseous techniques,
the damage has been described as reversible (Kanaa et a!. ,
2006) . Other complications are rare.
The use of PDL inj ections in two specific circum­
stances appears to be controversial. Some sources suggest
that primary teeth with underlying p ermanent succes­
sors should not be exposed to the pressures involved in
PDL inj ections in order to avoid damage to developing
teeth (Dudkiewicz, Schwartz, & Laliberte, 1987; Replogle,
Reader, Nist, B eck, Weaver, & Meyers, 1997) . Although
this caution has not been fully substantiated because of
ethical concerns of relevant research, it has not been fully
refuted, for the same reason. Recent evidence suggests
that PDL inj ections delivered with the Wand STA device
may not injure succedaneous teeth when performing PDL
injections because of the reduced pressures exerted (Ash­
kenazi, Blumer, & Eli, 20 1 0) . For further discussion, see
Box 15-5 •·
Local anesthetic inj ections, in general, are not con­
sidered invasive and therefore are not indications for an­
tibiotic prophylaxis. All intraosseous inj ections, however,
are considered invasive because they target medullary
bone. As with all other intraosseous procedures, infective

Al t hough it i s not known whether or not developing teeth
are at significant ri s k during PDL injections, i t known
that the pressures generated wi t h CCLAD devi c es are less
compared wi t h other syringes, particularl y when CCLAD
devi c es are set to their slowest deli v ery rates. The i s sue
seems to revol v e more around whether or not the potential
ri s k of damage to underl y ing permanent teeth is accept­
able when there are other excellent options that provi d e
profound anesthesia in children.
I f a speciali z ed syringe i s used for children, one spe­
ci f i c all y designed to provide reduced pressures i s the Child
Henke-Ject lntraligamental Syringe® (Henke-Sass Wol f,
Tuttlingen, Germany). It is possible for clinicians to custom­
ize hydraulic pressures wi t h this syringe for patient comfort.
Limits on pressure are maintained by inacti v ation of a pi s ­
ton, once preset l e vel s are reached. Fl ow cannot resume
until the pressure behind the solution drops bel o w the
selected level, which prevents excessi v e pressures. Despite
the ability of clinicians to control deli v ery pressures wi t h
the Henke-Ject, its manufacturer makes no claim regard-
ing its use in primary denti t ion with underl y ing permanent
•
t th
: . �� . �• • • • • • • • • • • • • • •
endocarditis and orthopedic premedication with antibiot­
ics is recommended for those at highest risk.
lntraosseous Tech n i q u e
The primary benefit o f intraosseous anesthesia is to pro­
vide anesthesia when other techniques have proven to
be inadequate or when profound anesthesia of specific
teeth is indicated (B lanton & Jeske, 2003; Brown, 2000;
C HAPTER 15 • S U PPLE M E NTAL TEC H N IQU ES A N D ADJU N CTIVE STRATEG I E S 305
Coggins et al. , 1996; Gallatin et al. , 2003 ; Replogle et al. ,
1997 ) . Secondary benefits include minimizing bleeding
when there are increased risks, limiting the extent of anes­
thetized areas, and decreasing total drug doses. Some have
suggested that intraosseous inj ections are most successful
when used as adjuncts for lA nerve blocks, particularly in
is molar areas (Dunbar et a!. , 1996; Reitz et a!., 1998b ). It has
been reported that supplemental intraosseous inj ections
improved the success rate of anesthesia in vital asymptom­
atic mandibular first molars up to 97 % (Daniel, Harfst, &
Wilder, 2008; Jastak, Yagiela, Donaldson, 1995 ; Malamed,
20 13; Nusstein et a!. , 1998) . Although less frequently used
in the maxilla, there have been occasions, particularly
during endodontic therapy, where intraosseous inj ections
have proven useful (Coggins et a!. , 1996) .
Cancellous, spongy bone (the compressible bone be­
tween adj acent tooth sockets) was originally accessed
with surgical round burs through the outer layer of bone
in the j aw. Several specialized devices are currently avail­
able, which facilitate penetration of the thin, however
dense, layer of bone (cortical plates) and provide access
to the spongy alveolar bone surrounding the dental plexus.
Anesthesia provided by these devices is localized to one or
two teeth.
•
• •• • • • • • • • • • • • • • • • • •
Field of Anesthesia
The areas anesthetized are minimal and include the
pulps of the teeth and their supporting structures im­
mediately adj acent to the sites of deposition. O ccasion­
ally, more widespread signs and symptoms develop (see
Figure 15-6 •).
Anatomical Factors
Intraosseous techniques involve the same alveolar bone
as PDL inj ections. Unlike PDLs, they require surgical
access to spongy bone. A thin layer of highly innervated
lntraosseous
Teeth anaathetlzed:
Individual tooth at
site of lnjectlon
Periodontium/Soft tl ..uea:
supporting structures
Immediately adjacent to
site of deposition
FIGURE 1 5-6 Field of Anesthesia for an Intraosseous Inj ection.
The field of anesthesia for an intraosseous injection is indicated by
the shaded area.
306 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E STH E S I A
connective tissue, the periosteum, covers and protects the
bone, and is also penetrated.
Technique Factors
Key factors for successful intraosseous inj ections are
discussed as follows.
Devices for lntraosseous Injection
There are a number of devices available for intraosse­
ous inj ection. They include the Stabident ® (Fairfax D en­
tal, Inc. ) , X-Tip ® ( D e ntsply M aillefe r ) , IntraFlow™
(Pro-Dex Micro Motors ) , and QuickSleeper (D ental Hi
Tech, France). These devices are shown in Figures 15-7 •,
15-8 •, 15-9 •, 15-10 •, and 9-38.
P E N E T R AT I O N S IT E The optimal p e netration site for
an intraosseous inj ection is in the most apical extent of
the attached gingiva between adj acent teeth. For device­
s p e cific t e ch n i q u e s , always c o n s u l t m a nufacture r s '
instructions (see Figure 15-llA •) . Chapter 20, " Insights
FIGURE 1 5-7 Stabident Intraosseous Anesthesia
Delivery System.
FIGURE 1 5-8 X-Tip Intraosseous Anesthesia D elivery
System.
fr o m S p e ci a l t i e s : O r a l S u r g e ry, P e ri o d o n t i c s , a n d
Endodontics," provides alternate descriptions o f this site.
In the molar region of the mandible, where cortical
plate thickness is greatest, the crestal third of the alveolar
process lies beneath the most apical extent of the attached
gingiva and is the area where the cortical plate of bone is
thinnest.
The site chosen should be distal to the tooth to be
anesthetized at an equal distance from the adj acent tooth.
It should approximate the apical extent of the attached
gingiva, which is approximately 2 mm below a line con­
necting the gingival margins of the teeth (Shimada &
Gasser, 1989) . Mesial penetration is acceptable but distal
penetration is recommended.
After withdrawal of the perforator p ortion of the
Stabident or X-Tip device, the n e e dle is intro duced
into the p erforation to deliver a local anesthetic drug
into the interdental medullary bone as demonstrated in
Figure 15-12 •· If an IntraFlow device is used, it is not nec­
essary to withdraw the perforator and insert a needle be­
cause the device contains both perforator and needle (see
Figure 15-13 • and Box 15-6 •).
N E E D L E PATHWAY The needle follows the perforation
through the cortical plate of bone into interproximal bone.
FIGURE 1 5-9 IntraFiow Intraosseous Anesthesia
Delivery System. Components of the IntraFiow device.
FIGURE 1 5-1 0 Assembled IntraFJow Device.
 C HAPTER
(A)
(B)
FIGURE 1 5-1 1 A - Penetration Site for an Intra osseous
Inj ection. The penetration site for an intraosseous inj ection
is indicated by the perforator (Stabident). B - Removing the
Perforator after Initial Penetration. The perforator is removed
prior to needle insertion with a Stabident.
Source: Courtesy of Albert "Ace" Goerig, DDS, MS.
(A)
FIGURE 1 5-1 2 Needle Insertion for Drug Delivery with a Stabident. After removal of the perforator portion, the needle is intro­
duced to deliver a local anesthetic drug. A - Needle inserted through perforation. B - Needle penetration demonstrated into spongy
bone.
Source: Courtesy of Albert "Ace" Goerig, DDS, MS.
15 • S U PPLE M E NTAL TEC H N IQU ES A N D ADJU N CTIVE STRATEG I E S 307
D E PO S I T I O N S I T E The deposition site is the interproxi­
mal bone underlying the cortical plate. Once penetration
through the cortical plate is "felt " by the clinician (for an
alternate description of this sensation, see Chapter 20) , the
deposition site has been reached (see Figures 15-13A and
15-13B).
Technique Steps
Apply the basic injection steps outlined in Chapter 1 1 and
summarized in Appendix 1 1-1. Additionally, apply the
guidelines listed in Box 15-6.
Periosteum overlying the mandible and maxilla is very
sensitive and pre-anesthesia is recommended for comfort
before performing any intraosseous technique.
For intraosseous inj ections, needles
N E E D LE S E L E CTI O N
and other armamentaria must be purchased for the spe­
cific system selected. All manufacturer instructions should
be followed.
Step 1- l f there i s no previous exi sting anesthesia of soft
tissue, anestheti z e the attached gingi v a first.
Step 2- Mark the penetration si t e by blanching wi t h a
blunt-tipped instrument.
Step 3 - Perforate the cortical plate and deposi t solution
into cancellous bone (thi s is painless when Step 1 has
been performed).
Note: Avo i d vasoconstri ctors (these d r u g s enter the CVS ra p i d ly)
a n d observe a l l m a x i m u m dose reco m m e n d a tions.
(B)
308 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E STH E S I A

(A) (B)
FIGURE 1 5-1 3 Initial Penetration and Delivery with the IntraFlow. The initial penetration (A) is performed in the same manner
as for Stabident and X-Tip devices. However, there is no need to remove the perforator. The drug is delivered directly through the
device into spongy bone ( B ) .
Source: Courtesy of Albert "Ace" Goerig, DDS, MS.

FIGURE 1 5- 1 4 Initial Perforation Using the X-Tip FIGURE 1 5-1 5 Needle Guide or "Guide Sleeve"
System. Placed for X-Tip System.

I NJECTIO N PROCE D U R E With pre-anesthesia in place, begin

perforation (see Figures 15-llA, 15-1 3A, and 15-14 •)
avoiding heat buildup because of friction. Once the cor­
tical plate has been perforated, insert the needle as rec­
ommended for the specific device being used (see Figures
15-12, 15-13B, 15-15 • , and 15-16 •) . As with the PDL
inj ection, aspiration is not necessary. B ox 15-7 • provides
suggested volumes of solutions when using the Stabident
system, as an example. It is important to refer to manu­
facturers' instructions at all times for proper use of these
devices. For an alternate description of this inj ection pro­
cedure, see Chapter 20, " Insights from Specialties : Oral
Surgery, Periodontics, and Endodontics. "
FIGURE 1 5-1 6 Needle Insertion Following Perforation
Using X-Tip System.
Confirming Anesthesia
Subj ective signs of anesthesia for intraosseous inj ections numb. The absence of a response to EPTs or to the appli­
are few. Patients may report a sense of numbness when cation of ice-cold temperatures can confirm anesthesia. In
biting down on the tooth or teeth anesthetized, or the soft Chapter 12, "Inj ections for Maxillary Pain Control I" see
tissues surrounding the tooth or teeth may feel somewhat Figures 12-7,12-8, and 12-9.

Mandible:
1 tooth: 0.45-0.6 ml (mesial or distal to tooth)
2 teeth: 0.6-0.9 ml (between the two)
3 teeth: 0.9 ml (distal to the middle tooth)
6 anteriors: one injection on each side, between canines
and premolars 0.9 ml per side
Maxilla:
1 : 0.45 ml
2: 0.45 ml
4 adjacent teeth: midway between 0.9 ml
Up to 8 teeth on one side: 1 .8 ml midway between
� S.o �r.c:: �a:a m e� 2.0��-
• - • • ,. • • • • • • • • • •
Obj ective signs include a lack of response to gentle
stimulation with an instrument and no pain during the
procedure for soft tissues or teeth. The absence of pain is
confirming.
Common Causes of Injection Failure
Inadequate cancellous bone in the central incisor region
may not allow this technique to be performed. Solution
is not able to diffuse easily through what is essentially a
cortical "sandwich " of bone with no intermediate spongy
layer.
Failures occur most frequently while clinicians are
learning this technique. Studies have shown it to be nearly
100% successful once clinicians gain confidence and expe­
rience and when it is used as an adjunctive technique. When
used as the initial appro ach to anesthesia, some stud­
ies have demonstrated only a 75 % success rate (Gallatin
et al. , 2000). With practice, success rates, along with skill
and confidence, tend to increase.
Troubleshooting
Penetration of the cortical plate distal to the tooth to be
anesthetized is more successful compared with mesial
sites when using these techniques. Choose alternate sites,
including mesial areas, if none is acceptable distal to a
tooth. If unable to perforate cortical bone quickly in any
site, an alternate site should be chosen without hesitation.
If no sites will allow easy perforation, choose an alternate
technique.
Technique Modifications and Alternatives
In some situations, the mandibular molar region is dif­
ficult to penetrate because of thick cortical bone, which
reduces the e ffective n e s s of intra o s s e o u s inj ections.
Alternatives to bone-perforating intraosseous inj ections
include non-perforating intraosseous inj ections (PDLs ) ,
C HAPTER 15 • S U PPLE M E NTAL TEC H N IQU ES A N D ADJU N CTIVE STRATEG I E S 309
nerve blocks, and reappointing after providing appropri­
ate medications.
Complications
As with all other intraosseous techniques, patients may ex­
perience postoperative soreness and sensitivity in the ar­
eas of inj ection.
Complications are rare and include root damage when
adj acent te eth are very close to one another and pre­
assessment failed to note this contraindication to the tech­
nique. Injury to the cortical plate is unique to intraosseous
techniques. Fortunately, this damage has been shown to be
reversible. B ecause the technique requires inj ury to bone
regardless of the perforating system, the healing process is
somewhat slow, although usually painless. Reported com­
plications include pain and swelling at the inj ection site as
well as bruising (Dudkiewicz, Schwartz, & Laliberte, 1987) .
•
Heart palpitations can be expected when vasocon­
• • • • • • • • • • • • • •
strictors are used. To avoid palpitations, use solutions
without vasoconstrictors ( Guglielmo et a l . , 1 9 9 9 ) . If
vasoconstrictors are selected, use minimal volumes and
greater dilutions, such as 1 :200,000 formulations. Accord­
ing to a 1993 comparison study, 85 % of inj ections with the
Stabident system and 93 % with the X-Tip resulted in per­
ceived increases in heart rate (Guglielmo et al. , 1999) .
lntrasepta l Tech n i q u e
The intraseptal technique is used to provide anesthesia of
the periodontium lingual to a tooth and can be particu­
larly useful when palatal tissues require anesthesia and
clinicians and/or patients wish to avoid palatal inj ections
(Malamed, 1982) .
This technique is also useful when soft-tissue anesthe­
sia and hemostasis are desired for periodontal procedures,
but PDL inj ections are contraindicated because of infec­
tion. It does not provide reliable pulpal anesthesia.
Field of Anesthesia
Anesthesia provided by the intraseptal technique involves
the bone, soft tissues, and other structures of the tooth in
the area in which it is administered. The anesthesia pro­
vided tends to be localized and specific to one or two teeth.
This technique also provides significant hemostasis when a
vasoconstrictor is administered. For some patients pulpal
anesthesia is achieved; however, it tends to be unreliable
or very short-term in nature (see Figure 15-17 •).
Anatomical Factors
The intraseptal technique involves alveolar bone, similar
to intraosseous and PDL inj ections. Unlike the PDL, in­
traosseous, and intrapulpal techniques, however, it does
not provide reliable pulpal anesthesia.
Technique Factors
Key factors for successful intraseptal inj ections are dis­
cussed as follows.
310 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E STH E S I A
lntraseptal
Teeth anesthetized:
unreliable pulpal
Periodontium/Soft tlaauea:
soft tissues and
perlodontium at
site of injection
FIGURE 1 5-1 7 Field of Anesthesia for an Intraseptal Inj ection.
The field of anesthesia for an intraseptal inj ection is indicated by
the shaded area.
P E N ETRATION SITE The penetration site is at the center of
the interdental papilla adj acent to the tooth to be treated
and below the height of the interdental papilla (about 2 mm)
but within the attached gingiva (note: insufficient attached
gingiva would preclude using this technique for any particu­
lar site). This is similarly represented by the penetration site
for an intraosseous injection in Figure 15-12B.
N E E D L E PATH WAY The nee dle advances through soft
tissue until bone is contacted and then is gently forced
deeper into the interdental bone.
The deposition site is just inside the
D E PO S I T I O N S I T E
cortical plate of bone. Unlike an intraosseous inj ection
(see Figure 15-16), however, no perforation is made in the
bone before needle insertion.
Technique Steps
Apply the basic inj ection steps outlined in Chapter 1 1 ,
"Fundamentals for Administration o f Local Anesthetic
Agents," and summarized in Appendix 1 1-1. Pre-anesthetize
the area if anesthesia is not already in effect at the penetra­
tion site. See Box 15-6 for a summary of steps.
N E E D L E S E L E CTIO N A 27-gauge needle (short) is recom­
mended, which is consistent with the negligible rate of
positive aspiration and the need for a needle with less flex­
ibility compared with 30-gauge needles.
I NJECTIO N PROCE D U R E Once the area has been anesthe­
tized using infiltration or any other technique, intraseptal
inj ections can be delivered with comfort and confidence.
Insert the needle in the center of the interdental papilla,
about 2 mm below the height of the attached gingiva but
still within the attached tissue. Saadoun and Malamed rec­
ommend orienting the bevel toward the apex (Saadoun &
Malamed, 1985 ) . The orientation of the needle is 45 de­
grees to the frontal plane, at right angles to the soft tissue.
The needle is advanced until bony resistance is met,
at which time pressure is applied to the syringe to force
the needle just barely deeper into the interdental septum.
Once within the septum, 0.2 to 0.4 mL of local anesthetic is
administered (0.2 mL each over 20 seconds) against what
should be considerable resistance, similar to that experi­
enced in PDL and palatal inj ections. Backflow of solution
and a failure to notice blanching when a vasoconstrictor is
used indicate that the needle is not deep enough.
Confirming Anesthesia
Subj ective signs of anesthesia for all intraosseous inj ec­
tions, including intraseptal inj ections, are few. The patient
may report a sense of numbness in the soft tissues on the
palatal aspects of the tooth or teeth where the intraseptal
inj ection was delivered. Typically, patients will report few
signs or symptoms of anesthesia.
Obj e ctive signs include a lack of response to gentle
stimulation with an instrument and no pain during the
procedure for the soft tissues. Significant blanching is the
best indicator of success. The absence of pain during the
procedure is often the only way to confirm anesthesia. If
hemostasis is desired , decreased bleeding confirms suc­
cessful procedures.
Common Causes of Injection Failure
Inadequate retention of solution and inadequate volumes
of solution are the most common causes of inj ection fail­
ure. Failures occur most frequently as clinicians are learn­
ing this technique.
Troubleshooting
It may be necessary to repeat the inj ection if anesthesia is
inadequate. Alternate techniques may be necessary, such as
intraosseous injections, PDL injections, AMSA nerve blocks,
NP nerve blocks, GP nerve blocks, and palatal infiltrations.
 C HAPTER 15 • S U PPLE M E NTAL TEC H N IQU ES A N D ADJU N CTIVE STRATEG I E S 311

Technique Modifications and Alternatives
Effectiveness is reduced for this technique in some situ­
ations. Mandibular molar regions, in particular, are more
difficult to penetrate because of the presence of thicker
cortical bone. Selecting penetration sites in this area can
be challenging if there is unusually dense bone.
Complications
Complications are rare. As with other intraosseous tech­
niques, patients may experience postoperative soreness or
sensitivity in the area of inj ection.
The procedure may not be appropriate when the roots
of adj acent teeth are very close to one another because
roots may be inadvertently injured.
Inj ury to the cortical plate is unique to intraosseous
techniques. Although more extensive inj ury has been
demonstrated to occur compared with nonintraosseous
techniques, damage tends to be reversible. Healing after
intraseptal inj ections tends to be a slow, painless process
but somewhat faster compared with intraosseous tech­
niques that use cortical perforators to access spongy bone.
It might be helpful to caution patients that they may expect
a little more soreness compared with other appointments.
Heart palpitations can be expected when vasocon­
strictors are used (Gallatin et a!., 2003; Wong, 200 1 ) . In or­
der to avoid or lessen palpitations, plain solutions or those
with greater dilutions, such as 1 :200,000 epinephrine for­
mulations are recommended.
The intrapulpal technique is the only nonintraosseous
technique discu s s e d in this chapter. This te chnique
can deliver effective anesthesia when the degree of in­
flammation in the pulp renders conventional methods
ineffective.
Field of Anesthesia
The area affected by intrapulpal inj ections is minimal and
is confined to pulpal tissues (see Figure 15-18 •) .
Anatomical Factors
Intrapulpal anesthesia relies on direct access to the
coronal or radicular pulp. In order for the inj ection to be
possible, it is assumed that endodontic access has already
been accomplished.
Technique Factors
Key factors for successful intrapulpal inj ections are dis­
cussed as follows.
P E N ETRATION SITE The penetration site is located in the
pulpal tissue of the pulp chamber or within the root canal
of the tooth (see Figure 15-19 •) .
N E E D L E PATHWAY The needle i s directed into the pulpal
tissue of the coronal chamber or root canal( s), as necessary
(see Figure 15-20 •). Anesthetic solutions are directed at
the remaining areas of vital nerve.

lntra p u l pa l Tech n i q u e D E PO S I T I O N S I T E The ideal site has been described as

The intrapulpal technique provides anesthesia for pulpally
involved teeth when other techniques have failed. Wong
reported that using lA nerve blocks in mandibular first
molars with irreversible pulpitis averaged only a 30% suc­
cess rate (Wong, 200 1 ) .
being wedged into the chamber or the root of the tooth
(Malam e d , 2004) . This technique provides anesthesia
in two ways, primarily as a result of pressure (pressure
anesthesia) and secondarily as a direct action of the drug
(see Figure 15-20).

lntrapulpal

Teeth anesthetized:

individual tooth pulp

at site of injection

Periodontium/Soft tissues:

none

FIGURE 1 5-1 8 Field of Anesthesia for an Intrapulpal Inj ection.

The field of anesthesia for an intrapulpal inj ection is indicated by the
shaded area.
312 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E STH E S I A
F I G U RE 1 5-1 9 Penetration Site for an Intrapulpal Inj ection.
A bur must be used to access the pulp prior to needle insertion.
F I G U R E 1 5-20 Modification for Intrapulpal Inj ections.
A sterile stopper can be positioned on the needle shaft to
maintain pressure while solution is deposited.
Technique Steps
Pre-anesthetize the area if anesthesia is not already in
effect at the penetration site.
N E E D L E S E L E CTI O N A 25- , 27- , 30-gauge short needle
may be used. Intravascular inj ection is not possible in the
pulp, and the needle is confined within the tooth; therefore,
needle gauge selection is directly related to providing a
needle that is small enough to fit into the chamber and ca­
nals without binding. Different gauges may be required on
the same tooth in various roots.
I NJECTI O N PROCE D U R EAfter endodontic access or par­
tial access has been accomplished, an intrapulpal inj ec­
tion can be perform e d . The patient should be warned
that there may be a brief but intense pain experienced;
however, this technique is effective at alleviating subse­
quent pain.
It may be useful to bend the needle to improve access.
B efore bending a needle, see Box 15-3 . Solution is admin­
istered at a slow rate, 0.2 mL over 20 seconds.
Confirming Anesthesia
Subj ective signs of anesthesia for intrapulpal inj ections
are few. Primarily, the patient reports that the toothache is
gone. A sense of numbness when biting down on the tooth
helps confirm profound anesthesia. Typically, patients will
report few signs or symptoms of anesthesia.
Obj ective signs include no response to gentle stimula­
tion with an instrument and no pain during the endodontic
procedure.
Common Causes of Injection Failure
Common causes of failure include too shallow a pen­
etration into the pulpal tissues resulting in backflow of
solution into the mouth versus within pulpal tissues; inad­
equate pressure generated by the solution; the degree of
inflammation or infection present; and clinician discom­
fort with the procedure.
Troubleshooting
Problems encountered include root canals that are nar­
rower than the circumference of the needle, which pre­
vents adequate access to the nerve; an intense initial pain
that quickly subsides; and clinician discomfort with the
brief but intense pain.
Technique Modifications and Alternatives
A useful modification when performing an intrapulpal in­
j ection is to insert the needle through a previously steril­
ized stopper from an unused cartridge. This can be done
without touching any part of the needle, and therefore
without risking needlestick inj ury by using two sterile
hemostats, one to hold the stopper and the other to hold
the needle as it is being inserted into the stopper. Once in­
serted onto the needle shaft, penetration is made while the
stopper is held tightly over the endodontic access opening
of the tooth. The pressures generated by the solution will
be greater compared with wedging the needle alone (see
Figure 15-20) .
Alternatives include intraosseous inj ections, PDL in­
jections, and Gow-Gates nerve blocks. In some cases it may
be necessary to defer care and allow pharmacotherapies to
reduce inflammation before reattempting treatment.
Complications
The experience of brief but intense pain associated with
this technique can be stressful. The use of appropriate
sedatives or nitrous oxide can diminish this effect for pa­
tients and indirectly relieve clinician concerns of causing
pain.
 C HAPTER
Adj u nctive Strateg ies
Onset™ Sodium Bicarbonate Buffering
Improvements in the areas of reducing the onset times of
anesthesia and the pain that is often associated with local
anesthetic inj ections have been facilitated with the intro­
duction of Onset, a buffering system for dental local anes­
thetic cartridges (Onpharma, CA) . Although medicine has
benefited for years from the ability to buffer anesthetic
solutions before use, dental administrations have been
frustrated by the otherwise overall convenience of the car­
tridge system. B efore the availability of Onset, there was
no practical way to buffer dental local anesthetic solutions
in cartridges before inj ection.
As previously explained in Chapter 4 , " Pharmacol­
ogy B asics," it is the neutral base or non-ionized local
anesthetic molecules that penetrate nerve membranes.
Two percent lidocaine with 1 : 1 00,000 epinephrine has a
pH of 3 . 3 to 5 .0. This is well below tissue or physiologic
pH because of the addition of sodium bisulfite preser­
vatives that are necessary to prevent vasoconstrictor
oxidation and shortened shelf life. Currently, Onset's
s o dium bicarbonate buffe ring system o nly provides
instructions for use with 2% lidocaine with, 1 : 1 0 0 , 0 0 0
epinephrine.
To clarify the impact of comparatively low pH val­
ues, Onpharma has added the following perspective to its
product inserts (Onpharma, 20 14) . *
A typical cartridge o f lidocaine with epinephrine con­
tains only 1 molecule o f de -ionized anesthetic for ev­
ery 10,000 molecules of ionized anesthetic . . . [C]loser
to physiologic p H [7.4] , more de-ionized anesthetic is
present. . . there is 2,500x more of the active form of the
anesthetic available than at p H 3 . 9 [the typical pH o f
lidocaine that is received from suppliers] .
Although the mechanisms for local anesthetic-related
pain, thought to be primarily due to acidity, and the posi­
tive effects of buffering on that pain remain unclear, stud­
ies have demonstrated that sodium bicarbonate buffering
with the Onset system reduces the experience of pain and
significantly improves onset times of anesthesia during
and following inj ections. It has been speculated that the
buffering system may act to reduce pain by either decreas­
ing the amount of tissue irritation that occurs after inj ec­
tion and/or by allowing faster onset of anesthesia, which
blocks nerve impulse generation and conduction more
rapidly than when buffers are not used (Burns et al. , 2006;
Talu et al. , 200 1 ) .
In addition to these m e chanisms, the carbon
d i o x i d e p r o d u c e d w h e n combining l o c a l a n e s t h e t i c
*Excerpt from "Science o f Buffering Lidocaine with Epinephrine."
Published by OnPharma Inc, © 2014.
15 • S U PPLE M E NTAL TEC H N IQU ES A N D ADJU N CTIVE STRATEG I E S 313
s o lutions with s o dium bicarbonate has b e e n demon­
strated to have an independent anesthetic effect on tis­
sues. Studies have speculated that the carbon dioxide
that is produced from this combination incre ases the
overall comfort of lidocaine inj ections ( C o ndouris &
Shakalis, 1 964 ) .
®
OraVerse Local Anesthesia Reversal
Ora Verse ® (phentolamine mesylate) (Septodont, Inc. ,
Louisville, CO) is the only pharmaceutical agent avail­
able for the reversal of soft-tissue anesthesia, which can
interfere with speaking, eating, and drinking for prolonged
periods. See Figure 17-6 for product example. Note the
unique color of the cartridge label and stopper. OraVerse
(phentolamine mesylate) , by Septodont Pharmaceutical,
was approved by the FDA on May 9, 2008. Early studies
have reported that sensations to the lips and tongue can
be regained in approximately half the time of typical den­
tal local anesthesia recovery (Hersh et al., 2008; Tavares
et al. , 2008) . D etailed pharmacological information on
OraVerse provided by Septodont Pharmaceutical can be
found in Box 15-8 •· The approval from the FDA does not
include the use of OraVerse in children younger than 6
years or weighing less than 33 lbs. The FDA requested that
additional investigation on this age group be completed
(Hersh & Lindemeyer, 20 10).
The active ingredient of OraVerse is phentolamine
mesylate, a nonselective alpha-adrenergic blocking agent
that is associated with countering the effects of epineph­
rine on tissues. The associated effect of this drug is vaso­
dilation of the vessels, which can allow for an increase in
the elimination and clearance of local anesthetic from the
deposition site.
In medicine, phentolamine is inj ected intravenously
at higher doses to produce acute lowering of blood pres­
sure (5 rug) (Tuncel & Ram, 2003 ) . It should be noted,
however, that in dentistry, phentolamine is used at nota­
bly lower doses (0.2-0 .8 rug) , not administered intrave­
nously, and has not been linked with major cardiovascular
changes (Hersh & Lindemeyer, 20 1 0 ; Lavio l a et a l . ,
2008).
For local anesthetic reversal, OraVerse is packaged in
the same manner as dental local anesthetic. Each 1.7-mL
cartridge of OraVerse contains 0.4 rug of phentolamine
m e sylate in 1 . 7-mL solution. The s o lution is inj ected
into the mucosa at the end of the dental procedure us­
ing the same location, volume, and inj ection technique
as the previous local anesthetic inj ection ( S eptodont,
20 1 1 ) .
There have been implications that OraVerse can re­
duce the incidence of self-inflicted, soft-tissue inj ury;
however, the manufacturer does not report or claim this
benefit (Hersh et al. , 2008, Hersh & Lindemeyer, 2 0 1 0 ;
Tavares et a l . , 2008) .
314 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E STH E S I A

The foll o wing information was gathered from clinical recommended dose for children: 33-66 l b s i s 0.2 mg (1 /2
data publi s hed in the Journ a l o f the A m e rican Dental cartridge); for children over 66 l b s and up to 1 2 years of
Association and from information provided by Novalar age the MRD i s 0.4 mg (1 cartridge). OraVerse i s not rec­
Pharmaceuti c al s . Before using OraVerse, the product in­ ommended for use in children less than 6 years of age or
sert should be consul t ed. weighing less than 15 kg (33 lbs).
Formulations for Use in Dentistry Relative Toxicity: Ora Verse is well tol e rated at the doses tested.
Ora Verse i s a steri l e , pyrogen-free, i s otonic sol uti o n for ad­ Metabolism: See publi s hed phentolamine mesylate
mini strati o n in gl ass dental cartri d ges that deliver 0. 4 mg li t erature.
phentol a mine mesyl ate in 1 . 7 ml of solution. The concen­ Excretion: Kidney
trati o n of the active ingredient (phentolamine mesyl ate) i n
OraVerse i s 0. 2 35 mg/ml. Excipients incl u de water for admin­ Vasodilator
istration, ethyl e nediaminetetraacetic acid (EDTA), D-mannitol ,
Vasoactivity:

sodium acetate, acetic acid, and sodium hydroxi d e. O n s e t of Actio n :Rapid

MRD (Maximum Recommended Dose) Half-Life: Approximatel y 2-3 hrs.
OraVerse was studied in a 1 :1 cartridge to cartridge rati o to P re c C e o r Cat C
gnan y at g y:
l o cal anestheti c solution. Safety During Lactation: Not studied
Prod u ct Wa r n i n g : Myocardial infarction and cerebrovas­
Amount o f Loca l Anesthetic
cular spasm and occl u sion have been reported following
Ad ministered Dose of Ora Verse
parenteral use of phentolamine, usually in association wi t h
1/2 Cartridge 1 /2 Cartridge (0.2 mg) marked hypotensive epi s odes producing shock-like states.
Tachycardia, bradycardia, and cardiac arrhythmias may oc­
1 Cartridge 1 Cartridge (0.4 mg) cur wi t h the use of phentolamine or other alpha-adrenergic
blocking agents. Al t hough such effects are uncommon wi t h
2 Cartridges 2 Cartridges (0.8 mg) OraVerse (phentolamine mesyl a te), clinicians should be
alert to the signs and symptoms of these events, particu­
OraVerse is admini s tered using the same l o cation(s) and larl y in patients wi t h a hi story of cardiovascular disease.
same technique(s) (infil t ration or block injection) used for 2008;
t n s ra i � a st t c s . T h a x 2.0��
Sources: O raVerse P ro d u ct I n sert , H ersh et a l . , Tavares et a l . ,

: . � � ���� : : . : �� �: ��� � . �� . �� � : : • • � .� . ����

• •

• • • • • • • • • • • • • • • • • • • • • • • • •• • • • • • • • • • • • • • • • • • • •

CAS E M A N AG E M E N T
John Jones
D e s p ite p u b l i s h e d s u ccess rates exce e d i n g 95% i n
m a xi l l a ry i nfi ltratio n s , re peated i nfi ltrati o n s fa i l e d i n
this patient ( B l a nton & J eske, 2003) . F u rth ermore, the
i nfi ltratio n s h a d been assessed and a d m i n iste red ac­
cu rately, which i n c l u d e d verificati o n of a pex l o cation
using rad iographs a n d a d e q u ate vesti b u l a r h e i g ht for
the penetratio n sites.
A d iffe rent a p p ro a c h , one that circumvented u n ­
known a n ato m i c barriers, was decided u p o n . T h e soft­
tissue a n esth esia t h a t deve l o p e d over #4 fo l l owi n g
t h e third infi ltratio n with a rtica i n e enabled a P D L i njec­
tion to be a d m i n iste red comfo rta b l y fro m the b u cca l
aspect of t h e toot h . T h i s s e q u e n ce q u i ckly p rov i d e d
p rofo u n d p u l p a l a n est h e s i a of #4, a n d a resto rative
proced u re on the tooth was su bsequ ently com p l eted .
Accord i n g to t h e g ratefu l patie nt, t h i s was t h e fi rst
time ever that tooth #4 had been treated comfo rta bly.
Case Discussion: Any n u m b e r of a h ost of a n a ­
to m i c variati o n s m a y h ave b e e n res p o n s i b l e fo r t h i s
fa i l u re , i n c l u d i n g accessory o r a b e rrant i n n e rvati o n ,
denser-t h a n - n o r m a l maxi l l a ry b o n e i n t h e a rea a bove
#4, a p ro m i n e nt zyg o m at i c p rocess, a l i n g u a l -fa c i n g
d i l a ce ra t i o n of t h e a p ex of t h e r o o t of t h e tooth ,
p hys i o l o g i c b a r r i e rs to d iffu s i o n , a n d fasc i a l p l a n e s
that d i rected sol ution away fro m t h e target area.
Fort u n ately, obta i n i n g p u l p a l a n esth esia i n cases
l i ke t h i s i s not d e p e n d e n t on an exact k n o w l e d g e
of t h e c a u s e o r c a u s e s of t h e fa i l u re . U n d e rsta n d ­
i n g w h e n a n ato m i c v a r i a t i o n s a re l i ke l y t o sabota g e
a p ro c e d u re , h oweve r, c a n b e c r i t i c a l to s u c c e s s .
Re peated i nfi ltratio n s of # 4 , as confi r m e d by t h i s pa­
tie nt's p revi o u s experien ces over decades of d e nta l
treat m e nt, d i d n ot res u l t i n p u l p a l a n esth e s i a . A n
a p p roach t h a t c i rcu mve nts barriers to a n esthesia was
n e cess a ry and worked we l l . As a res u lt of his g rati­
t u d e to t h e st u d e n t fo r t h e comfo rta b l e p roce d u re,
h e i n s isted o n rece i v i n g a l l fut u re treat m e n t at the
u n ive rsity c l i n ic.
 C HAPTER 15 • S U PPLE M E NTAL TEC H N IQU ES A N D ADJU N CTIVE STRATEG I E S 315

Chapter Questions
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Coggins, R., Reader, A., Nist, R., Beck, M., & Meyers, W. J.
(1996) . Anesthetic efficacy of the intra osseous inj ection in
maxillary and mandibular teeth. Oral Surgery Oral Medicine
1 . The rate of deposition of local anesthetic drugs in
Oral Pathology Oral Radiology & Endodontics, 81 (6), 634-641.
intraosseous, intrapulpal, and PDL inj ections is best Condouris, G. A., & Shakalis, A. (1964) . Potentiation of the
represented by which one of the following? nerve-depressant effect of local anesthetics by carbon dioxide.
a. 0.1 mL over 20 seconds Nature, 204, 57.
b. 0.2 mL over 10 seconds Daniel, S. J. , Harfst, S. A., & Wilder, R. (2008) . Mosby's den­
c. 0.2 mL over 20 seconds tal hygiene: Concep ts, cases, and competencies (2nd ed.).
d. 0.1 mL over 30 seconds Philadelphia: Mosby Elsevier.
Dudkiewicz, A., Schwartz, S., & Laliberte, R. (1987).
2. Which one of the following techniques does not typi­ Effectiveness of mandibular infiltration in children using the
cally provide reliable pulpal anesthesia? local anesthetic Ultracaine (articaine hydrochloride) . Journal
a. Intraosseous of the Canadian Dental Association, 53, 29-3 1.
b. Intrapulpal Dunbar, D., Reader, A., Nist, R., B eck, M., & Meyers, W. J.
c. Intraseptal (1996) . Anesthetic efficacy of the intra osseous inj ection af­
d. PDL ter an inferior alveolar nerve block. Journal of Endodontics,
22(9), 481-486.
3. Which one of the following is not recommended as an Frank, J. E. (2005). Diagnosis and management of G6PD
anesthetic approach in irreversible pulpitis? deficiency. American Family Physician, 72, 1277-1282.
a. The Stabident system Gallatin, E., Stabile, P. , Reader, A., Nist, R., & B eck, M. (2000).
b. PDL injections Anesthetic efficacy and heart rate effects of the intraosse­
c. Higher concentrations of lidocaine ous inj ection of 3% mepivacaine after an inferior alveolar
d. The IntraFlow system nerve block. Oral Surgery Oral Medicine Oral Pathology Oral
Radiology and Endodontics, 89(1 ) , 83-87.
4. What is the approximate success rate of inferior al­ Gallatin, J. , Reader, A., Nusstein, J. , Beck, M., & Weaver, J.
veolar nerve blocks, according to Wong, in pulpally (2003). A comparison of two intra osseous anesthetic tech­
involved teeth? niques in mandibular posterior teeth. Journal of the American
a. 1 0 % Dental Association, 134( 1 1 ) , 1476-1484.
b. 20% Guglielmo, A., Reader, A., Nist, R., B eck, M., & Weaver, J.
c. 30% (1999). Anesthetic efficacy and heart rate effects of the
d. 40% supplemental intraosseous injection of 2% mepivacaine with
1 :20,000 levonordefrin. Oral Surgery Oral Medicine Oral
5 . Which one of the following statements is true regard­ Pathology Oral Radiology and Endodontics, 87(3), 284-293.
ing PDL inj ections? Hersh, E.V., & Lindemeyer, R. G. (20 10). Phentolamine mesyl­
a. Solution diffuses through the periodontal ligament ate for accelerating recovery from lip and tongue anesthesia.
to the dental plexus. Dental Clinics of North America, 54, 631-642.

b. The orientation of the bevel is critical to success of Hersh, E.V. , Moore, P.A., Papas, A.S., Goodson, J.M., Navlata,
the procedure. L.A., Rogy, S., Rutherford, B., Yagiela, J.A. (2008) . Reversal
of soft-tissue local anesthesia with phentolamine mesylate in
c. The technique is only u s e ful as an initiating
adolescents and adults. Anesthesia Recovery Group. Journal
technique. of the American Denta1 Association. 139(8) , 1080-1093.
d. Solution diffuses through alveolar bone to the den­ Hochman, M. N. (2007) . Single-tooth anesthesia: pressure­
tal plexus. sensing technology provides innovative advancement in the
field of dental local anesthesia. Compendium, 28( 4 ) ,186-188,
190, 192-193.
References Jastak, J. T. , Yagiela, J. A., & Donaldson, D. (1995). Local anesthe­
Ashkenazi, M., Blumer, S . , & Eli, I. (20 10). Effect o f computer­ sia of the oral cavity. Philadelphia: Saunders.
ized delivery intraligamental inj ection in primary molars Laviola, M., McGavin, S.K., Freer, G.A., Plancich, G. , Woodbury,
on their corresponding permanent tooth buds. International S.C., Marinkovich, S., Morrison, R., Reader, A., Rutherford,
Journal of Paediatric Dentistry, 20( 4), 270-275. R.B., Yagiela, J.A. (2008). Randomized study of phentolamine
Blanton, P. , & Jeske, A. (2003, June) . The key to profound local mesylate for reversal of local anesthesia. Journal of Dental
anesthesia -Neuroanatomy. Journal of the American Dental Research, 87, 635-639.
Association, 134, 755-756. Malamed, S. F. (1982). The periodontal ligament (PDL) inj ection:
Brown, R. (2000). Intraosseous anaesthesia: A review. Oral An alternative to inferior alveolar nerve block. Oral Surgery
Health, 3, 7-14. Oral Medicine Oral Pathology, 53(2), 1 17-121.
Burns, C. A., Ferris, G. , Feng, C., Cooper, J. Z., & Brown, M. D. Malamed, S. F. (2004) . Handbook of local anesthesia (5th ed.). St.
(2006). Decreasing the pain of local anesthesia: A prospective, Louis: Elsevier Mosby.
double-blind comparison of buffered, premixed 1 % lidocaine Malamed, S. F. (20 13). Handbook of local anesthesia (6th ed.). St.
with epinephrine versus 1 % lidocaine freshly mixed with epi­ Louis: Elsevier Mosby.
nephrine. Journal of the American Academy of Dermatology, Nusstein, J. , Reader, A., Nist, R., Beck, M., & Meyers, W. J.
54( 1 ) , 128. (1998) . Anaesthetic efficacy of the supplemental intra osseous
316 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E STH E S I A
inj ection of 2 % lidocaine with 1 : 1 00,000 epinephrine in irre­
versible pulpitis. Journal of Endodontics, 24, 487-491.
Onset (Sodium Bicarbonate Inj . , neutralizing additive solution),
Rev. 1 1/11 (LS0 13-D), Onpharma Prescription information
available from Onpharma, USA, Los Gatos, CA; www.
onpharma.com. Accessed January 19, 2014.
Oraverse (phentolamine mesylate) injection, Rev. 04/11 (2604-4) ,
Septodont Prescription information available from Septodont,
USA, Lancaster, PA; www.septodontusa.com. Accessed Janu­
ary 19, 2014.
Quinn, C. L. (1998) . Inj ection techniques to anesthetize the diffi­
cult tooth. Journal of the California Dental Association, 26(9),
665-667.
Reitz, J. , Reader, A., Nist, R., B eck, M., & Meyers, W. J. (1998a).
Anesthetic efficacy of a repeated intraosseous inj ection given
30 min following an inferior alveolar nerve block/intraos­
seous injection. Journal ofthe American Dental Society of
Anesthesia, 45(4), 143-149.
Reitz, J. , Reader, A., Nist, R., B eck, M., & Meyers, W. J. (1998b ).
Anesthetic efficacy of the intraosseous inj ection of 0.9 mL
of 2% lidocaine ( 1 : 100,000 epinephrine) to augment an
inferior alveolar nerve block. Oral Surgery Oral Medicine
Oral Pathology Oral Radiology and Endodontics, 86(5),
516-523 .
Replogle, K., Reader, A., Nist, R., B eck, M., Weaver, J. , &
Meyers, W. J. (1997). Anesthetic efficacy of the intra osseous
inj ection of 2 % lidocaine ( 1 : 100,000 epinephrine) and 3 %
mepivacaine in mandibular first molars. Oral Surgery Oral
Visit www.pearsonhighered.com/healthprofessionsresources to access the student resources that accompany
this book. Simply select Dental Hygiene from the choice of disciplines. Find this book and you will find the
complimentary study tools created for this specific title.
Medicine Oral Pathology Oral Radiology and Endodontics,
83( 1 ) , 30-37.
Rifkind, J. B. (20 1 1 ) . Management of a broken needle in the pter­
ygomandibular space following a Vazirani-Akinosi block: Case
report. Journal of the Canadian Dental Association, 77, b64.
Saadoun, A. P. , & Malamed, S. (1985). Intraseptal anesthesia in
periodontal surgery. Journal ofthe American Dental Associa­
tion, 111 (2), 249-256.
Shimada, K., & Gasser, R. (1989). Anatomical record:
Advances in integrative anatomy and evolutionary biology.
The Anatomical Record, 224(1 ) , 177-182.
Talu, H., Yanyali, A., Karbas, L., Alp, B., & Caglar, Y. (20 0 1 ) .
Effect of warming and buffering lidocaine o n pain during fa­
cial anesthesia. Annals of Ophthalmology, 33( 1 ) , 43.
Tavares, M., Goodson, J.M., Studen-Pavlovich, D., Yagiela,
J.A., Navalta, L.A., Rogy, S., Rutherford, B., Gordon, S.,
Pappas, A.S., Soft Tissue Anesthesia Reversal Group. (2008).
Reversal of soft tissue local anesthesia with phentolamine
mesylate in pediatric patients, Journal of the American Dental
Association, 139(8), 1095-1 104
Tuncel, M., & Ram, V. C. (2003). Hypertensive emergencies:
Etiology and management. American Journal of Cardiovascu­
lar Drugs 3, 21-31.
Umbreit J. (2007). Methemoglobin - it's not just blue: A concise
review. American Journal of Hematology, 82, 134-144.
Wong, J. A. (20 0 1 ) . Adjuncts to local anesthesia: Separating fact
from fiction. Journal of the Canadian Dental Association, 67,
391-397.
 (f)
c

3
* * For mandibular PDLs,
3
lingual sites o re easiest OJ

* * *Or, choose where Any point at is -<

wedged against root and is Associated
tissues ore a l ready
anesthetized completely confi n ed with in the periodontal liga­ periodontiu m 0
ment; blanching and the absence of bockflow --+-.
Figure 1 5-2
should be observed upon deposition (f)
1 5-3
c
"""0
"""0
({)
Periodontium/Soft
tissues:
3
A position in which the tip of the needle is ({)
wedged i nto the pulp chamber or root canol of None :J
the tooth to be anesthetized r-+
re 1 5-20 OJ
l ntroosseous Needles ore �
The most o icol extent of
provided with the ottoc ed mucosa t-----:----:---i---t
the half way between two :J
'--- ·
armamentari u m adjacent teeth
selected Figure 1 5- 1 2A
({)
()
r-+
0
:J
(f)

l ntroseptol 27, gouge shot Center of the

interdental pa pilla adja­
cent to the tooth to
be treated
Figure 1 5- 1 2 B

I n t h e center of t h e interdental b o n e adjacent

to the g i ngiva l , osseous, and/or tooth structures
to be treated
1 5- 1 2B

� •oose volumes provided a re minimum recommendations for pulpal anesthesia.

"" Modified from: 1 ) Melamed S.F., Handbook of local anesthesia, ed 5, St Louis, 2004, Mosby; 2) Jastak JT, Yagiela J.A., Donaldson D, Local anesthesia of the oral cavity.
Philadelphia, 1 995 W.B. Saunders; 3) Daniels S.J., Harfst S.A., Wilder R.S., Dental hygiene: concepts, cases and competencies, 2nd edition, St Louis, 200 7, Mosby
F i e l d of An esth es i a
Su pplemental I njections
I ntrasepta l

Teeth anesthetized :
l ntra p u l p a l
u n reliable p u l pal
Teeth an esthetized:

individual tooth p u l p
Periodonti um/Soft tissues:

at s ite o f i njectio n
soft tissues and

period onti um at
Periodonti um/Soft ti ss u e s :
site of i njection
none

l ntraosseuos PDL

T-th anesthetized: Teeth anesthetized :

i ndividual tooth at i ndivid ual tooth at

site of i njection s ite of i nj e ction

Pe riodontiu m/Soft tissues: Pe riod ontium/Soft tissues:

supporti n g structure s a ssociated period onti u m

i m medi ately adjace nt to

site of deposition
Courteey of:

318
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . @· · · · · · · · · · · · · · · · · · · · · · · · · · · · · ·
Tro u b l esh ooti n g I n a d e q u ate
�m estm esi�a

O BJ E CT I V E S KEY T E R M S

• Defi n e a n d d i scuss t h e key terms i n t h i s c h a pte r. a b errant i n n e rvati o n s 325

a ccess o ry i n n e rvat i o n s 325
• D i sc u ss t h e p ri m a ry rea s o n s fo r i n a d e q u ate l o ca l a n esth es i a .
d i u rn a l b o d y rhyt h m 32 1
• Describe t h e physi o l og i c a l a n d a n ato m i c a l b a s i s i ntraosseo u s i njecti o n s 327
of i n a d e q u ate a n esthesi a . tachyphylaxis 324

• Deve l o p criti ca l th i n ki n g s ki l l s t o h e l p ove rco m e fru strati n g

a n est h etic c h a l l e n g es .

• Deve l o p a n d a p p l y strate g i e s fo r a d d ress i n g i n a d e q u ate

a n esth esia .
320 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E STH E S I A

CAS E S T U DY
Phillipe Giradot
Some suggested reading on the topic of inadequate
P h i l l i p e G i ra d ot is a 2 2 - ye a r- o l d exch a n g e s t u ­
d e n t w h o is i n exce l l e n t h e a lth a n d m a i nta i n s a n
anesthesia incl u des:
a ct i v e r e g i m e n of p h y s i c a l a ct i v ity a n d r e g u l a r 1.L o c a l An esthesia of th e Ora l Cavityby Jastak, J. T.,
h e a lth care. Desp ite h i s d e d icati o n t o p reventi o n , Yagiela, J. A . , & Donaldson, D.
2.Inadequacy of Inferior Alveolar Ne rve Blo ck, Exp loring
by Madan, G. A., Madan, S. G . , &
h e h a s a vo i d e d reg u l a r d e n ta l ca re d u e to p a s t
th e Alterna tives
exp e r i e n ces of p a i n , p a rticu l a rly i n t h e m a n d i b l e ,
Madan, A. D.
desp ite atte m pts by at l e ast 1 0 c l i n i c i a n s to a n es­
3.Th e Inadequacy of Local A n esth esia i n Acute
th etize h i m .
Infla m m ation by Brown, R. D.
H e p rese nts with a n a g g i n g toothache i n t h e vi­
4.Th e Possible Role of th e Mylohyoid Nerve in
cin ity of # 1 9, which has a l a rg e and obvious ca rious M a n dibular Posterior Tooth Sensation by Frommer,
l e s i o n . D u ri n g q u esti o n i n g , h e avoids eye contact J., Mele, F. , & Monroe, C. J.
a n d g rips the arms of the c h a i r. With some prom pt­ 5.ln tra osseous Injection for Profo u n d A n esthesia o f the
i n g , he re l ates h i s past exp e r i e n ces with p a i n d u r­ Lower Molar by Pearce, J.
i n g d e n ta l treat m e n t a n d h is fea r of expe r i e n c i n g 6.Why Ca n 't Yo u Ach ieve Adequate Regio n a l A n esth esia
s i m i l a r p a i n . O n h i s l a st v i s it, h e reca l l s t h a t h e in th e Presence of I n fe ction ? by Najjar, T.
7.Difficu lties in Achieving Local A n esthesia by Kaufman,
E . , Weinstein, P., & Milgrom, P.
received a n u m be r of " s h ots " ( n i n e) a n d that t h e
treatment sti l l h u rt desp ite the n u m ber o f ti m es h e
8.Th e Missed Infe rior Alveolar B lo ck: A New Look a t a n
s a i d h e w a s poked with the need l e .
O l d Problem by Mill e s, M.
9.A Pilot Study of th e Clin ica l Problems of Regiona lly
An esth etizing th e Pulp of an Acutely Infla m e d
Man dib ular M o l a r by Wallace, J., Michanowicz, A . ,
I ntrod uction Mundell, R . , & Wil s on, E .
Complete reference citations are included at the end of
ti c tr
All clinicians have experienced inadequate local anesthesia • •

: . � � . � �� � ; •
(Meechan, 1999) . The term inadequate as it is applied to
local anesthesia refers to the inability to induce effective • • • • • • • • • • • • • • • • • • • • • • • • • • • • • •

conduction blockade to allow comfortable therapy. Even

when conduction blockade is effective, inadequacies can
occur due to psychological factors or postoperative effects
of pain-free procedures. This latter situation illustrates that
local anesthetic failure from a patient perspective does not
always occur during therapy.
Meechan summarizes the causes of local anesthetic
inadequacy in which comfortable therapy is not possible
as either clinician or patient dependent, the former related
more to the choice of technique and drug and the latter re­
lated more to anatomical, psychological, and pathological
factors (Meechan, 1999).
Most local anesthetic procedures performe d after
thorough patient assessment are effective, and success
rates are typically high. When profound anesthesia is
n o t achieved after an initial inj ection, repe ating the
same inj ection usually provides adequate anesthesia
although re-inj ection may also fail. In fact, despite the
high rate of success of re-inj ection with the same tech­
nique, inadequacies are seen as inevitable. The causes of
inadequate anesthesia have been explored in numerous
pe er-reviewed articles, some of which are suggested in
B ox 16-1 •.
When local anesthetic inadequacies occur, not only
are the experiences painful for patients, but confidence in
clinicians can be undermined. Strategies to overcome in­
adequate anesthesia are useful in building and preserving
strong patient-clinician relationships, although they are
not completely successful in all circumstances.
While patients may occasionally blame themselves for
not getting numb and there may be some truth in that as­
sumption, clinicians are keenly aware that it is their respon­
sibility to provide adequate anesthesia. Understanding
that all techniques occasionally fail to provide adequate
anesthesia is a key motivation in the development of strat­
egies to enhance success.
Blanton and Jeske have stated that neuroanatomy is
the "key to profound local anesthesia" (Blanton & Jeske,
2003a) . Their point is liberally reinforced in the litera­
ture. For example, studies have reported difficulties with
inferior alveolar nerve blocks due to a bifid pattern, each
branch of the nerve having a separate foramen (Blanton &
Jeske, 2003a; Lew & Townsend, 2006) .
Failure to appreciate neuro anatomy and its variabil­
ity is not the only cause of anesthetic inadequacy, however.
Bony prominences and dense bone, atypical fascial planes,
highly vascular areas, ligamenta! deflection, circadian
(diurnal) influences (see B ox 16-2 •) , and a host of other
physical and chemical barriers can be responsible for anes­
thetic inadequacy.
Although inadequate volumes of solution may be
a cause of failure, depositing excessive volumes of so­
lution in an attempt to overwhelm nerve membranes

Despite the use of al t ernati v e techniques and strategies,
there are occasions when adequate anesthesia i s not pos­
sibl e during a particular appointment and rescheduling
i s preferable for both clinician and patient. I f reschedul­
ing i s agreed upon, i t has been suggested that circadian
rhythms may influence an indi v idual's susceptibility to local
anesthesia (Malamed, 2006; Panza, Epstein, & Ouyyumi,
1 991 ). The term is frequentl y used
d i u r n a l body rhythm
to describe the variable response to drugs during different
times of a day (Meechan, 1999).
In the event of unsuccessful anesthesia, rescheduling
an appointment during a di fferent time of day could prove
useful (Malamed, 2006). For exampl e , i f the failed appoint-
ment occurred in the afternoon, a morning appointment
•
c d ug t
: . ��� . �� � . :�� �� .
• • • • • • • • • • • . •
compromises safety. Clinicians can achieve more reliable
success by understanding barriers that may be present and
developing their skills with alternative techniques.
This chapter explores strategies for successful local
anesthesia and factors relating to inadequate anesthesia,
and possible causes, as well as approaches to overcome
them. While alternative techniques will be identified in this
chapter for each factor discussed, specific details for per­
forming these techniques will be found in Chapters 12-15,
" Inj ections for Maxillary Pain Control I," " Inj ections for
Maxillary Pain Control II - Palatal Approach," "Inj ections
for Mandibular Pain Control," and "Supplemental Tech­
niques and Adjunctive Strategies."
Defi n i n g Success
The term successful, similar to the term inadequate, has been
used in many different ways when discussing local anesthe­
sia, making it difficult to arrive at a generally accepted def­
inition. For example, does success have the same meaning
to clinicians and patients? Were procedures accomplished
comfortably or were they accomplished despite some dis­
comfort? Was pain experienced early in an appointment
or later, after initial satisfactory levels of pain control?
Problematic in any discussion of successful pain control
is that the pain experience is subj ective, as discussed in
Chapter 2, "Fundamentals of Pain Management."
Published studies use a variety of phrases such as the
absence ofpain, no pain during therapy, well-tolerated, and
comp letely successful, describing results with modifiers
such as most, many, and compared with others. Analyses
of variance (ANOVA) and visual scales (VAS) are used
to analyze, quantify, and report on pain or its absence (see
Box 16-3 •). Clinically reproducible results assess the effi­
cacy of techniques, drugs, and behavioral modifications in
C HAPTER 16 • TRO U B LE S H O OTI N G I N A D EQUATE A N E STH ESIA 321
AN OVA and VAS are frequentl y used research tool s when
studying pain. Anal yses of variance assess and weigh the
to the overall variations that have
impact of e a ch varia ble
been demonstrated or discussed, as they relate to the
outcomes of studies. Vi s ual scal e s are assessment tools
that gi ve relative information regarding the percei v ed in­
tensity of pain. These are expressed on a scal e from 1 to 1 0,
wi t h 1 representing no pain and 1 0 representing the worst
pain the patient has ever experienced. See Chapter 2,
"Fundamental s of Pain Management," for an example of a
A S h·e· • •
: . � . : : V:��:-.8���� ���:� ��;� .�a�i�� .s.c�/�: ..... •
pain control. Tabulated results may be used to formulate
•
and corroborate conclusions.
• Specific measures selected in studies to assess the ab­
• • • • • • • • • • •
sence of pain vary as well and include the use of electric
pulp testing applied to teeth at specific reporting intervals
and reports of pain experienced during procedures. Still
others rely on evaluator and cohort interviews, reaction
surveys, or both (Certosimo & Archer, 1996) .
However success is defined, troubleshooting anes­
thetic inadequacy is an important clinical skill. The dis­
cussion of possible causes and strategies that follows is
intended to provide insights for troubleshooting local an­
esthetic inadequacies and to highlight the most common
categories. Although suggestions in this discussion have
been drawn from multiple sources, it is acknowledged that
experienced clinicians may employ additional, successful
strategies that are not included here.
Ad m i n istration-Related Factors
Local anesthetic success may be influenced by a number
of factors. Those related to the administration include
delivery devices, drugs, and clinical judgment.
Device-Related Factors
In general, the devices used for administration of local an­
esthetics include syringes, cartridges, and needles. While
there are numerous inj ection devices available, most have
little impact on anesthetic success. Additionally, there are
very few needle-related issues in most procedures.
The following discussions are examples of rare device­
related factors that can contribute to inadequacy.
Needle Bevel Considerations
Although needle bevel orientations are considered by
most to be non-critical factors related to anesthesia,
success-specific orientations are recommended in some
techniques (Daniel & Harfst, 2007; Malamed, 20 13). Some
consider it beneficial to make bevel adjustments in order
to place anesthetic solutions as close as possible to target
322 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E STH E S I A
nerves. In deeper penetrations, when bevel orientations
are ignore d , deflections away from targets may occur.
(Malamed, 20 1 3 ) . For example, some recommend that
bevels in Vazirani-Akinosi techniques face the midline,
away from the mandible, in order to facilitate deflection
toward the mandible (Malamed, 20 13).
Needle Deflection Considerations
The higher the gauge of needles, the greater their flex­
ibility and deflection in tissues (Robison et al . , 1984) .
Although many clinicians choose to use 27-gauge needles
out of concern for patient comfort (even though this bene­
fit has not been corroborated) , a 25-gauge needle does not
deflect as much in deeper penetrations (Hamburg, 1972;
Malamed, 2006) . Although deflection is common when
deposition sites are some distance from penetration sites,
problems with inadequate anesthesia due to deflection are
uncommon (Malamed, 20 13).
Quality o f Cartridge Contents
On rare occasions, anesthetic solutions may fall below min­
imum standards for clinical effectiveness. Cartridges of lo­
cal anesthetics with vasoconstrictors are expected to have
a minimum limit of 90 % of the vasoconstrictor effective
and a pH of no lower than 3 . 3 in order to be considered
reliably effective (Lew & Townsend, 2006; Panza, Epstein,
& Quyyumi, 1991). Despite excellent industry standards, at
least one study demonstrated that entire batches of drugs
have at times fallen below these thresholds when tested
immediately upon receipt (Lew & Townsend, 2006; Panza,
Epstein, & Quyyumi, 1991). Although there is no easy and
practical way for offices and clinics to test cartridges for
meeting minimum standards when they arrive, if a par­
ticular batch is repeatedly failing to provide profound and
durable anesthesia, replacement should be considered.
It is important to understand that anesthetic solu­
tion integrity and efficacy are not solely the responsibil­
ity of the manufacturer. It is more likely that damage to
solutions occurred during shipping, handling, or storage.
Product storage facilities and end users must avoid ex­
treme temperatures and improper handling and storage.
Solutions should be stored in dark, room-temperature
locations.
Unfortunately, the antioxidant preservatives that are
necessary to maintain the effectiveness of the vasocon­
strictor also lower the pH of solutions. In general, the lon­
ger a solution containing vasoconstrictors is stored before
use, the greater the degradation of the drugs in the solu­
tion and the higher its acidity. Not only is acidified solution
less likely to produce profound anesthesia, but it is more
likely to produce discomfort during administration.
Clinician Judgment
In order to provide profound anesthesia, adequate vol­
umes of solution must be deposited to block nerve im­
pulses. Volumes necessary vary depending on the anatomy
of the area into which solution is deposited , individual
responses to local anesthetic drugs, and the length of
anticipated treatment.
Volume Considerations According to Anatomy
The total volume of anesthetic drug administered must
be adequate to flood targeted neural membranes. Certain
techniques, such as the Gow-Gates mandibular nerve
block, require greater initial volumes for sufficient diffu­
sion to the target area. Others, such as buccal nerve blocks,
where solution is placed directly over the nerve, require
very little solution.
Volume Considerations According to Individual
Responses
Individual responses to local anesthetic drugs are also im­
portant. For example, an individual who states "I always
take more" or "That stuff lasts forever on me" provides
valuable information that is not available from physical
assessment. When planning drug doses, patient concerns
should be addressed.
Volume Considerations According to Length of
Anticipated Treatment
Volumes administered should take into account the length
of anticipated tre atment. Thirty minutes of soft-tissue
anesthesia will often require less volume compared with
1 hour of pulpal anesthesia in the same area . It is im­
portant to establish adequate anesthesia for procedures
involving roots structures particularly in hygiene therapy.
Anesthesia of s oft tissues alone may not be adequate
without durable pulpal anesthesia.
Ps y cholog ica l Barriers
Some of the most frustrating local anesthetic inadequacies
can be attributed to psychological factors. In the absence
of any known physiological or anatomical factors, some
patients may relate that local anesthesia is not very ef­
fective for them, whereas others report an excessive fear
of inj ections. Others are fearful of specific aspects of in­
jections, such as having no personal control, the fact that
needles are involved, fear of insufficient anesthesia, or of
long-lasting residual anesthesia and are expressed by some
as phobias. For further discussion on inj ection phobias, see
Chapter 18, " Insights for Fearful Patients." Some psycho­
logical barriers are hard to assess, as discussed in the ex­
ample in Box 16-4 •·
Physica l and Chem ica l Barriers
Many physical and chemical barriers can interfere with
successful anesthesia by decreasing the concentrations of
drugs at targeted areas of nerve membranes. This most
commonly occurs due to physical barriers such as liga­
ments and fascia, which can deflect solutions and due to
chemical changes in the tissues such as decreases in pH.

A si t uation that devel o ped in a pri v ate office illustrates the
inexplicable nature of some barriers in denti stry. Following
eight inferior al v eolar injections, with three different drugs,
a pati e nt continued to report inadequate anesthesia of the
mandibular quadrant. Both clinician and patient agreed to
reschedule.
After making a second appointment, the pati e nt walked
to her car. As she inserted the key into the lock she fel t as if
"lightning had struck". Signifi c ant signs and symptoms of
anesthesi a devel o ped immediatel y. She went back into the
office and the procedure was completed that day.
Al t hough it remains to be explained whether this
was a physiol o gical or psychol o gical reaction, when ap­
proached with the problem, two experts, a cogni t i v e psy­
chol o gist and a neurologist, offered the following possible
explanations:
1 . The neurologist suggested that it was a psychol o gi­
cal reaction stemming from the patient's anxiety over
treatment that day. Once it was determined that treat­
ment would not take place, the anestheti c took effect.
2. The cogni t i v e psychol o gi st suggested that it was a
physiol o gical reaction brought on by the metal -to­
metal contact as the key was placed in the lock.
A third explanation i s that the two events were coincidental
an t t n e �l �a s e es h e i
� • � . � � � � : � � � : : ��� � �� . : � � �� . � � : �� . � . � �··
•
Physical Barriers to Successful Anesthesia
Dense bony prominences, shallow vestibules, dilacerations,
and soft tissues such as ligaments can physically block so­
lutions or deflect them away from ideal deposition sites.
Shallow vestibules and bony prominences may prevent
adequate diffusion in infiltrations. Palatal dilacerations
can increase bony distances through which solutions must
diffuse to reach root apices. Ligaments can deflect solu­
tions away from ideal sites. Inferior alveolar nerve blocks
may be unsuccessful when needle penetration is too me­
dial or too shallow, or the sphenomandibular ligament
deflects solution away from the nerve (Jastak, Yagiela,
& D onaldson, 1995b, 1995c) . During infiltrations, fascial
planes may create similar barriers and may be responsible
when ideal deposition sites fail to provide profound anes­
thesia. D ense bone overlying the roots of teeth and bony
curvatures create greater bony distances between depo­
sition sites and nerves. This may prevent solutions from
reaching the nerves in sufficient quantity to produce pro­
found anesthesia. Unusually small foramina can prevent or
limit the volume of local anesthetic solution that can pass
through the opening. This may occur with the infraorbital
(IO) and incisive nerve blocks where it is necessary that
solution diffuse through foramina for success. Regional
nerve blocks and intraosseous inj ections (such as the peri­
odontal ligament [PD L] ) can overcome the maj ority of
these obstacles.
C HAPTER 16 • TRO U B LE S H O OTI N G I N A D EQUATE A N E STH ESIA 323
Chemical Barriers to Successful Anesthesia
Chemical barriers include those existing in the tissues
before inj ection and those caused by injury to tissues dur­
ing inj ection. Inflammation in the area of inj ection from
any cause lowers pH, which can prevent the formation of
sufficient numbers of base molecules. See Box 16-5 • for
further discussion on the impact of inflammation. Vascular
inj ury may flood deposition sites and surrounding areas,
thereby diluting anesthetic solutions and lowering pH as
the inflammatory response is triggered.
The presence of inflammation adversel y affects the success
of l o cal anestheti c injections. Two common explanations
for this phenomenon are increased vascular permeability,
which promotes systemic absorption of drugs and de­
creases their concentrations, and increased tissue acidity
(acidosi s ), which limi ts the number of neutral base mol­
ecul e s available to penetrate nerve membranes. The l o ss
of anestheti c effecti v eness in the presence of inflammation
relies heavil y on the latter explanation that an acidic envi­
ronment i s created during inflammation and suppresses
the production of neutral base molecules.
Changes in pH due to inflammation have been
characteri z ed as bri e f and relati v el y minimal (Brown, 1 981 ;
Ueno, et al., 2008). In addit ion, ti s sues are thought to
have significant buffering capaci t i e s and rather than being
diminished during inflammation, these capaci t i e s appear
to be enhanced (Brown, 1 981 ; Capogna et al . , 1 995;
Quinn, 1 998; Rood, 1 977; Tsuchi y a et al., 2007; Ueno, et al.,
2008).
The assumption that elevated hydrogen ion concen­
tration during inflammation i s the primary cause of l o cal
anestheti c ineffecti v eness has been challenged by some
researchers. Ueno, Mi z ogami, et al. (2008) state that "ti s sue
acidosis i s not essentiall y responsibl e for the l o cal anes­
thetic failure associated wi t h inflammation." They speculate
that non-hydrogen substances, including some negativel y
charged ions produced by inflammatory cells known as
peroxyni t ri t es, may be responsible for local anestheti c inef­
fecti v eness in infl a med ti s sues (Tsuchiya et al., 2007; Ueno,
Mi z ogami, et al . , 2008; Ueno, Tsuchi y a, et al . , 2008).
Sodium bicarbonate, the innate buffering agent used
by ti s sues to maintain normal pH l e vel s , when added to
l o cal anestheti c cartri d ges has been demonstrated to de­
crease the onset time and pai n associated wi t h injections
and to increase the depth of anesthesia (Malamed & Falkel,
201 2). There i s al s o specul a tion that carbon dioxide liber­
ated during the buffering process has an earl y anesthetic
effect due to rapid diffusion through nerve sheaths and may
be responsible for the faster onsets observed (Catch love,
1 972). The brief but immediate effect of raising the pH of
injected ti s sues i s speculated to be responsible for the
demonstrated efficacy of buffering solutions even in inflam­
matory environments (Tsuchiya et al., 2007; Ueno, et al.,
20 )
� . . �� �• • • • • • • • • • • • • • • •• • • • • • • • • • • • • • • • • • •
324 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E STH E S I A

Vascular inj ury may play an important role in the In local anesthesia, tachyphylaxis refers to the inad­
following example: When an initial inj ection with a local an­ equacy of subsequent administrations of local anesthetics
esthetic containing a vasoconstrictor such as 2% lidocaine (in the same appointment) to prolong the duration, extent,
with 1 : 100,000 epinephrine proves unsuccessful, many cli­ and intensity of the anesthetic effect (Lipfert, 1989) . This
nicians follow with another inj ection of 2% lidocaine with phenomenon can also be described as occurring after pre­
epinephrine. Using sodium bicarbonate ( O nset™, On­ viously profound anesthesia has been achieved.
pharma, Los Gatos, CA) can decrease the time of onset and Tachyphylaxis is most likely to occur once anesthe­
increase the potential for success of the repeat inj ection. tized tissues have returned to normal levels of sensation
See Box 16-6 • for further discussion on buffering local an­ (Malamed, 20 1 3 ) . The most successful re-administrations
esthetics. Taking into consideration the potential change in of local anesthetic drugs are those delivered before the
pH, another alternate approach that addresses the lowered return of any sensations (Malamed, 20 13).
pH would be to re-inj ect using a drug with a higher pH The causes of tachyphylaxis include localized tissue
such as 3 % mepivacaine plain. See Box 16-7 • for further edema in the area of inj ection and localized hemorrhage,
discussion of this strategy. Techniques to overcome barriers both of which prevent sufficient concentrations of base
of inflammation include the use of alternate inj ections such molecules near the nerves for anesthesia to develop suc­
as nerve blocks instead of infiltrations, intraosseous tech­ cessfully (Lipfert, 1989; Lipfert, Holthusen, & Arndt, 1989;
niques, and intrapulpal anesthesia. In endodontic therapy, Malamed, 20 1 3 ) . For further discussion of tachyphylaxis,
higher concentrations of epinephrine are sometimes useful. see Box 16-8 •·
TACH Y P H Y LAXIS In general terms, tachyphylaxis is syn­
onymous with what is known as rapid drug tolerance, the
need for increasing doses in order to achieve similar thera­ Anatom ical Va riations
peutic effects. This is what occurs, for example, when in­ Unexpected anatomical variations that are neither vis­
dividuals require 60 mg of codeine in order to achieve an ible nor palpable can sabotage even the most careful
equivalent pain relief previously provided by 30 mg. technique. If root anatomy has been accurately assessed

The introduction of a buffering system for dental l o cal an­ A typical cartridge of l i docaine wi t h epinephrine
estheti c cartridges (Onpharma's Onset) has brought about contains onl y 1 molecule of de-ioni z ed anestheti c for
improvements in the areas of reducing the onset times and every 1 0,000 molecules of ioni z ed anestheti c . . . cl o ser
depth of anesthesia and the pain that i s often associated to physiol o gic pH, more de-ioni z ed anestheti c i s pres­
wi t h l o cal anestheti c injections (Burns et al., 2006; Malamed ent . . . At . . . physiologic pH . . . there i s 2,500x more
& Falkel, 201 2; Talu et al., 2001 ). Al t hough medicine has of the acti v e form of the anestheti c available than at
benefited for years from the ability to buffer anesthetic pH 3.9 [the typi c al pH of lidocaine that is recei v ed
solutions before use, dental admini s trations have been from suppl i ers]. http: //www.onpharma.com/ScienceON.
complicated by the otherwi s e overall convenience of the html, accessed March 1, 201 4.
dental cartridge system. Cartridge deli v ery has discour­ Mechanisms for local anesthetic-related pain, thought
aged practi c al methods of buffering while preserving the to be primarily due to acidity, and the positive effects
integri ty and efficacy of the drugs. Onpharma's Onset mi x­ of buffering on that pain remain unclear. Studies have
ing system has resol v ed this challenge (see Figure 1 6-1 •). demonstrated that sodium bicarbonate buffering wi t h
As previ o usl y expl a i n ed in Chapter 4, "Pharmacol o gy Ba­ the Onset system reduces the experience of injection
si cs," it is the neutral base or non-ionized l o cal anesthetic mol ­ pain. It has been speculated that buffering may act to
ecul es that penetrate nerve membranes. Neutral base forms reduce pain either by decreasing the amount of tissue
of l o cal anesthetic mol e cul e s are consi d ered to be 4000 times irritation that occurs after injection or by allowing faster
more l i pid sol u bl e compared to cationic forms (Mal a med & onset of anesthesia, which blocks nerve impulse gen­
Falkel , 2012). Two percent li d ocaine with epinephri n e, the onl y eration and conduction more rapidly than when buffers
drug for which instructions are provi d ed when usi n g Onset's are not used.
sodium bi c arbonate bufferi n g system, has a pH of 3. 3-5. 0 . In addi t ion to these mechanisms, carbon dioxide
Thi s i s well bel ow tissue or physiol o gic pH of 7.4 due to the produced when combining l o cal anesthetic solutions
addit i o n of sodium bi s ulfite preservatives that are necessary to with sodium bicarbonate has been demonstrated to have
prevent vasoconstrictor oxi d ati o n and shortened shel f life. an independent anesthetic effect on tissues (Catch love,
To cl a ri fy the impact of comparati v el y l o w pH values, 1 972; Condouris & Shakalis, 1 964; Malamed & Falkel,
Onpharma has added the following perspecti v es to its 201 2; Raymond, Wong, & Strichartz, 1 989). Studies have
websi t e:* speculated that carbon dioxide produced from this
combination increases the overall comfort of lidocaine
i je i s
•
* Excerpt from " S ci e n ce o f B u ffer i n g L i d oca i n e with Ep i nephri n e " •

: : � � • � • • : .� �� :�� � � . . � . �� � � :
l i s ed b
.
n a n
• • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • •

On , <:t r" r ,.,a
Buffe ring Guid e
(A)
(B)
(C)
FIGURE 1 6-1 Onset Buffering System. A- The Onset system
provides cartridges of sodium bicarbonate, a unique mixing
device, and a clinical dosing guide. B - The components needed
to buffer dental local anesthetics include the proprietary mix­
ing pen, cartridge connector, cartridge of sodium bicarbonate,
and a standard cartridge of anesthetic. C - Once assembled, the
mixing pen allows a small volume of anesthetic to be replaced
by sodium bicarbonate. The cartridge of anesthetic must then be
used immediately.
C HAPTER 16 • TRO U B LE S H O OTI N G I N A D EQUATE A N E STH ESIA 325
The weakest vasodilator of all dental l o cal anesthetic
drugs is 3% mepi v acaine, which makes i t a useful drug
when vasoconstrictors cannot be used. Its usefulness may
also apply beyond that abili ty. I f an ini t ial injection of 2%
lidocaine is followed with 3% mepivacaine, there may
be an increasing likelihood of success for the following
reasons:
1 . There is 50% more drug per volume of a 3% solution
(30 mg/ml) compared wi t h 2% solutions (20 mg/ml),
providing a greater suppl y of base molecul e s.
2. Depositing 3% mepi v acaine raises the pH at the de­
position si t e. Each pH increase of amounts to a one
decrease in available hydrogen ions, provi d ­
tenfold
i n g a greater supply of base molecules. Because i t is
the base form of the l o cal anestheti c molecule that
di ff uses through the nerve membrane, conduction
blockades may be enhanced. The time i t takes for
the innate tissue-buffering process to return tissues
to normal pH (7 .4) is al s o important when discussing
the differences between the injections of l o w pH and
high pH solutions. Following an injection of a low pH
solution (e.g., 3.5), it takes a longer time to return to
a normal pH of 7.4 compared wi t h the time required
after an injection of a high pH solution (e.g., 6.0).
From a practical standpoint, when comparing the in­
jection of a l o cal anestheti c solution with a relati v el y
low pH to one wi t h a relati v el y high pH, the high pH
drug wil l be effective sooner (Malamed, 201 3). The pH
of 3% mepi v acaine varies from 4.5 to 6.8, and the pH
of 2% lidocaine, 1 :1 00,000, epinephrine varies from
3.3 to 5.5.
3. The mepiv acaine administration takes advantage of
the vasoconstri ction of the l o cal vessels already in
pl a ce due to the epinephrine in the lidocaine solution,
•
: . .
and mepivacaine's duration is enhanced.
. . . . . . . . . . . . . . . •
. . . . . . . . . . . . . . . . . . . . . .
and all other factors have been observed, fascial planes
may cause inadequate anesthesia. Fascial planes can
deflect solution away from ideal deposition sites, result­
ing in inadequate volumes of solution to achieve anesthe­
sia. Conversely, depositing in a less-than-ideal site may
achieve success due to fascial planes that direct solution
to the intended target.
Atypical Innervation Patterns
Innervation p atterns are reliable from an anatomical
standpoint. Although this is generally true, there are some
variations that are expected and some that are entirely
unexpected. Unexpected variations are highly unusual
and are referred to as aberrant innervations. Accessory
innervations may be defined as typical, and therefore ex­
pected, variations.
326 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E STH E S I A

addressing accessory innervation are well recognized and

include those that address incomplete anesthesia in spe­
cific areas of the maxilla and mandible.

Some authors report that tachyphylaxi s occurs only Considerations for Inadequate Maxillary
infrequently, whereas others believe i t occurs in almost
every repeated injection to some extent. Al t hough in some Anesthesia

instances drug tol e rance can be adequatel y explained, the This s e ction will discuss factors unique to maxillary
mechanisms of tachyphylaxi s are not well understood in techniques.
l o cal anesthesia. These mechanisms do not appear to be
related to mode of administration, technique variations, PSA N E RVE BLOCK Some branches of the posterior supe­

or indi v idual drug characteri stics, including whether or not rior alveolar nerve enter the maxilla medial to the usual
the drugs are short or l o ng acting. Specul a tion has cen­ location and innervate the palatal roots of molars and, occa­
tered on pharmacokinetics more than pharmacodynamics sionally, premolars (Blanton & Jeske, 2003a; DuBrul, 1980) .
(Lipfert, 1989). Some sources suggest that fibers from the greater palatine
Diminished response to addi t ional doses of local an­ nerve also provide similar accessory innervation (Meechan,
estheti cs does not appear to resul t from reduced effecti v e­ 1999). Regardless of the source of the accessory innervation,
ness of the drugs at the nerve membrane. On the contrary,
the drugs have been shown to actuall y increase in effec­
a greater palatine nerve block will effectively anesthetize

ti v eness with repeated administrations (Lipfert, Hol t husen,

atypical branches and remedy incomplete anesthesia of af­

& Arndt, 1989). The onl y certainty is that the l a ck of under­

fected maxillary molars and premolars.
standing of this phenomenon does li ttl e to l e ssen frustra­ PDL inj ections are also effective in this situation. It is
tion among clinicians and patients. suggested that three to four sites will provide the best cov­
Tachyphyl a xi s i s most likely to occur once anesthe­ erage of maxillary molars, with at least one site located on
ti z ed ti s sues have returned to normal level s of sensation the palatal aspect of the tooth. It has been suggested that
(Malamed, 201 3). The most successful re-administrations articaine is useful in PSA blocks or associated PDL inj ec­
of l o cal anestheti c drugs are those deli v ered before the tions due to its more effective diffusion to the palatal roots
return of sensations (Malamed, 201 3).
any (Lima-Junior et al. , 2009) .
Possible causes of tachyphyl axi s in l o cal anesthesia
incl u de decreases in l o cal tissue pH, edema, l o cal hemor­ M SA N E RV E B L O C K Middle superior alveolar nerves
rhage, and cl ot formation (Malamed, 201 3). Inadvertent are missing in a significant percentage of the population.
puncture of a vessel , for example, may resul t in l o cali z ed Clinicians are aware of this variant and adapt by routinely
bleeding into the ti s sues, and the resul t ant pool of blood
may present a physi c al barrier. The same puncture may
administering an infiltration over the mesiobuccal root of

al s o dilute the solution to a l e ss than therapeutic concen-

the maxillary first molar (Blanton & Jeske, 2003a; DuBrul,
•

t ati ( � e 0 1 ) • 1980; Jastak, Yagiela, & D onaldson, 1995a; Loetscher &

: . : . � � . � � ��. � � � . : : • • • • • • . •• . • . • • . • . • • • • • •
Walton, 1988) .

ASA N E RVE B LOCK The anterior superior alveolar nerve

Aberrant Innervations block is a highly successful procedure but is subj ect to two
maj or sources of inadequate anesthesia. The first is an­
Most inadequacies due to aberrant innervations result
terior cross-innervation in which the incisors of one side
in a complete lack of anesthesia of the targeted tissues.
may receive fibers from the contralateral ASA nerve. To
Often these situations can never be fully explained; for
achieve complete anesthesia, one of the following options
example, consider a patient who reports never experi­
should be considered:
encing anesthesia to the mandible regardless of the local
anesthetic techniques used. It is possible that this patient 1. Infiltration over the same side central incisor (benefi­
is receiving aberrant innervation from nerve fibers origi­ cial for pulpal and soft-tissue therapy)
nating in other than the trigeminal ganglion . Although 2. Contralateral ASA nerve block
controversial, it has been speculated that some patients
3. P-ASA nerve block
may receive innervations to the mandible from the cervi­
cal nerves. The second occurs when bone in the anterior max­
Overcoming inadequacy due to aberrant innervation illa is unusually dense, the vestibule has very little vertical
requires alternative techniques that bypass them. The ma­ height, or the maxilla has an exaggerated curvature over
j ority of aberrant innervation inadequacies, for example, the roots of the teeth. All may result in deposition too far
can be addressed with PDL inj ections. from the nerve. B oth IO and ASA nerve blocks anesthe­
tize the ASA nerve while the IO nerve block also typically
Accessory Innervations anesthetizes the MSA, when present. The inability to block
Incomplete anesthesia is a common consequence of acces­ the ASA nerve through infiltration can be remedied by
sory innervation (Blanton & Jeske, 2003a). Strategies for performing an IO nerve block.

Another alternative is the AMSA nerve block that
effectively anesthetizes the anterior and middle superior
alveolar nerves and palatal tissues from the anterior mid­
line through the first and, in some cases, the second molar.
PDLs are also an effective alternative. They are suc­
cessful for most teeth, however may be less effective for
canines with unusually long roots.
PALATAL I N N E RVAT I O N OF M AXI LLARY CE NTRAL I N CI S O R S
It has been demonstrated that fibers of the nasopala­
tine nerve may j oin with the maxillary dental plexus to
innervate the central incisors. In order to achieve com­
plete maxillary central incisor anesthesia, an NP nerve
block may be required (Blanton & Jeske, 2003a). A PDL
inj ection may also achieve complete anesthesia in this
situation.
Considerations for Inadequate Mandibular
Anesthesia
This s e ction discusses factors unique to mandibular
techniques.
lA nerve blocks
I N F E R I O R A LV E O LA R N E RV E B L O C K
have a relatively high incidence of inadequate anesthesia
(Malamed, 20 1 3 ) . Subj ective signs and symptoms of an­
esthesia may be misleading. D espite a profound sense of
anesthesia, adequate anesthesia may be absent. Possible
reasons include accessory innervations to pulps from
(Blanton & Jeske, 2003b; Moini, 2008) :
1. Mylohyoid nerves
2. Buccal nerves
3. Lingual nerves
4. Contralateral incisive and mental nerves
5. Sensory fibers traveling with the motor fibers of the
muscles of mastication
6. Bifid inferior alveolar nerves
7. B ranches from the cervical plexus (to the anterior
teeth)
Perhaps the most documented of the accessory in­
nervations is from the mylohyoid nerve, the incidence of
which has been reported as approximating 60 % (Blanton
& Jeske, 2003a). For information on performing a supple­
mental mylohyoid nerve block, see the mylohyoid nerve
block technique in Box 14-8.
PDL inj ections are invaluable in the mandible and
may overcome nearly all of the challenges mentioned pre­
viously. Although PDL inj ections are useful as a primary
technique, they are perhaps even more useful as supple­
mental techniques when other techniques have failed.
PDL inj ections of mandibular second molars can provide
effective mandibular blocks in some situations.
Other helpful techniques for overcoming acce s ­
sory innervation are Gow-Gates nerve blocks, which are
C HAPTER 16 • TRO U B LE S H O OTI N G I N A D EQUATE A N E STH ESIA 327
administered in the superior segment of the pterygo­
mandibular space and Vazirani-Akinosi blocks, which
are administered intermediately between the lA and
Gow-Gates deposition sites (see Figure 14-45) .
Considerations for lntraosseous Anesthesia
Intraosseous injections that involve perforations of cor­
tical plates of bone are useful in overcoming inadequate
anesthesia. Unlike PDL inj ections, intraosseous inj ections
require perforation of the overlying periosteum and corti­
cal plate of bone before deposition. This allows solution
to diffuse directly through spongy alveolar bone to the
dental plexuses in the area. As discussed in Chapter 1 5 ,
" S upplemental Techniques a n d Adj unctive Strategies,"
specialized intraosseous devices and handpieces pro­
vide access to the spongy bone underlying cortical plates.
These techniques appear to be most effective when initial
anesthesia (pre-anesthesia) is already in effect (Malamed,
20 13).
I ntravascu lar I njection
Intravascular inj ections can contribute t o failed anesthesia
because solutions are deposited directly into vessels and
removed from intended target areas. Performing multiple
aspirations and aspirations in more than one plane will
minimize this possibility.
I nfla m m ation
Local anesthetic drugs are packaged primarily i n cationic
form. As they diffuse through healthy tissues with pH val­
ues near 7.4, base molecule concentrations increase. In the
presence of inflammation, base molecule formation may
be significantly diminished. Insufficient numbers of base
molecules for adequate penetration of nerve membranes
may result in inadequate or nonexistent anesthesia. Using
nerve blocks to avoid areas of inflammation usually over­
comes these chemical barriers. When blocks are either
impossible or ineffective, comfortable therapy may not
be possible. The greatest challenges to profound anesthe­
sia may present when treating highly inflamed ("hot")
teeth requiring endodontic therapy. Intraosseous and
intrapulpal techniques and/or higher concentrations of
drugs may be the only recourse if pain relief is urgent and
is impossible to achieve through commonly used blocks
and infiltrations. Pre - anesthesia is recommended for
these inj ections. Some sources state that pre-anesthesia
does not increase success rates, whereas others describe
pre-anesthesia as necessary for reliable success (Blanton
& Jeske, 2003b; Cannell & Cannon, 1976; Kleber, 2003;
Lilienthal, 1975 ; Pearce, 1976 ) . For optimal patient com­
fort, pre-anesthesia seems a reasonable approach when
the rationale for performing an intraosseous inj ection is
to control pain.
328 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E STH E S I A

CAS E M A N AG E M E N T
Phillipe Giradot
Aft e r a c h i ev i n g p a i n re l i ef with a n i n fe r i o r a l veo l a r
n e rve b l ock, a n e l ectric p u l p teste r confirmed that a n ­
esthesia was n ot p rofo u n d o n # 1 9 . Alth o u g h t h e l i p
a n d c h i n were n u m b, # 1 9 was not.
The G ow - G ates n e rve b l o c k p rov i d e d a w i d e r
a re a of a n est h e s i a b e c a u s e t h e a n est h et i c s o l u t i o n
was d e posited m u ch h i g h e r i n t h e pte ryg o m a n d i b u ­
l a r s p a ce, we l l a b ove t h e l ocatio n fo r lA b l ocks. T h e
e nti re tru n k o f t h e i n fe r i o r a lveo l a r n e rve w a s a n es ­
t h e t i z e d , i n c l u d i n g t h e m y l o hyo id a n d l i n g u a l n e rve
fi b e rs (a n d u s u a l l y t h e b u cca l n e rve fi b e rs ) , a n y of
w h i c h co u l d h ave p rovided a ccessory i n n e rvat i o n to
tooth # 1 9 .
M r. G i ra d ot d i d n o t re m e m b e r h a v i n g to k e e p
h i s m o uth o p e n after t h e p rev i o u s i nj e cti o n s , w h i c h
w a s a g o o d i n d i ca t i o n t h a t a G ow - G ates h a d n o t
b e e n atte m pted . H e c o o p e rated we l l , a n d t h e p ro ­
c e d u re w a s c o m p l et e d u s i n g 2 % l i d o c a i n e w i t h
1 : 1 00,000 e p i n e p h ri n e . With i n 1 0 m i n utes, h e
stated t h a t h e h a d n e v e r b e e n t h at n u m b i n h i s l ife
a n d t h e e l e c t r i c p u l p teste r c o n fi r m e d p rofo u n d
a n esth esi a .
Alth o u g h it is l i ke l y fro m his descri ptio n that P D L
i njecti o n s h a d b e e n atte m pted p revio u s l y, tech n i q u e
c o n s i d e ra t i o n s a re critica l fo r routi n e s u ccess. T h e
d e g ree o f d iscomfo rt h e exp e r i e n ced afte r receiving
sh ots i n the g u ms i n d icates that they may h ave been
performed tra u m atica l ly, with excessive p ressu res and
too q u ickly.
P h i l l i p e was g ratefu l for what he te rmed the o n ly
comforta b l e d e n ta l a p p o i nt m e n t h e h a d eve r expe­
r i e n ced and h e made a p p o i nt m e nts to ret u r n fo r his
routi n e care.
Case Discussion: I t is u n l i ke l y that this p a t i e n t
received s u bsta n d a rd a n esth e s i a . T h e n u m be r of c l i ­
n i c i a n s atte m pt i n g a n esth e s i a , a l o n e , s u g g ests t h a t
d iffe rent a p p roaches were atte m pted . N o n e had been
effective. In order to dete rm i n e whether o r n ot a p a r­
ticu l a r tech n i q u e has been atte m pted in the past, it is
h e l pfu l to q u estion patie nts reg a rd i n g aspects of tech­
n i q u es t h at d iffe r fro m lA n e rve b l ock tech n i q ues. I n
M r. G i radot's case, he d i d not reca l l kee ping h i s m o uth
open after any i njecti ons. He did rem e m be r sh ots be­
side the tooth and that the sites h u rt a l ot afterwa rd .

� h. c:l.P.t.� r. . 9.LJ.��� i () .rl � . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

. . _ _
4. Possible successful approaches when an inferior
alveolar nerve block fails to provide complete and
1 . Inadequate anesthesia may typically be caused by all profound pulpal anesthesia are:
of the following, except: a. PDL inj ections
a. Accessory innervation b. Mylohyoid nerve blocks
b. Inflammation c. Gow-Gates blocks
c. Poor manufacturing processes d. All of the above
d. Freezing of cartridges during shipping 5. Two inj ections of 2% lidocaine, 1 : 1 00,000 epineph­
2. Infiltration (supraperiosteal) anesthesia over the rine (total lidocaine = 72 mg) have failed to provide
apex of #9 has failed to achieve adequate anesthesia. adequate anesthesia. Useful supplemental alterna­
Which one of the following is not a likely possibility? tives, regardless of the location or technique, include
a. Cross-over innervation from the contralateral ASA all of the following, except:
b. Bony obstructions a. 3 % mepivacaine
c. Dense bone b. PDL inj ections
d. Unseen inflammation c. Mylohyoid blocks
d. 2% mepivacaine, 1 :20,000 levonordefrin
3. The relative acidity of tissues into which anesthetic
drugs are inj ected is related to the efficacy of a drug 6. By which of the following mechanisms do intraosse­
in the following manner: ous techniques work?
a. An excess of hydrogen atoms enhances neutral a. They are propelled through tissues to nerves and
base molecule formation nerve trunks
b. A pH-driven increase in cationic concentrations b. They rapidly diffuse through bony tissue to nerve
decreases the rate of success trunks
c. A pH-driven increase in cationic concentrations in­ c. They slowly diffuse through bony tissue to nerve
creases the rate of success trunks
d. A decrease in pH increases the number of neutral d. They slowly diffuse through bony tissue to dental
base molecules plexuses

7. Where is the deposition site for the Gow-Gates nerve
block located relative to the inferior alveolar nerve
block?
a. At the same level in the pterygomandibular space
b. At a higher level in the pterygomandibular space
c. B elow the inferior alveolar nerve block
d. B elow the Vazirani-Akinosi block but above the
IA block
8. Some nerve blocks require far greater volumes of
solution compared with others.
a. True
b. False
References
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Loca l An esth esi a Com p l i catio n s

a til d M a til a g·e·rmr e r.ut!

O BJ E CT I V E S KEY T E R M S

• D efi n e a n d d i scuss t h e key terms i n t h i s c h a pte r. adverse eve n ts 332

a dverse rea ct i o n s 332
• I d e ntify a n d d i scuss t h e m ost co m m o n adverse loca l eve n ts
ageusia 339
that m a y occu r d u ri n g a n d afte r l o ca l a n esthetic d ru g
a n g i o e d e m a 349
a d m i n i strati o n s . co m p l ications 332
• I d e ntify a n d d i scuss t h e cate g o ries of adverse systemic dysest h e s i a 339
events that m a y occu r d u ri n g a n d afte r l o ca l a n esth etic d ru g e m b e d d e d n e e d l e s 337
a d m i n i strati o n s . h e m at o m a s 333
h u b b i n g 336
• Eva l u ate a n d d i scuss a p p ro p ri ate res p o n ses a n d m a n a g e m e n t
hyp eresth esia 339
o f adverse l o ca l eve nts.
hyper- respo n d e rs 345
• Eva l u ate and d i scuss a p p ro p ri ate res p o n ses and m a n a g e m e n t hypers e n s itivity 348
o f adverse syste m i c eve nts. h y p o g e u s i a 339
hypo-res p o n d e rs 345
• Eva l u ate and d i scuss p roto co l s fo r t h e m a n a g e m e n t of over-
i d i osyncratic 350
dose a n d a l l e rg i c eve nts.
m et h e m o g l o b i n e m i a 350
• D efi n e i d i osyncratic events and a n a l yze th e i r m a n a g e m ent. occ u l t h e m at o m a s 333
D i sc u ss and apply a p p ro p riate p reve ntive strate g i e s to avo i d overdose 332
a n esth e s i a c;9 m p l i ctJti o n s . p a rest h e s i a 338
tris m u s 335

331
332 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E STH E S I A
CAS E S T U DY
Ashley Smith
Ash l ey S m it h , a stu d e n t " patient" fo r a d e n ta l hy­
g i e n e l o c a l a n esth e s i a l a b o ratory sess i o n , had n o
co m p l i cati n g fa ctors a n d n o re l ative o r a b s o l ute
co ntra i n d i cations to receivi ng a poste rior su perior
a lveo l a r ( P SA) n e rve b l o c k . Fo l l ow i n g n e e d l e i n ­
sertion fo r a PSA b l ock, t h e stu d e n t " c l i n i cia n " re­
ported a positive a s p i ration at the d e positi o n site.
In res p o n s e , t h e n e e d l e t i p was re positi o n e d a n d
a secon d aspiration test was perfo r m e d . Fo l l ow i n g
a negative res u lt, the c l i n ician a d m i n iste red the lo­
ca l a n esthetic sl owly. Before the p l a n n ed dose h a d
been d e l ivere d , Ash l ey deve l oped l o c a l ized swe l l ­
i n g i n h e r cheek n e a r t h e site o f t h e i njecti o n .
I ntrod uction
Adverse events o r reactions related t o the administration
of drugs have been defined as undesired effects that occur
in response to their pharmacologic actions (Horlocker &
Wedel, 2002; Pickett & Terezhalmy, 2006). This definition
can be expanded to include events that surround admin­
istrations of drugs described in terms of their local or sys­
temic effects or as complications.
Local complications occur more frequently than
systemic complications and may include anything from
postop erative soreness to prolonged anesthesia. The
maj ority of adverse events related to local anesthesia in
dentistry involve mild reactions such as p o stoperative
discomfort in the area of inj ection, syncope, pain from
patient s elf-inj ury, and mild inflammation following
muscle penetrations. These usually present as no more
than limited inconveniences or short-term management
situations.
Systemic reactions such as overdose, allergy, and idio­
syncratic response occur far less frequently but are gener­
ally more serious. Although fewer serious adverse events
may be expected, clinicians must be prepared to respond
appropriately if and when they occur. It has been reported
in the literature that peripheral nerve blocks, in particular,
have been associated with the highest incidence of sys­
temic toxicity (Cox, Durieux, & Marcus, 2003 ) . D espite
this reported incidence, which includes statistics from mul­
tiple health professions, local anesthetic drug administra­
tion in dentistry appears to be relatively safe, with a very
low overall risk and rare occurrence of life-threatening
events (Haas, 1998; Malamed, 20 1 3 ) . In a 1999 study in­
volving over 1 ,000 healthy subj ects undergoing oral sur­
gery, for example, it was found that there were no reported
adverse events despite administrations that exceeded
overdose thresholds in a majority of the subjects (Lustig &
Zusman, 1999) .
A primary responsibility of dental clinicians is to
recognize and respond to adverse events that occur before,
during, and after the administration of local anesthetics.
Practice acts may differ on the extent of emergency train­
ing required of dental professionals but all are expected
to recognize and respond to local and systemic adverse
events, including life-threatening emergencies when they
occur. Product monographs for all of the anesthetic drugs
used in dentistry make similar statements regarding clini­
cian responsibility when administering local anesthetics
(see Box 17-1 •).
Morbidity and Mortality
Catastrophic outcomes following local anesthetic drug ad­
ministrations in dentistry are very rare. Dental local anes­
thesia has been characterized as being extremely safe, with
estimates of more than 300 million administration proce­
dures each year in the United States (Malamed, 20 13). In
one report of complications following the administration
of local anesthetics for 2,731 dental patients, nearly half of
whom had at least one significant risk factor, severe com­
plications (bronchospasm and seizure) occurred in only
two cases or 0.07 % (D aublander, Miller, & Lipp, 1997 ) .
When adverse events are recognized a n d addressed in a
timely manner, significant morbidity and mortality are un­
likely (Moore & Hersh, 20 10).
Reports o n localiz e d complication rates are l e s s
frequent in reviewed literature. M a n y of t h e available
complication studies provide pertinent information; how­
ever, information provided is usually related to a spe­
cific complication or population instead of an overall
incidence rate.
This chapter examines the local and systemic compli­
cations of local anesthesia, prevention strategies (when
available ) , and appropriate response and management
protocols.
WAR N I N G S
DENTAL PRACTI T IONERS WHO EMPLOY LOCAL
ANESTHETIC AGENTS SHOULD BE WELL VERSED IN
DIAGNOSIS AND MANAGEMENT OF EMERGENCIES
WHICH MAY ARISE FROM THEIR USE. RESUSCITATI V E
EQUIPMENT, OXYGEN AND OTHER RESUSCITATI V E
DRUGS SHOULD BE AVAILABLE FOR IMMEDI ATE USE.
*XYLOCAINE i s a trademark of DENTS PLY Pharma­
ceuti c al; manufactured by Novocol Pharmaceuti c al of
Canada, Inc., Cambridge, Ontario, Canada, for DENTSPLY
Pharmaceuti c al.
Source: Li doca i n e H C I a n d ep i n ep h r i n e i nj ection p rescri ption
i nformation (Rev 1 2/1 1 ), D E NTS P LY ava i l a b l e from D E N TS P LY
• •
: • • � �. � . � � � • • � .� : : ��- • • • • • • • • • • • • • • • • • • • • •
P h r a eu i a , U S , o k
 C HAPTER
Loca l Com p l ications
Local complications of local anesthetic drugs involve
tissue inj uries that occur before, during, and after the ad­
ministrations of topical and inj ectable local anesthetic
drugs. Some causes are obvious, such as injuries that result
in the formation of hematomas. Others are less obvious,
such as the development of neuropathies, where multiple
theories have been proposed to explain the etiology of
neural inj uries that sometimes occur during local anes­
thetic administrations (Pogrel & Thamby, 2000) .
Hematoma
Hematomas are formed from the leaking of blood from
vessels into surrounding tissues (Ibsen & Phelan, 2014) as
a result of inadvertent nicks of blood vessels during inj ec­
tions. If the injury to a vessel is minor, bleeding into tissue
spaces surrounding the injured vessel may not be noticed.
When a more significant inj ury occurs in a larger vessel,
particularly an artery, the development of a hematoma can
be rapid and dramatic. The most likely occurrence follows
posterior superior alveolar and division 2 (maxillary tu­
berosity approach) nerve blocks. This is due to the proxim­
ity of the pterygoid plexus of veins and maxillary arteries
to the target sites in the infratemporal and pterygopala­
tine fossae (Blanton & Jeske, 2003 ) . Figure 17-1 • shows
swelling that occurred moments after insertion during a
PSA inj e ction . Overall, hematomas occur infrequently.
Inferior alveolar (IA) nerve blocks along with mental inci­
sive nerve blocks are associated with lesser risks compared
with PSA nerve blocks but relatively high risks compared
with other inj ection techniques due to the proximity of
their associated vasculature. Hematomas occurring during
F I G U R E 1 7-1 Initial swelling from a hematoma.
Immediate swelling during a PSA injection.
Source: Courtesy of Ashley Diteman.
17 • LOCAL A N E STH ESIA C O M PLICATI O N S A N D MANAG E M ENT 333
or after lA nerve blocks frequently have no extraoral signs
due to the ability of the pterygomandibular space to con­
ceal large quantities of blood (Malamed, 20 1 3 ) . Those oc­
curring near the mental foramen tend to be more visible
because they occur near the chin where bruising may be
more obvious. Fibrous attached tissues of the palate tend
to limit the extent of hematomas that occur there, as dem­
onstrated in Figure 17-2 •·
S o m e clinicians b e lieve that p o s itive aspirations
significantly increase the incidence of hematoma forma­
tion. This may not be the case considering that nicking a
vessel can occur as needles penetrate to depth, but hema­
tomas can also occur well after aspiration when needles
are withdrawn, regardless of the results of aspiration.
Although a positive aspiration indicates that a vessel was
penetrated, the maj ority of penetrations result in too lit­
tle bleeding for noticeable hematoma formation (Haas,
1998) .
Failure to achieve adequate anesthesia in lA nerve
blocks has been attributed to the formation of hematomas
(Scheinfeld et al. , 20 1 3 ; Trager, 1979) . Hematomas may
interfere with the development of anesthesia by diluting
the drugs, by transporting them from intended target areas,
and by initiating inflammatory responses that lower pH. In
the case of lA nerve blocks, clinicians may not be aware
that hidden or occult hematomas exist, in which case trou­
bleshooting the lack of profound anesthesia after adminis­
tration can be frustrating. This may be the situation when
successive lA nerve blocks fail to establish anesthesia.
Alternative techniques such as Gow-Gates nerve blocks
or periodontal ligament (PDL) inj ections (see Chapter 16,
" Troubleshooting Inadequate Anesthesia " ) can place
drugs away from these hematomas.
Although uncommon, infection and trismus have
occurred following hematoma development (Haas, 1998) .
While the clinical course of healing is marked by very
noticeable discoloration of the face, the maj ority of he­
matomas heal uneventfully and re quire no additional
treatment.
FIGURE 1 7-2 Palatal Hematoma. Hematomas of the
palatal are generally well confined.
334 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E STH E S I A

P R E V E N T I O N OF H E M ATO MAS Taking into account the

number of dental inj ections administered daily, hematomas
are rare (Pogrel & Thamby, 2 0 0 0 ) . Clinicians can help
maintain this low risk by observing a few relatively simple
precautions. Minimizing the number of needle penetra­
tions is recommended, considering that one penetration
involves a certain degree of risk; two penetrations double
the risk; three triple the risk; and so on. Avoiding trauma in
general is also important, as any aspect of an inj ection that
traumatizes tissues increases the risk of hematoma (Haas,
1998). This can be accomplished by maintaining good ac­
cess, observing appropriate angulations and penetration
depths, and avoiding rapid penetrations and bowing of
Pati e nts on anti c oagulant therapy are at increased risk of
extensive hematoma formation. Aspirin, warfarin, and cl o p­
idogrel (Piavix) are commonl y used anti c oagulants. Some
patients are on high doses or may be taking combinations
including al l three drugs, as was the case with this patient.
After a single PSA injection, this patient developed
a vigorous hematoma and was referred to an oral sur­
geon, who placed the compression dressing seen in
Figure 1 7-3A • · The patient was subsequentl y admitted to
a nearby hospi tal. In contrast to Ashley in the chapter case
study, this is a rare event.
•

needles.
PSA nerve blocks, in particular, should be avoided if Al t hough PSA nerve blocks have been described as
patients are taking blood thinners. Hematomas that occur preferable to infil t rations, especiall y when mul t iple molars
require anesthesia, exceptional bleeding risks may con­
traindicate their use. Infil t rations are excellent substi t utes
in the presence of anticoagulant therapy can be extensive
and may require additional therapy. Some have required
• for PSA nerve blocks in patients wi t h increased risks due
hospitalization. A case history of a vigorous hematoma
to the rel a tivel y minimal risk of hematoma formation.
formation after a single PSA inj ection on a patient tak­
• Al t hough infil t rations (supraperiosteal injections) can sig-
ing multiple anticoagulants is discussed in Box 17-2 and
•,
•
ni ficantl y decrease bleeding risks, an overall risk-reward
shown in Figure 17-3 which illustrates the benefit of anal y sis is important when making decisions whether to
careful pre-anesthetic assessment. treat patients such as this one, particularly in a typical
Consultation with a patient's physician before per­ office or clini c al setting. The combination of aspirin,
forming local anesthetic procedures can be useful for pa­ warfarin, and clopidogrel is unusual and shoul d raise
tients on anticoagulant therapy as discussed in B ox 17-2 concerns of signi ficant bleeding risks, regardless of the
and shown in Figure 17-3, which once again illustrates the procedure or l o cal anestheti c technique contemplated.
Figures 1 7-38 • and 1 7-3C • show the progressive
h ea d re i f t o a
benefit of careful pre-anesthetic assessment.
• • � �� �� . . � � � �� �� � . �� ����: .� .' , , , • • • , •
•

Aside from the risk of hematoma formation, an impor­

• , , •
tant benefit of careful anatomical assessment, observing

(A) (B) (C)

FIGURE 1 7-3 Extensive Hematoma. A - This atypical, extensive hematoma required the placement of a compression bandage. This
patient was on anticoagulant therapy, which complicated the situation. B - Bruising lingering around the eye and mouth. C - Fully
healed several weeks later.
 C HAPTER
appropriate technique, and minimizing the number of pen­
etrations is enhanced patient comfort.
R E S PO N S E TO A N D MANAG E M ENT OF H E MATOMAS Early
recognition and response to a developing hematoma can
alter its clinical course. A hematoma's extent is limited by
the degree of flexibility of the tissues into which the blood
is emptying. Clinicians can create an opposing force by
applying pressure and keeping the pressure in place long
enough for clotting to begin. In the absence of deliberate
pressure or when pressure is ineffective, tissue resistance
must approximate the pressure of the blood pouring from
the vessel before blood will cease entering the tissues. In
situations where surrounding tissues are flexible, larger he­
matomas can develop. Where tissues are less flexible, such
as in the palate or when pressure is applied, hematomas
tend to be more limited in size. Protocol for the manage­
ment of hematomas is summarized in Box 17-3 •·
Trismus
From a neurological standpoint, trismus is defined as a
motor disturbance of the trigeminal nerve (Dorland 's
Illustrated Medical D ictionary [D orland 's] , 2009; Jastak,
Yagiela, & Donaldson, 1995 ) . It is more simply described
as an inability to open the mouth. Broadly considered, it
has many etiologies and contributing etiologies, including
tetanus (lock j aw) , tumors, bony ankylosis, fracture, for­
eign bodies, fascial space infections, and enlarged coronoid
processes (Jastak, Yagiela, & Donaldson, 1995 ) . As a con­
sequence of local anesthesia, however, its primary causes
are hemorrhage and muscle trauma following needle pen­
etrations (Jastak, Yagiela, & Donaldson, 1995).
Protocol for the management of hematomas includes:
Earl y recognit ion and response:
1 . Be alert to the possibility of hematoma formation
2. Respond to ini t ial signs of swelling
a. Discontinue treatment
b. Appl y pressure and i c e (i f i c e is available, you can
appl y pressure wi t h i c e)
c. Do not inci s e and drain hematomas
3. Once the hematoma has stopped expanding:
a. Instruct the patient to apply ice intermittentl y for
the next 6 hours
b. Instruct the patient to avoid anti c oagulant pain re­
lievers such as aspirin
c. Advi s e the patient regarding the potential for brui s ­
i n g and discoloration
d. Advise the patient to noti fy you immediatel y of any
change, especiall y the development of signs and
� • • • • • . :�:���� �f. i � f��t�� n. � r. l �� i�e•d•j�� �:�� i �: • • • .li
s tissues, causing pain. Pain can occur due to the irritating
17 • LOCAL A N E STH ESIA C O M PLICATI O N S A N D MANAG E M ENT 335
Trismus is a relatively common complication of local
anesthetic inj ections (Haas, 1998) . Inj uries sustained in­
volve the muscles of mastication and blood vessels of the
infratemporal fossa (Jastak, Yagiela, & Donaldson, 1995).
In addition to physical trauma due to needle movements,
local anesthetic toxicity to skeletal muscle has also been
demonstrated (B enoit, Yagiela, & Fort, 1980; Malamed,
20 1 3 ) . Causes of trismus include not only physical and
chemical trauma to muscle tissue but also physical trauma
to blood vessels (Jastak , Yagiela, & D onaldson, 1995 ) .
Contaminants o n needles may result i n local infection and
trismus.
The most frequent muscle to experience trismus is the
medial pterygoid. It can be inj ured by all three common
approaches to mandibular nerve block, the inferior alveo­
lar, Gow-Gates, and Vazirani-Akinosi techniques (Haas,
1998). The lateral pterygoids and temporalis muscles are
less frequently involved (Haas, 1998) .
Bleeding, toxicity of anesthetic solutions, and direct
physical injury to muscle tissues are all suspect when tris­
mus occurs following local anesthetic inj ections (Haas,
1998) .
PREVENTION OF TRI S M U S The occurrence of trismus can
be minimized by decreasing the number of penetrations,
changing needles frequently (especially whenever tips
may be barbed), and assuring that needle contamination
does not occur before penetration (Haas, 1998; Stacy &
Hajj ar, 1994) .
R E S P O N S E TO A N D M A N AG E M E N T O F TR I S M U S In the
response to management of trismus, instruct patients to:
1. Apply hot, moist towels approximately 20 minutes
every hour (5 minutes on, 10 minutes off) .
2. Use analgesics for discomfort, particularly ibuprofen,
if appropriate.
3. Open and close the mouth gradually and repeatedly
to maintain mobility of the temporomandibular j oint.
A useful exercise suggested by some dental clinicians
includes placing the tip of the tongue behind the max­
illary central incisors. With the tongue held in place,
the mouth is opened and closed at regular intervals
throughout the day.
4. Monitor for signs of infection that may require anti­
biotics, such as increasing heat, redness, elevated tem­
peratures, and pain.
5. Refer to an oral surgeon or physician if signs and
symptoms fail to improve, or worsen (Haas, 1 9 9 8 ;
Norholt et a!. , 1998) .
Pain on Injection
There are many possible causes of pain on inj ection .
Needle penetrations o f well-innervated anatomical tissues
can cause pain. Rapid deposition of solution can distend
and acidic nature of local anesthetic solutions and can also
336 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E STH E S I A

occur if solutions are too cold or too hot compared with

oral temperatures. Although each of these factors has the
potential to cause pain, the maj ority of the time they do
not when topical anesthetics are used, deposition rates are
slow, and muscles are relaxed (Haas, 1998; Malamed, 20 13).
P R E V E N T I O N O F PAI N O N I NJ E CTI O N
venting pain on inj ection include:
1. Adequate pre-anesthesia
a. Appropriate topical anesthesia
b. Pressure anesthesia techniques for needle pen­
etration in palatal tissues
2. Slow rate of deposition of local anesthetic solution
a. Adhere to recommended maximum rates
b. Adjust to one-third the normal rate or slower for
Strategies for pre­
� . . � · · : � . . �� �� ��� u.l � �:e.a ��:� ��c�:·
Occasional "hubbing" may be necessary in order to con­
tact bone when there i s excessi v e flaring or an unusually
large mandible. Long needles (31 or 32 mm) may barely
reach deposition targets for mandibular nerve blocks in
these indiv idual s . In these instances, maximum insertion
may be necessary and acceptable. I t i s prudent practi c e,
however, when maximum insertion is necessary, to wi t h­
draw slightl y (approximatel y 4 mm) in order to l e ave a por­
tion of shank visible (see Figure 1 7-4 • ). This reduces the
ri s k of needl e breakage and provi d es a portion of shank to
g r s p i h fo e
• • • •Ji • • • • • •

deposition in palatal tissues

3. When administrating solutions with and without vaso­
constrictors, administer plain solutions first
4. If a particular drug causes a burning sensation, sub­
stitute with other appropriate drugs (H aas, 1 9 9 8 ;
Malamed, 20 13).

R E S PO N S E T O PAI N O N I NJECTIO N Pain on inj ection is not

uncommon. When deliberate attempts to control pain on
inj ection are made, pain is usually eliminated. Following
the b asic steps for inj ections outline d in Chapter 1 1 ,
"Fundamentals for Administration o f Local Anesthetic
Agents," will help assure comfortable inj ections in most
cases.
FIGURE 1 7-4 Reducing Risks for Needle Breakage.
Broken Needles Leave a length of the shaft visible to reduce the risk of
Although rare, needle breakage has occurred after unex­ needle breakage and to provide a portion of shank to
pected patient movements. Factors that increase risks for grasp should breakage occur.
needle breakage include using needles of higher gauges in
deeper penetrations, bending needles at hubs, and needle
penetrations to hubs (Haas, 1998; Malamed, 20 1 3 ) . While 3. Use long needles for deeper penetrations.
needle breakage is not common today, litigation is possible 4. Use lower gauge needles.
should it occur.
5. Avoid excessive forces on needles (such as when repo­
Clinicians should
P R E V E N T I O N OF N E E D LE B R E A KA G E sitioning, or when needles are bowed).
choose needle gauges and lengths that are appropriate 6. Avoid excessive numbers of penetrations with the
for the depths of penetration and types of tissue through same needle.
which needles will pass. This helps prevent insertion to 7. I f b e n d i n g is d e si re d , * av o i d b e n d i n g at h u b s
hubs, which are the weakest point on needles, a practice (Bedrock, Skigen, & Dolwick, 1999; Bhatia & Bounds,
referred to as bobbing. Choosing needles with adequate 1998; Haas, 1998; Malamed, 20 1 3 ; Marks, Carlton, &
length reduces risks of needle breakage that result from McDonald, 1984; Zeiter, Cohen, & Casap, 2002).
hubbing. Sudden patient movements when needles are
hubbed are more likely to break needles compared with
R E S P O N S E T O A N D M A N A G E M E N T OF B R O K E N N E E ­
movements where hubs are not touching the mucosa.
D L E S Appropriate response to broken ne e d le s may
Leveraged pressures at maximum insertion are applied
b e critical to maintain p o s itive patient relationships
directly against the hub/needle shaft j unction. Some ex­
(Ethunandan et al. , 2007; Haas, 1998; Orr, 1983). Although
ceptions to this guideline are discussed in Box 17-4 •·
these occurrences are rare, in the event of a broken needle,
Prevention strategies to avoid undue stre s s e s o n
needles include the following:
* O SHA's bloodborne p athogens standard on bending and recapping
1. Inspect needles before use. contaminated needles is provided in Box 17-5 •· See Figure 9-1 1 for an
2. Avoid inserting needles to hubs. example of the hazards of recapping bent needles.

patients frequently seek litigation (Malamed, 20 1 3 ) . It
may be argued whether a particular embedded needle
fragment should be removed, however, breakage must be
recognized, located, and documented (B edrock, Skigen, &
Dolwick, 1999) .
Additional precautions and responses include:
1. Have a sterile hemostat readily available whenever
drugs are administered with needles.
2. Do not allow patients to close their mouths if break­
age occurs (closing can draw the needle further into
tissues).
3. If the needle is visible, remove it with a hemostat.
4. If the needle is not visible:
a. Inform the patient that a needle has broken and a
nonretrievable segment is embedded in the tissues.
b. Refer patients to an oral and maxillofacial surgeon
for immediate evaluation.
c. Keep accurate records of location, needle size, any
unforeseen events precipitating the breakage, and
patient communication.
5. Where possible, any remaining unembedded frag­
ments of the needle should be sent to the surgeon who
is evaluating the situation.
Surgical removal may not be indicated because of the
potential for extensive tissue damage that can result dur­
ing removal. Retaining needle fragments might ultimately
When choosing to bend needl e s prior to injection (before
needl es are contaminated), it is important to note that this
practi c e may create both di ff i c ul ty and hazards for safel y
recapping needles after the procedure. OSHA's blood­
borne pathogens standard [29 CFR 1910.1 030(d)(2)(vii ) (A)]
prohibi ts the bending, recapping or removal of contami­
nated needl e s and other contaminated sharps unless the
employer can demonstrate that no al t ernati v e i s feasible or
that such action i s required by a speci f i c medical or dental
procedure.
The standard al s o provi d es an exception where an
"employer can demonstrate that no al t ernati v e i s feasible
or that such action i s required by a speci f i c medical or den­
tal procedure. Such bending, recapping or needle removal
must be accomplished through the use of a mechanical
devi c e or a one-handed technique" [29 CFR 1 91 0.1 030(d)
(2)(vii ) (B)].
The preamble to the bloodborne pathogens standard
notes that the administration of incremental doses of a
medication is one medical procedure, among others, to
which this exception refers [56 641 1 8 (1 991 )].
FR
·This information was accessed at U.S. Department of
Labor, Occupational Safety & Heal t h Administration, www
h a g o · rc 4
� •� � . � . : . � � . � :�: : .
• • • • . . • • . • . IIi
• •
C HAPTER 17 • LOCAL A N E STH ESIA C O M PLICATI O N S A N D MANAG E M ENT 337
cause less tissue damage than removal. When preparing a
patient for referral to an oral surgeon, choose terms such
as evaluation rather than removal in order to better align
patient expectations with a surgeon's eventual actions. As
an example of the difficulty in guessing the ultimate dis­
position of an embedded needle fragment, one relatively
recent case cited an initial decision to leave a needle in the
tissues but was reversed 6 months later when the buried
fragment became symptomatic (Ethunandan et a!. , 2007).
D espite the precaution of using language that does
not conflict with a surgeon's later advice to a patient, it
is unlikely today that a surgeon will opt to leave a needle
fragment in the tissues (see Box 17-6 •) .
Self-Injury
It is important for dental professionals to advise patients,
parents, and caretakers of the risk of self-injury when areas
of the mouth are anesthetized with inj ections that provide
extensive soft-tissue anesthesia, especially because the risk
of injury can continue for some time after a patient leaves
the dental chair. Figure 17-5 • shows an example of a post­
anesthesia lip bite.
In the event of lingering anesthesia, there is a subse­
quent risk of biting oral soft tissues following treatment
and from drinking or eating hot foods. These are common
causes of mucosal trauma following local anesthesia in
children and occasionally in adults (Cousins et a!. , 2008) .
Accidental or intentional self-inflicted inj uries can be
painful and may take several days to heal. In children and
those with mental disabilities, soft-tissue biting and chew­
ing may cause severe lip, cheek, or tongue trauma due to a
lack of self-awareness of the dangers of biting (Malamed,
The remove-or-not-to-remove debate
e m b e d d e d need l es
currentl y favors removal. Clinical judgment is important,
particularl y as i t relates to being able to accuratel y locate
a needle. This has become easier wi t h the abili ty to ob­
tain cross-sectional scans of affected areas and reference
needle insertions before exposing radiographs.
Removal addresses the possibility of needl e migra­
tion toward larger blood vessels in the head and neck.
Other concerns incl u de pain, infection, psychological di s ­
comfort wi t h having a foreign body embedded in the jaw,
and the abili ty to percei ve the needle during mandibular
movement.
Needles that are not removed typically devel o p what
have been described as fibrous cocoons or scars around
them that generall y restrict significant migration, but some
authori t i e s have suggested that the lingering possibility of
needle migration and li t igation argue strongl y for removal.
• • • • • • • • •
338 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E STH E S I A

(A)
FIGURE 1 7-5 Lip Bite Following Local Anesthesia.

20 13). Severe injury to labial soft tissues has been reported

as a result of self-inflicted trauma that has required surgi­
cal correction in some cases (Akram, Kerr, & McLennan,
2008; Chi et al. , 2008; College et al., 2000). The occurrence
of self-inflicted soft-tissue trauma is observed most often
in younger patients, with lower lips most frequently af­
fected. In a study of 320 pediatric dental patients, the in­
cidence of accidental trauma and oral injury was 1 8 % in
children under the age of 4, 1 6 % between the ages of 4
and 7, 1 3 % between the ages of 8 and 12, and 7 % in older
children (College et al., 2000) . It is important to note that
these investigations may be limited and may represent
specific patient types and regional discrepancies that could
impact the reported incident rates.
P R E V E N T I O N OF S E LF-I N J U RY Prevention of self-inj ury
has traditionally centered around communicating the risks
to patients and caregivers, with visual reminders placed
on areas of exposed skin for those at greatest risk, such as
warning stickers on foreheads.
It is common for clinicians to use verbal communica­
tion and stickers or temporary tattoos on children's fore­
heads, hands, and/or arms to warn caregivers of the risks
of self-inj ury. This strategy has been reasonably effective;
however, the risks can be present for extended periods after
verbal and visible warnings have been forgotten or ignored
and stickers have been prematurely removed or misplaced.
Recent studies have suggested that the use of an an­
esthetic reversal agent, phentolamine mesylate (a va­
sodilator) , by reducing the residual soft-tissue duration
of anesthesia, may result in fewer self-inflicted inj uries.
•
Figure 17-6 shows an example of the unique packaging
and features of the phentolamine mesylate product cur­
rently available, OraVerse ® (Septodont, Inc, Lancaster, PA) .
While this suggestion h a s n o t b e e n confirmed, a recent
study evaluating complication rates with local anesthetic
administration and reversal revealed an improvement in
safety outcomes when phentolamine mesylate was ad­
ministered to p ediatric dental p atients (B oynes et al. ,
20 12) . Ora Verse is discussed in more detail in Chapter 19,
"Insights from Pediatric Dentistry."
OraVerse'"
G.!M¥��� �·-·· -····
(B)
FIGURE 1 7-6 Ora Verse Product Example. A - OraVerse
is the only pharmaceutical agent available for the reversal of
soft-tissue anesthesia. B - OraVerse cartridges have unique
translucent green labels and blue end-caps (top) to avoid confu­
sion with local anesthesia drug cartridges (bottom - lidocaine).
Source: Courtesy of Septodont, USA.
M A N A G E M E N T OF S E L F - I N J U RY When s e lf-inj ury is
identified during or soon after an appointment, a cold
pack should be applied over the injured tissue to reduce
swelling. If notification is delayed (the day following an
appointment) , a warm pack can be recommended to stim­
ulate circulation and promote healing. Anecdotal reports
suggest that applying 0.12% chlorhexidine solution to the
outer areas of traumatized tissues with cotton-tipped ap­
plicators may improve healing. Antibiotics are usually not
indicated and are prescribed only in the unlikely event
of infection (Ashkenazi, B lumer, & Eli, 2005 ; Chi et al. ,
2008) . For further discussion of management of self-inj ury
for pediatric patients, refer to Chapter 19.
Paresthesia
Paresthesia is a broad term for a number of related but
clinically diverse neurological effects that all result from
nerve inj ury. It has b e e n defined as an altered sensa­
tion and/or as a persistent p artial or complete numb­
ness (D aniel, Harfst, & Wilder, 2007). It may be further
 C HAPTER 17 • LOCAL A N E STH ESIA C O M PLICATI O N S A N D MANAG E M ENT 339

defined in terms of its potential to affect taste if the chorda

tympani nerve is involved.
Other frequently associated terms include hyperesthe­
sia and dysesthesia, which refer to an increased sensitiv­
ity to stimuli and the sensation of pain from non-noxious Direct trauma (Chen & Horowi tz, 2006; Crean & Powi s ,
1 999; Stacy & Hajjar, 1994)
•

Drug-induced apoptosi s (increase in the rate of pro­

stimuli, respectively. Ageusia and hypo geusia refer to

grammed cell death) (Park et al., 2005)

the absolute and relative losses of the ability to perceive •
•

sweet, sour, bitter, or salty substances due to chorda tym­

Detergent effects (due to possible neural membrane
l y si s ) (Ki t agawa, Oda, & Totoki , 2004)
•
pani injury, otherwise referred to as altered taste sensations
or perversions. Unfortunately, the basis of the vulnerabil­
Pressure from l o cali z ed edema (due to hemorrhage
invol v ing the neural sheath) (Pogrel, Bryan, & Regezi,
•
•
ity of particular nerves to the development of paresthesia
and the etiology of paresthesia are not clear (Pogrel et al. , 1 995; Rayan et al., 1 988)
2003). Higher l o cal anestheti c drug concentrations (Haas &
Lennon, 1 995; Smit h & Lung, 2006)
•
The lingual nerve is most frequently involved in par­
esthesias that follow dental inj ections (Haas & Lennon, : Vasoconstri ctors and their preservati v es (Pogrel &
h b · 20 )
•
•

: -� ��- : . . �� •
1995 ) . A possible explanation has been proposed, which
suggests that the fascicular pattern of the lingual nerve • • • • • • • • • • • • • • • • • • • • • • • • • • • • •

compared with the inferior alveolar nerve may make it

more susceptible, particularly near the lingula, where de­
position occurs (Pogrel et al., 2003). The lingual nerve has
been found to be unifascicular in this location in approxi­
mately 33 % of individuals, which has been speculated to
increase its vulnerability to paresthesia (Pogrel et al., 2003).
Although neurotoxicity of anesthetic drug solutions
has been demonstrated, with cautions attached to higher
concentrations of drugs, it has not been proven to be a
definitive cause of paresthesia (Haas & Lennon, 1995;
Koizumi et al. , 2006; Malamed, Gagnon, & LeBlanc, 200 1 ) .
O n e study that examined rat mental nerve tissue several
hours after direct inj ection of 4% articaine with 1 : 1 00,000
epinephrine into the nerve found that articaine is not toxic
to nervous structures and that further studies are neces­
sary to explain the possible relation between articaine
inj ection and paresthesia (B aroni et al. , 20 1 3 ) . In some
instances, paresthesia follows direct trauma from surgery
or needle injury (Blanton & Jeske, 2003) . In others, it oc­
curs after what were described as routine procedures with
no indications of injury at any time during the procedures
(Paxton et al. , 1994; Pogrel & Thamby, 2000).
In addition to routine procedures, surgical trauma, and
neurotoxicity from local anesthetic drugs, other suggested
etiologies include the chemical effects of sulfite preserva­
tives used for vasoconstrictors, detergent actions of local
anesthetic drugs, increased apoptotic activity, and vasocon­
strictor toxicity (Chen & Horowitz, 2006; Crean & Powis,
1999; Kitagawa, Oda, & Totoki, 2004; Park et al. , 2005;
Pogrel & Thamby, 2000; Stacy & Hajj ar, 1994) . Some pro­
posed etiologies are included in Box 17-7 •, which illustrate
the ongoing nature of the discussion regarding paresthesia.
Although the subj ect of ongoing research, the overall
risk of paresthesia is thought to be low, regardless of the
drug or concentration (D anish Medicines Agency, 2006;
D ower, 2007; Lustig & Zusman, 1999) . Based on data
from the American D ental Association and other sources,
the apparent risk of local anesthesia-related paresthe­
sia ranges from approximately 1.0-2.3 cases in 1 million
(Haas, 1998; Haas & Lennon, 1995 ; Malamed, 20 13; Pogrel
et al. , 2003; Pogrel & Thamby, 2000) . Table 17-1 • provides
information on the relationship between specific drug con­
centrations and reported incidences of paresthesia.
Put into perspective, it has been estimated that 1 in ev­
ery 3,000 individuals in the United States will be struck
by lightning in their lifetimes (National Geographic News,
October 8, 2010), and the risk of developing vaccine-related

Table 1 7-1 I n c i d e nce of Pa resthesia

Drugs Concentration Reported Paresthesia Injection Technique (Nerve Reported Paresthesia

(%) Incidence I nvolvement) Incidence

0.5 1 : 1 ,200,000 IA nerve block 1 :26,0 00-1 :800,000

2 1 : 1 ,200,000 Involving lingual nerve 70% of cases

3 1 : 1 ,200,000 Involving lA nerve 30% of cases

4 1 : 500,000 No data No data

Note: All values are approximations as reported in the literature.

Source: Haas (1998), Haas and Lennon (1995), Malamed (2004) , Pogrel et al. (2003), and Pogrel and Thamby (2000).
340 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E STH E S I A
poliomyelitis is approximately 1 in 750,000 (Racaniello,
2006) .
P R E V E N T I O N O F PAR E STH E S I A In the absence of clearly
defined etiology (see Box 17-7), preventive strategies tend
to focus on approaches that appear to lower risk (Lustig &
Zusman, 1999; Malamed, 20 13; Pogrel et al., 2003). There is
no reliable strategy for avoiding damage that may result in
paresthesia during inferior alveolar nerve blocks; however,
it is possible to avoid situations in which paresthesia is re­
portedly more likely to occur. Because the lingual nerve is
most frequently involved, using high block techniques to
avoid lingual nerve injury has been recommended when
using 4% drugs (see Boxes 17-8 • and 17-9 •) (Hawkins,
2006).
Needle tips in dentistry are so small that severing
nerves is unlikely (Smith & Lung, 2006) . The inferior al­
veolar and lingual nerves, the most frequently involved
in paresthesia, are both similar in size and much larger
than the tip of even the largest needle (25 gauge) com­
monly used in dentistry (Haas, 1998). Even though sever­
ing nerves is unlikely with dental needles, the possibility
of nerve injury from needles exists, especially if they have
been barbed (Blanton & Jeske, 2003 ) . When a patient is
in obvious distress during an inj ection, the procedure
Persi stent paresthesi a after dental care i s a rare event,
wi t h publis hed occurrence varying from 1 in 140,000 to 1
in 4,1 59,848 (Moore & Haas, 201 0). This dichotomy in esti-
mated rate of occurrence i s troublesome and appears to
refl e ct uncertainti e s based on conflicting data and conflict-
ing i n terpretati o ns of data. Gari sto and colleagues, based
on paresthesi a s occurring subsequent to dental l o cal anes-
theti c i n jections administered in the United States from
1 997 to 2008, concl u ded that "paresthesia ari s ing from a
l o cal anestheti c injection al o ne i s a rare event" (Gari sto
et al., 201 0). Because most paresthesi a s are temporary,
permanent paresthesi a s are considered very rare. Arti c aine
received special attention in the Gari sto study because it
was responsibl e for the highest proportionate number of
paresthesi a s even though it was introduced in 2000, nearl y
3 years after the beginning of the study period. Pril o caine
was the onl y other drug to exceed the average occurrence
rate. Gari sto and col l eagues noted that both arti c aine and
pril o caine share 4% formulations. I t i s generall y agreed that
the occurrence of l o cal anesthesia-related neuropathy (i n
this case paresthesi a ) i s rare; therefore, data from random-
ized trial s may not include enough study subjects to val i date
the occurrence of this complicati o n (Hill e rup & Jensen,
2006). Moore and Haas pointed out that data collected
retrospectivel y may be fragmented and could possibly
demonstrate bias; therefore, there is not an authoritative
amount of empiri c al evidence to explain the rel a tionship
between paresthesi a and 4% articaine soluti o ns (Moore &
� � a.a � , .2.0 � �)� � u·rt·h � :�� r� ,. t�� : �� r �.a �� v.i : i �a ��� �� : k: n·g·
• •
Al t hough not substanti a ted, some strategies that are com­
monly employed to reduce the risks of paresthesia include:
1 . Observe slow drug deposition recommendations.
2. Reduce volumes by 50%.
3. Use Gow-Gates or Vazirani - Akinosi techniques in place
•
f f r r a ve a r o c · •
: . � �� � : � . � . �� � �� : � �� . ��
• . • • • •• . • • . • • • • • • •
should be discontinued and a new needle and either a
new pathway or a different technique should be used. It
has been reported that there is a nearly 4% likelihood of
traumatizing the lingual nerve every time a conventional
mandibular nerve block is administered. Fortunately, the
significant majority of these injuries were found to resolve
within 2 weeks (Harn & Durham, 1990) .
Barbed needle tips, in particular, have the capacity to
inflict damage to all structures, including nerves (Stacy &
Hajj ar, 1994) . In a 2000 prospective study of permanent
nerve damage, it was reported that in the vast maj ority
of inferior nerve blocks in which the nerve was directly
Committee of the European Union, based on the experi e nce
of 57 countri e s with articaine administered to approxi m atel y
100 mill i on indiv idual s annually, found no basis for modifying
i n formati o n regarding articaine's use (Stenver, 2006).
Pogrel and coll e agues pointed out previousl y that
the majority of paresthesias are associated wi t h the lingual
nerve (Pogrel et al., 2003). Lingering questions regard-
ing arti c aine's neurotoxi c potential can be bypassed by
avoiding traditional lA nerve bl o cks, the technique wi t h
the greatest likelihood to invol v e paresthesia. This would
appear to be a reasonable prevention approach. Because
Gow-Gates nerve blocks, for example, have not result ed in
any reportedly higher incidence of paresthesia wi t h artie-
aine, they would appear to be reasonable al t ernati v es to lA
nerve blocks wi t h arti c aine (Hawkins, 2006).
Considering unresol v ed questions as to the cause(s) of
these paresthesias a cautious approach to admini s tration
i s suggested. Until further research i s completed it i s sug-
gested to avoid arti c aine for mandibular inferior al v eolar
nerve blocks. Arti c aine remains a dependable anestheti c
agent. Its diffusion properties make i t an excellent anes-
theti c of choice for most strategies for providing maxil-
lary and mandibular anesthesia (Abdul wahab et al., 2009;
Boynes, 2010; Paxton & Thome, 201 0). I t also provi d es a
supplemental al t ernati v e for inadequate l A nerve blocks
(mandibular infil t ration wi t h articaine) and a modest sup-
plemental al t ernati v e when the l A nerve block fails during
irreversible pulpi t i s treatment (Kanaa et al., 2006; Matthews
• • • • • •
ta
� . � · ·. :o.o:); . . . . . . . . . . . . . . . . . . . . . . . . . . IIi
. . . .
 C HAPTER
contacted by the needle, barbed or not, there were no
long-term effects (Pogrel & Thamby, 2000). The creation
of barbs on needle tips by contact with bone that would
indicate damage occurred after full penetration was not
found to account for the maj ority of permanent pares­
thesias because it appeared that most of the paresthesias
occurred on penetration rather than withdrawal (Harn &
Durham, 1990; Stacy & Hajj ar, 1994) .
The experience of an electric shock did not predict the
development of symptomatic nerve damage either. It has
been estimated that between 3 % and 7 % of the time, elec­
tric shocks are experienced during inferior alveolar nerve
blocks (Harn & Durham, 1990; Pogrel et al., 1995 ) . It is
reasonable to assume that the incidence is actually higher
because some inj ections will not result in noticeable nerve
"shocks" even when nerves are contacted by needles. This
may occur, for example, when needles are being with­
drawn and the nerve is already anesthetized or when clini­
cians anesthetize ahead of needles while penetrating. Even
without considering these likely unrecognized inj uries,
the cited incidence of 3% to 7% exceeds the incidence of
paresthesia due to all local anesthetic drug inj ections by a
considerable margin.
Evidence demonstrates there is no reliable strategy for
preventing paresthesia. Even surgical trauma, which many
consider to be the most unequivocal of etiologies, may not
always be responsible. As pointed out in one discussion on
paresthesia, it may be impossible to state that paresthesia
is the result of nerve injury during surgery when the injury
could have occurred during the administration of the local
anesthetic, before the surgery (Pogrel & Thamby, 2000) .
R E S PO N S E TO PAR E STH ESIA Response to the initial noti­
fication of paresthesia should be rapid and should convey
Upper/lower Arch
FIGURE 1 7-7 Example of Paresthesia Documentation Chart.
Source: Example of "Paresthesia Documentation Chart." Copyright © by VELscope LED
Dental, Inc. Used by permission of VELscope LED Dental, Inc.
17 • LOCAL A N E STH ESIA C O M PLICATI O N S A N D MANAG E M ENT 341
sympathy and concern. It has been recommended that the
clinician who administered the inj ection speak personally
with the patient and arrange for him or her to return to the
office or clinic as soon as possible (Haas, 1998) .
PA R ESTH E S I A M A N A G E M E NT The lack of a universally
accepted etiology may confuse the discussion of paresthe­
sia somewhat but the protocol for its management is clear.
Current protocol includes the following:
1. Speak personally with and reassure the patient.
2. S chedule an appointment to evaluate as s o o n as
possible.
3. Document the conversation.
4. Examine the patient; determine and record the extent
and degree of the deficit.
5. Diagram the extent of the loss by recording where
sensation begins and ends and the nature of the loss
(numbness, partial numbness, tingling, burning, pain,
taste perversion, loss of sweet, sour, salty, or bitter
sensations, etc. ) . Figure 17-7 • provides a sample
chart for mapping paresthesia, and Figures 17-8 • and
17-9 • demonstrate a method for tracking changes
over time.
6. Explain that paresthesias may last for a while but the
vast maj ority improve over time.
7. Review and update the map at follow-up appoint­
ments to document resolution, which reassures pa­
tients, particularly those who need visible reassurance.
Follow-up appointments should be spaced far enough
apart to allow slow healing to take place. Follow-up
appointments that are too close together may tend to
discourage patients.
Tongue - Lateral View
Tongue - Underside
342 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E STH E S I A

Tongue - Lateral View

LEFT
U 31 � H U V H � � n H 21 � 1 9
18 17

Upper/Lower Arch Tongue - Underside

FIGURE 1 7-8 Documentation of Initial Extent of Paresthesia.

Source: "Documentation of Initial Extent of Paresthesia." Courtesy © VELscope LED
Dental, Inc. Used by permission of VELscope LED Dental, Inc.

8. Refer to an appropriate specialist if improvement
does not occur or the situation deteriorates.
9. If future therapy is anticipated in the affected area, use
an alternate inj ection technique (Boynes, 2010; Daniel,
Harfst, & Wilder 2007; Hass, 1998; Malamed, 20 13).
Facial Nerve Paralysis
Local anesthetic techniques can result in anesthesia of
the facial nerve ( CN VII ) , as it travels through the pa­
rotid gland (Haas, 1998; Malamed, 20 13). While it does not
provide parotid innervation, it does innervate structures
peripheral to the gland, including the muscles of facial
expression and regions inferior to the eye and around the
mouth and chin.
During lA blocks, overinsertion of needles can penetrate
the capsule surrounding the deep lobe of the parotid gland. If
anesthetic drugs are deposited into the gland, the facial nerve
can be anesthetized. This can usually be prevented by con­
firming bony resistance when administering lA nerve blocks,
to assure that needle tips are not inserted into the gland.

Tongue - Lateral View

RIGHT LEFT
32 31 � U U V H � � 23 H 21 � 1 i 1
8 17

Upper/Lower Arch Tongue - Undenaide

FIGURE 1 7-9 Documentation of Partial Resolution of Paresthesia over Time.

Source: "Documentation of Partial Resolution of Paresthesia Over Time." Copyright © by
VELscope LED Dental, Inc. Used by permission of VELscope LED Dental, Inc.
 C HAPTER 17 • LOCAL A N E STH ESIA C O M PLICATI O N S A N D MANAG E M ENT 343

If the facial nerve is anesthetized, unilateral paralysis 5. Document the incident.

of the face will result. This typically will last only as long 6. Follow up as indicated.
as the anesthetic is in effect. Some mistakenly refer to this
temporary lack of function due to facial nerve anesthesia Postanesthetic Mucosal Lesions
as B ell's palsy, which refers to an unexplained idiopathic Postanesthetic lesions include those resulting from infectious
unilateral facial p aralysis that can p ersist for months or suspected immune processes and those resulting from
or occasionally may be p ermanent (Jastak, Yagiela, & direct injury to the mucosa (Haas, 1998; Malamed, 2013).
Donaldson, 1995). Lesions with an infectious etiology, such as herpetic
Vazirani-Akinosi nerve blocks can also result in facial ulcers, or a suspected immune or autoimmune etiology,
nerve paralysis when needles are over-inserted. The facial such as aphthous ulcers, can develop following anesthetic
paralysis seen after Vazirani-Akinosi nerve blocks has the inj ections. Herpetic lesions occasionally appear after in­
same pattern, behavior, and distribution as that which de­ j e ction, particularly in the palate. They present as small,
velops after lA nerve blocks. multiple ulcerations in the vicinity of the inj ection. There
In some individuals, the facial nerve is located close is sometimes an inability to discriminate between herpetic
to target areas of lA and Vazirani-Akinosi nerve blocks. and aphthous lesions in the palate because aphthous le­
In these individuals, observing recommended insertion sions, although typically solitary, larger, and found on non­
depths and confirming bony resistance (for lA nerve keratinized mucosa, may also present as small, multiple
blocks) may not prevent the development of facial nerve ulcerations on keratinized tissue (Ibsen & Phelan, 20 14) .
anesthesia (Malamed, 20 13). These are known as herpetiform aphthous ulcerations or
Due to eye involvement, reflex activity can be com­
promised; however, tears will continue to be produced.
lesions (see Figure 17-10 •).
A past history of labial her­
p etic outbreaks or of recurrent aphthous ulcerations is
Protection is recommended over the affected eye until re­ helpful in discriminating between the two. By definition,
flex activity returns to normal (Malamed, 20 13). ulcerations involve both epithelial and connective tissue
injury and tend to be quite painful, especially to hot and
Patients who
R E S PO N S E TO FAC I A L N E RV E PA RALY S I S
acidic foods. There is usually no difference in the healing
experience facial nerve paralysis are primarily concerned
pattern of the ulcers regardless of the cause.
with the duration of the dysfunction, any lasting effects,
Overly vigorous hemostasis from high concentrations
and avoidance of the event in the future. Reassurance can
of vasoconstrictor or desiccation from topical anesthetic
be offered that paralysis will last only as long as the drug's
left in contact with mucosa for extended periods can lead
effects, consistent with individual recovery patterns after
to necrosis and ulceration . These lesions, similar to her­
local anesthesia. Patients who repeatedly experience facial
petic and aphthous ulcerations, tend to be painful and sen­
nerve paralysis after lA nerve blocks may be advised that
sitive to certain foods and beverages, especially those that
recurring paralyses after dental inj ections indicate ana­
are acidic. Patients should be instructed to alert clinicians
tomical predispositions and alternative techniques will be
if lesions occur and are slow to heal, or if pain increases,
used in the future.
signaling the possibility of infection.
PREVENTION OF FACIAL N E RVE PARALYSIS Strategies that
P R E V E N T I O N OF P O STA N E ST H E T I C M U C O S A L L E S I O N S
have been found useful in preventing facial nerve anesthe­
Unfortunately, there i s no prevention for the develop­
sia include:
ment of herpetic or aphthous lesions. Patients sometimes
1. Observe proper injection technique. understandably suspect that the clinician might have
2. Avoid depositing solution in lA nerve blocks without
confirming bony resistance.
3. Use smaller gauge needles to avoid deflections away
from bone.
4. Avoid needle overinsertion in Vazirani-Akinosi nerve
blocks.
5. Use alternate techniques such as PDL and infiltration
inj ections.

MANAG E M ENT OF FACIAL N E RVE PARALYSIS Steps in the

management of facial nerve paralysis include:
1. Discontinue treatment.
2. Reassure the patient.
FIGURE 1 7-1 0 Herpetiform Aphthous Ulcerations.
3. Remove contact lens, if present. Palatal aphthous ulcerations following a palatal
4. Place a patch over the affected eye. inj ection.
344 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E STH E S I A
FIGURE 1 7-1 1 Post-inj ection Necrosis. Signs of necro­
sis following a GP injection.
caused some kind of inj ury that is responsible for their
postoperative pain. They may be reassured, however, by
recognition of postanesthetic lesions at follow-up visits and
by brief explanations as to possible etiologies. Individuals
who are susceptible to cold sores, for example, are often
unaware that they can occur intraorally after inj ections.
Unlike herpetic and aphthous lesions, n e crosis is
largely preventable (see Figure 17- 1 1 •) . The following
strategies are effective for reducing the risks of necrosis:
1. Avoid epinephrine concentrations of 1 :50,000 espe­
cially in attached gingiva.
2. Avoid excessive durations of topical anesthetic con­
tact as recommended in the product instructions.
3. Avoid excessive blanching by allowing sufficient time
for solution to diffuse into tissue during deposition;
tissues should not turn "stark white" in appearance.
4. Avoid extensive distention of tissues by allowing suf­
ficient time for solution to diffuse while depositing;
tissues should not bulge or "balloon" with too much
solution.
Figure 17-11 shows post-injection necrosis following a
greater palatine (GP) inj ection and Figure 17-12 • shows
trauma following an AMSA inj ection.
FIGURE 1 7-1 2 Post-inj ection Trauma. Signs of local
trauma developed approximately 1 minute into the
deposition for an AMSA injection.
M A N A G E M E N T OF PO STA N E ST H E T I C M U CO S A L L E S I O N S
Whereas prevention may o r may not be possible, manage­
ment is. Various over-the-counter (OTC) medications are
available and tend to relieve discomfort during the early
phases of healing. When postanesthetic lesions occur, the
following steps should be observed:
1. D etermine previous history of herpetic or aphthous
lesions
2. Recommend an OTC medication to coat the lesion
(with or without topical anesthetic), taking care not to
spread the infection if it is herpetic.
a. Recommend applying the medication before each
meal to protect the lesions from additional injury
and applying otherwise as recommended in the
product instructions.
3. Recommend to avoid spicy and acidic foods.
4. Recommend OTC pain relievers as needed (pain usu­
ally lasts for 2-3 days).
Whereas the best indicators of extraoral healing are
" crusting over" and scarring, scars do not typically form
on mucosa, and reduced sensitivity indicates that new con­
nective tissue (granulation tissue) has begun to form over
the ulcer.
Infections
Due to the availability of sterile and disposable arma­
mentarium and to federal and state mandates of standard
precautions in dental facilities, postoperative infections
are rare today (Malamed, 20 1 3 ; Pogrel & Thamby, 2000).
Contaminated needles, along with other devices if handled
improperly, represent the greatest threat of iatrogenic infec­
tion. Normal flora do not represent a significant threat de­
spite their transport into deeper tissues with every needle
penetration because their small numbers are easily removed
by the body's immune system (Haas, 1998; Malamed, 20 13).
Exceptions may occur in severely immunocompromised in­
dividuals and when the tissues to be penetrated are infected
before insertion. Elective treatment might not be possible
for some immunocompromised individuals or might be pos­
sible only with prophylactic antibiotics. A physician consult
is recommended. Should the anticipated area of penetra­
tion be infected before inj ection, there is a greater chance
of deeper spread of the infection and penetration in these
areas should be avoided (Haas, 1998).
Manifestations of postanesthetic infections include
pain and trismus, although overt signs and symptoms are
rare (Haas, 1998; Malamed, 20 13 ) . If trismus persists beyond
3 days, infection should be considered (Malamed, 20 13).
P R E V E N T I O N OF P O S TA N E S T H E T I C I N F E CT I O N S The
following strategies are effective for reducing the risks of
infection from injection:
1. Use only sterile, uncontaminated needles.
2. In the presence of infection, use a new needle for each
penetration.
3. If extraoral contamination occurs, discard the needle.
 C HAPTER
4. If intraoral contamination occurs (other than oral tis­
sues), discard the needle.
5 . In immunocompromised individuals, apply antiseptics
to penetration sites or use antibiotics after consulta­
tion with the patient's physician.
MANAG E M E N T O F PO STAN E STH ETIC I N F E CTI O N S When
postanesthetic infections occur, the following steps should
be observed:
1. Schedule an evaluation appointment as soon as possible.
2. Prescribe antibiotics as appropriate.
3. Document the infection and the prescription.
4. Schedule follow-up appointments until the infection is
resolved.
Ocular Complications
D uring the course of local anesthetic administration,
other nerves may be unintentionally affected resulting
in anesthetic complications of the eye (Boynes, Echeverria,
& A d d u l w a h a b , 20 1 0 ; N g e o w, S h i m , & C h a i , 2 0 0 6 ;
Penarrocha-Diago & Sanchis-Bielsa, 2000). Symptoms of
this rare complication have been described most often as
blurring of vision and temporary blindness. In addition,
anesthesia of motor neurons in the optic area can result
in pupil dilation, drooping of the eyelid, and double vision
(Boynes, 20 10). Generally, symptoms develop immediately
after inj ection of the anesthetic solution and last for sev­
eral hours. These symptoms are attributed to anesthetic
solution reaching the orbit or cavernous sinus through
distribution, diffusion, and/or venous and arterial trans­
port directly or via retrograde blood flow (B oynes, 20 10;
Lee, 2006; Horowitz et al. , 2005).
While these complications may be stressful to patients
and clinicians, permanent injury to tissues, nerves, and eyes
is unusual; however, there have been reports of permanent
blindness occurring. Clinicians must be prepared to apply
preventive measures and to rapidly identify and respond
to ocular complications, including appropriate treatment
and referral (Walsh, 1957).
P R E V E N T I O N O F O C U LA R C O M P L I CATI O N S To prevent
ocular complications, it is important to aspirate frequently
before depo siting solution when aspiration is recom­
mended. S olutions should also be administered slowly
(Cooley & Cottingham, 1979) .
M A N AG E M E N T O F O C U LAR C O M P L I CATI O N S Although
ocular complications are rare, they can be severe and, at
the very least, can provoke understandable anxiety in pa­
tients. It is therefore imperative that clinicians understand
the proper management of these cases (Lee, 2006; van der
Bijil & Meyer, 1998) .
The following steps should be applied:
1. Reassure the patient that these complications are usu­
ally transient.
2. Covering the eye will restore functional monocular vision
and protect the cornea for the duration of the anesthesia.
17 • LOCAL A N E STH ESIA C O M PLICATI O N S A N D MANAG E M ENT 345
3. Arrange for the patient to be escorted home.
4. Refer to an ophthalmologist if the complication lasts
longer than 6 hours.
5. Continue regular follow-up procedures.
S y stemic Com p l ications
Systemic complications from local anesthetic drugs, with
the exception of syncope, occur less frequently compared
with local complications. When they occur, non-syncopal
systemic complications manifest primarily as overdoses, al­
lergic responses, and idiosyncratic reactions. In addition to
discussions of these complications, two other systemic con­
ditions previously discussed in Chapter 10, "Patient Assess­
ment for Local Anesthesia," atypical plasma cholinesterase
and methemoglobinemia, will be discussed briefly here.
Of the three non-syncopal systemic complications,
overdose, allergy, and idiosyncratic reaction, overdose oc­
curs most frequently (Malamed, 20 1 3 ) . Overdoses may
be defined as administrations of drugs that result in signs
and symptoms of CNS and CVS depression (Horlocker &
Wedel, 2002) . It is suspected that some of the overdoses ex­
perienced occur due to intravascular administration (Hor­
locker & Wedel, 2002). Not all individuals will respond
adversely to inadvertent intravascularly administered
doses, however (Lustig & Zusman, 1999; Malamed, 20 13).
The maj ority of overdose reactions occur as a result
of systemic absorption of excessive volumes of drugs.
Many individuals do not respond with adverse systemic
signs and symptoms to local anesthetic drugs until much
higher than recommended doses are administered. They
are referred to as hypo-responders (Lustig & Zusman,
1999; Malamed, 20 1 3 ) . Other individuals may respond
adversely when less than maximum recommended doses
have been administered and are referred to as hyper­
responders. Importantly, regardless of the response level,
an individual's threshold for adverse reaction to a local
anesthetic drug is considered normal for that individual
(Malamed, 20 13).
Allergic reactions to amide local anesthetic drugs are
rare. Allergy to esters are less rare and typically associated
with topical anesthetics. They can manifest both locally
and systemically. An important distinction between aller­
gic reactions and overdose reactions is that allergic reac­
tions are not dose-dependent.
Adverse events that have no known etiology also oc­
cur and are known as idiosyncratic reactions.
Syncope
Anxiety as well as perceived or real distress can result in
abrupt loss of consciousness, or syncope. Syncope usually
is the result of insufficient perfusion of oxygenated blood
within the brain (cerebral ischemia secondary to inade­
quate cerebral perfusion) . Anxiety is frequently cited as the
main cause of syncope but other factors should be consid­
ered, including hyperventilation, postural hypotension, se­
vere cardiac disorders, and drug interactions (Jastak, 1995).
346 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E STH E S I A
Stress reduction protocols can be helpful for preventing
adverse events such as syncope. See Appendix 10-2.
Management of Syncope
The goal of treatment when syncope occurs is to restore
adequate oxygenated blood and circulation within the
brain. Supplemental oxygen is recommended for patients
experiencing syncope. The supine position is recommended
because it places the patient's brain and heart at the same
level. The legs should be elevated slightly to enhance the
venous return of blood to the heart to quickly restore ad­
equate cerebral circulation (Malamed, 2007). Loosen any
tight-fitting clothing that could restrict breathing.
The exception to the supine position occurs when
pregnant mothers experience syncope. It is not uncom­
mon for pregnant females to lose consciousness when do­
ing nothing other than lying on their backs. Depending on
the size and position of the fetus and how far along the
pregnancy, the supine position can compromise blood flow,
especially venous return to the heart through the inferior
vena cava (Malamed, 2007). Rather than placing pregnant
patients in supine positions, rolling them onto their right
sides has been recommended (Malamed, 2007).
Instituting these procedures usually reverses the ef­
fects of syncope; however, should non-responsiveness per­
sist, additional protocols including CPR and emergency
transport may be necessary.
O ccasionally, convulsions may occur in response to
brain hypoxia. Attention should focus on patient safety as
soon as convulsions are recognized, including placing pa­
tients in supine positions with all instruments and other
potentially harmful items cleared from the area and pa­
tients protected from injury (Little et al., 20 13).
Patients may continue to exhibit signs and symptoms
of syncope (pallor, clamminess, and weakness) for several
hours after the event. A return to baseline should be con­
firmed before dismissal.
The following steps serve as a guideline for the man­
agement of syncope:
1. Activate emergency protocols.
2. Place the patient in a supine position, with legs slightly
elevated and brain and heart at the same level.
3. Administer supplemental oxygen.
4. Monitor vital signs until baseline is achieved.
5 . Provide patient safety from injury if convulsive activ-
ity occurs.
6. Observe for pallor, clamminess, and weakness.
7. Dismiss with escort or emergency transport as indicated.
8. Document the incident.
Overdose
The overdose potential of local anesthetic drugs differs
with each drug. For example, one study demonstrated that
higher blood levels of articaine were necessary compared
with lidocaine before signs and symptoms of overdose
were noted and that when overdose developed from artic­
aine it was observed to be less severe (Tetzlaff, 2000). Bupi­
vacaine is known for its nearly equal toxicities to the CNS
and CVS, yet Albright reported in 1979 that in a handful of
cases of bupivacaine toxicity, CVS collapse preceded any
evidence of CNS toxicity (Horlocker & Wedel, 2002) .
T H E PAT H O P H Y S I O LO G Y O F L O C A L A N E ST H E T I C O V E R ­
D O S E Overdoses are t h e result of t h e pharmacological
actions of the local anesthetic drugs on the CNS and CVS.
They occur due to either intravascular deposition or non­
intravascular administration of excessive doses, both of
which interfere with normal ionic exchange across neural
membranes of the CNS and CVS.
Typical initial effects of drug overdose result from de­
pression of inhibitory pathways in the CNS, resulting in early
excitation. Inhibitory depression occurs due to a concentrat­
ing effect of the drugs in the well-vascularized limbic brain
(Tetzlaff, 2000). Some drugs such as lidocaine and bupiva­
caine in very high quantities may not produce early excita­
tion in overdose, beginning instead with signs and symptoms
of depression (Malamed, 20 1 3 ; Tetzlaff, 2000). Continued
overdosing depresses both inhibitory and excitatory path­
ways, resulting in signs and symptoms of CNS depression. If
overdosing continues, it can lead to seizures, CVS depression,
and eventually coma and respiratory and cardiac arrest. With
some exceptions, CVS depression occurs only after higher
overdose levels of a drug have been reached in the blood.
CVS effects of overdose involve several mechanisms.
These primarily affect myocardial contractility and con­
duction volumes, causing an interrelated decrease of both.
D ecreased contractility and conduction volumes can lead
to bradycardia, arrhythmias, and, finally, asystole (the ab­
sence of a heartbeat) . Factors that may complicate recov­
ery from higher overdoses include electrolyte imbalances,
hypoxia, and acidosis (an abnormal increase in body fluid
acidity) (Levsky & Miller, 2005).
Overdoses are reversed once normal metabolic path­
ways eliminate enough of the circulating drug for levels
to drop below overdose thresholds. At that time, signs and
symptoms of overdose diminish or cease. Predisposing fac­
tors to overdose include physical status, concomitant med­
ications, and genetics.
I N I T I A L S I G N S A N D S Y M PTO M S OF L O C A L A N E ST H E T I C
OVE R D O S E The initial signs and symptoms of overdose
have been described as a manifestation of central nervous
system excitation. These may include ringing in the ears, a
metallic taste in the mouth, increased anxiety, and circum­
oral tingling or numbness (Malamed, 20 13; Mulroy, 2002) .
Intravascular inj ections may result in rapid develop­
ment of these signs and symptoms because blood con­
centrations in the brain have been stated to be higher
after intravascular inj ections than from any other source
(Mulroy, 2002) . Fortunately, the same abundant perfusion
of blood to the brain that hastens the onset of the early
 C HAPTER
signs and symptoms of overdose in intravascular inj ections
tends to decrease the duration of the overdose (drug levels
quickly diminish, provided the cardiovascular system re­
mains relatively unimpaired) (Mulroy, 2002).
When overdoses are caused by absorption of exces­
sive volumes of drug, the development of overdose tends
to be more delayed (Mulroy, 2002). This is moderated by
factors such as the presence or absence of vasoconstric­
tors, the vascularity of areas into which drugs are inj ected,
the physical status of patients, and the class of drug. Drugs
that are rapidly metabolized in the blood have shorter
overdose courses versus those metabolized in the liver (a
relatively long process) . Signs and symptoms nevertheless
will be similar when overdoses occur.
LAT E R S I G N S A N D S Y M PTO M S O F L O C A L A N E ST H E T I C
OVERDOSE A s overdose continues and progresses, previ­
ously unopposed excitatory pathways are depressed and
signs and symptoms of CNS depression prevail. These
may include twitching and tremors, slurred speech, fatigue,
unconsciousness, and seizures (Malamed, 20 1 3 ; Mulroy,
2002) . If drug levels continue to rise, coma, respiratory ar­
rest, and cardiac arrest are possible (Mulroy, 2002) . One
approach to reversing cardiovascular collapse experienced
after overdose from local anesthetic drugs is discussed in
Box 17-10 •·
P R E V E N T I O N O F LOCAL AN E STH ETIC O V E R D O S E To pre­
vent local anesthetic overdose, the following guidelines
are recommended:
1. Establish maximum doses based on weight and physi­
cal status, before inj ection.
2. Aspirate whenever there is a possibility of intravascu­
lar deposition.
3. Administer all doses slowly.
4. Re-aspirate throughout inj ections.
Research on a weight loss supplement, lntralipid, has sug­
gested that i t may aid in reversing the cardiovascular ef­
fects of local anestheti c overdose (Weinberg et al., 1 998).
Resusci t ation wi t h Intra lipid has had promising resul ts in
treating cardiovascular depression experienced after
bupivacaine, ropi vacaine, and l e vobupi v acaine-i n duced
cardiovascular collapse (Foxall et al., 2007; Rosenblatt et al.,
2006). Several studies have suggested that infusions of 20%
(Intra lipid) have contributed to CVS toxi c i ty reversal and
may even have aided in seizure reversal (CNS toxi c ity rever­
sal ) (Foxall et al., 2007).
The abili ty of this supplement to provi d e reliable,
li fe-saving rescue in emergency si t uations i s still under in-
vestigation, and its potential usefulness in dental overdose
s t t n s nk h s t Ca ar y 0 )
• •
: . : �� :� � : . � . ���� �: � : . ��� � . :� �. � . �� � �� : : . •
17 • LOCAL A N E STH ESIA C O M PLICATI O N S A N D MANAG E M ENT 347
Several strategies can help prevent overdoses in den­
tistry. In addition to accurate pre-inj ection assessment of
physical status to determine safe maximum dosages, the
most important technique strategy is to administer drugs
slowly (no more than one cartridge per minute) (Malamed,
20 13). Some clinicians believe aspiration is more important
than slow administration. Although the point might not be
worth arguing because aspiration and slow deposition are
both critical safety factors, it appears that negative aspira­
tion is not an absolutely reliable indicator that needle tips
are not in vessels (Malamed, 20 1 3 ; Mulroy, 2002) . When
aspiration is negative but the needle tip is located within a
vessel, only slow deposition can minimize the potential ad­
verse effects of intravascular administration because slow
deposition allows for greater dilution.
If a needle tip is located intravascularly and aspira­
tion is performed, a false-negative aspiration can be ob­
served if the positive pressure of aspiration creates suction
on the inside of the vessel wall that blocks the blood from
entering the lumen of the needle. Aspirating in two planes
can decrease the incidence of false-negative aspiration
and intravascular inj ection , but it cannot guarantee its
elimination.
Early
R E CO G N IT I O N O F LOCAL A N E ST H E T I C O V E R D O S E
signs and symptoms of overdose overlap with signs and
symptoms of anxiety in dental patients. This is particu­
larly true with articaine, mepivacaine, and prilocaine when
excitatory phases precede CNS depression and when va­
soconstrictors are included in solutions. When overdose
occurs, these excitatory phases precede CNS depression. It
is not unusual to have a talkative, apprehensive patient in
the dental chair who may display many of the signs and
symptoms of overdose when there is no overdose. Impor­
tant distinctions, however, help discriminate between the
manifestations of anxiety and true overdose. Circumoral
tingling or numbness, in particular, would not be due to
the effects of unilateral anesthesia or of anxiety. In addi­
tion, relaxation techniques can reverse the signs and symp­
toms of anxiety but are unlikely to be effective in response
to a progressive overdose. Finally, a progression of depres­
sive signs and symptoms is suggestive of an overdose.
Initial signs and symptoms of overdose include the
following:
1. Metallic taste
2. Increased anxiety
3. Circumoral tingling or numbness
A list of the signs and symptoms of local anesthetic
overdose is illustrated in Table 17-2 • and for vasocon­
strictors see Table 17-3 •·
M A N AG E M E N T O F LOCAL A N E STH ETIC OVER­
D O S E Overdose reactions may occur within minutes to
up to an hour or more from the time of administration
(Jastak, Yagiela, & Donaldson, 1995). Generally, the more
delayed the onset, the less severe the reaction.
348 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I O N OF LOCAL A N E STH E S I A

Table 1 7-2 S i g n s and Sym pto m s of loca l An esthetic

Overdose (Prog ressive O rd e r)

Central Nervous System Card iovascu lar System

In response to mild overdose, the following guidelines are
Lightheadedness Hypertension recommended:
Tinnitus Tachycardia
1 . Acti v ate emergency protocol s , as needed
Confusion
2. Reassure
Circumoral numbness
3. Observe
Muscle twitching Decreased contractility and 4. Monit or
Auditory and visual cardiac output Dental procedures may continue (i f tol e rable), or the
hallucinations Hypotension patient may be dismi s sed. The patient may not need an
escort if full recovery has occurred; however, an escort or
e r c t a �r nd a -
li
•

: . .�� � � � '! . � � �� : ��: �� : . :� � � �

Tonic-clonic seizures Sinus bradycardia
Unconsciousness Ventricular dysrhythmias • • • • • • • • • • • •

Respiratory arrest Circulatory arrest

Sources: Jastak, Yagiela, and Donaldson (1995), Little et al. (20 13), and
Malamed (2004) .
Mild overdoses may require no more than monitoring
while providing supportive measures until drug levels fall
below overdose thresholds. Moderate to severe overdoses
can require aggressive management, including rapid re­
sponse, appropriate positioning (especially in the event
of clonic-tonic seizures), and activation of the emergency
system. For a quick reference of guidelines on the manage­
ment of overdoses, see Boxes 17-11 • and 17-12 •·
Clinicians should be prepared to implement the CABs
(Circulation, Airway, Breathing) of basic life support and
appropriate positioning of the patient.
Allergy
A maj or difference between overdose and allergy is that
allergies are not dose-dependent. Allergy, also referred
to as hypersensitivity, involves localized or systemic, cell­
mediated, and/or humoral responses to antigens, in any
Table 1 7-3 S i g n s and Sym pto m s of Va soco n strictor
Overdose
concentration. Hypersensitivities to local anesthetics can
manifest both locally and systemically and are classified as
immediate (Type I) or delayed (Type IV) responses (Ibsen &
Phelan, 20 14; Malamed, 20 13).
Systemic allergic reactions can be life threatening and
require prompt response. Fortunately, the amide drugs in
dentistry today have very low allergenic potentials. They also
have low cross-reactivity; in other words, if a patient is aller­
gic to one amide, he or she often has no adverse response
to others. Allergy testing should precede further administra­
tions once hypersensitivity has been identified, and it should
include testing for sensitivity to possible alternatives.
Unlike amides, all esters have a common metabolite
para-aminobenzoic acid (PABA) , the suspected allerge d
in ester hypersensitivities (Tetzlaff, 2000). Esters in den­
tistry are primarily used as topical anesthetics. An allergic
reaction to one ester precludes the use of all esters.
Local anesthetic molecules are considered too small
to act as antigens, but their binding preference for pro­
teins, which largely explains their actions in sodium ion
channels, also provides sufficient size to allow them to be­
come antigenic (Jastak, Yagiela, & Donaldson, 1995).

Cardiovascular System

Generalized signs of fear Serious elevation in blood

and anxiety pressure and heart rate In response to moderate to severe overdose, the following
Nausea Cardiac dysrhythmias guidelines are recommended:
Restlessness Premature ventricular
1 . Acti v ate emergency protocol s
Heart racing contractions
2. Administer oxygen (to prevent seizures that can occur
In tense anxiety Ventricular tachycardia
because of a l a ck of 02)
Weakness Ventricular fibrillation
3. Administer diazepam (Valium) or midazolam (Versed),
Tremor Circulatory arrest
if a seizure devel o ps
Severe headache Stroke
4. Perform CPR when necessary
Hyperventilation
5. Prevent patient injury due to seizures
Palpitation
6. Moni t or vital signs
Shaky
7. Pati e nt di s mi s sal wi t h escort or/emergency transport '
•

as indicated
•
Sources: Jastak, Yagiela, and Donaldson (1995), Grimes (20 14), and •

Ltttle et a!. (20 13). : . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

 C HAPTER
Allergy may also occur due to sulfite preservatives in
vasoconstrictor-containing local anesthetic solutions. If a
patient is allergic to sulfites, solutions with vasoconstric­
tors should not be used. Allergy to epinephrine is impossi­
ble because the epinephrine in local anesthetics is identical
to endogenous epinephrine. An allergy to the epinephrine
found in local anesthetic solutions would be incompatible
with life; however, on rare occasions, patients have experi­
enced allergic reactions to the bitartrate in local anesthetic
solutions, the typical salt form of epinephrine in dental
cartridges (Kohase & Umino, 2004) . Despite the presumed
physiologic impossibility, it is not unusual for patients to
report they are allergic to adrenalin . The sensitivity they
may have experienced, although not allergenic in etiology,
limits epinephrine's future use for them and may be the
basis of a fear of dentistry.
In addition to drug allergies, latex components of lo­
cal anesthetic drug cartridges have been speculated to be
possible causes of allergic reactions. These components
are discussed in detail in Chapter 9, " Local Anesthetic
D elivery Devices." Latex components of local anesthetic
drug cartridges currently manufactured for use in North
American have been voluntarily replaced with latex-free
components.
LOCALIZ E D A L L E R G I C R EACT I O N S Localized allergic re­
actions to local anesthetic drugs occur most frequently af­
ter topical anesthetic application (see Figure 17-13 •) and
manifest as Type IV reactions (Ibsen & Phelan, 20 14) . They
are usually limited and respond well to antihistamine ther­
apy. The majority have occurred due to the metabolic by­
product of esters, para-aminobenzoic acid (PABA). Allergic
reactions typically occur in response to topical anesthetics
within 30-60 minutes of tissue contact (Malamed, 20 1 3 ) .
Despite this rapid reaction, some onsets may be delayed,
occurring hours after a patient has been dismissed. There
is concern that contact allergy to lidocaine topicals may be
increasing (Tucker, 2007). Several patients in a recent report
experienced positive reactions to lidocaine topical and to
FIGURE 1 7-1 3 Localized Allergic Reaction. Signs of localized
allergic reaction following the placement of topical anesthetic.
17 • LOCAL A N E STH ESIA C O M PLICATI O N S A N D MANAG E M ENT 349
inj ectable lidocaine in all concentrations, suggesting a true
allergic reaction versus an irritant effect (Tucker, 2007).
Hives (urticaria) are associated with many conditions,
including reactions to antigens (Ibsen & Phelan, 20 14).
They present as well-demarcated swellings on the skin
usually accompanied by itching and can occur after local
anesthetic administration (Malamed, 20 13). A similar, but
less frequent allergic manifestation to anesthetics is known
as angioedema (Ibsen & Phelan, 20 14). Angioedema and
urticaria are different in that angioedema is not usually
accompanied by itching due to involvement of less super­
ficial vessels (Ibsen & Phelan, 20 14). Either may occur
rapidly after inj ectable or topical anesthetic administra­
tion, in which case patients should be closely monitored.
Close monitoring is important in local allergic reac­
tions in order to recognize the possible progression from
local to systemic events. Whereas most complications man­
ifest with only local tissue changes, some local anesthetic
allergic reactions can progress to systemic events (Jastak,
Yagiela, & Donaldson, 1995). Clinicians should be alert to
possible progressive worsening of the signs and symptoms
of localized allergy (see Figure 17-13 ) , especially respira­
tory distress.
R E S P O N S E TO LOCA L IZ E D A L L E R G I C R EACTI O N S Rapid
recognition and response to developing localized allergic
reactions can alter the extent of the reaction. It is also im­
portant to remove any remaining traces of a topical drug
and discontinue its use.
PREVENTION O F LOCALIZE D ALLERG I C EVE NTS To prevent
local allergic events:
1. Avoid medications that have induced allergic reac­
tions in the past
2. Avoid same-class topical preparations that previously
induced hypersensitivities
3. Consult with previous providers whenever patients re­
port past allergic experiences
4. Refer for allergy testing if patients report past aller­
gies or symptoms
5. Document in patient records
M A N AG E M E N T OF LOCALI Z E D A L L E R G I C E V E NTS In re­
sponse to local allergic events, the following guidelines are
recommended:
1. Schedule the patient immediately to evaluate possible
postoperative allergic lesions/reactions
2. Recommend OTC B enadryl or prescribe diphenhydr­
amine as appropriate
3. Refer for allergy testing, depending on signs and
symptoms
4. Send samples of anesthetic and of non-anesthetic sub­
stances that also contacted the site
5. Document in the patient record
350 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I ON OF LOCAL A N E STH E S I A
Systemic Allergic Reactions
Although less frequent, systemic reactions to local an­
esthetic drugs and solutions are far more serious. These
reactions may be in response to local anesthetic drugs
themselves, sulfite preservatives in solutions, or, in the case
of esters, the byproduct of ester hydrolysis, PABA.
R E S PO N S E TO SYSTE M I C A L L E R G I C R EACTI O N S Recogni­
tion and prompt response are critical when allergic reac­
tions occur. Any delay allows a progressively deteriorating
situation that may result in respiratory and cardiovascular
arrest. Epinephrine reverses bronchial constriction and
peripheral vasodilation and is not, itself, an antigen. It is
important to note that epinephrine's effectiveness is lim­
ited to relatively short intervals due to its rapid biotrans­
formation. Clinicians must be prepared to deliver repeated
doses until emergency medical personnel arrive.
PREVENTION O F SYST E M I C ALLERGIC REACTI O N S Systemic
reactions to known allergens can be prevented by obtain­
ing information during health history reviews. Specific
questions related to previous allergic reactions can provide
guidance, either as direct evidence or in provoking further
questioning or referrals to allergists.
B ecause of the possibility of allergic reactions to pre­
viously nonallergenic substances and the nearly universal
exposure of the population to a wide variety of allergens,
there is no way to predict or prevent unprecedented aller­
gic reactions. The exception to this unpredictable pattern
occurs when there may be cross-reactivities, which should
be investigated whenever a positive response has been
noted to a history of allergy to any amide anesthetic.
MANAG E M ENT OF SYSTE M I C ALLERGIC REACTI O N S Type
I hypersensitivities may manifest as localized reactions
(localized anaphylaxis) and systemic reactions (general­
ized anaphylaxis). B oth are similar in a number of ways.
The most important similarity in this discussion, how­
ever, is that the reaction occurs within a short time, any­
where from seconds to hours after exposure to an antigen
(Malamed, 20 13).
Localized anaphylaxis has the potential to become
systemic and should be monitored for the development of
systemic signs and symptoms, especially peripheral vasodi­
lation, which can lead to hypovolemic shock, a generalized
rash, and difficulty breathing due to constriction of the air­
way (see Box 17-13 •) .
Systemic allergic reactions are life-threatening emer-
gencies and require prompt responses, including:
1. Terminate treatment
2. Activate emergency protocols
3. Administer oxygen
4. Administer epinephrine, 0.3 mg (0.15 mg for a child)
intramuscularly or subcutaneously
5. Administer diphenhydramine, 50 mg (25 mg for a
child)
In the event of generali z ed anaphyl axi s , signs and symp­
toms will progress through phases that include:
1 . Skin reactions-itching, flushing, hi ves
2. GI /GU reactions-cramps, vomi t ing, diarrhea, nausea,
incontinence
3. Respiratory-chest tightness, cough, wheezing,
dyspnea, laryngeal edema
4. CVS-palpi t ations, lightheadedness, tachycardia,
hypotension, unconsciousness, arrest
Source: " P ro g ress i o n of S i g n s and Sym pto m s i n G e n e r a l ized A n a -
p h y l a x i s , " by Sta n l ey F . M a l a m e d fro m H A N D B O O K O F L O C A L •
: �� ��� �� � � � � � : � � � � �0.1 :·�
ES l i e d b E s v e r,
.
S
. . • • . . . • . • • . . • . . • •
6. Transfer to a hospital via ambulance. If appropriate,
following observation and consultation with the pa­
tient's medical provider, patients may be dismissed
with a prescription for diphenhydramine or an appro­
priate substitute. The need for an escort should be de­
termined by the medical provider or hospital.
7. Medical consultation before subsequent therapy, in­
cluding allergy testing (Malamed, 20 13)
Idiosyncratic Events
Adverse events may occur that have no known etiology.
These are referred to as idiosyncratic events and are likely
of genetic origin. The varieties of signs and symptoms that
may occur resemble those seen in overdose and allergy
and require responses that are appropriate to the particu­
lar signs and symptoms that develop (Malamed, 20 13).
Atypical Plasma Cholinesterase
As discussed in Chapter 10, atypical plasma cholinester­
ase impairs the metabolism of esters. Prescreening for this
genetic trait is the primary preventive measure. Because
esters are no longer packaged in cartridges, they are rarely
used in dentistry as inj ectable drugs. The most common
current use of esters in dentistry is in topical anesthetics
such as benzocaine and tetracaine. These preparations are
easily avoided by using topicals containing lidocaine, prilo­
caine, or dyclonine hydrochloride.
Methemoglobinemia
Methemoglobinemia is a condition characterized by a
diminished oxygen-carrying capacity of blood. Patients
who have genetic predispositions, bre athing problems
such as asthma, bronchitis, emphysema, heart disease, and
patients who smoke are at greater risk for complications
related to methemoglobinemia. Methemoglobinemia
may also occur in non-predisposed individuals. In addi­
tion to other chemical substances, both prilocaine and
benzocaine are known inducers and must be avoided in
 C HAPT E R
susceptible individuals (Abu-Laban et a!. , 2003; Centers
for Disease Control and Prevention [CD C] , 1994; FDA
Patient S afety News, 2006; Institute for S afe M e dical
Practices [ISMP] , 2002) . Although typical doses in den­
tistry do not seem to be problematic, warnings from the
FDA in response to recent serious incidents with benzo­
caine spray, and a history of numerous warnings associ­
ated with prilocaine, have reinforced the need for caution
(Abu-Laban et a!., 2003). There are many reports of met­
hemoglobinemia associated with both drugs (FDA Mod­
ernization Act of 1997; FDA Patient Safety News, 2006;
ISMP, 2004 ) . Although not mentioned in these FDA re­
ports, articaine in large doses was reported in a limited
number of case reviews to induce methemoglobinemia
(Sambrook et a!., 20 1 1 ) .
Methemoglobinemia occurs when hemoglobin en­
counters a chemical or an agent that changes its molec­
ular structure to methemoglobin, which has a decreased
affinity for oxygen. The net effect of having too many
molecules of methemoglobin in the blood is that red
blood cells will have a reduced ability to provide oxygen
to the tissues. When the level of methemoglobin reaches
certain levels, cyanosis can be observed, usually at the lips
and nail beds. If methemoglobin levels continue to rise,
symptoms can become severe and life-threatening (See
Table 17-4 •) .
Treatment for methemoglobinemia usually o ccurs
during an emergency room visit with the intravenous infu­
sion of methylene blue (1-2 mg/kg) (Trapp & Will, 20 10).
For more information on methylene blue and an example
of a genetic predisposition to methemoglobinemia, see
Box 17-14 •·
Table 1 7-4 S i g n s a n d Sym pto m s Associated
with M et h e m o g l o b i n e m i a
Percentage of
Methemog lobin i n
Blood Signs and Sym ptoms
Less than 2 Normal amount in blood
2-15 None
15-20 Cyanosis
20-30 Headache, dizziness, syncope,
tiredness, increased heart rate
30-50 Confusion, tiredness, increased
heart rate, and breaths per minute
50-70 Abnormal heart rhythm, seizure
activity, coma
More than 70 Death
Sources: Trapp and Will (2010) and Wright, Lewander, and Woolf (1999).
17 • LOCAL A N E STH ESIA C O M PLICATI O N S A N D MANAG E M ENT 351
Methylene blue is a concentrated dye that works with
a naturall y occurring enzyme known as NADPH to
change the mol e cular structure of methemoglobin
back to hemoglobin (Umbrei t , 2007). Methylene blue
requires the availabili ty and presence of NADPH to
reverse methemoglobinemia. Individuals with glucose-
6-phosphate dehydrogenase deficiency (G6PD) l a ck the
abili ty to produce NADPH (Trapp & Will 201 0; Umbreit,
2007). This X-I inked inheri t ed di s order usuall y affects
persons of Middle-Eastern, Medi t erranean, Asian, or
African lineage, and nearl y 400 million people are affected
globall y (Frank, 2005). Anestheti c agents associ a ted wi t h
methemoglobinemia should not be used in patients wi t h
•
P
: .�� .� •
.
• • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • •
Methemoglobinemia can be a serious complication
of local anesthetic administration. Preventive measures
should include a thorough risk-benefit analysis and avoid­
ance of benzocaine and prilocaine for any patients with
previously known susceptibility.
Needle Phobia
During the administration of local anesthesia, the most
frequently encountered systemic reactions have a psycho­
logical basis (Jastak, 1995 ) . In addition to syncope, many
patients suffer non-syncopal reactions surrounding dental
appointments including avoiding them entirely because of
needle phobia, as discussed in depth in Chapter 2, "Fun­
damentals of Pain Management" (Dionne, Gordon, &
McCullagh, 1998 ) . Needle phobia is considered a formal
medical condition affecting approximately 1 0 % of the
world's population (Hamilton, 1995). Management of den­
tal phobias is discussed in Chapter 18, "Insights for Fearful
Patients." Additional discussion on needle phobia is pro­
vided in Box 17-15 •·
An extensi v e revi e w of needle phobia provided evidence
that this condi t i o n is both l e arned and inherited (Sokolowski ,
Giovannitti, & Baynes, 201 0). I n the majority of phobic
patients, needle phobia usually ari s es as a negati v e experi ­
ence at the dental offi c e or wi t h another medical provider
during childhood. This learned fear in childhood can
progress over time into a phobia that l e ads to anticipa­
tory anxiety. In addit ion to the l e arned process, there are
genetic indications for the physiol o gic reaction to needl e
puncture that ari s e from primi t i v e impul s es of survi v ability
•
( � �o� s k � : va i :t , & � y n · 2�; �) .....•
•
: . � �� . :� . �� : . . � . �� .
. . . .
• •
352 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I ON OF LOCAL A N E STH E S I A
CAS E M A N AG E M E N T
Ashley Smith
A l t h o u g h s o m e w h a t d r a m at i c i n a p p e a ra n ce , t h e
h e m ato m a p resented i n t h i s case is m o re typ ica l of
m a ny that d eve l o p fo l lowi ng denta l i njecti ons, i n both
exte nt a n d co u rse of h e a l i n g . U n l i ke the case h i g h ­
l i g hted i n t h e text o f t h i s c h a pter, w h e re t h e patient
was ta k i n g th ree a nticoa g u l a nts, t h e re were n o co m ­
p l i cating fa cto rs a n d n o contra i n d i cati o n s to t h e u s e
of a P S A n e rve b l ock.
Case Discussion: The h e m ato m a seen i n F i g u re 1 7-1
occu rred i m m ed iate ly fo l l ow i n g a positive aspi ration
at o pti m u m p e n etrat i o n d e pth and a n g l e fo r a PSA
nerve b l ock. Of particu l a r interest i n this series of pho­
t o g ra p hs a re t h e time seq u e n ce, t h e a p pe a r a n ce of
the h e m at o m a at va r i o u s sta ges of h e a l i n g , and t h e
length o f time for reso l utio n . Fig u re 1 7-1 4 shows the • which occu r over time, under the ski n .
FIGURE 1 7-1 4 Progression of a Hematoma-Day 1 + .
Progression of swelling a few minutes after observing the
initial swelling.
Source: Courtesy of Ashley Diteman.
h e m atom a a few m i n utes after deve l o p m ent. This was
the approxim ate extent of the swe l l i n g a n d represents
t h e p o i n t at w h i c h t h e i ntravasc u l a r p ressu res h ave
been e q u a l ized by the p ress u res exerted by the d is­
tended tissues of the face. One week later, the swe l l i n g
is sti l l present b u t h a s d iffused somewhat into adjacent
tissues, providing a smoother o utl i n e (Fig u re 1 7-1 5 •).
H e m atomas a re affected by g ravity. N otice how t h e
swe l l i ng has d ropped below the mandible in its inferior
extent. Two weeks later (Fig u re 1 7-1 6 •), the o utl ine is
even sm ooth er, m u ch l ess a n g u l a r compared with the
appearance on the day of development, and the bruise
is m uch more obvious, demonstrating typical shades of
ye l l ow, b rown, and purple (Fig u re 1 7-1 7 •).These co l­
o rs reflect the changes in the appearance of the blood,
FIGURE 1 7-1 5 Progression o f a Hematoma-1 Week
Later. The swelling is still present but has diffused into
adjacent tissues.
Source: Courtesy of Ashley Diteman.
 C HAPT E R 17 • LOCAL A N E STH ESIA C O M PLICATI O N S A N D MANAG E M ENT 353

FIGURE 1 7-1 6 Progression of a Hematoma - -2 FIGURE 1 7-1 7 Progression of a Hematoma - 2 Weeks+

Weeks Later. After 2 weeks, the outline is smoother Later. Demonstrating typical shades of yellow, brown, and
compared with day one; however, the bruise is much purple, these colors reflect the changes in the appearance
more obvious. of the blood, which occur over time, under the skin.
Source: Courtesy of Ashley Diteman. Source: Courtesy of Ashley Diteman.

As h e m at o m a s h e a l a n d b r u i s i n g becomes m o re res p o n s i b l e fo r t h e red d i s h - b l u e co l o r, b i l iverd i n fo r

v i s i b l e , c o l o r c h a n g es a re d u e to t h e b r e a k d o w n of t h e g re e n , a n d b i l i ru b i n t h e ye l l ow. H e m os i d e r i n is
h e m o g l o b i n , its meta b o l ites ( b i l iverd i n and b i l i r u b i n ) , responsi b l e fo r the b rown co l o r.
a n d h e m os i d e ri n . T h e b r e a kdown of h e m o g l o b i n is

Chapter Questions b. The patient is likely suffering from a drug overdose

· · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · ·
due to excessive administered doses.
1 . A clinician is administering an IA nerve block be­ c. The patient is likely suffering from a drug overdose
fore therapy when the patient suddenly j erks and the due to intravascular administration.
needle breaks. The embedded portion is not visible. d. The patient is likely suffering from an allergy to
What should the clinician do? lidocaine.
a. Attempt removal 3. Allergies to topical anesthetic drugs that cause mucosal
b. Refer for removal signs and symptoms hours to days after exposure are
c. Reappoint to remove once the needle has devel­ explained best by which one of the following reactions?
oped a fibrous cocoon around it a. Delayed hypersensitivity
d. Refer for evaluation b. Anaphylaxis
2. A second cartridge of 2% lidocaine has been admin­ c. Angioedema
istered for an IA nerve block when the 160-lb patient d. Immunopathology
becomes anxious and states that she doesn't feel well, 4. A patient calls several days after an IA block and
even a little nauseous. She becomes less anxious as reports that numbness is still present along with some
she becomes increasingly fatigued, her speech be­ annoying, occasional sharp pains. Which of the fol­
comes slurred, and she reports a numb feeling all lowing terms best describes what is occurring?
around her mouth. Which one of the following state­ a. Paresthesia, anesthesia
ments best describes these observations? b. Paresthesia, hypoesthesia
a. The patient is likely suffering from severe anxiety c. Paresthesia, dysesthesia
and fatigue. d. Anesthesia, hyperesthesia
3 54 S E C T I O N IV • C LI N I CAL A D M I N I STRAT I ON OF LOCAL A N E STH E S I A
5. Which of the following responses is most appropriate
after rapid tissue swelling is noticed after a PSA block?
a. Get an ice pack and then place pressure on the area
with the ice pack.
b. Place pressure on the area for 10 minutes and then
continue working.
c. Place pressure on the area while someone else
looks for ice; terminate procedure.
d. Reassure the patient and continue with planned
therapy once numb.
6. Of the following possible adverse reactions, which
one occurs most frequently?
a. Allergy
b. Idiosyncratic response
c. Overdose
7. Considering all of the following measures for pre­
venting overdose, which one is most important?
a. Calculating doses
b. Slow administration
c. Aspiration
d. Reassuring patients
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Annals of Emergency Medicine, 34, 646-656.
Zeiter, R., Cohen, C., & Casap, N. (2002). The implications of
a broken needle in the pterygomandibular space: Clinical
guidelines for prevention and retrieval. Pediatric Dentistry, 24,
153-156.
C h a pter 1 8 I n s i g h ts fo r Fea rf u l Pati e n ts

Chapter 1 9 I n s i g hts f ro m Ped i a t r i c D e n t i st ry

Chapter 20 I n s i g h ts f ro m S p e c i a l t i e s : O ra l S u rg e ry, P e r i o d o n t i cs , a n d
E n d o d o n t i cs
 AGNES SPADAFORA, RDH, BS

O BJ E CT I V E S KEY T E R M S

• Defi n e a n d d i scuss t h e key terms i n th i s c h a pte r. a n x i ety 359

b e h av i o ra l control 362
• D iffe renti ate between t h e terms fear; anxiety, and p hobia . b e h av i o ra l i n d icators of
• Exp l a i n t h e eti o l og y a n d deve l o p m e n t o f fea r a s it re lates to fea r 36 1
p a i n a n d pa i n m a n a g e m ent. b i o fe e d b a c k 364

• D i scuss the p ri m a ry so u rces fo r reco g n i z i n g a n d assess i n g fea rs . c o g n itive control 36 1

control 36 1
• A p p l y t h e fu n d a m e n ta l concepts of treatm e n t fo r fea rfu l a n d
d e b riefi n g 362
a nx i o u s patients. d e e p b reath i n g 363
• R e l ate a patient's sense of contro l to his o r her exp e r i e n ced e l ectric p u l p teste r (E PT) 364
l eve l of fea r o r a nxi ety. fea r 359
focu s i n g atte n t i o n 362
• Exp l a i n fo u r u sefu l types of contro l fo r a nx i o u s patients receiv­
g r a d u ated expos u re 364
i n g i nj e ct i o n s .
g u i d e d vis u a l izati o n or
• D i sc u ss a n d d e m o n strate physica l re l axat i o n a n d co p i n g s ki l l s , g u i d e d i m a g e ry 36 1
i n c l u d i n g d e e p b reath i n g a n d m u s c l e re l axati o n . i nfo r m a ti o n a l control 36 1
p a i n 360
• Te ach physica l re l axati o n a n d co p i n g s ki l l s t o patients.
p a i n m a n a g e m e n t 360
• Apply a p p ro p ri ate fea r m a n a g e m e n t strate g i e s and co p i n g
p h o b i a 360
s ki l l s t o t h e a d m i n i strati o n o f l oca l a n esthetics. p h ys i o l o g i c a l i n d i cators of
• Describe and exp l a i n t h e b e n efit of re h e a rsa l s , ti m e struct u r­ fea r 36 1
i n g , a n d b i ofeed back to fea rfu l patie nts. pos itive co p i n g
state m e n t 362
• Describe b e n efits and tech n i q u es fo r testi n g l o ca l a n esthetic
p rog ressive m uscle re l axati o n
effective n ess.
( P M R) 363
• Describe t h e m a n a g e m e n t of a n esthetic fa i l u re , i n c l u d i n g re h e a rs a l s 363
psych o l og i ca l m a n a g e m e n t o f t h e patient a n d tech n i ca l retro sp ective control 362
rea ssess m e n t . se lf-re p o rt 360
syste m a t i c
d e s e n s itizati o n 363
t i m e structu r i n g 364

358

CAS E S T U DY
Lydia O'Kaine
M rs . Ly d i a O ' Ka i n e , a 3 3 - ye a r- o l d fe m a l e , p re ­
sented fo r denta l care with a ch ief co m p l a i nt o f u n ­
h a p p i n ess o v e r the esthetics o f tooth # 7 . The i n itia l
i nterview reve a l e d that s h e h a d not seen a d e ntist
in 6 years. H e r m e d i c a l h i story was n o n -contri b u ­
tory, exce pt fo r smoking o n e p a c k o f ciga rettes p e r
d a y fo r 1 5 years. M rs . O ' Ka i n e i n d i cated t h a t s h e
h a d tried t o q u it seve ral t i m e s b ut fou n d the h a b it
" re laxing a n d e njoya b l e . "
A t t h e i n itia l exa m , i nfo rmati o n a b o ut h e r l ast
d e nta l visit was o bta i n e d . Lyd i a re p o rted that t h e
l o w e r right m o l a rs " h a d cavities a n d needed treat­
m e nt" and that the c l i n i ci a n had to sto p treatment
seve ra l times to g ive h e r m o re a n esthetic. S h e a lso
stated that she " n ever rea l ly fe lt n u m b , " but s h e
w a s a b l e t o " to u g h it o u t " a n d t h e treatm ent was
com p l eted . The a d d iti o n a l i njectio n s were very d if­
ficu lt fo r h e r because "they b u r n ed . " Lyd i a stated
she is now q u ite a p p re h e n sive about p a i nfu l i njec­
tions and a d d iti o n a l ly she is concerned a bo u t the
effective n ess of the a n esthetic. Lyd ia i n d i cated that
b efo re her l ast exp e r i e n ce she had n ot received
reg u l a r denta l care but had n ot h a d p ro b l e m s with
i njections o r a n esth esia . After this experience Lyd ia
did n ot retu rn to h ave tooth #7 treated , and the
cavity is now vis i b l e but asym pto m atic.
Findings at the i n itial exa m included the fo l l ow­
i n g : caries in #7, #8, a n d # 1 3 a n d a m issi ng restora­
tion in #3 1 . D u ri n g her periodonta l exa m , c h ro n i c
g i n g ivitis w a s a p p a rent i n the maxi l l a ry anterior re­
g i o n . Because of tiss ue sensitivity, fu l l m o uth p rob­
ing was not co m p l eted . Iso l ated p ro b i n g reve a l e d
5- to 6- m m pocket depths in the maxi l l a ry a n d m a n ­
d i b u l a r m o l a rs . M o d e rate s u p ra g i n g iv a l ca l c u l u s
w a s p resent o n t h e l i n g u a l o f t h e l ower a nteriors.
The proposed treatm ent p l a n included oral hyg i e n e
i n str u ct i o n s , fo u r q u a d ra nts of s ca l i n g a n d r o o t
p l a n i n g w i t h a n esthesia, fl u o r i d e t h e ra py a n d p re­
scriptions, and resto ration of #7, #8, # 1 3, and #3 1 .
I ntrod uction
This chapter discusses the use o f local anesthesia for pa­
tients that are known as fears patients. Despite the empha­
sis on the management of exceptional fear, there are many
discussions within this chapter that apply when anesthetiz­
ing all patients. Fear and anxiety are by no means unique
to this segment of the dental patient population, especially
when needles and drugs are involved. As reported in the
literature, approximately 40 % of patients presenting for
dental care experience some level of anxiety related to
C HAPT E R 18 • I N S I G HTS FOR F E A R F U L PAT I E NTS 359
appointments, whereas another 1 2 % to 20 % are extremely
anxious or fearful (De Jongh et al., 1995 ; Sohn & Ismail,
2005). Despite dramatic improvements in dental technol­
ogy, this pattern of fear has not changed over time (Smith
& Heaton, 2003). Anxiety and fear produce both psycho­
logical and physiological changes that can affect the abil­
ity to receive local anesthetics and their effectiveness once
received. When asked to rank the most fearful elements
of dentistry, patients consistently place needles at or near
the top of surveys. It has been found that nearly 1 in 20
individuals avoids dentistry because of fear of inj ections
(Milgrom et al., 1997; Milgram et al. , 1988) .
Local anesthesia failures can magnify the problem. Fail­
ure rates were demonstrated to be as high as 14 % during
dental appointments in one report (Weinstein et al. , 1985).
More than 2 % of the patients involved were unable to com­
plete treatment because of the inadequacy of the anesthesia
(Weinstein et al., 1985). There figures compare closely with
the results of a 1984 survey of dentists, which revealed diffi­
culties administering adequate anesthesia in approximately
1 3 % of patients over a 5-day period (Kaufman, Weinstein, &
Milgram, 1984). The actual percentage of the failures with at
least a partial psychological etiology is unknown, but there
is reason to suspect that there is at least some psychological
influence on the effectiveness of local anesthetic drugs. The
manner in which dental fear and anxiety can contribute to
local anesthesia failure will be clarified in this chapter. As
one clinician commented, "Why is it that I always seem to
miss the blocks on my most anxious patients?"
Some clinicians emphasize the benefits of oral health
when attempting to motivate fearful patients. Many of
these patients are aware of the benefits of oral health, but
the prospect of good oral health, alone, is not sufficient to
enable them to tolerate treatment. This chapter focuses
on strategies and skills that lower psychological barri­
ers to treatment. A principle known as treat the fear first,
developed and elaborated by Milgrom, Weinstein, and
Heaton in their text, Treating Fearful Dental Patients: A
Patient Management Handbook, will be highlighted.
Term i nology and Fea r Development
The terms fear, anxiety , and phobia are often used inter­
changeably. In order to better understand the differences
between these terms, particularly as they are used in the
dental fears literature, they will be defined as follows
(Milgrom, Weinstein, & Heaton, 2009) :
Fear is an emotional response to an immediate threat
or danger. Reactions to perceived danger include ( 1 ) un­
pleasant cognitions that something terrible will happen,
(2) physiological changes (tachycardia, perspiration, nau­
sea, hyperventilation) , and (3) overt behaviors such as
shaking, pacing, and rapid speech. This layered response is
often referred to as fight or flight.
Anxiety is an emotional response to a threat or danger
that is not immediately present or is unclear. Anxiety may
lead to the same cognitive, physiological, and behavioral
360 SECTION V • S P E C IAL C O N S I D E RATI O N S F O R LOCAL A N E STH ESIA
responses as fear. Anticipatory anxiety may occur hours or
days before an actual dental appointment.
Phobia, as described in the American Psychiatric As­
sociation's D iagnostic and Statistical Manual of Mental
Disorders, is a persistent, irrational fear of a specific object
or situation that results in a compelling desire to either
avoid the situation or endure it with dread (American Psy­
chiatric Association , 2000) . Phobias can interfere with a
person's ability to function. In dentistry, phobias are likely
to interfere with the achievement of oral health, often re­
sulting in pain and suffering when oral health is neglected.
The terms strategy, skill, response, and reaction may be
helpful for clinicians when presenting methods for modi­
fying behaviors in the dental environment. The follow­
ing definitions will apply to these terms ( The American
Heritage® Dictionary of the English Language [American
Heritage Dictionary] , 2000):
Strategy is defined as a plan of action intended to
accomplish a specific goal.
Skill refers to a proficiency acquired or developed
through training or experience.
Response refers to a reply, an answer, or a reaction to
a specific stimulus.
Reaction is a response to a stimulus.
Local anesthetic drugs are used in dentistry to control
and manage pain. Unfortunately, the very act of adminis­
tering local anesthetics is often perceived as too painful
to endure by patients who are excessively fearful of inj ec­
tions. Pain management for these individuals entails their
ability to cope with and tolerate treatment, in addition to
the proper administration of local anesthetic.
Before discussing pain management in these individu­
als, it is important to define the term pain. As a positive
experience, pain has a primary benefit of alerting an indi­
vidual to injury. Most definitions, and this discussion, focus
on the overwhelmingly negative aspects of pain, which are
well articulated in the following definition provided by the
International Association for the Study of Pain (IASP) : *
Pain: A n unpleasant sensory and emotional experience
associated with actual or potential tissue damage, or de­
scribed in terms of such damage. Pain is always subj ec­
tive. Each individual learns the application of the word
through experiences related to inj ury in early life. It is
unquestionably a sensation in a part or parts of the body,
but it is also always unpleasant and therefore also an
emotional experience. Many people report pain in the
absence of tissue damage or any likely pathophysiologi­
cal cause; usually this happens for psychological reasons.
There is usually no way to distinguish their experience
from that due to tissue damage if we take the subj ective
*"Definition of Pain" by Harold Merskey from CLASSIFICATION
OF CHRONIC PAIN: DESCRIPTIONS OF CHRONIC PAIN
SYNDROMES AND DEFINITIONS OF PAIN TERMS. Copyright ©
1994 by IASP Press. Used by permission of IASP Press.
report. If they regard their experience as pain and if they
report it in the same way as pain caused by tissue dam­
age, it should be accepted as pain. This definition avoids
tying pain to the stimulus. (Merskey, B ogduk, 1994)
For additional information on this topic see Chapter 2,
"Fundamentals of Pain Management."
The Development of Fear
Fear of dentistry is complex (Milgrom,Weinstein, & Heaton,
2009) . The most common cause for the development of
dental fear is through direct negative experience, usually of
pain or fright, to a perceived threat of harm. The experi­
ence of pain or fright, alone, does not necessarily lead to
exceptional fear and avoidance of dentistry. The manner in
which a clinician manages a patient's emotional reaction
to pain (or the anticipation of pain) is a more important
determinant of whether or not dental fear develops.
The !ASP's definition of pain describes the experience
as occurring with or without tissue damage. In the absence
of injury, the causes of pain can be hidden from clinicians.
In the absence of obvious injury, it is the patient, alone, who
determines whether or not pain has been experienced. This
self-determination can lead to emotional reactions arising
from unpleasant experiences perceived by patients. The re­
sponse of clinicians and their behavior in the face of these
reactions can be critical. If clinicians fail to understand or
respond to patient concerns, or if they belittle patient reac­
tions, fear is a likely result. This is especially true when a
patient has no ability to control stressful and fearful situ­
ations. Clinicians who are empathetic, on the other hand,
can respond in ways that inhibit the development of fear.
Recog n izing Fea r and Anxiety
Studies have demonstrated that even dental p ersonnel
who recognize fear and anxiety in patients often do not
address the problem in order to avoid making matters
worse (Corah, O ' Shea, & Ayer, 1985). Before administer­
ing anesthetics, it is important to assess a patient's past
experiences. This will provide information about their ex­
pectations and about the possibility of fear and anxiety af­
fecting the administration.
There are three primary sources for assessing patient
anxiety and fear before and during stressful dental experi­
ences according to Milgrom, Weinstein, and Heaton: self­
report, behavioral indicators, and physiological indicators
(Milgrom, Weinstein, & Heaton, 2009) .
Self-report is the principal method for obtaining infor­
mation about a patient. It allows patients to express both
negative and positive aspects regarding past dental experi­
ences. Information may be obtained in one-on-one inter­
views or by using simple questionnaires that may include
some of the following questions: How long has it been
since your last dental visit? What kind of treatment did
you receive? How did it go? Are there any concerns about
receiving inj ections? Is there anything that you would like
to do or not do during today's appointment? What will
make receiving an inj ection easier for you?

Behavioral indicators of fear include overt signs such
as pacing the waiting room, fidgeting, wringing hands, or
gripping the arms of chairs until knuckles turn pale ("white
knuckles"). Patients may talk incessantly in order to avoid
dental treatment. Signs of fear in the operatory also include
opposite responses such as quiet, nonresponsive postures.
Physiological indicators of fear include perspiration,
changes in respiration, shallow breathing, and increased
heart rate and blood pressure. Patients also frequently hold
their breath during injections. Unfortunately, the increased
tension caused by holding one's breath actually lowers pain
tolerance. Sensitivity generally increases, and procedures are
commonly more uncomfortable throughout. The perception
of increased patient sensitivity and discomfort could encour­
age clinicians to administer anesthetics more rapidly (to get it
over with), which can cause even greater discomfort.
Fou ndations of Treatment
There are three concepts t o consider when developing strat­
egies for treating fearful patients: the patient-clinician re­
lationship, the patient's sense of control over a potentially
threatening environment, and the patient's ability to cope
with a stressful situation. Interactions between clinicians
and patients take place throughout the process of providing
dental care. Every aspect of treatment takes place within the
framework of those interactions. A patient's sense of con­
trol and the ability to cope are essential to tolerating dental
procedures that are perceived as aversive, such as injections.
Without control and coping skills, fearful patients may worry
that experiences will surpass the limits of their endurance.
Trust in the Patient-Clinician Relationship
Once a fearful patient has been identified, building a trust­
ing relationship is critical to successful treatment. Dentistry
is a social interaction, and research has shown that a clini­
cian's personal attributes and professional behaviors impact
patients' attitudes toward dentistry (Corah, O'Shea, & Bis­
sell, 1985). Dental fear can develop from painful and fright­
ening experiences, especially when clinicians are perceived
as unaware of or unconcerned with physical and emotional
suffering. Because one of the primary means by which pa­
tients are able to assess clinician competence is through the
strength of their interpersonal behavior, it is important for
clinicians to set the stage early for positive perceptions.
Interpersonal rapport, open two-way communication,
empathy, and professional competence are important to
establishing trust. Patients should be encouraged to ex­
plain their fears and concerns, to express likes and dislikes,
and to ask questions. Fearful patients frequently need help
learning to be assertive and to express their needs. Good
communication is an important means for fearful patients
to begin to exercise control over what is perceived as a po­
tentially threatening situation.
Enhancing a Sense of Control
C ontrol has been define d as "the belief that one has
at o n e ' s d i s p o s a l a r e s p o n s e that can infl u e n c e the
C HAPT E R 18 • I N S I G HTS F O R F E A R F U L PAT I E NTS 361
aversiveness of an event" (Thompson, 1981 ) . An impor­
tant tenet of psychology recognizes that when an indi­
vidual perceives a situation as harmful or threatening over
which he or she has little control, fear increases. When an
individual believes there is at least some control over the
stressful situation, both fear and the need to exercise con­
trol decrease. An important corollary to this tenet is that
fearful patients have low pain tolerances. It is important to
provide patients with a means of control over situations in
order to decrease fear and increase pain tolerance.
Thompson ( 1 9 8 1 ) has identified four methods for
providing patients with control: informational, cognitive,
behavioral, and retrospective. Milgrom, Weinstein, and
Heaton (2009) have elaborated on the use of these four
types of control in the dental situation as well.
Informational control communicates to the patient
what to expect of an imminent aversive procedure. The in­
formation is best delivered as a simple description immedi­
ately before treatment with the emphasis on the sensations
that the patient will experience. This helps fearful patients,
especially those who have avoided dentistry for a long time,
to know what to expect, to understand that any sensations
they experience are normal, and to avoid being alarmed by
them. In addition, prior knowledge of aversive events and
how long the events will last helps fearful patients tolerate
them. Without this information, patients may remain vigi­
lant and tense, alert to the next painful occurrence.
It is helpful to furnish patients with the following: simple
descriptions of the steps involved in procedures, sensations
they can expect, estimates of the time allowed for each step,
and suggestions as to ways in which they can participate in
the process or at least speed it along. Furnished rationale
should be limited to benefits of procedures rather than blow­
by-blow descriptions; for example, the slow delivery of anes­
thetics is explained as having a motive of "increased comfort"
and rubber dams are placed to "improve safety." Some fear­
ful patients may benefit from more detailed descriptions, es­
pecially if they need reassurance of clinician competence. All
pretreatment discussions should be prefaced by determina­
tions of how much each patient wishes to know.
Cognitive control involves mental maneuvers through
which patients can lessen their fearful, negative thoughts and
their reactions to these thoughts. It is sometimes referred to
as relaxing the mind and includes distraction, guided visual­
ization, focusing attention, and positive coping statements.
Distraction strategies are familiar to most and are the easi­
est to use. Patients may listen to clinician story-telling or
use audio devices with headphones for music, audio books
(selected by patient) , video devices, or audiovisual glasses.
Table 2-2 suggests additional distraction techniques.
Distraction has its limitations and does not work well
for more than the mildly anxious patient because of the
passive nature of the patient's role. Highly fearful patients
need stronger interventions to keep worst-case scenarios
from replaying in their heads.
Guided visualization or guided imagery provides pa­
tients with active roles and greater control over recurring
negative thoughts by replacing them with mental images of
362 SECTION V • S P E C IAL C O N S I D E RATI O N S F O R LOCAL A N E STH ESIA
pleasant scenes or scenarios. Clinicians can encourage pa­
tients to engage as many senses and memories as possible
while speaking in slow, relaxed voices. If patients choose
to imagine beach scenes, for example, clinicians may ask
patients if they can feel the warm breezes, hear the palm
leaves rustling, smell the tropical flowers, and see the sun­
light sparkling on the waves. This use of suggestion and
positive images to relax the mind is very similar to tech­
niques applied in the practice of hypnosis. A short discus­
sion of hypnosis can be found in Chapter 2, "Fundamentals
of Pain Management." Patients who have experience with
this type of relaxation training should be encouraged to
use those skills in the dental environment. Sample scripts
for guided visualization can be found in Appendix 2-1.
Focusing attention is a technique used to prevent what
are known as anticipatory anxieties or thoughts of what
might happen during treatment. Through this technique,
clinicians are able to redirect patient attention to the ex­
perience of the moment by checking in frequently and
providing rest breaks. Questions such as "How is it going
right now ? " and "Is anything hurting you? " can be help­
ful. Fearful patients are often so worried about what might
happen or what has happened in the past that they have a
hard time recognizing that they are "okay" in the present.
Of equal importance, they might overlook the difference
between the present experience and past experiences.
Positive coping statements are statements or phrases
that replace negative thoughts, such as "This is awful," "I
don't like this," " I wish I were somewhere else ! " Patients
are coached before treatment to select phrases that are
positively worded and relevant. They repeat these phrases
silently throughout procedures, whenever they become
anxious or to prevent the resurgence of negative thoughts.
These phrases do not have to be complex. Simple affir­
mations such as "I can do this," "This isn't so bad," "I will
make it," or "I'm a capable person, I can get through this"
can be very effective at competing with negative thoughts.
Behavioral control allows patients to take actions to
lessen, shorten, or terminate stressful situations. One of
the most familiar of these is the use of a hand signal to
stop procedures. Fearful patients should be given permis­
sion to discontinue procedures for any reason, including
escalating anxiety. The same signal can be used to indicate
a willingness to proceed with treatment once the patient is
ready to resume. In this way, patients remain in complete
control of procedural progress. It is important to acknowl­
edge their control by responding to their signals. Even a
single failure to respond to a signal can completely negate
its benefit, both at the time and in the future.
Planned rest breaks can also be beneficial for fearful
patients. Even when patients indicate they would like to
push on and "get done," it is important to give breaks in or­
der to allow them to catch their breath before proceeding.
D ebriefing or retrospective control, introduced in
Chapter 2, "Fundamentals of Pain Management," is the
post-treatment discussion of the appointment experi­
ence. Fearful patients may have had a difficult time get­
ting through appointments. They might be distraught and
apprehensive after inj ections. They might have interrupted
the inj ection or might not have been willing to proceed in
the first place. Rather than analyzing failure, an inability to
proceed can be viewed as an opportunity to help patients
reinterpret events and to note progress to date. For exam­
ple, patients who are able to receive injections despite emo­
tional upset should be praised for completing procedures
that are difficult for them. Patients who signal clinicians to
stop mid-inj ection can receive positive reinforcement for
the assertiveness they have gained in learning to control
the situation and put their needs above all. Patients who
were unable to proceed at all can receive positive rein­
forcement for their willingness to initiate the process.
D ebriefing is also an opportunity to solicit feedback
from patients regarding the aspects of appointments that
were helpful and those that were not.
Patient Strategies and Coping Skills
When working with p atients who are fe arful and who
find particular aspects of dentistry threatening, it is help­
ful to make them see the clinician as one who is interested
in making the experience as comfortable and pain free
as possible. It should be emphasized that pain control is
most effective and easiest to achieve in relaxed patients.
Patients benefit from learning skills and strategies to help
them relax physically and mentally in order to increase
their tolerance for dentistry (Bobey & Davidson, 1970) .
It is useful to deter­
R E LAXAT I O N : R O L E A N D F U N CT I O N
mine whether or not patients have any previous experience
with relaxation training or coping skills and whether or not
they have been used successfully in other situations. These
skills can be transferred to the dental environment with a
little practice. If the patient has not previously used any re­
laxation strategies, it is important to emphasize that relax­
ation is a learned skill and that effectiveness increases with
practice. It can be helpful to explain the role and function of
physical relaxation to the patient. Its use in the dental envi­
ronment is based on the principle that it is impossible to be
physically relaxed and psychologically anxious at the same
time (Jacobson, 1938). The questions in Box 18-1 • may be
used to survey patient relaxation skills. If the patient has no
previous experience with relaxation techniques, and does
• Do you find i t di ff i c ul t to rel a x in the dental chair?
Do you find yoursel f tensed up and sti ff during certain
•
dental procedures?
•
I f so, which speci f i c procedures?
Do you have a problem wi t h gagging while taking x-rays
•
or other procedures?
•
• Do you find i t di ff i c ul t to breathe or swall o w during an
injection or other dental treatment?
•
Is there anything you can do to help yoursel f relax in the •
: dental chair?
•
: . . . . . . . . . . . . . . . . . . . .• . . . . . . . . . . . . . . . . . . .

not know how to relax, the clinician will need to teach the
appropriate skills for the patient to cope with treatment.
Deep breathing is a familiar relaxation technique that
can be taught by means of a simple demonstration. Patients
can actively reduce their levels of fear and anxiety using this
technique. At the same time, it helps to prevent counter­
productive breathing, which can lead to hyperventilation,
dizziness, and loss of control. When insufficient air reaches
the lungs, the blood is poorly oxygenated and this contrib­
utes to anxiety, fatigue, and depression and can make cop­
ing with a stressful dental procedure more difficult.
The technique of deep breathing is introduced by ex­
ample, encouraging patients to learn without feeling silly ,
a s follows. Let the patient know that i t i s important not to
hold his or her breath during the procedure or inj ection.
Proper breathing allows the anesthetic to be administered
slowly, which is essential for comfort. Suggest practicing
before proceeding with the inj ection.
I would like you to:
1. inhale slowly and deeply to the count of 5, filling the
lungs with air
2. hold the breath for 1 second
3. slowly exhale to the count of 5, feeling the tension re­
lease while sinking into the dental chair.
It is helpful to count aloud on each inhale and exhale.
A gentle hand on the patient's shoulder, along with calm­
ing tones, can help to regulate the timing of the breaths
to make sure they are not too rapid or shallow. A slight
downward hand movement on the shoulder should coin­
cide with each exhalation. This continues until the patient
is relaxed and ready to receive the inj ection. Once the in­
jection begins, the clinician coaches the patient to breathe
deeply and slowly by counting aloud as before.
PROG RESSIVE M U SCLE RE LAXATION Progressive muscle re­
laxation (PMR) is another coping skill that most patients can
learn quickly and effectively (Jacobson, 1938). The body of­
ten responds to anxiety and stress by tensing muscles, which
actually heightens anxiety. Muscle relaxation, on the other
hand, reduces tension and competes with and blocks anxiety.
"Toughing it out" is not an effective way to cope with anxi­
ety and fear. Muscles that are tensed increase the likelihood
of experiencing what is known as a startle reaction. Startle
reactions can blur the difference between the anticipation
of pain and the actual experience. The confusion that ensues
can compromise patients' abilities to report pain accurately.
Muscle relaxation is learned by tensing and relaxing
different muscle groups throughout the body. This not only
helps relieve tension but also allows patients to under­
stand which areas are most tense. Clinicians can explain
and demonstrate the following:
1. inhale and tense the leg muscles
2. exhale while releasing the leg tension
3. inhale and tense the arm and hand muscles
4. exhale and release the hand and arm tension, allowing
them to go limp.
C HAPT E R 18 • I N S I G HTS FOR F E A R F U L PAT I E NTS 363
These steps can be repeated for the head, neck, and
shoulders.
A second quick and useful method is to introduce and
practice two cycles of deep breathing with the patient and
then combine it with muscle relaxation:
1. have the patient inhale deeply to the count of 5 and
squeeze and tense all the body muscles
2. on the initiation of the exhale begin to release the ten­
sion in all the muscles as the patient sinks into the chair.
Deep breathing and muscle relaxation not only allow
patients to have active roles during the administration
of local anesthetics, they also help to enhance cogni­
tive control over negative thoughts as patients focus on
their breathing and the clinician's voice guiding them.
Patients can be encouraged to practice at home and to
use the techniques in other stressful situations. Physi­
cal relaxation techniques are the simplest to teach and
the most straightforward for patients to learn. When pa­
tients have developed reasonable proficiency with those,
it may be helpful to introduce the technique of guided
visualization as described above to relax the mind. Table
2-3 provides suggestions for preparing patients for guided
visualization.
Practica l App l i cations
Rehearsals
After patients have been introduced to relaxation skills,
rehearsals provide opportunities to practice the new skills
while simulating the steps involved in actual dental pro­
cedures. Rehearsals allow patients to master control over
anxiety-provoking situations while relieving everyone of
the burden of having to accomplish any treatment. Deep
breathing, muscle relaxation, and guided imagery can all
be used by patients to calm themselves as aversive stimuli
are progressively introduced, from least to most anxiety­
producing. This process of decreasing fear and anxiety to
stimuli in a step-by-step fashion is referred to as system­
atic desensitization.
A desensitization rehearsal for local anesthesia, for
example, can begin with a patient practicing deep breath­
ing. When calm, the clinician can place topical anesthetic.
Reminding the patient to continue with the relaxation
technique, the syringe can be introduced with the cap still
covering the needle. The syringe is positioned in the pa­
tient's mouth and held there for the time it would take to
complete the inj ection.
While continuing to remind the patient to breathe
deeply, a cap-off rehearsal can be followed by the actual
inj ection if the patient is willing to proceed. Alternatively,
during a cap-off rehearsal, the patient uses a prearranged
hand signal to indicate his or her willingness for the clini­
cian to proceed with administering the actual inj ection. It
should be remembered during this process that each suc­
cessive step is increasingly challenging for the patient and
an unwillingness to continue at any point should be greeted
with acceptance and with praise of the progress made.
364 SECTION V • S P E C IAL C O N S I D E RATI O N S F O R LOCAL A N E STH ESIA
Treatment rehearsals are very similar to "tell-show­
do" techniques used to introduce new procedures to young
children. In both instances, the techniques allow what is
known as graduated exposure in order to let anxious pa­
tients know what to expect and to help them determine
when they are ready to proceed.
Rehearsals for some can be as simple as a onetime
review of the steps involved in a procedure. For others,
systematic desensitization of every step can be repeated
until they are ready and willing to go on to the next (see
the CARL program for desensitization of needle inj ection
phobia described later in this chapter) .
In an actual appointment using systematic desensitiza­
tion, patients can visualize each fearful stimulus before be­
ing presented with it, while using their coping skills (deep
breathing, muscle relaxation, positive coping statements) .
This approach allows patients to gain confidence in their
ability to cope. If the technique starts at a manageable
level and the steps are small enough, patients are much
more likely to succeed. Extremely fearful patients may
require multiple sessions before receiving inj ections. It is
important to stop any time patients tire of the process. This
will allow clinicians to recognize and praise the progress
made without exhausting patients and perhaps causing
them to lose their willingness to continue at a future time.
Time Structuring
When rehearsing local anesthetic procedures, it is useful to
consider what is referred to as time structuring. This is a pro­
cess whereby patients are informed of the time it will take
to administer a particular injection. In this method, patients
are continually apprised of injection progress by stating the
inj ection is one-fourth complete, one-third complete, three­
quarters complete, and finished. Many anxious patients find
this helpful. This is also an appropriate time to remind fear­
ful patients that one important reason for administering an­
esthetics slowly is out of concern for patient comfort.
Biofeedback
Biofeedback can be useful in addressing the physiological
changes that occur during stressful situations, such as in­
creases in heart rate. It has been used successfully in the
past to modify these responses. Subj ects have been able to
lower their blood pressure by observing it on a monitor,
for example, after having been given instructions to con­
centrate on lowering it, with no instructions on how to do
so (Kristt & Engel, 1975).
A simple heart rate monitor can be used by patients to
monitor their heart rate and anxiety. Patients may be en­
tirely unaware of the effect of anxiety on their heart rates.
The ability to visualize the effects of relaxation on their
heart rates reinforces the effectiveness of coping mecha­
nisms and their ability to compete with anxiety.
Testing the Effectiveness of Anesthesia
Patients may fear n e e dles, the sensations of drugs as
they are delivered into tissues, or inadequate anesthesia.
Recalling from previous discussions that more than 1 4 %
o f patients reported inadequate anesthesia during dental
procedures and over 2% reported pain to the extent that
they were unable to complete procedures, fear of inad­
equate anesthesia seems relatively pervasive.
The electric or electronic pulp tester (EPT) may be
useful much of the time but is particularly useful when
patients have reported a history of inadequate anes­
thesia. See Figure 18-1 • · The EPT is designed to test
the vitality of teeth by using an electric current. It is a
self-contained, battery-powered unit with a digital read­
out scale that registers from 0 to 80, with 80 indicating
a complete lack of vitality. The EPT consists of a wand
into which a sterilized tip is inserted and a ground lead,
typically attached to the wand with what is called a lip
clip. Rather than place the clip on the patient's lip, it
is equally effective and increases the patient's sense of
control, when the patient is asked to hold the clip firmly
between two fingers (see Figure 18-1 ) . The device is ac­
tivated when the tip is placed on a nonrestored , dried
area of a tooth after having been coated sparingly with
toothpaste ( a conducting medium) . Electricity flows to
the tooth when the circuit has been completed. A light
o n the wand indicates that a g o o d contact has b e e n
establishe d . T h e l e v e l of stimulus gradually incre ases
autom atically starting at 0 and continuing to 8 0 . If a
reading of 80 is registered and unnoticed by the patient,
the anesthesia is presumed to be profound.
The proce dure that incorporates EPTs is a simple
one. First, explain the function and purpose of the EPT
to the patient. It is important for patients to understand
that they have complete control over the process be­
cause they can drop the clip at any time, which imme­
diately stops the flow of electricity. After administering
the anesthetic and waiting an appropriate period for its
FIGURE 1 8-1 Testing for Adequate Anesthesia. Electric pulp
testing devices can be a reliable method to reassure patients
that adequate anesthesia has been established prior to initiating
treatment.
Source: Courtesy of Marilynn Rothen, RDH, MS.

onset, test for effectiveness with the EPT. The expected
sensation can be described in advance as a glowing, tin­
gling, warm, cold, or pulsating feeling. It is best to avoid
the word painful when describing the sensation. It is also
useful to remind patients that they will feel nothing if
the tooth is profoundly anesthetized. It can be helpful
to demonstrate the EPT on a nonanesthetized contralat­
eral tooth as a basis for confirming that the anesthetized
tooth is truly anesthetized.
If the EPT confirms that the tooth is not profoundly
anesthetized, additional anesthetic can be administered
using the same technique or a different or supplemental
technique. The tooth is then retested with the EPT and the
process is repeated until there is no response to a reading
of 80 on the device. This can be very reassuring to patients.
It is not unusual for patients anxious about inadequate an­
esthesia to request the EPT before every treatment involv­
ing the administration of anesthetic.
When an EPT is not available, an ultrasonic device or
other instrument may be used. The instrument or device
selected should be used along with a time structuring tech­
nique in order to assure the patient of profound anesthesia.
It is explained to the patient that the instrument will touch
the tooth to the count of 1 and will be removed, for feed­
back. Feedback from patients should differentiate between
the sensations of sharp and painful versus vibration and
awareness. If the patient remains comfortable to the count
of 1, the protocol should be repeated to the count of 2, then
to the count of 5. After reaching 5, treatment may begin.
Some very anxious patients may request that the counting
continue during treatment. They may consider the count of
5 to be the limit of their tolerance and the break at each
count of 5 allows tension to subside while patients catch
their breath. This process assures them that they have a safe
stopping point in case they begin to feel pain.
Protocol for Managing Anesthetic Failure
D espite the use of the EPT, strategies to reduce fear and
anxiety, and carefully planned inj ection techniques, pa­
tients may not be adequately anesthetized on occasion.
If this o ccurs, subsequent discussions should focus on
solutions to the problem rather than on emotional re­
actions. The discussion should begin with reassurance
that no treatment will begin until profound anesthesia
has been achieved and should continue with reassur­
ance that this has happened before and was successfully
addressed. It is further emphasized that providing pro­
found anesthesia is the clinician's responsibility and any
of a variety of factors can affect the success at a particu­
lar day and time.
When encountering this problem, clinicians should
consider whether or not fear has been adequately ad­
dressed. B ecause fear and lack of control can lower a
patient's pain tolerance, sensitivity can actually increase
if past experiences were not adequately addressed. Ac­
cording to Milgrom, Weinstein, and Heaton (2009) , "Fear
can lead to inadequate anesthesia and inadequate anes­
thesia during treatment can increase fear." Following fear
C HAPT E R 18 • I N S I G HTS FOR F E A R F U L PAT I E NTS 365
reassessment (patient's sense of control and use of relax­
ation techniques) and reassurances that no treatment will
begin until profound anesthesia has been confirmed, the
patient is guided through the process of developing real­
istic expectations about the sensations that will be expe­
rienced even when anesthetized. For example, pressure
and awareness (of an instrument) , although provoking
feedback to the brain, are expected sensations and are not
considered painful stimuli by most. Fear of being hurt will
lead the patient to believe that any sensation is the precur­
sor to pain. The patient needs guidance in developing the
ability to report pain accurately by distinguishing between
the anticipation of pain, sensations of instrument touch,
and actual pain.
Factors that can preclude the development of pro­
found anesthesia include infection in the area to be anes­
thetized, excessive fatigue, or physical pain elsewhere in
the body, as well as the factors discussed in Chapter 16,
"Troubleshooting Inadequate Anesthesia," which also ap­
ply to fearful individuals. Patients in pain, regardless of
the nature of the pain, are more sensitized to new stimuli
despite taking analgesics to treat the pain. The fatigue of
bearing other pain can also decrease a patient's ability to
cope with difficult situations.
When encountering inadequate anesthesia, it is best
to reassess the technique. Is there anatomical variation
and was it appropriately addressed? Was an ade quate
volume of anesthetic used? Were variations in p atient
response taken into consideration when assessing ap­
propriate dosing? Would other techniques be helpful
at this point, such as Gow- G ates nerve blocks, higher
penetration sites for inferior alveolar blocks, intraos­
seous techniques, or p eriodontal ligament inj ections ?
Another factor w h e n assessing for adequate anesthe­
sia is whether or not to use a vasoconstrictor. Control­
ling fear and anxiety with adequate anesthesia is made
easier with the use of vasoconstrictors. Not only is dif­
fusion of local anesthetic solution to centrally located
pulpal fibers more likely when vasoconstrictors are used
(they keep local anesthetics in the area of the nerve
longer and have even been demonstrated to have some
ane sthetic propertie s ) , but the anesthesia is more du­
rable and doesn't wear off as quickly. Vasoconstrictors,
when appropriate, also help to maintain blood pressures
within he althy ranges by increasing the effe ctiveness
of p ain control (decreasing endogenous epinephrine) .
Conversely, using anesthetics without vasoconstrictors
may convince fearful p atients that p ain might b e ex­
pected at future appointments if the anesthesia was not
effective or wore off before the end of treatment. In ad­
dition to the possibility of tachyphylaxis, future anesthe­
sia may b e ineffective because p atients will n o longer
remain desensitized to all the stimuli.
A final approach might be to schedule an appointment
with the exclusive goal of determining which techniques
will provide ade quate anesthesia for the challenging
area, known as an anesthetic testing protocol. No treat­
ment is scheduled. Without the pressure to "get numb "
366 SECTION V • S P E C IAL C O N S I D E RATI O N S F O R LOCAL A N E STH ESIA

for treatment, many patients are better able to manage
their anxiety, decreasing their sensitivity to stimuli and
increasing the potential for anesthesia effectiveness. The
anesthetic testing protocol appointment may use any and
all relevant techniques in order to determine which tech­
niques provide the most effective anesthesia.
Post-op Anesthetic Recovery
In addition to expectations for inj ections and treat­
ment, dental fears p atients need re alistic expectations
for postoperative periods. S oreness is not unusual, espe­
cially after generous amounts of anesthesia have been
administered and where more than one technique was
u s e d . In order to provide these p atients with control
over the post- op recovery period, it is important for
them to be prepared in advance with recommendations
for handling p ain from routine trauma and inflamma­
tion, including taking anti-inflammatory me dications
before the recovery of the tissues from anesthesia. In re­
ceiving the recommendation that they take these medi­
cations while the anesthetics are still in effect, patients
can understand that p o stop erative sensations are nor­
mal and expected.
Nitrous Oxide-Oxygen Sedation for Anxiety
Control during Dental Injections
Nitrous oxide- oxygen sedation is sometimes used for
fearful and anxious patients. It is not the intent of this
chapter to discuss the details of the use of nitrous oxide
sedation except to say that it is not a substitute for good
behavioral management skills when working with fearful
patients. Introducing nitrous oxide-oxygen sedation when
an appointment is not going well is unlikely to result in
success. It is far better to introduce nitrous oxide when
patients have time to become accustomed to its sensa­
tions and when it can be titrated to comfortable levels
before commencing treatment. Patients who demand high
levels of control over situations and who are distrustful
of dentistry often make poor candidates. In contrast, oth­
ers who are more receptive to the use of adj unctive pain
control may benefit greatly. For a detailed discussion on
the administration of nitrous oxide-oxygen sedation see
Chapter 2 1 , " Fundamentals for the Administration of
Nitrous Oxide-Oxygen sedation."
desensitization as described earlier. The desensitization
protocol consists of three active components: First, cop ­
ing responses such as deep breathing, muscle relaxation,
guided imagery, and p o s itive coping statements are
provide d . Second, a hierarchy of fearful stimuli is gen­
erated. The third, and final, step involves the presenta­
tion of fearful stimuli in order of increasing aversiveness
(Coldwell et al. , 1998).
Although not necessarily a true hierarchy, the hierar­
chy of fearful stimuli for the anesthetic inj ection is bro­
ken down into seven segments (Table 18-1 •) . Patients
proceed through e ach segment in logical order rather
than strictly by increasing levels of aversiveness. At first,
patients watch a video of a model patient learning coping
skills. Patients then observe the actor viewing and holding
an anesthetic syringe without the needle or cartridge at­
tached. At the end of the first video segment, patients rate
their anxiety on a scale of 1 to 9. If the self-rating score is
4 or less, patients are ready to move to the next segment.
If the score is more than 4, patients repeat the segment un­
til their level drops to 4 or less. The program is self-paced,
with individual sessions limited to 45 minutes. Patients re­
turn as often as necessary to complete the seven segments.
In the seventh and final segment, patients view the model
patient receiving and coping with an actual inj ection (see
Table 18-1) .
Table 1 8-1 Content o f t h e CARL Prog ra m Exposu re
H i e ra rchy S e g m ents
Segment 1 Explanation of local anesthetic, viewing
and holding the syringe.
Segment 2 Discussion of the needle, including
the length, flexibility, only required to
insert a short distance.
Segment 3 Discussion of topical anesthetic,
demonstration of its use and numbing
action.
Segment 4 Topical anesthetic is applied to the
injection site and its numbing action is
demonstrated.

The CAR L Program

Segment 5 The inj ection procedure is
The CARL ( Computer Assisted Relaxation Le arning) demonstrated to the patient with the
program, developed at the University of Washington cap on the needle.
and tested in a randomly controlled clinical trial in pri­
vate dental offices to establish efficacy, may in the fu­ Segment 6 The inj ection procedure is
ture be available online for p ersonal use to treat dental demonstrated to the patient with the
inj ection fear (He aton et a l . , 20 1 3 ) . The program is a cap off the needle, but the injection is
prime example of the potential for technology to lower not actually given.
barriers to dental treatment by providing patients with
Segment 7 An inj ection is administered to the
a means to begin to address their fear before present­
model patient.
ing to the d e ntal office. The program uses system atic
 C HAPT E R 18 • I N S I G HTS FOR F E A R F U L PAT I E NTS 367

CAS E M A N AG E M E N T for comfo rt. U s i n g the tip of a periodontal p robe, the

tissue at the i njecti on site ca n be touched l i g htly after
Lydia O'Kaine the a p p l ication of the t o p i c a l and ca n be co m p a red
Lyd i a 's treatment p l a n s h o u l d i n c l u d e strate g i e s a n d with t h e tiss u e o n t h e contra l atera l side to d e m o n ­
co p i n g s ki l l s to " treat t h e fe a r fi rst, " before t h e a d ­ strate t h e effective ness o f t h e topica l .
m i n istration of loca l a n est h etic. O n ce s h e is a b l e t o T h e seq u e n ce o f steps fo r a d m i n iste r i n g t h e i n ­
receive a n i nj e cti o n comfo rta b l y, it wi l l be i m p o rtant j e cti o n i s exp l a i n e d to t h e p a t i e n t . I t is s u g g ested
to ass u re h e r that p rofo u n d a n esth e s i a h a s b e e n at­ t h a t a re h e a rs a l w i l l a l l o w Lyd i a to p r a ct i c e h e r
ta i n e d before treatment by using a tech n i q u e such as n ew d e e p b re a t h i n g a n d m u s c l e r e l axati o n co p i n g
the EPT to confirm the effectiveness of the a n esth esia. s ki l l s . S h e is i n t ro d u ce d to t h e u s e of h a n d s i g n a l ­
A p p o i n t m e nts a re sch e d u l e d fo r fo u r q u a d ra nts i n g t o control both t h e sta rt a n d stop o f t h e i njection
of sca l i n g a n d root p l a n i n g . S h e is i n fo r m e d t h a t at p ro ce d u re . She is coached when p r a ct i c i n g her re­
h e r fi rst a p p o i ntment fo r sca l i n g a n d root p l a n i n g , the l axati o n s ki l l s and is i n fo r m e d that o n ce s h e is com­
c l i n i c i a n wi l l i n t rod uce tech n i q ues to h e l p her to be fo rta b l e , s h e can raise her hand to i n d i cate that she
m o re comfo rta b l e d u ri n g i njectio n s . is ready to b e g i n t h e re h e a rsa l . If t h e re h e a rsa l is a
The fi rst appointment b u i l ds ra pport b y d iscussing s u ccess, t h e a ctu a l i nj e cti o n ca n p ro c e e d fo l l owi n g
specific concerns about rece ivi ng i njections. The clini­ t h e s a m e p rotocol w i t h n o c h a n g e s o r s u r p rises fo r
c i a n exp l a i n s that t h e re a re tech n i q ues that patie nts t h e patient.
ca n use to keep themse lves comfo rta b l e d u ri n g an i n ­ O n ce t h e a p p ro p r i ate a m o u nt of a n esthetic has
jecti o n . Lyd ia is q u esti o n e d as to whether o r not s h e b e e n a d m i n iste red , verifyi n g p rofo u n d a n esth e s i a is
has used any re laxation ski l ls i n other situations. Having the n ext ste p . T h e E PT o r u ltraso n i c i n str u m ent may
no previous specific experience, the c l i n ician describes be used with time structuring (count of 1 , 2, 5) to con­
to Lyd i a the ro l e and fu n ction of deep b reath i n g a n d fi rm that t h e a rea to be treated is a d e q u ately a n es­
m u s c l e rel axati o n . T h e c l i n i c i a n d e m o n strates e a c h th etize d . During treat m e nt, if t h e re is a n y i n d i cati o n
ski l l a n d practices them with Lyd i a . It is reco m m ended o f p a i n o r d isco mfo rt, the treatment s h o u l d sto p a n d
to Lyd ia that s h e practice them at home a n d that she a d d it i o n a l a n e st h et i c s h o u l d b e a d m i n i ste r e d , fo l ­
rem e m b e r to use them i n other stressfu l situations. l owed b y repetitio n o f t h e a n esthetic testi ng p rotoco l .
I nfo r m a t i o n i s p ro v i d e d a b o u t the b e n efits of T h ro u g h o ut treatme nt, the c l i n i c i a n m o n itors patient
t o p i ca l a n est h etics and slow a d m i n istrati o n of d ru g s comfo rt, applying behavioral m a n a g e m ent ski l ls.

Chapter Questions c. That clinicians never recommend treatment pa­

· · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · ·
tients cannot tolerate.
1 . There is a new patient in the chair. During appropriate d. That clinicians are professionals and know what is
introductions including handshaking, it is noticed that best for patients.
the patient's hands are clammy and he has perspiration
on his upper lip. He appears very stiff and responds 3. Providing patients with information is an impor­
with a brief yes or no to attempts to engage him in tant means of increasing their sense of control
conversation. When deciding whether or not he is ap­ in the dental environment. When providing in­
prehensive about the dental treatment he is scheduled formation to a fearful p atient about an aversive
to receive, the most appropriate strategy would be to: procedure:
a. Try to distract the patient by offering to let him a. The clinician should explain how steps taken dur­
watch a movie or listen to music. ing the procedure are necessary for the benefit of
b. Get the nitrous oxide-oxygen sedation ready just in the clinician's work.
case. b. The emphasis should be on the scientific rationale
c. Check out the observations made by asking the for the treatment, procedures , materials, and/or
patient about possible concerns regarding dental equipment used.
treatment. c. It is better not to tell the patient what will happen
d. Avoid saying anything about dental anxiety or fear because it might make the patient more fearful.
because it might upset the patient and risk not be­ d. The p r o c e d u r e s h o u l d be d e s crib e d in simple
ing able to get the scheduled treatment completed. terms, including the sensations the patient will
experience s o that the patient knows what to
2. Establishing trust in the patient-clinician relationship expect.
is especially important for fearful dental patients be­
cause they need to learn: 4. It is important to have the skills and confidence
a. How to pay for services provided. necessary to teach anxious and fearful patients how
b. How to be assertive. to relax in the dental chair. When a patient learns
368 SECTION V • S P E C IAL C O N S I D E RATI O N S F O R LOCAL A N E STH ESIA
the physical relaxation skills of deep breathing and
muscle relaxation:
a. The patient benefits by having an active means to
relieve the discomfort, both physical and mental,
which is experienced as a result of anxiety.
b. The clinician benefits because it is easier to achieve
pain control in a relaxed patient.
c. Neither the clinician nor the patient benefits be­
cause these skills are too difficult to teach and to
learn in the stressful dental setting.
d. Both a and b
5. Patients who are fearful of dental inj ections can
benefit from having the opportunity to rehearse the
procedure before receiving the actual inj ection. The
obj ective of the rehearsal is to:
a. Find out if the patient is sincere about wanting to
overcome his dental fears.
b. Allow the p atient to learn how his role and the
clinician's role are synchronized before proceeding
with the inj ection and treatment.
c. D etermine the treatment plan for the patient by
gaining knowledge about which treatments the pa­
tient will be capable of tolerating.
d. Test the patient for intolerance and allergies to lo­
cal anesthetics.
6. Some patients will report a history of receiving dental
care without being adequately anesthetized. They
may not be anxious about the inj ection procedure,
but will be reluctant to proceed with treatment after
the administration of local anesthetics. Despite soft­
tissue signs and symptoms of anesthesia, they do not
believe the teeth are numb. The next step for these
patients should be to:
a. Verify that the tooth is adequately anesthetized by
testing, preferably with an electronic pulp tester
(EPT) , before beginning treatment.
b. Reassure the patient that the correct amount and
type of anesthetic has been used for the area of the
mouth to be treated.
c. Reassure the patient that if pain is felt in the tooth,
treatment will cease the minute the hand signal to
stop is given.
d. Give the patient more anesthetic to be on the safe
side before attempting to proceed with treatment.
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Corah, N. L., O'Shea, R. M., & Ayer, W. A. (1985). Dentists'
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De Jongh, A., Muris, P., Schoenmakers, N. , & Ter Horst, G.
(1995). Negative cognitions of dental phobics: Reliability and
validity of the dental cognitions questionnaire. Behaviour
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Heaton, L. J. , Leroux, B. G. , Ruff, P. A., & Coldwell, S. E. (20 13).
Computerized dental injection fear treatment: A randomized
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· · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · @ · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · ·

I n sig hts fro m Ped i atri c De ntistry

GREG PSALTIS, DDS
SEAN BoYNEs, DMD, MS, DAs

O BJ E CT I V E S KEY T E R M S

• Defi n e a n d d i scuss key terms i n t h i s c h a pte r. age-a p p ro p riate

term i n o l ogy 370
• A p p l y t h e p ri n c i p l es of l o ca l a n esth etic d ru g toxicity to co m ­
b e h aviora l g u i d e l i nes 3 7 1
p ute safe d o ses fo r ped iatric patie nts based o n body we i g ht.
b i l atera l m a n d i b u l a r
• R e l ate effective a n esth esia to the m a n a g e m e n t of p e d i atric b l ocks 3 7 7
b e h a v i o r. m a n d i b u l a r i nfi ltratio n 3 7 7
positive feedback 3 75
• P rov i d e a g e-a p p ro p ri ate exp l a n at i o n s of the l o ca l a n esth esia
posta n esthetic tra u m a 3 72
exp e r i e n ce fo r ped iatric patients.
tri g g e r words 370
• Describe i njection tech n i q u e m o d ificat i o n s fo r s m a l l ch i l d re n . voca l d istraction 3 75
• Recog n i ze a n d m a n a g e posta n esth etic tra u m a .

• D i scuss t h e s u p p o rtive ro l e o f d e n ta l as s ista nts i n s u ccessfu l

a n esth e s i a d e l ivery fo r ch i l d re n .
370 SECTION V • S P E C IAL C O N S I D E RATI O N S F O R LOCAL A N E STH ESIA
CAS E S T U DY
Jaden Harris
J a d e n H a rris, a h e a lthy 4-ye a r-o l d c h i l d , weig h i n g
45 l bs, h a s co m p l eted h i s fi rst visit t o t h e d e ntist.
H e p resented with exte nsive caries and is i n need
of s i g n ifi ca nt resto rative treat m e nt . The fo l l ow­
ing resto rative n e e d s have been d e te r m i n e d fo r
J a d e n , w h i c h wi l l req u i re a n u m be r of loca l a n es­
thetic i njectio n s .
1 . Resto rati o n s : Tooth #A O L, C = D L, J MO,
= =
K MO, M
= =F, S DO =
2 . P u l poto my with sta i n l ess steel crowns: Tooth # B
and L
D u r i n g J a d e n 's i n itial exa m i n ation, he was ve ry co­
o p e rative and a p p e a rs to be receptive to the d e n ­
ta l staff a n d treatm ent.
I ntrod uction
Children perceive their world i n real terms. I f their experi­
ences in a dental facility have been painful and negative,
they are less likely to return as willing patients. On the
other hand, when their experiences have been positive and
pain-free, children can be excellent patients. Young chil­
dren, in particular, will not be persuaded by any possible
benefits of oral health if a visit to the dentist is equated
with pain.
This chapter discusses philosophical and practical
approaches to pediatric dental care. Although many cli­
nicians consider treating children to be challenging, a well­
managed child can be the best patient of the day.
The Ped iatric Denta l Patient
Appropriate Terminology for Successful Anesthesia
The acceptance of care by children and the gratitude of
their parents/guardians and caregivers can be fulfilling.
When treated appropriately with effective and comfort­
able local anesthesia, children will be receptive to care.
Administering local anesthesia for children is not com­
plicated, but it does require specific technical and verbal
skills that can be characterized as significantly different
compared with the skills needed for most adults. Similar to
other techniques in dentistry, local anesthetic techniques
in children are more demanding from a communication
standpoint. In order to achieve optimum success, the pro­
cess of local anesthesia must be a harmonious blend of
skilled delivery and skilled communication.
Unlike adults, children usually do not have precon­
ceived fears about inj ections because they do not know to
expect them. This is especially true when pediatric dental
facilities do not look like other medical facilities. Pediatric
clinicians recognize the advantage of working with a blank
slate instead of with experienced patients. This is the result
of a deliberate process. Part of the success of local anesthe­
sia requires preparation before appointments; moreover,
it requires the involvement of key players other than pa­
tients, including parents/guardians and caregivers. When
key players have been prepared, children are more likely
to be receptive to the actual procedures. It is critical that
key players know and use appropriate terminology in or­
der to avoid frightening children before procedures. When
provided with age-appropriate terminology and rationale
for their use, the odds of successful anesthetic experiences
are significantly increased. Once aware of appropriate lan­
guage, key players can avoid trigger words that can un­
dermine the success of appointments. It is important for
clinicians to be comfortable with the selected words in
order for them to be used with ease. Although some may
consider it silly or even deceptive, pediatric dentists are
keenly aware that appropriate terminology can be a key
factor in the success of dental appointments for children.
For some examples and suggestions of appropriate termi­
nology, refer to Table 19-1 •.
Use of age-appropriate terminology will depend on
the developmental level of the child in addition to the
age. The term sleepy juice, for example, may work well for
preschool patients. As children grow, sleepy juice may no
longer be appropriate and a more mature phrasing such
as I am going to make your tooth and lip fall asleep may be
more effective. The language should be consistent with the
child's level of comprehension and maturity. Later, as the
child ages, the words can reflect increasing maturity such
as I am going to get your teeth numb. In every description,
trigger words such as shot and needle have been replaced
with terms that are more easily accepted by young patients
and are equally useful for adults. The exact ages to make
the transitions are based on individual levels of matu­
rity and understanding. There are no hard and fast rules.
Table 1 9-1 S u g g ested Te rm i n o logy for Ped iatric
Patients
Traditional Term Alternative Term
Local anesthetic Sleepy juice
Needle/syringe Sprayer
Numb feeling Fat/sleepy lip/tongue/cheek
Shot/inj ection Put teeth to sleep*/spray
sleepy juice
Topical anesthetic Jelly stick/"sleepy gel"
Wearing off Lip/tongue/cheek waking up
*Because some children have had their pets "put to sleep," it should
be made clear that the child will remain awake. Only the lip, tongue,
and teeth will "go to sleep" for a while and they will wake up soon.

A relatively easy way to decide is for the clinician to con­
sider the self-impact of the language; in other words, are
the words flowing easily or do they seem a bit silly with a
particular child?
In addition to their concerns for their children, par­
ents/guardians and caregivers often bring their own dental
fears to the child 's appointment. Coaching is essential if
they are present during any portion of a dental visit. It can
be helpful to outline behavioral guidelines for observers.
If they wish to observe, they need to be silent observers,
allowing the child's attention to be focused on the clini­
cian. In this way, parents are not distracting to children and
children are more cooperative.
Awareness of facial expressions, body postures, and
movements can be crucial to the success of local anes­
thesia in pediatric dentistry. This applies equally to office
personnel, parents/guardians and caregivers. Calm, neutral
expressions convey the important visual message that all
is going well. Knitted brows and narrowed eyes or grimaces
can raise concerns that something is amiss. Slow, measured
movements are equally important because they arouse
fewer negative responses. Gentle touches on the shoulders
are reassuring as are gentle hand-holding (as opposed to
tight gripping) and gentle ankle stroking by the parent or
guardian. These nonverbal cues enhance a child's sense of
comfort and safety.
Drug Toxicity and Agent Selection
One of the most important considerations when treating
pediatric patients is the potential for drug toxicity due to
the relatively low body weight of small children and the im­
maturity of their organs. Overall, dose-dependent toxicity
reactions in dentistry are most frequently reported in chil­
dren (Goodson & Moore, 1983; Reynolds, 1987). Several
possible theories as to why excess dosing occurs with this
population include the following: the disproportion of
orofacial anatomy to a child's body weight (larger head
compared with body) that may require larger volumes
of anesthetic to achieve effect; failed anesthesia leading
to multiple inj ections; the inadequacy of pain assessment
scales due to some patients perceiving the numb feeling as
pain; lack of or improper calculation of maximum recom­
mended dose; and/or improper administration procedures
(Armfield & Milgram, 20 1 1 ; Hersh, Helpin, & Evans, 1991 ;
Jastek, Yagiela, & Donaldson, 1995; Moore & Hersh, 20 10).
Whatever the cause, it is important for clinicians to under­
stand the risks associated with anesthetic administration
through sound knowledge and familiarity with anesthetic
agents and their maximum recommended doses. It is im­
perative that clinicians follow appropriate dosing guide­
lines and never exceed the MRD for weight and/or age.
A list of maximum cartridges and dose calculations can
be found in Chapter 5 , "Dental Local Anesthetic Drugs,"
Chapter 6, "Vasoconstrictors in D entistry," and Chapter 7,
" D o se Calculations for Local Ane sthetic S olutions."
B o x 19-1 • addresses maximum dose calculations for
obese children.
C HAPT E R 19 • I N S I G HTS F R O M P E D IATR I C D E NTI STRY 371
Obese children pose unique chall e nges when establi s h­
ing appropriate doses for l o cal anestheti c drugs. When
a young child has the body weight of an adul t , the usual
dosing guidelines not onl y not appl y but likely do
m ay
not appl y. Obesity is recurrentl y reported as a complicat­
ing factor during dental care (Cheymol, 2000; Ebbeling,
Pawlak, & Ludwig, 2002; Pi s chon et al., 2007; Reilly, Boyl e ,
& Craig, 2009). A large amount of adipose tissue in the oral
cavi ty can make it diffi c ul t to identi fy a patient's intraoral
anatomy, an essential assessment for l o cal anesthetic ad­
ministration, and it can decrease the field of vi e w (Reilly,
Boyl e , & Craig, 2009). Obesity al s o al t ers the di s tribution
and elimination of drugs that may influence dosing and
increase the occurrence of complications (Cheymol, 2000;
Ebbeling, Pawlak, & Ludwig, 2002).
Consul t ing standard milligram per pound tables in or­
der to cal c ul a te safe doses for these children can be prob­
lematic. Unfortunatel y, there are no cl e ar-cut, separatel y
stated guidelines for local anestheti c dosing in obese
children. Current medical research, however, has found
that i t i s advi s able to use the ideal body weight (IBW) when
cal c ulating doses of medicinal agents for patients consid­
ered to be obese (Bouillon & Shafer, 1 998; Leykin et al.,
2004). IBW i s a stati stical formula that uses combinations
of height, weight, gender, and/or frame si z e to determine
the optimal weight that i s associated wi t h low mortality for
the average person. There are many IBW formulas avail­
able, the easiest of which to use is the body mass index
(BMI ) (Lemmens, Brodsky, & Bernstein, 2005). The majority
of these formulas are somewhat complicated; however,
tables and/or calculators can be found on the Internet, and
• most smartphone
carriers have IBW phone apps available
for download. These calculators and apps have simpli fied
the IBW process, allowing users to plug in simple informa­
tion such as height, weight, and age to recei v e an IBW
score. It should be noted that while providing guidance
this currentl y is not a veri f i e d tool for safe dose
m axim um
cal c ul a tion in denti stry; therefore, remaining alert to the
development of adverse events and dosing below the
MRD are paramount whenever local anestheti c drugs are
a
� • •d.� i � i �t.e :e•d• t� .t � �s•e•c•h :l � r.e � .• • • • • • • • • • • • • • • • • . IIi
Mepivacaine without a vasoconstrictor (3 % mepiva­
caine plain) seems to be associated with a higher number
of local anesthetic toxicity reports compared with other
agents (Goodson & Moore, 1983 ; Hersh, Helpin, Evans,
1991 ; Moore & Goodson, 1985; Virts, 1999) . This seemingly
higher toxicity may be due to the lack of a vasoconstric­
tor, which increases systemic absorption. Pharmacokinetic
evaluation has revealed that anesthetic blood levels of 3 %
mepivacaine without a vasoconstrictor peak at a more rapid
rate than an equivalent amount of 2% lidocaine, 1 : 100,000
epinephrine and surpass plasma levels by a nearly three­
fold margin, following maxillary infiltration inj ection
(Goebel, Allen, & Randall, 1978, 1980; Moore & Hersh,
372 SECTION V • S P E C IAL C O N S I D E RATI O N S F O R LOCAL A N E STH ESIA
20 10). Considering that 3% mepivacaine plain is frequently
used in pediatric dental care, this can be of concern.
The frequent use of 3 % mepivacaine plain in pediat­
ric dentistry is rooted in reports of mepivacaine having a
shorter duration, which reduces the occurrence of some­
times severe postanesthetic trauma such as lip, cheek, and
tongue biting; however, while the durations of pulpal anes­
thesia with mepivacaine without epinephrine are shorter
than those of 2% lidocaine with 1 : 1 00,000 epinephrine,
the duration of soft-tissue anesthesia for these two agents
has been reported to be nearly identical (Hersh et al., 1995;
Moore & Hersh, 20 1 0 ) . This is key because it has been
demonstrated that soft-tissue anesthesia is responsible for
nearly all biting and chewing injuries.
Postoperative Trauma (Lip/Cheek/Tongue Biting)
A considerable concern with pediatric oral anesthesia is
the occurrence of self-inflicted soft-tissue inj uries, such
as the lip bite shown in Figure 19-1 • · These types of
(A )
(B)
F I G U R E 1 9-1 Lip Tauma. A-Injury occurred within 15 minutes
of leaving the office. B-Patient came the day following treatment
for evaluation . .
inj uries are considered to be some of the most common
local anesthesia complications in children. The incidence
of self-inflicted soft-tissue trauma following local anes­
thetic administration has been reported to occur from
3 % to 16 % of the time (B oynes et al . , 20 1 3 ; Chi et al. ,
2008; College et al. , 2000). The majority of these compli­
cations are considered mild and, occasionally, moderate
in o ccurrence ; however, severe events have b e e n re­
ported, including complete amputation of the lower lip
(Akram, Kerr, & Mclennan, 2008; B oynes et al. , 20 1 3 ) .
D espite every effort of p e diatric dental teams to pre­
vent postanesthetic self-inj ury (trauma) , children will
occasionally test anesthetized oral tissues by biting them,
causing significant trauma. The inj ured tissues can ap­
pear red or red and white, and there may be significant
edema present (see Figure 17-5) (Ashkenazi, Blumer, &
Eli, 2005 ) . If notified of a self-inj ury soon after an ap­
pointment, a cold p ack should be recommended over
the inj ured tissue to reduce swelling. If the notification
occurs the day following an appointment, a warm pack
can be recommended to stimulate circulation and pro­
mote healing. If the patient returns to the dental office
or clinic, anecdotal reports have suggested that admin­
istering 0 . 1 2 % chlorhexidine solution to the outer area
of the tissue trauma with cotton-tipped applicators has
yielded improved healing. Antibiotics are usually not in­
dicated and are prescribed only in the unlikely event of
infection (Ashkenazi, B lumer, & Eli, 2005 ) . If the inju­
ries are first evaluated by physicians, it is not unusual for
them to prescribe antibiotics because of the rather dra­
matic clinical appearance of these inj uries, which closely
resemble infections. It should be noted that the use of
the alpha adrenergic receptor antagonist, phentolamine
mesylate (Ora Verse ® ) (Septodont, Inc, Lancaster, PA) ,
may provide a n option i n decreasing soft-tissue inj uries
by decreasing the duration of soft-tissue anesthesia (see
Box 19-2 •) .
Perspective on Articaine for Pediatric Patients
In general, articaine 4 % with epinephrine 1 : 10 0 ,0 0 0 or
1 :200,000 demonstrates an appropriate level of safety
and efficacy for use during pediatric dental care. Onset
time and duration of action are suitable for clinical use
and comparable to other local anesthetic agents used in
pediatric dentistry (Malamed, Gagnon, & Lablanc, 2000;
Ram & Amir, 2006). Worldwide, articaine has acquired the
maj ority of the dental market in many countries (Paxton
& Thome, 20 1 0 ; Schertzer, 20 0 0 ) . In addition, it is used
with frequency in pediatric care in many countries includ­
ing the United States (B rickhouse et al., 2008; Wright,
Weinberger, & Friedman, 1989).
Articaine is believed by some to be more effective in
its ability to diffuse through bone compared with other
amide anesthetic solutions, thus having improved efficacy
especially as it relates to mandibular infiltration (Ab­
dulwahab et al. , 2009; Kanaa et al. , 2006; Vree & Gielen,
2005 ) . In 20 1 0 , a meta-analysis evaluating 1 0 published
 C HAPT E R 19 • I N S I G HTS FROM P E D IATR I C D E NTI STRY 373

OraVerse was granted Food and Drug Administration ap­

proval for dental application in May 2008 with the indi c a­
tion of soft-ti s sue anesthesia reversal as a resul t of dental
l o cal anestheti c administration (Hersh & Li n demeyer, 2010).
The unique packaging is shown in Figures 19-2 • and 1 7-5.
It should be noted that current FDA approval does not
incl u de the use of OraVerse in children weighing l e ss than
33 l b s or younger than 6 years of age (OraVerse Package
Insert, 201 1). The acti v e ingredient of OraVerse i s phentol ­
amine mesylate (PM), an al p ha adrenergic bl o cker. Phen­
tolamine mesylate opposes the effects of norepinephrine
and epinephrine, maintaining blood vessel dilation and not
allowing the alpha receptors to ini t i a te bl o od vessel wall
constri ction (Chobanian et al., 2003). Its use in denti stry
relates to the init iation or progression of vasodilation in FIGURE 1 9-2 OraVerse Anesthesia Reversal Agent.
areas where local anestheti c was admini s tered, enhancing OraVerse is packaged with unique green labels and blue
the cl e arance of anestheti c from the injection si t e (Moore
et al., 2008). Pivotal research concl u ded that the use of
stoppers to avoid confusion with local anesthetic cartridges.

phentolamine mesylate reduced soft-ti s sue anesthesia Source: Courtesy of Septodont, USA.

and hastened pati e nts' return to normal l i p sensation by anesthesia, the ability to reduce these complications
approximatel y 1 . 4 hours following mandibular bl o ck and would likel y improve the dental experience. A theoreti c al
maxillary infil t ration injections, and improved the return link has been inferred between the reversal of soft-tissue
to normal tongue sensation by approximatel y 1 .1 hours anesthesia and a reduction in soft-tissue injury (Hersh et
foll o wing mandibular block injections (Hersh et al., 2008; al., 2008; Hersh & Lindemeyer, 201 0; Moore & Hersh, 201 0;
Tavares et al., 2008). Further anal y si s revealed that the Tavares et al., 2008). A recent study evaluating complica­
percentage of pati e nts that experienced an earl i er return tion rates wi t h local anestheti c administration and reversal
to normal lip sensation was signifi c antl y higher for those in a portable school - based dental deli v ery system reveal e d
recei v ing OraVerse during the study (see Figure 1 9-3 •) an improvement in safety outcomes when phentolamine
(Hersh et al., 2008). mesyl a te was admini s tered to pediatri c dental patients
In light of the frequency of sel f-inflicted and some­ (Boynes et al., 201 3). The patients who did not recei v e
times severe soft-ti ssue trauma following dental l o cal PM in thi s study experienced the majority of soft-tissue
Mandible Maxilla
(n=244) (n=240)
1 00 /
l l
�0 75 �0 75 v ...
"'� "'�
2:- 2:- ..
"'5 "'5
.....
:!
50 .....
:!
50 v
1: 1:
·!a .!
· 75
�
/--
0.. 59
...
0 25 0 25 v
� �

0 /
7
2 27
�
I
25
/
0-30 3 1 -60 6 1 -90 0-30 3 1 -60 6 1 -90
Time after Injection (min) Time after Injection (min)

I D OraVerse D Control (sham injection) I

FIGURE 1 9-3 Percentage of Complete Return of Lip Sensation with Ora Verse
Source: "Percentage of Complete Return of Lip Sensation with OraVerse®." Copyright © by Septodont USA. Used by permission
of Septodont USA.
374 SECTION V • S P E C IAL C O N S I D E RATI O N S F O R LOCAL A N E STH ESIA
injuries and were more likely to experience a complication.
l t should be noted that overall complication rates for all
groups invol v ed i n the anal y si s were considered low. lnves-
tigators concluded that the safe administration of dental
care wi t h l o cal anesthesia is clearl y feasible wi t h or wi t hout years of age and more than 66 lbs; and one-half cartridge
the admini s tration of PM; however, the use of PM improves
safety outcomes, especiall y as it relates to sel f-inflicted
soft-tissue injuries.
OraVerse is deli v ered using the same l o cation(s)
and same technique(s) used for the administration of
local anesthetic. Dosing of the agent is at a 1 :1 ratio.
For example, i f one-half a cartridge of local anesthetic is
: admini s tered, one-hal f of a cartridge of OraVerse should
.............. .................... ... .............. .............................•
. .
studies, involving 1 , 146 subj ects, evaluated the efficacy
of articaine formulations in comparison to lidocaine
2% w/epinephrine 1 : 1 0 0 , 0 0 0 (Paxton & Thome, 20 1 0 ) .
The meta-analysis implied a distinct advantage to the
use of articaine. As it relates to pediatric care, articaine
may decrease the likelihood of needing additional inj ec­
tions while providing a dependable drug for mandibular
infiltration, especially in adole scents. Articaine pack­
age inserts state that safety and efficacy have not been
evaluated in subj ects under the age of four, which has led
many providers to avoid articaine in this patient popula­
tion (Septodont, 2010).
As with all anesthetics, clinicians should have a sound
knowledge of the risks and benefits of any drugs that are
used and should communicate these risks and benefits to
patients, parents/guardians, and caregivers. An ongoing
point of controversy within dental delivery is the rare oc­
currence of paresthesia. Persistent numbness after dental
care is extremely rare and, according to some authorities,
is most often the result of surgical trauma (B agheri et al. ,
20 10). Of the five inj ectable anesthetic agents, prilocaine
and articaine, both 4% solutions, are most often associ­
ated with reports of paresthesia. A recent publication ,
however, stated that because of t h e limitations a n d bias
of currently available research there is no absolute proof
that a cause and effect relationship exists between these
4% solutions and paresthesia (Moore & Haas, 20 1 0 ) ;
however, i t has been suggested that caution may be ad­
visable when blocking the mandible with 4% drugs be­
cause the maj ority of p aresthesias are associated with
direct mandibular block inj ections. During the course of
treatment, it is the responsibility of clinicians to under­
stand the risks versus the benefits of different agents and
to provide patients with the opportunity to ask questions
concerning care. More information on the pharmacology
and adverse occurrences with articaine formulations can
be found in Chapter 5 , "Dental Local Anesthetic Drugs,"
and Chapter 17, " Local Anesthesia Complications and
Management."
be admini s tered using the same technique for admini s tra-
tion. Maximum recommended doses (MRD) for OraVerse
are as follows: two cartridges for adul t s and adolescents
1 2 years of age and older; one cartridge for patients 6-1 1
for children 6 years of age and older weighing 33-66 lbs
(Ora Verse Package Insert, 201 1 ). The adverse reactions
reported during the clinical trials occurred less than 3%
of the time. The most commonl y observed include post-
procedural pain, injection-sit e pain, tachycardia, and
headache (Hersh & Lindemeyer, 201 0). As wi t h all agents
that are used in practice, the package insert should be •
reviewed at regular intervals.
. . .
Use of Topical Anesthetics
Like adults, children want their dental visits to be as com­
fortable as possible. The youngest children may not be
able to verbalize this desire, but they are definitely able
to make it known when things are not comfortable. The
anesthetic sequence typically sets the tone for an appoint­
ment. It is important that procedures start well. Topical an­
esthetic techniques are effective for preventing discomfort
during needle penetration.
Topicals are available in a variety of flavors. Allow­
ing children to choose a flavor and to actually smell the
topical before placement can create a sense of familiar­
ity with the agent and is likely to put the child at ease.
Gels and ointments tend to be easy to control and place
with cotton applicators. They pose far less concern for
potential aspiration compared with liquids and sprays.
If using aerosol sprays, metered dose systems are advis­
able (Palm, Kirkegaard, & Poulsen, 2004) . See Chapter 8,
" Topical A n e sthetics." Rese arch ers have fo und that
some children prefer topical anesthetic patches (Wu &
Julliard, 2003 ) .
D rying t h e mucosa with a 2 x 2 cotton pad before
placement of the topical enhances its effectiveness. It is im­
portant to allow adequate time for topicals to take effect.
The onset time for most agents ranges between 30 seconds
and 5 minutes (Pinkham et al. , 1994) . Inj ecting before topi­
cals have a chance to work risks pain and management dif­
ficulties. B ox 19-3 • provides examples of other uses for
topical anesthetics for children.
Topical anestheti cs may also be useful for comfortable rub­
ber dam cl a mp placement and to anestheti z e the tissue
• tretaining eextremel y mobile primary teeth to allow children •
th i et r t c t h o e
: . � :���� . . � : :� . � �� ���� : ��� � • • .� ." . • • • • • • • •

Management Techniques for Pediatric
Dental Injections
From the perspective of technique, inj ection steps for
children do not differ significantly from those for adults.
Because children are more likely to react and move dur­
ing anesthetic procedures, managing their behavior during
inj ections is considered to be more of an art form than a
technique. Mastering this art benefits both clinician and
child and sets the stage for a positive dental experience.
In particular, it is important to:
1. Prepare the child with appropriate terminology.
2. Prepare child with show-tell-do communication (dem­
onstrate and explain before doing) .
3. Use a tone of voice that is reassuring yet assertive
enough to prohibit bargaining.
4. Use passive restraint. The dental assistant places one
hand over the child's hands (which should be placed
on the child's stomach) in case of quick reactions by
the child to the procedure. The other hand is placed on
the child's forehead to guard against sudden or unex­
pected movements (see Figures 19-4 • and 19-5 •).
5. Pass the syringe out of the child's line of sight.
6. Some clinicians may use pre-warmed anesthetic car­
tridges (see Box 19-4 •) .
7. Describe t h e sensations of anesthesia t h e child will
feel before onset. For example, at the onset of a man­
dibular block, an appropriate comment might be that
the side of the tongue will start to tickle.
8. Always inj ect the solution slowly, administering a few
drops ahead of the needle to allow anesthesia to pre­
cede the tip of the needle.
FIGURE 1 9-4 Preparing for Unexpected Movements. The
child is asked to place the hands on his or her stomach. The as­
sistant places one hand over the child's hands to respond in case
of quick reactions by the child during the injection.
Source: Courtesy of Greg Psaltis, DDS.
C HAPT E R 19 • I N S I G HTS FROM P E D IATR I C D E NTI STRY 375
FIGURE 1 9-5 Gently Stabilize the Child's Head. The assistant
places one hand on the child's forehead (in addition to over
the child's hands) to guard against sudden or unexpected move­
ments during the inj ection.
Source: Courtesy of Greg Psaltis, DDS
9. Explain to parents/guardians and caregivers, and to
the child when appropriate, that the lips, cheek, tongue,
and teeth will remain asleep for a period of time after
the appointment is over. Be sure they understand the
risks of postoperative traumatic injury.
10. When indicated, comfortable palatal anesthesia can be
achieved by first completing a facial infiltration, then
penetrating slowly through the interdental papilla, and
administering a few drops of solution ahead of the nee­
dle until the palatal tissues have been initially numbed.
Following these steps, proceed with standard palatal
inj ection techniques (see Chapter 13, " Inj ections for
Maxillary Pain Control II - Palatal Approach").
Behavioral Management Techniques
Two useful behavior management techniques include
vocal distraction and positive feedback. Vocal distraction is
the process of keeping the child focused on the clinician's
voice rather than on the dental procedures. Distraction
can be created by a calm, reassuring, and informative nar­
rative that is continuous throughout the procedure. When
children have a focus other than an actual procedure,
inj ections are more likely to succeed.
Other means of distraction can include a variety of
stimuli. One device designed for this is called B uzzy ®
(MMJ Labs LLC, Atlanta, GA) . This simple toy-like de­
vice provides audible (buzzing sound) and sensory (cold
and vibration) stimuli. The vibration and cold may act as
gate control stimuli as well as cognitive distraction. Some
children may do well with these types of distraction (see
Figure 19-6 • ) .
Positive feedback for specific desirable behaviors
can also be helpful. General statements such as "what a
good patient you are or you're being so brave today" are
less helpful compared with statements regarding specific
376 SECTION V • S P E C IAL C O N S I D E RATI O N S F O R LOCAL A N E STH ESIA

Warming cartridges before use is intended to reduce the

incidence of pain on injection. Some suggest the practi c e
may be effecti v e (Bainbridge, 1 991 ; Courtney, Agrawal, &
•

Revington, 1999). One meta-anal y si s determined that

warming had a signi ficant impact on reducing percei v ed
injection pain and should be done before administration (A)
(Hogan et al., 201 1).
Others hold li ttle esteem for the practi c e, especiall y
when the ri s k of administering overheated solution is in­
troduced to an otherwi s e negl i gibl e risk of tissue damage
due to cartridge temperature (Malamed, 201 3). In addition,
vasoconstri ctors in warmed cartridges may l o se some of
their effecti v eness, particul a rl y if they have been stored in
warming devices for extended periods (Malamed, 201 3).
When the practi c e of warming is utili z ed, approved el ec­
tronicall y controll e d medical devices are suggested in order
to avoid excessive temperatures (see Figure 19-7 •l. Car­
tridges shoul d not be stored in heating devi c es for l o ng peri ­
ods of ti m e regardl ess (DiMarco & Bassett, 201 2). It has been
noted that even after having been subjected to repeated
sterilizati o n cycl e s, both lidocaine and epinephrine remained
effective as l o ng as recommended temperature cycl e s were
followed (Courtney et al., 1999). However, manufacturers will
o r t e ve s of t l t n s •

� : ;�� �� � � : � . ��e�� . ��� · · ��� �� �� � :� . .

.

• • • • •

aspects of the procedure that are going well. For example,

the clinician might say, "thank you for holding your head
so still for me." Positive feedback becomes a learning tool
for the child. Children learn how to be successful patients
and how to be active participants in the procedure when
feedback praises them for behavior that is beneficial.
Additional patient management strategies that may be
useful when treating children can be found in Chapter 2, (B)
"Fundamentals of Pain Management."

I njection Tech n iq u e Va riations

for Ch i l d ren
Showing or Hiding the Needle
Although some clinicians advocate showing needles to
children, many young patients do not respond favorably
to this approach. Children are far less likely to respond to
something they cannot see. This technique does not rely on
favorable responses from children. During the anesthetic
procedure, continuous and calming communication with
the child will usually gain his or her cooperation. This is an
example of vocal distraction. Occasionally, a child may ask
to see the needle after the inj ection, at which time the cli­
nician can hold the syringe in the child's view, concealing
the capped needle in the palm while pointing to the empty (C)
cartridge, explaining that it is where the sleepy juice came FIGURE 1 9-6 Buzzy. Device designed to stimulate a gate­
from. Children are usually satisfied with this explanation. control response, and provide cognitive and sensory distraction
Although it has been suggested that children have a prefer­ with both audible and sensory stimuli (buzzing sound, vibration
ence for the appearance of the Wand device (see Chapter 9, and cold).

FIGURE 1 9-7 Electronically Controlled Cartridge Warming
Device.
Source: Courtesy of Practicon.
"Local Anesthetic Delivery Devices"), the simplest way to
avoid the issue is to keep all inj ection armamentarium out
of the child's eyesight (Kuscu & Akyuz, 2006).
Anatomical Differences
Primary tooth roots are typically shorter than the roots of
their permanent successors. Basic techniques for pediatric in­
jections vary somewhat compared with the same techniques
for permanent teeth because of the decreased insertion depths
needed. Although the depths are shallower, the penetration
sites for primary teeth are analogous to the sites of penetra­
tion for permanent teeth in most cases; for example, the tar­
get for a primary maxillary infiltration is above the apex of
the root. Extra-short (10 mm) needles that would usually be
too short for maxillary adult infiltrations may be adequate for
reaching this site in many children.
In inferior alveolar nerve blocks, the position of the
mandibular foramen in children is inferior to its eventual
(A)
FIGURE 1 9-8 Mandibular Infiltrations. Mandibular infiltrations can be useful for basic restorative procedures in young children due
to their thinner cortical plates and very porous bone, allowing for easy diffusion of anesthetic solutions.
Source: Courtesy of Greg Psaltis, DDS and Royann Royer RDH.
C HAPT E R 19 • I N S I G HTS FROM P E D IATR I C D E NTI STRY 377
adult location. Studies have demonstrated that this occurs
because of the remodeling of the ramus during growth
(Kanno et al. , 2005).
B I LAT E RAL M AN D I B U LAR B L O C K S When planning treat­
ment for children, it is considered beneficial to treat half
a mouth at a time in order to minimize the total number
of appointments. One way to accomplish this is to deliver
bilateral inferior alveolar blocks at one appointment, com­
pleting mandibular treatment. Many consider this prob­
lematic because of the lack of control of oral functions. A
recent study however found that the incidence of postoper­
ative lip-biting actually decreased in children who received
bilateral mandibular blocks compared with those who re­
ceived unilateral blocks (College et al. , 2000). It was specu­
lated that, following a unilateral mandibular block, children
are more inclined to test the funny (numb) side by chewing
their lips. Further research is needed on this topic, however,
before it can be considered a standard of care.
Mandibular Infiltration
Pediatric patients have thinner cortical plates and more
porous bone, allowing for easy diffusion of anesthetic
solutions. For this reason, mandibular infiltrations are
commonly used for many simple restorative procedures
(Malamed, 20 1 3 ) . Some mandibular extractions can also
be accomplished with infiltrations. When children require
pulpotomies or stainless steel crowns, the technique is less
reliable and mandibular blocks remain the best choice.
The mandibular infiltration technique is very similar
to the technique for maxillary infiltration. Once adequate
topical anesthesia has been obtained, the patient's lip is
retracted and the tip of the needle is placed into the mu­
cobuccal fold. With the lip retracted upward, the tip of the
needle can be enveloped or captured by the tissue. This
will minimize sensations due to needle penetration. Figure
19-8 • demonstrates an infiltration of a mandible molar.
Only a small volume of anesthetic (0.6-0.9 mL per tooth
or one-third to one-half of a cartridge) is necessary to
(B)
378 SECTION V • S P E C IAL C O N S I D E RATI O N S F O R LOCAL A N E STH ESIA
CAS E M A N AG E M E N T
Jaden Harris
T h e fo l l ow i n g strate g y fo r m a n a g i n g J a d e n 's treat­
ment is suggeste d :
1 . R esto rati o n s : Tooth # A = O L, C = D L, J
K M O , M F, S D O
= = =
2 . P u l potomy w i t h sta i n l ess ste e l crow n s : Tooth # B
and L
Fi rst a p p o i ntme nt: B e g i n t re a t m e n t i n t h e m a n d i ­
b l e fo r # K, L , a n d M u s i n g 1 . 8 m l 2% l i d o ca i n e with
epinephrine.
Rationale: Sta rti ng with the m a n d i b u l a r l eft q uad­
rant ca n have the advantage of ass u r i n g p rofo u n d
a n esth esia fo r a fi rst-t i m e experience. Beg i n n i n g
with a n e rve b l ock tech n i q u e c a n ass u re comfo rt
i n t h e p l a c e m e n t of t h e r u b b e r d a m , e s p e ci a l ly
the c l a m p . Also, this q u a d rant is o n e of two q u a d ­
r a n ts i n g reatest n e e d of treatm e n t . Oth e r fa c­
tors being e q u a l , this strategy add resses both the
prio rity needs of the patient and the re l i a b i l ity of
a n esth esia .
M a ny c l i n icians p refe r t o sta rt with t h e maxi l la , as­
s u m i n g that i nfi ltrati o n s a re e a s i e r i nj e cti o n s fo r
c h i l d re n to to l e rate. T h e seq u e n ce of b eg i n n i n g
treatment with a nesthetic proce d u res i n t h e m a n ­
d i b l e m a y s e e m u n us u a l to s o m e ; h oweve r, t h i s
c a n b e a v e ry s u ccessfu l a p p ro a c h . T h e fa ctor
that i n fl u e n ces t h i s seq u e n ce of a p p o i n t m e nts is
obtain adequate local anesthesia. The primary advantage
of this technique is that anesthesia of large areas of the lip
and tongue can be avoided. It has been suggested by some
that soft-tissue trauma may not be reduced by the use of
mandibular infiltration anesthesia (American Academy of
-�.h. ti).P.t.E! r. . 9.l1.��� i () .Jl � . . . . . . . . . ...... . . . ....... . . . .. . .. . . . . . . . ... .
_ _
1 . Why is it generally more critical to consider toxicity of
local anesthetics in pediatric patients than in adults?
a. Children react differently to local anesthetic agents
than adults
b. Local anesthetic doses are based on body weight
c. Appropriate anesthetic agents for children are dif­
ferent than for adults
d. Crying and screaming may allow more rapid anes­
thetic uptake
2. How does excellent anesthesia serve as a manage­
ment tool for children?
a. Restorative procedures become tolerable, if not
pain-free
r u b b e r d a m c l a m p p l acement. M a ny ch i l d re n d o
very we l l w i t h proce d u res u nt i l t h e p l a ce m ent of
= MO, the c l a m p . M a n d i b u l a r b l ocks may be bette r to l ­
e rated b y ch i l d ren than p a l ata l i njections t o avoid
d isco mfo rt fro m c l a m p p l ace m e nt. Therefore, th is
s e q u e n ce may b e p refe rred to p rovi d e a m o re
favora b l e fi rst a n esthesia expe rience.
Second appoi ntment: #A, B, and C u s i n g 1 . 8 ml 4%
a rtica i n e with e p i n e p h r i n e .
Rationale: T h i s is the oth e r " h i g h prio rity" q u a d ­
r a n t . If trust h a s now been esta b l is h e d , t h e c h i l d
wi l l m o re l i ke l y accept t h e p a l at a l i nj e cti o n n e c­
ess a ry to m a ke c l a m p p l acement comfo rta b l e fo r
tooth #A. P a l ata l a n esthesia is a l so i n d i cated fo r
t h e m ax i l l a ry sta i n l e ss ste e l crow n s . Oth e r a p ­
p roaches t o p rovid i n g a n esthesia fo r pa l ata l g i n ­
g iva a re d iscussed i n C h a pter 8 .
Third appointment: # J a n d S, fo r t h i s a p p o i nt m e n t
use a tota l o f 1 . 2-1 . 8 m l 4% a rtica i n e w i t h e p i n e p h ­
rine for i nfi ltrati ng both J a n d S .
Rationale: By m a ki n g t h e fi n a l resto rative v i s i t
b r i ef, w i t h s i m p l e p r o ce d u res, t h e c h i l d i s l e ft
with t h e m e m o ry of a s h o rt, easy a p p o i nt m e n t .
B e c a u s e both restorat i o n s req u i re i n fi ltrati o n s ,
0 . 6-0 . 9 m l p e r t o o t h w i l l res u l t i n a d e q u a te
a n esthesia .
Pediatric D entistry, 2006-2007) . Others disagree, finding
the incidence of lip-biting to be reduced when techniques
with more limited areas of anesthesia such as infiltrations or
PDLs have been administered versus nerve blocks (Ashke­
nazi et al., 2005).
b. Clamp placement for rubber dam is simplified
c. Quadrant (or half-mouth) treatment can be com­
pleted in one visit
d. All of the above
3. In which of the following ways do anatomical
variations affect the choice of inj ection techniques for
children?
a. Roots of primary teeth are generally shorter than
permanent tooth roots
b. The cortical plate is thicker and less porous in chil­
dren than in adults
c. The inferior alveolar foramen is often more supe­
rior in children than adults
d. All of the above

4. Which of the following describe ways in which an as­
sistant can play a vital role in the successful adminis­
tration of local anesthetics to children?
a. Showing the patient the needle to prepare the
child
b. Calming the parent during the inj ection by explain­
ing what is happening
c. Placing one hand on the child's forehead and the
other on the child's hands for safety
d. None of the above
5. Which of the following are benefits of using age­
appropriate terminology and specific positive feedback
during the successful anesthetic administration in
pediatric patients?
a. Using understandable terms to demystify the
child's experiences
b. Using specific positive feedback teaches children
what is expected and going well
c. Avoiding frightening (or "trigger") words to reduce
the chance of resistance
d. All the above
6. Which of the following is true when considering inj ec­
tion techniques in children?
a. Mandibular infiltrations rarely work for children
b. D eposition of anesthetic solutions for mandibular
blocks are more inferior compared with adults
c. Long needles are usually necessary
d. All of the above are true
7. When children traumatize soft tissues immediately
following inj ections, what is the best management?
a. Place a cold pack immediately
b. Place a warm pack immediately
c. Always put the child on an antibiotic for infection
d. a and c
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Visit www.pearsonhighered.com/healthprofessionsresources to access the student resources that accompany
this book. Simply select Dental Hygiene from the choice of disciplines. Find this book and you will find the
complimentary study tools created for this specific title.
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Palm, A. M., Kirkegaard, U. , & Poulsen, S. (2004, November/
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tions: Quantitative reviews. Dental Clinics ofNorth America,
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· · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · ® · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · ·

I n sig hts fro m S peci a lti es : O ra l S u rg e ry,

P.e r.iodo m�i cs, a m d Em d·o·d·o·m�i·cs
MELANIE LANG, DDS, MD
WILLIAM c. LUBKEN, DMD
MARK HOCHMAN, DDS
ALBERT "ACE" GOERIG, DDS, MS

O BJ E CT I V E S KEY T E R M S

• Defi n e a n d d i scuss key terms i n t h i s c h a pte r. h e m ostasis 385

i nte rpa p i l l a ry i njections 385
• Describe the choice of need les in o ra l a n d maxi l l ofa cia l s u rgery.
l ntra F i ow 386
• D i scuss the po p u l at i o n s w h o a re at g reatest risk fo r l o ca l a n es­ i ntraosseous i njections 386
thetic toxi city. i ntra p u l p a l i njecti on 387
• Exp l a i n t h e effects of i nfl a m matio n/infecti o n on l o ca l n e e d l e tract infecti ons 382
Sta b i d e nt 386
a n esth etics.
X-Tip 386
• D i scuss a l l e rg i c res p o n ses with l o ca l a n esth etics .

• Determ i n e treatm ent o pti o n s fo r patie nts with tru e a l l e rg ies to

l o ca l a n esth etics .

• D i scuss i n fe r i o r a l ve o l a r n e rve b l ock com p l i cati o n s , i n c l u d i n g

n e rve I nJ U ri e s .

• D i scuss c o n c e r n s w i t h use of 4% l o ca l a n esthetic a g e nts.

• Determ i n e effective treatment options for m a n d i b u l a r a n esth esia
i n periodontics.

• Determ i n e effective treatm e n t o pti o n s fo r m a xi l l a ry a n esth esia

i n periodontics .

• D i scuss h e m o stasis i n periodo ntics.

• D i scuss ways i n which a n esth eti c c h a l l e n g e s a re a d d ressed in

e n d od o ntics.

• D i scuss the ro l e of to p i ca l a n esth etics i n endodontic a n esth esia.

• D i scuss tech n i q u es fo r m a n a g i n g excessive fea rs i n e n d o d o n ­

tic patie nts.

• D i scuss the ben efits of i ntraosse o u s and i ntra p u l p a l a n esth e s i a

tech n i q u e s i n e n d od o n tics.

• D i scuss p reca u t i o n s fo r t h e u se of vasoco n stri ctors i n i n traos­

seo u s and i n tra p u l p a l a n esth esia tech n i q u e s.

381
382 SECTION V • S P E C IAL C O N S I D E RATI O N S F O R LOCAL A N E STH ESIA
I ntrod uction
This chapter provides insights from three additional spe­
cialty areas in dentistry. The purpose of presenting multi­
disciplinary insights is to develop an understanding of the
importance of local anesthesia in these settings and the
unique challenges encountered from the point of view of
dental specialists.
I nsig hts from O ra l an d M axi l lofacial
S u rgery
Local anesthesia is critical to the practice of oral and maxil­
lofacial surgery (OMFS). It would be impossible to provide
effective and successful intraoperative or postoperative pain
management without it. Many referrals to OMF surgeons
are motivated by local anesthetic failures in other settings,
such as patients for whom anesthesia was unsuccessful.
Other patients are referred because of complications related
to local anesthesia or because they have serious concurrent
medical conditions that complicate its administration.
Specific challenges encountered in OMFS local anes­
thesia administration include safe management of patients
of all ages with diverse medical backgrounds who may
require extensive treatment (e.g. , full mouth extractions).
Minor to life-threatening infections are also encountered.
Achieving adequate local anesthesia in the presence of
these infections while limiting the potential for needle
tract infections (infections spread along needle pathways)
and compensating for anatomical difficulties with asso­
ciated trismus and airway patency concerns are serious
and significant challenges encountered by OMF surgeons
(Maestrello, Abubaker, & Benson, 2007).
Although inhalation and intravenous sedation, as well
as general anesthesia, are common in OMFS, effective lo­
cal anesthesia plays an important supplemental role, assist­
ing in providing effective intraoperative pain management
and allowing for lighter general anesthesia and sedation.
Local anesthetics with vasoconstrictors also provide he­
mostasis, whereas longer-acting local anesthetics provide
postoperative pain control and a more comfortable transi­
tion to oral and intravenous analgesics.
Selection of Armamenta r i u m
Oral and maxillofacial surgeons typically use the five in­
j e ctable local anesthetics available to other dental spe­
cialists and clinicians, although some may occasionally
access other local anesthetic drugs, such as ropivacaine
and levobupivacaine.
Desirable Local Anesthetic Properties
Whether considering surgical procedures performed by
oral surgeons, periodontists, endodontists, pedodontists,
or general practitioners, an understanding of the onset
times, durations of action and relative potencies of specific
local anesthetics is important in the surgical setting. See
Chapter 4, "Pharmacology Basics," for more detailed ex­
planations of these properties.
D U RAT I O N B upivacaine and tetracaine are both highly
protein bound and therefore have long durations of action.
Long-acting local anesthetics are frequently used in OMFS
to assist with initial postoperative analgesic management.
B upivacaine, when used for regional nerve blocks, lasts
an average of 5 hours in the maxilla and 8 hours in the
mandible.
POTE N CY Lidocaine and bupivacaine are frequently used
concurrently in OMFS. Lidocaine provides a rapid onset
and bupivacaine provides a long duration. B ecause bupi­
vacaine is the more potent local anesthetic, a 0.5 % solu­
tion will obtain comparable depths of local anesthesia
compared with a 2 % solution of lidocaine.
N E E D LE C H O I C E In OMFS, 25- or 27-gauge long needles
are typically used for all local anesthetic techniques. Long
needles are preferred because they allow all types of den­
tal inj ections to be completed without changing needles.
Loca l Anesthetic Toxicity
and Maxi m u m Dosing
I n the OMFS setting, clinicians often face local anesthetic
challenges due to the extent of treatment or to associated
infections, either of which may increase the difficulty of
achieving adequate local anesthesia. It is therefore criti­
cal for clinicians to have a thorough understanding of the
clinical manifestations of local anesthetic toxicity as well
as an ability to quickly and accurately calculate the maxi­
mum dosing of the local anesthetic they are using.
Pediatric Considerations for Dosing
In the pediatric population, it is easier to exceed maximum
doses of local anesthetics because of smaller body mass.
In general, the pharmaceutical industry is not required to
perform drug testing on the pediatric population. Varia­
tions in age and weight make the manufacturers reluctant
to recommend maximum pediatric doses. This leaves the
selection of pediatric doses to the clinical judgment of cli­
nicians after performing standard calculations and taking
into account health status, including the immaturity of pe­
diatric organ systems.
A preferred local anesthetic in OMFS that is safe
for use in the pediatric population is 2% lidocaine with
1:100,000 epinephrine. For in-depth discussions on pediatric
dosing, see Chapter 7, "Dose Calculations for Local Anes­
thetic Solutions," and Chapter 19, "Insights from Pediatric
Dentistry."
Anxiety and Fea r
Oral or intravenous sedation is frequently used in OMFS
to reduce anxiety in patients who have difficulty achiev­
ing profound local anesthesia. B enzodiazepines such as
 C HAPT E R 20 • I N S I G HTS FROM S P E C IALTI E S : O RAL S U R G E RY, P E R I O D ONTI C S , A N D E N D O D O N T I C S
triazolam, midazolam, diazepam, lorazepam, and alpra­
zolam are most often prescribed or administered because
they have relatively quick onsets and wide margins of
safety. Unfortunately, in addition to their adjunctive role
in reducing perioperative anxiety, benzodiazepines can
also decrease the toxic threshold of any local anesthetics
administered. Specific strategies for managing dental anx­
iety and fears can be found in Chapter 2, "Fundamentals
of Pain Management," and Chapter 18, "Insights for Fear­
ful Patients."
Vasoconstrictor Considerations
The concurrent use o f a vasoconstrictor can allow for an
increase in the maximum dose that can be safely admin­
istered. Epinephrine also has the potential to counteract
vasodilating �2 receptors, which allows it to act as a pure
a-adrenergic stimulant accounting for its usefulness in
providing excellent hemostasis in surgery.
Adverse reactions can occur when administering vaso­
constrictors with a number of other drugs, including tricy­
clic antidepressants (TCAs) , beta-adrenergic antagonists,
volatile anesthetics, cocaine, and other vasoconstrictors.
This potential is of particular concern for psychiatric pa­
tients, cardiac patients, and suspected drug users.
Tricyclic antidepressants (TCA ) , such as amitripty­
line, increase the availability of endogenous norepineph­
rine. This can lead to an exaggerated response in heart
rate or blood pressure when epinephrine or levonordefrin
is administered with local anesthetics. TCAs also block
the muscarinic and a-adrenergic receptors, which directly
depress the myocardium. This concern is greatest during
the first 14-21 days of TCA use and appears to have the
most significant effect when levonordefrin and imipramine
(Tofranil) are used concomitantly. The same concern was
originally thought to exist with monoamine oxidase inhibi­
tors, but this is no longer thought to be the case.
A potential dysrhythmic effect exists between the in­
halation anesthetic agent halothane (Fluothane) and epi­
nephrine or levonordefrin through stimulation of both
alpha and beta receptors. The greatest potential for this
adverse reaction exists in the first 10 minutes of halo­
thane administration; therefore, OMF surgeons typically
wait at least 1 0 minutes following induction of a general
anesthetic with halothane before injecting local anesthetic
drugs.
Loca l Anesthetics i n I nfla m m ation
a n d I nfection
Achieving effective local anesthesia i n the presence of
inflammation and/or infection is a common challenge in
OMFS.
Products of inflammation lower the surrounding tissue
pH (e.g., purulent exudates have a pH of 5 .5-5.6). At this
more acidic pH, the numbers of base molecules necessary
for passage of the anesthetic into the nerve membrane
383
The effecti v eness of local anesthesia in the presence of
infection i s frequentl y compromi s ed by changes in tissue
pH. The following suggestions may increase successful an­
esthesia outcomes:
• Allow additional time for the local anestheti c to take
effect.
•
Use a greater amount of local anestheti c to help over­
come acidity created by the infection. (Make sure that
•
maximum doses are not exceeded.)
Use a regional nerve block away from the area of
inflammation.
•
Discard the needl e after penetrating in or near an area
of inflammation/infection.
• •
Consider potential secondary innervations to the area
(e.g., myl o hyoid nerve in the mandible).
•
Use a local anesthetic agent wi t h a higher pH.
Alkalini z e the local anestheti c by adding sodium bicar­
•
•
bonate immediatel y before the injection.*
•
Use intravenous sedation or general anesthesia.
I f the infection i s minor, consider antibioti c s and
•
rescheduling.
•
'Sodium bicarbonate decreases the a cidity o f the a n esthetic solu­
tion and the tiss ues into which it is injected, p roviding sign ificantly
greater n u m b e rs of initia l base m o lecules th a n were p rovided in
th e m a n u fa ctured so lutio n . Alkalin izing (buffering) local a n esth et­
ics with sodium bicarbonate has been difficult a n d inconvenient
when o n ly ste rile, sealed cartridges a re available. This technique
has been simp lified with the availability of Onset from Onpharma,
discussed in Chapter 1 6, " Tro u b leshooting Inadequate A n esthe­
sia . " Wh en m e dica l via ls of loca l a n esth etics a re a va ilable (often
, the case in OM FS), buffering is q u ite easy and very effective for ,
: . �� . � � : : . � �: : . . : ���: � : : ��:� : • • � : . � . : : . � •
i ro i ne t s a ou c i n l n d i f ct d t s u e
may be significantly reduced. Inflammatory exudates may
also enhance nerve conduction action potentials, making
blockage of sensory nerve impulses more difficult. In ad­
dition, blood vessels in the area of inflammation may be
dilated, leading to a more rapid uptake of the anesthetic
agent from the area of inj ection. These changes can lead
to delays in onsets of anesthesia, inadequate depths of an­
esthesia, and the potential for local anesthetic blood lev­
els to be elevated. Considerations for the management of
local anesthesia in the presence of infection are listed in
Box 20-1 •.
Needle tract infection is a potential complication of
inj ection into infected tissues. Although penetration into
infected tissues can be avoided by using more distant re­
gional nerve blocks, whenever there is a possibility of a
needle having passed through infected tissues, it should
be discarded immediately after use to prevent inadvertent
reuse.
S evere trismus is sometimes seen in inflammation
and infection. Trismus has been mentioned previously as a
painful condition that impairs the extension of the muscles
384 SECTION V • S P E C IAL C O N S I D E RATI O N S F O R LOCAL A N E STH ESIA
of mastication leading to decreased ability to fully open
the mouth. Limitation in opening can follow trauma, local
anesthetic inj ections, and temporomandibular j oint prob­
lems and ankylosis.
Limited opening can p o s e anatomical difficulties
with standard conventional inferior alveolar (IA) nerve
block techniques and especially with the Gow-Gates ap­
proach, which requires patients to open fully. In situations
of severe trismus, an extraoral nerve block or an intraoral
high nerve block technique (Vazirani-Akinosi) where
the mouth remains closed during its administration is
recommended.
Another serious concern with more severe progressive
infections, such as Ludwig's angina, is the potential for air­
way compromise. Management and control of the airway
is the first priority in these situations. These patients are
typically treated with a general anesthetic in a hospital set­
ting. B efore induction of general anesthesia, airway man­
agement is initiated with conscious fiberoptic intubation
or a possible surgical airway. In this setting, supplemental
local anesthesia is administered once the airway is secure.
Loca l Anesthetic Allerg ies
As previously mentioned in Chapter 4 , "Pharmacology
Basics," and Chapter 8, "Topical Anesthetics," true allergic
reactions to amide local anesthetics are rare. Sensitivity to
ester-type local anesthetics is more common. Most topical
local anesthetics contain the esters benzocaine, butamben,
or tetracaine, and similar to amide topicals in multiuse
containers, many contain paraben preservatives. In OMFS,
cocaine, an ester topical anesthetic, may be used on the
nasal mucosa to assist with hemostatic control due to its
vasoconstrictive properties.
Latex allergies have become more common and should
be considered when using local anesthetics. The needle­
puncture diaphragm of dental cartridges and multidose
vials may contain latex. In latex-allergic patients a latex­
free syringe should be used. Increasingly, manufacturers
are producing anesthetic cartridges and vials with no latex,
including the diaphragms. These may be used in place of
more cumbersome multidose dispensing techniques. When
local anesthetic solutions are drawn up from multidose
vials, rubber diaphragms should first be removed.
Documentation of true local anesthetic allergic reac­
tions is based on clinical history (e.g., allergic dermatitis,
asthmatic attack , systemic anaphylaxis) and use of in­
tradermal testing with preservative-free local anesthetic
solutions without vasoconstrictors by an appropriate
healthcare provider. History of hypotension associated
with syncope or rapid he art rate after administration
of a local anesthetic may be confused with an allergic
reaction but is more suggestive of an inadvertent intra­
vascular inj ection and the associated vasoconstrictor or
a psychogenic-vagally me diated reaction. Options for
treatment of patients with local anesthetic allergies are
provided in Box 20-2 •·
When it is determined that a patient has a true l o cal anes­
thetic allergy, the following suggestions may increase suc­
cessful anesthesia outcomes:
Allow addit ional time for the local anestheti c to take
effect.
•
Following allergy testing, use an al t ernate local anes­
thetic (Bartfield, Weeks, & Raccio-Robak, 1 998).
•
•
1 % Benadryl (diphenhydramine hydrochloride)
0.09% benzyl alcohol
•
General anesthesia
•
•
•
•
: . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
I nferior Alveolar Nerve Block
Com p l ications and Nerve I nj u ries i n
O ra l S u rgery
One of the most common local anesthetic inj ections per­
formed by OMF surgeons is the lA nerve block. Despite
the frequent use of lA nerve blocks, they are considered
to be one of the more technically difficult inj ections due
to anatomical constraints and variability and there are a
number of potential complications. Local complications
related to lA nerve blocks include vascular, neural, osse­
ous, connective tissue, and muscular inj ury from needle
penetration and deposition of the anesthetic and/or local
hemorrhage. Systemic complications related to lA nerve
blocks include syncope, hypersensitivity, overdose, toxicity,
allergy, and other intravascular anesthetic reactions.
Transient and long-term nerve inj uries have been
reported related to cranial nerves II-VIII. Adverse neu­
rologic complications affecting local and more distant
neurologic tracts have been reported related to lA nerve
block inj ections. These neurologic complications include
cranial nerve paralysis and anesthesia of cranial nerves
II-VIII as well as cervical sympathetic blockade (Fish,
Mcintire, & Johnson, 1989) .
Although uncommon, a neurological complication
of lA nerve blocks is p aresthesia of the lingual nerve.
Jorgensen and Hayden reported that the lingual nerve does
not slide away when encountered by anesthetic needles
because the nerve is attached to the interpterygoid fascia.
With the mouth open, this fascia is stretched, holding the
lingual nerve in place (Smith & Lung, 2006) . Harn and
Durham reviewed the incidence of lingual nerve trauma
after conventional lA nerve block anesthesia in 2,289 pa­
tients who received 9,587 inj ections (Smith & Lung, 2006) .
They reported a 3.62% probability of lingual nerve trauma
each time a conventional lA nerve block is administered,
with a 14.99 % probability of a post-inj ection complication
after trauma to the lingual nerve. Less commonly reported
complications include chorda tympani nerve injury, optic
 C HAPT E R 20 • I N S I G HTS FROM S P E C IALTI E S : O RAL S U R G E RY, P E R I O D ONTI C S , A N D E N D O D O N T I C S
nerve atrophy, and paralysis of cranial nerves III, IV, VI,
VII, and VIII (Gray, 1978; Harn & Durham, 1990; Paxton
et al. , 1994; Pogrel & Thamby, 20 00; Tomazzoli-Gerosa,
Marchini, & Monaco, 1988) . Haas and Lennon retrospec­
tively reviewed 143 cases of inj ection-related mandibular
paresthesia in dental patients unrelated to surgery, over
a 2 1-year period. Paresthesia was most often reported
after administration of 4% local anesthetic agents, artic­
aine or prilocaine (Haas, 2006) . According to Haas, the
incidence of p ermanent paresthesia from all local an­
esthetics is approximately 1 :785 , 0 0 0 (Haas & Lennon,
1995a, 1995b ). The incidence for lower concentrations
(0.5 % , 2 % , and 3 % ) is approximately 1 : 1 ,20 0,000. After
administering 4% concentrations, it increases to approxi­
mately 1 :500,000 (Paxton et al., 1994; Stoelting & Miller,
2000; Tomazzoli-Gerosa, Marchini, & Monaco, 1988). See
Chapter 17, " Local Anesthesia Complications and Man­
agement," for a more detailed discussion on paresthesia's
causes and incidence.
I nsig hts from Periodontics
A relatively high percentage of patients experience dis­
comfort from root sensitivity during and after periodontal
treatment. This is true for surgical and nonsurgical proce­
dures requiring an ongoing need for profound anesthesia.
In addition, hemostasis is desirable for most periodontal
treatments.
Hemostasis in Periodontics
Hemostasis is an important consideration in periodontal
surgery where visualization of exposed defects is critical to
their correction. Control of bleeding can usually be accom­
plished with anesthetic solutions containing no more than
1 : 100,000 epinephrine or 1 :20,000 levonordefrin. The use
of 1 :50,000 epinephrine solutions may be useful at times
for hemostasis in periodontal surgery, particularly in pala­
tal infiltrations. For the maj ority of procedures, however,
this higher concentration of vasoconstrictor increases risk
without providing significant benefit.
An alternative to using an anesthetic solution with
an increased concentration of vasoconstrictor is to use a
computer-controlled local anesthetic delivery (CCLAD)
system that allows for greater diffusion of ane sthetic
solution by using a low-pressure gradient as discussed in
Appendix 9-5 . The increased diffusion property of con­
trolled low-pressure and regulated fluid flow rate moves
a greater volume of anesthetic through cortical bone and
into medullary bone space. This provides improved hemo­
stasis and greater visibility of the surgical site.
Maxillary Techniques in Periodontics
Unless a division 2 (true maxillary) nerve block is admin­
istered, hemi-maxillary anesthesia requires anesthetizing
several different nerves. This can be accomplished with a
minimal amount of anesthetic and a minimal number of
inj ections. For quadrant anesthesia, the posterior superior
385
alveolar inj ection can be administered, depositing from 0.9
to 1.8 mL (one-half to one cartridge) depending upon the
duration needed. An ASA and MSA or IO nerve block
will complete the anesthesia of the teeth in the quad­
rant. Palatal tissues must be anesthetized separately using
greater palatine and nasopalatine nerve blocks unless an
anterior middle superior alveolar (AMSA) nerve block is
administered.
Anesthesia of the palate is one of the greatest chal­
lenges to comfortable administration in periodontal pro­
cedures. The AMSA nerve block is particularly useful in
these procedures because fewer inj ections will be neces­
sary in order to provide wide areas of anesthesia, both
pulpal and soft tissue. Very slow deposition of local anes­
thetic solution following good topical anesthesia will effec­
tively anesthetize the palate with an AMSA nerve block
on one side to the midline. It is easy to follow the diffusion
of the anesthetic solution in the tissues by observing the
expanding area of blanching. Whenever additional anes­
thesia is needed in the palate, inserting the needle within
an area of blanching or previous blanching and depositing
a small amount of anesthetic slowly can eliminate discom­
fort. The AMSA inj ection has the advantage of anesthetiz­
ing not only the palate but also the facial gingiva, from the
premolars to the midline in addition to the pulps of the
teeth in the area. To accomplish this, usually no more than
two-thirds to three-quarters of a cartridge is necessary.
Mandibular Techniques in Periodontics
In the mandibular arch, anesthesia usually involves nerve
block techniques that provide the deepest and most exten­
sive anesthesia using the least amount of local anesthetic
drug. Although the IA nerve block is popular, the Gow­
Gates and Vazirani-Akinosi techniques are preferred by
some clinicians. The mental incisive nerve block inj ection
can also be delivered effectively for those cases involving
only structures anterior to the molars. After administra­
tion of a mental incisive nerve block, the lack of lingual
anesthesia can be problematic, especially for periodontal
procedures. Anesthesia of lingual tissues can be provided
by slowly infiltrating the papillary areas (interpapillary
inj e ctions) after facial anesthesia has been established.
This approach has the advantage of providing hemosta­
sis (if vasoconstrictors are used) to the anesthetized area
and is particularly helpful for procedures such as gingival
grafting.
I nsig hts from Endodontics
M any patients who require root canal therapy present
with pain and swelling, an environment in which anesthet­
ics are not as effective as they are in healthy, noninfected
tissue. Nerve blocks in these circumstances have been
more effective at providing profound anesthesia compared
with infiltrations, but neither is always able to provide reli­
able profound anesthesia for root canal therapy, which, as
a consequence, has developed a very painful reputation.
386 SECTION V • S P E C IAL C O N S I D E RATI O N S F O R LOCAL A N E STH ESIA
The Use of Anesthetics in Endodontics
The introduction of articaine has decreased the incidence
of pain in endodontics to some extent. Because of its pre­
sumed ability to penetrate efficiently through bone, at
times mandibular teeth can be adequately anesthetized
by infiltration (Dudkiewicz, Schwartz, & Laliberte, 1987;
Kanaa et al. , 2006). Whereas lA nerve blocks are contro­
versial with articaine, Gow-Gates and Vazirani-Akinosi
nerve blocks are not known to involve increased risks of
paresthesia with articaine and can be performed when ar­
ticaine is preferred (Hawkins, 2006). Lidocaine and mepi­
vacaine are both quite effective as well. In the maxilla,
infiltrations with articaine sometimes anesthetize the en­
tire tooth including the palatal roots of the molars with­
out administering separate palatal injections (Kanaa et al.,
2006; Vree & Gielen, 2005).
Topical Anesthetics i n Endodontics
Topical anesthetics are placed at penetration sites to pre­
vent pain during penetrations with needles. They are also
useful, for example, on palatal gingiva to ease rubber dam
clamp placement. Some topicals, such as lidocaine, prilo­
caine, and benzocaine, when combined with tetracaine, are
particularly effective.
Managing Fear in Endodontics
B ecause of its painful reputation, ordinary levels of dental
fear are magnified when the term root canal is mentioned.
Anxiety can intensify typical levels of fear, particularly of
inj ections. It is important to take a few minutes to address
this fear, which can have at least two maj or benefits, eas­
ing patient anxiety and increasing the success of local an­
esthesia. It is also important to avoid criticism of neglect,
including the length of time since the last appointment. In­
stead, patients should be warmly encouraged and praised
for investing in their oral health and for keeping their ap­
pointments. Specific strategies for managing dental anxi­
ety and fears can be found in Chapter 2, "Fundamentals of
Pain Management," and Chapter 18, "Insights for Fearful
Patients."
lntraosseous Injections in Endodontics
Intraosseous inje ctions are supplemental inj ections fol­
lowing infiltration or nerve block inj ections that provide
immediate and predictable profound anesthesia, especially
when the initial anesthesia has been inadequate. This is
particularly beneficial in endodontics when there is con­
siderable inflammation and infection present in tissues
surrounding an abscessed tooth. Specific technique in­
structions are discussed in Chapter 15, " S upplemental
Techniques and Adjunctive Strategies."
S olution is deposited into cancellous bone spaces
surrounding a tooth. In order to reach cancellous bone,
four layers must be penetrated : epithelium and its un­
derlying connective tissue, periosteum, and cortical bone.
Pre-anesthesia will desensitize the epithelial layer and its
underlying connective tissue as well as the periosteum sur­
rounding the bone. Cortical bone lacks sensory innerva­
tion and can be perforated painlessly once the other layers
are anesthetized.
There are three essential steps when administering
intraosseous inj ections, anesthetizing the attached gin­
giva, perforating the cortical plate, and depositing anes­
thetic into cancellous bone around the tooth. Although
those with more experience did not find it to be particu­
larly challenging, this was accomplished using a surgical
round bur to perforate the cortical plate. While some still
prefer this technique, the difficulty with the bur approach
is that it is necessary to renegotiate the perforation with
the needle once the bur has been withdrawn from the
tissues.
Commercial products such as the Stabident and
X-Tip have guide sleeves that remain in place after perfo­
ration and direct needles into the perforations. With these
products, there is rarely a reason to use a round bur for
intraosseous inj ection access. One system, the IntraFiow
device, does not require withdrawal after perforation.
A CCLAD device for intraosseous inj ections with con­
trolled flow rates, the Quicksleeper, also does not require
withdrawal after perforation. These systems are discussed
in Chapter 9, " Local Anesthetic D elivery D evices," and
demonstrated in Chapter 15, "Supplemental Techniques
and Adj unctive Strategies." Anesthetic solution is de­
posited immediately on perforation of the cortical plate.
Although some clinicians prefer round bur perforation,
these innovative systems are much easier for novices to
master.
Before discussing the intraosseous technique, it is im­
portant to comment on the benefit of radiographs. These
provide accurate assessments of the spacing between ad­
j acent roots in the identified area, assuring that the spac­
ing between roots is adequate. If the roots are too close
together, another site must be chosen, one or two teeth
distal or mesial to the tooth that is to be treated, in order
to avoid damage when perforating.
lntraosseous Technique
B egin by imagining a horizontal line along the gingival
margins of the teeth in the area and a vertical line through
the interdental papilla. A point about 2 mm apical to the
intersection of these lines is usually a suitable site for a
lateral perforation. This has also been described as being
located j ust barely within the most apical portion of the
attached gingiva. It is more successful to inj ect distal to
the tooth to be anesthetized rather than mesial; however,
in most cases, a mesial inj ection will provide adequate
anesthesia.
It is very important to use a gentle "pecking" motion
versus a long, continuous movement while penetrating in
order to avoid overheating the cortical bone (Malamed,
20 1 3 ) . Overheating can result in postoperative soreness
 C HAPT E R 20 • I N S I G HTS FROM S P E C IALTI E S : O RAL S U R G E RY, P E R I O D ONTI C S , A N D E N D O D O N T I C S 387

and potential infection of the bone and overlying gingiva The duration of anesthesia with intraosseous inj ec­
(Malamed, 20 13). tions is short. Typical pulpal durations range from 15 to
If using the Stabident system, hold the syringe in a 30 minutes. Durations will vary depending on the spe­
"pen-grip" manner and angle the needle in the direction cific drug, the presence or absence of a vasoconstrictor,
in which the drill was withdrawn from the bone. The inj ec­ and individual metabolism. If sensitivity returns before
tion needle should be allowed to engage the cortical bone procedures have been completed, a small volume of an­
with only very light pressure to avoid " digging" into it esthetic can be deposited after renegotiating the perfora­
(binding) or bending. If the needle does not pass through tion (0.4 mL) .
the perforation easily, a modified inj ection needle may be Most patients will have little to no postoperative
used. This needle has a flattened tip, which is quite effec­ symptoms, including pain. In rare cases (less than 5% ) ,
tive because no sharp bevel is necessary in intraosseous patients may experience localized swelling with o r with­
techniques that by necessity have pre-perforated path­ out infection, which heals uneventfully or occasionally re­
ways of insertion. The lack of a bevel minimizes binding quires antibiotics.
of the needle tip in bone.
If using the guide sleeve provided with the X-Tip sys­ lntrapulpal lnjections in Endodontics
tem, gently insert the inj ection needle into the predrilled The intrapulpal injection is used exclusively for endodon­
channel. If using the IntraFlow, the perforator retracts and tics. This inj ection is administered for discomfort experi­
the needle is inserted without moving the device from the enced when the pulp is invaded by a bur or instrument
perforation. With the Quicksleeper, the controlled per­ despite the presence of otherwise profound anesthesia.
foration is made with a specialized needle, which is then It can be administered only after access to the pulp has
used for drug delivery. been made. To ensure good back-pressure and complete
One-third of a cartridge (0.6 mL) of solution should be anesthesia, the initial opening into the pulp chamber
slowly deposited (0.6 mL over 60 seconds) into the cancel­ must be very small. This is ideally no larger than the size
lous bone. Diffusion through bone is efficient but not rapid. of a one-half round bur or a 330 pear-shaped bur. The ini­
Slow deposition is mandatory to allow for easy diffusion tial opening should be directed toward the largest canal
and to avoid discomfort at the time and postoperatively. in the tooth, which is the distal canal on lower molars and
Vasoconstrictors should be avoided or minimized. Studies the palatal canal on upper molars. Once the needle has
have demonstrated that the cardiovascular system effects been inserted into the opening, one-half to one full car­
of vasoconstrictors in intraosseous techniques are imme­ tridge of anesthetic (0.9-1.8 mL) is administered slowly.
diate and p ervasive. If necessary, dilutions of 1 :200,000 The choice of drug is not important because it is primar­
epinephrine may be used. When using vasoconstrictors, pa­ ily the pressure of the inj ection that provides the anes­
tients should be warned to expect temporary rapid heart­ thetic effect (VanGheluwe & Walton, 1997).
beats, which will pass quickly. Plain solutions can be used Additional technique considerations for these inj ec­
and will not produce these effects but will also have shorter tions can be found in Chapter 15, " S upplemental Tech­
durations. niques and Adjunctive Strategies."

.�.h. c:a.P..t.� r. . 9.lJ.���.i.e>.rl � . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3. Which one of the following is not a local anesthesia
consideration in oral and maxillofacial surgery when
1 . Which one of the following methods of adjusting treating an infected patient?
doses of local anesthetic drugs for children is recom­ a. Use a greater amount of local anesthetic to help
mended in this chapter? overcome acidity created by the infection (Make
a. Clark's rule sure that maximum doses are not exceeded.)
b. The Rule of Inference b. Use a regional nerve block away from the area of
c. Young's rule inflammation
d. Heuristic rule c. Use a local anesthetic agent with a lower pH
d. Discard the needle after inj ecting in or near an area
2. Specific challenges in oral and maxillofacial local an­ of inflammation/infection
esthesia include all of the following, except:
a. Frequent management of oral infections, some of 4. Which one of the following is not an adverse event
which are life threatening following local anesthetic inj ections?
b. Limiting the potential for needle tract infections a. Trismus
c. Achieving adequate local anesthesia in the pres­ b. Normal durations of numbness
ence of these infections c. Postoperative soreness
d. All of the above d. Infection
388 SECTION V • S P E C IAL C O N S I D E RATI O N S F O R LOCAL A N E STH ESIA

5. Which one of the following is not an option for treat­
ment of patients with true local anesthetic allergies?
a. Use of an alternate local anesthetic
b. 1 % B enadryl ( diphenhydramine hydrochloride )
c. 0.09 % benzyl alcohol
d. 0.1 % sodium benzoate
6. Systemic complications related to lA nerve block in­
clude all of the following except:
a. Hematomas
b. Syncope
c. Overdose reactions
d. Allergic reactions
References
Bartfield, J. M . , Weeks, S . , & Raccio-Robak, N . (1998). Random­
ized trial of diphenhydramine versus benzyl alcohol with epi­
nephrine as an alternate to lidocaine local anesthesia. Annals
of Emergency Medicine, 32, 650-654.
Dudkiewicz, A., Schwartz, S., & Laliberte, R. (1987). Effective­
ness of mandibular infiltration in children using the local
anesthetic Ultracaine (articaine hydrochloride) . Journal of the
Canadian Dental Association, 53, 29-3 1.
Fish, L. R., Mcintire, D. N. , & Johnson, L. (1989). Temporary pa­
ralysis of CN III, IV, and VI after a Gow-Gates injection. Jour­
nal of the American Dental Association, 119( 1 ) , 127-130.
Gray, R. L. M. (1978). Peripheral facial nerve paralysis of dental
origin. British Journal of Oral Surgery, 16(2) , 143-150.
Haas, D. A. (2006). Articaine and paresthesia: Epidemiologic stud­
ies. Journal ofthe American College of Dentistry, 73(3), 5-10.
Haas, D. A., & Lennon, D. (1995a) . Local anesthetic use by den­
tists in Ontario. Journal of the Canadian Dental Association,
61 (4), 297-304.
Haas, D. A., & Lennon, D. (1995b ) . A 21 year retrospective study
of reports of paresthesia following local anesthetic admin­
istration. Journal of the Canadian Dental Association, 61 ( 4),
319-330.
Ham, S. D., & Durham, T. (1990) . Incidence of lingual nerve
trauma and post inj ection complications in conventional
mandibular block anesthesia. Journal of the American Dental
Association, 121 (10), 519-523.
Hawkins, M. (2006, October) . Local anesthesia: Technique and
pharmacology, problems and solutions. ADA Annual Session
'
Las Vegas, NV.
Jorgensen, N. B., & Hayden, J. (1980, February). Sedation, local and
general anesthesia in dentistry. Philadelphia: Lea & Febiger.
Kanaa, M. D., Whitworth, J. M., Corbett, I. P., & Meechan, J. G.
(2006). Articaine and lidocaine mandibular buccal infiltration
anesthesia: A prospective randomized double-blind cross-over
study. Journal of Endodontics, 32, 296-298.
Maestrello, C. L., Abubaker, A. 0., & Benson, K. J. (2007). Lo­
cal anesthetics. In A. 0. Abubaker & K. J. Benson (Eds.), Oral
and maxillofacial surgery secrets (2nd ed., pp. 65-74). St. Louis:
Mosby.
Malamed, S. F. (20 13). Local anesthetic considerations in dental
specialties. In S. F. Malamed (Ed.), Handbook of local anesthe­
sia (6th ed., pp. 277-291 ) . St. Louis: Mosby.
Paxton, M. C., Hadley, J. N. , Hadley, M. N. , Edwards, R. C., &
Harrison, S. J. (1994). Chorda tympani nerve injury following
inferior alveolar inj ection: A review of two cases. Journal of
the American Dental Association, 125, 1003-1006.
Pogrel, M. A., & Thamby, S. (2000). Permanent nerve involve­
ment resulting from inferior alveolar nerve blocks. Journal of
the American Dental Association, 131, 90 1-907.
Smith, M. H., & Lung, K. E. (2006) . Nerve injuries after dental
inj ection: A review of the literature. Journal of the Canadian
Dental Association, 72( 6), 559-564.
Stoelting, R. R., & Miller, R. D. (2000). Local anesthetics. In R.
R. Stoelting & R. D. Miller (Eds.), Basics of anesthesia (4th
ed., pp. 132-142). New York: Churchill Livingstone.
Tomazzoli-Gerosa, L., Marchini, G., & Monaco, A. (1988).
Amaurosis and atrophy of the optic nerve: An unusual com­
plication of mandibular-nerve anesthesia. Annals of Ophthal­
mology, 20, 170-171.
VanGheluwe, J. , Walton, R. (1997). Intrapulpal injection: factors
related to effectiveness. Oral Surgery, Oral Medicine, Oral Pa­
thology and Oral Radiology, 83(1 ) , 38-40.
Vree, T. B., & Gielen, M. J. (2005). Clinical pharmacology and
the use of articaine for local and regional anaesthesia. Best
Practice & Research Clinical Anaesthesiology, 1 9, 293-308.

Visit www.p earsonhighered.com/he �lthprofessionsresources to access the student resources that accompany
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C h a pter 2 1 F u n d a m e n ta l s fo r t h e Ad m i n i st rati o n of N i t ro u s
O x i d e- Oxyg e n S e d a t i o n
· · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · � · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · · ·

Fu n d a m e nta l s fo r th e Ad m i n istrati o n
o] � iiErtous Oxid e-Ox�g·e -ril �-Le�d�a1f i o lil SEAN BovNES, DMD, MS, DAs
ROYANN ROYER RDH, MPH

O BJ E CT I V E S KEY T E R M S

• Defi n e a n d d i scuss key terms i n t h i s c h a pte r. a lveo l i 3 93

a m b i e n t gases 409
• D efi n e a n d d i scuss t h e p h y s i ca l a n d c h e m i c a l p ro p e rties of
a n a l g e s i a 397
n itro u s oxi d e a n d oxy g e n (N 20-02) . b ro n c h i o l i 3 93
• I d e n tify t h e m a i n co m po n e n ts of N 20-02 d e l ivery syste m s . chro n i c o bstructive p u l m o n a ry

• D e m o n strate a b a s i c u n d e rsta n d i n g of t h e p ro p e r m a i nte­ d isease (COPD) 3 98

co n d u ct i o n t u b i n g 405
n a n ce of N 20-02 eq u i p m e n t to i n c l u d e i nfect i o n contro l p ro­
c o p p e r t u b i n g 40 1
ced u res, co m m o n m a l fu n cti o n s , a n d a p p ro p ri ate co rrect i o n s
cystic fi b rosis 3 98
a n d p reca uti o n s fo r safe u s e .
d e e p sedati o n 3 9 1
• D e m o n strate t h e ste ps i n a d m i n i stra t i o n o f N 20-02 sedati o n . d iffu s i o n hypoxia 3 94
• Descri be t h e effects o f N20 o n t h e centra l n e rvous syste m expi rati o n 3 94
fl ow m eters 403
(CNS), g a stro i n testi n a l system (G I ) , a n d t h e ca rd i ovascu l a r
g e n e r a l a n esth e s i a 3 9 1
syste m .
hyp erca r b i c d rive 4 1 4
• Describe a n d d i scuss i n d i cati o n s fo r N 20-02 sedati o n . hypoxic d rive 4 1 4
• D e s c r i b e a n d d i sc u s s c o n t ra i n d i ca ti o n s t o N 20-02 s e d a ti o n . i n s p i rati o n 3 93
l a rynx 3 92
• I d e ntify a n d resp o n d t o pote n ti a l adverse re a cti o n s with
m a n ifo l d 3 9 9
N 20-02 sedati o n .
m axi m u m exposu re l i m it 409
• I d e n tify a n d d i scuss s i g n s a n d sym ptoms t o observe w h e n m i n i m a l sedation 3 9 1
m o n itori n g N20-02 sedati o n . m i n i m u m a lve o l a r
• I d e ntify a n d res p o n d t o s i g n s a n d sym ptoms o f N 20-02 c o n ce ntrat i o n 3 9 7

ove r-sed a ti o n . m i n ute vo l u m e ( m i n ute

venti l a t i o n ) 3 94
• C a l c u l a te a n d re c o rd a cc u rate p e rce n t a g e s of N 20-02 m o d e rate sedati o n 3 9 1
d e l i v e re d . n a s a l h o o d 405
• I d e n tify pote n ti a l effects o f N 20 abuse. n itro u s oxi d e 3 9 1
occu pati o n a l expos u re 4 1 4
• State t h e cu rre n t l aws a n d statutes i n yo u r j u ri sd i ct i o n a s they
p h a ry n x 3 92
re l ate to a d m i n i strati o n and m o n ito ri n g of N 20-02 sedati o n .
p i n i n d ex safety system 402
• State t h e cu rre n t N I O S H a n d ADA occupati o n a l expo s u re p n e u m o t h o rax 4 1 4
l i m its of N 20 i n t h e worki n g e n v i ro n m e n t . re g u l ator 403
rese rvo i r bag 403
res p i rato ry system 3 9 1
scave n g i n g syste m s 407
sedation 3 9 1
ti d a l vo l u m e 3 94
t i m e-we i g hted
d o s i m etry 409
tra ce gases 409
t ra c h e a 3 93

390
 C HA PT E R 21 • F U N D A M E NTALS FOR T H E A D M I N I STRATI O N OF N ITRO U S OXI D E-OXYG E N S E DATI O N
I ntrod uction
Local anesthesia, nitrous oxide-oxygen (N20-02) sedation,
and general anesthesia are common, well-recognized strat­
egies for controlling pain and anxiety in dentistry ( Boynes,
20 1 1 ) . The American Dental Association ( ADA) has con­
sistently reaffirmed its commitment to the safe and effec­
tive administration of all three of these modalities and
provides guidelines to the profession on their use as well
as for education and training of dental healthcare provid­
ers in pain and anxiety management ( ADA, 2007a).
Sedation may be defined as a state of calm induced by a
drug or other tranquilizing substance. Nitrous oxide-oxygen
sedation is a valuable option for patients who experience
difficulties receiving treatment due to a lack of adequate
coping skills and/or high levels of anxiety. This chapter pro­
vides an introduction to the fundamentals of dental N20-0z
sedation, including the anatomy and physiology of the respi­
ratory system as it relates to N20-0 2 sedation, indications
and contraindications, appropriate delivery armamentarium,
and techniques for its administration.
The benefits of administering N20-02 sedation in
dentistry are many. Equally important are significant lim­
itations to its administration. Although for the most part
avoidable and rarely insurmountable, limitations require
appropriate education of staff and patients. Despite educa­
tion and strategies to overcome limitations to the adminis­
tration of N20 sedation, some individuals may respond in
unpredictable ways to stress and anxiety. It is possible that
N20-0 2 sedation alone or in combination with local anes­
thesia may prove insufficient to allow these patients to tol­
erate therapy. Whenever an appointment can be enhanced
with other techniques to reduce these exceptionally stress­
ful and difficult situations where pain control is not or
cannot be achieved with local anesthetics and NzO-O z
sedation, other strategies may achieve greater success. See
Chapter 18, " Insights for Fearful Patients." Table 21-1 •
provides a brief discussion of benefits, limitations, and pre­
cautions associated with the use of N20-02 sedation.
Nitrous oxide sedation addresses both fear and pain
and provides a mild amnesia that tends to shorten the per­
ception of appointment length. It can also increase levels
Table 2 1 -1 Ben efits, L i m itatio ns, and Preca utions of N itro u s Oxide-Oxyg e n Sedation
Benefits
• Addresses both fear and pain
• Provides mild amnesic affects, including the perception of a
quick passage of time
• Facilitates positive behaviors in pediatric patients
• Allows easy titration of gases delivered to patient
• Provides rapid onset of sedation: 30 seconds to 5 minutes
• Provides short recovery times once N20 delivery is
discontinued: 3-5 minutes
391
of tolerance and cooperation, particularly in young chil­
dren if they are tired, restless, fearful, or ill-tempered when
they arrive for their appointments. Other benefits when
administering N20-0 2 include easy titration of gases,
rapid onset, and short recovery times.
In recently published ADA Guidelines, four levels of
sedation/anesthesia are defined: general anesthesia, deep
sedation, moderate sedation, and minimal sedation ( ADA,
2007b).
General anesthesia is a drug-induced loss of con­
sciousness during which p atients are incapable of be­
ing aroused, even with painful stimulation. The ability to
maintain ventilatory function is often impaired.
Deep sedation is a drug-induced state of depressed
consciousness accompanied by partial or complete loss
of protective reflexes, including the inability to continu­
ally maintain an airway independently and/or to respond
purposefully to physical stimulation or verbal command.
Moderate sedation is a depression of consciousness
during which patients can respond purposefully to verbal
commands, either alone or accompanied by light tactile
stimulation.
Minimal sedation is a minimally depre s s e d level
of consciousness in which a patient is able to indepen­
dently and continuously maintain an airway and respond
normally to tactile stimulation and verbal commands
( ADA, 2007b ) . In minimal sedation, selected drugs and
techniques should carry wide enough safety margins that
unintended loss of consciousness never occurs.
Minimal sedation produces diminished pain and anxi­
ety and a depressed level of consciousness while patients
remain aware of their surroundings. This is the intended
use of N20-0 2 sedation in dentistry. At this level of seda­
tion, patients maintain the ability to respond to both phys­
ical and verbal stimulation and are able to independently
maintain open airways.
Nitrous oxide sedation is effective for alleviating anxi­
ety in patients who might otherwise avoid dental treatment.
According to one source, 23 million people with dental fear
were more willing to see a dentist when some form of seda­
tion was offered ( Dionne et al. , 1998) . A survey of recent
Lim itations and Precautions
• Expresses variable effects on individual patients; ineffective
for some
• Increases costs
• Requires education to safely administer and monitor
sedation
• Requires routine equipment monitoring and maintenance
• Requires monitoring to prevent environmental exposure
392 S E C T I O N VI • N IT R O U S OXI D E-OXYG E N S E DAT I O N
dental school graduates reported that 93.7 % perceived a
need for sedation services within their respective patient
populations (Baynes, Lemak, & Close, 2006).
Nitrous oxide has multiple mechanisms of action that
underlie its varied pharmacological properties. Nitrous ox­
ide is capable of providing not only analgesic and anxiolytic
benefits but anesthetic (loss of sensation) benefits as well.
Findings to date indicate that the analgesic effect of N20
(reduction or relief of pain) is opioid in nature and, like
morphine, may involve a myriad of neuromodulators in the
spinal cord. Mechanisms involved in its anxiolytic and anes­
thetic actions remain less clear (Emmanouil & Quack, 2007).
Current Use in Dentistry
The proportion of dentists who actually use different
pharmacologic approaches to pain and anxiety control
was the subj ect of a 2007 ADA Survey of Current Issues in
Dentistry, in which questionnaires were sent to 5,775 general
dentists and dental specialists in the United States (ADA,
2008). Sixty-two p ercent did not provide any sedation
services. Of those providing sedation, the maj ority (70 % )
selected N20-02 inhalation sedation a s their commonly
used modality of sedation care. Sixty-five percent of the
general anesthesia users were oral and maxillofacial sur­
geons, whereas 24 % were general dentists, the second high­
est category. The profession is currently observing a trend
in which more non-dentist clinicians are administering and/
or monitoring N20-02 sedation (B aynes, 20 1 1 ; Michigan
Department of Community Health, 20 12).
Anatomy, Physiology,
a n d Pha rmacology
Anatomy and Physiology Involved in N20 Sedation
Th e
A N AT O M Y A N D P H Y S I O LO G Y O F R E S P I RAT I O N
primary function of the respiratory system is to ex­
change oxygen ( 0 2 ) and carbon dioxide ( C02 ) across
FIGURE 2 1 -1 Anatomy and Pathway of Respiration in the Lungs. A- Basic
lung anatomy. B - Structures of bronchus. C- Internal view of alveolus.
pulmonary/capillary membranes. The design of the system
allows this function to be p erformed continuously and
with minimal effort. Respiration is driven involuntarily by
the medulla oblongata in the brainstem and voluntarily by
the cerebral cortex. Nitrous oxide exchange uses the same
pathways as normal respiration (see Figure 21-1 •).
Upper Respiratory System Respiration begins with the
nose. The function of the nose is to warm and humidify air
and filter foreign particles. Conditions that cause or con­
tribute to nasal obstruction such as allergic rhinitis, upper
respiratory tract infections, colds, sinusitis, influenza, and
deviated septa must be considered before the administra­
tion of N20-0 2 sedation. In other words, patients must be
able to breathe well through their noses.
Inhaled gases move from the nose to the pharynx. The
pharynx is a muscular tube 12-14 em long that is divided
into three regions, the nasopharynx, oropharynx, and
laryngopharynx. The nasopharynx is the uppermost part of
the pharynx and extends from the lower skull to the soft
palate. The oropharynx contains the tonsils and opening of
the mouth and is a continuous structure from the oral cav­
ity to the soft palate and epiglottis. The laryngopharynx,
from the epiglottis to the cricoid cartilage, comprises what
is referred to as the larynx (see Figure 21-2 •) .
The epiglottis, a n upright flap o f cartilage lying behind
the tongue in front of the opening to the larynx, allows air
to pass into the deeper portions of the respiratory system.
During swallowing, it folds back to cover the entrance to
the larynx, preventing food from entering the windpipe.
Although primarily thought of as an organ of communica­
tion or voice box, the larynx is also an important regula­
tor of respiration. As a valve separating the windpipe, or
trachea, from the upper digestive tract, it is essential for
effective cough maneuvers and in preventing aspiration
during swallowing. An important feature in this area, the
piriform recess, is a deep cavity found on either side of the
larynx that directs food around it.
 C HA PT E R 21 • F U N D A M E NTALS FOR T H E A D M I N I STRATI O N OF N ITRO U S OXI D E-OXYG E N S E DATI O N 393

N asal cavity

Pharynx

Laryngopharynx

Bronchus

Lam ina propria

(connective
tissue)

A i r space

U<--- Squamous
epith e l i u m

Alveolar Structure
FIGURE 2 1 -2 Review of Upper and lower respiratory system anatomy.

The larynx is covered by a shield-shaped thyroid carti­
lage and a ring-shaped cricoid cartilage. The area between
the thyroid and cricoid cartilages (cricothyroid ligament)
can be penetrated for emergency respiration access when
upper airways are occluded (cricothyrotomy) . The vestibu­
lar folds of the larynx prevent entry of foreign objects into
the lungs. Contact with these tissues produces a cough re­
flex. It is important to note that under normal N20-0 2 se­
dation levels the cough reflex is not affected.
Lower Respiratory System The lower respiratory system
begins at the trachea, a muscular tube about 1 1 em long
that is contiguous with the larynx. The trachea begins at
the sixth cervical vertebra, divides into two branches the
right and left bronchi, and is surrounded by cartilaginous
rings; the lumen of this very important breathing passage­
way is maintained by these rings.
The carina is located at the junction of the trachea and
the left and right bronchi. Foreign obj ects are often found
in the carina. It is a secondary backup for reflex-defensive
cough initiation. The right bronchus is about 2.5 em long
and deviates about 25 degrees from the trachea. The left
bronchus is about 5 em long and deviates at about 45 de­
grees. The right bronchus divides into three branches that
link three upper lobes, two middle lobes, and five lower
lobes. The left bronchus divides into two branches and
links five upper lobes and four lower lobes.
Bronchioli are the smaller subdivisions of the branched
bronchial tree, approximately 1 mm or less in diameter.
They differ from bronchi in that they have cuboidal epithe­
lial cells and no cartilage plates. In the case of asthma, the
bronchiole can constrict because of the absence of carti­
lage rings and the presence of muscle tissue. This can make
expiration very difficult (see Figure 21-3 •).
Alveolar ducts are the finer ramification of the air
passages at the ends of the respiratory bronchioles. There
are approximately 1.5-2 million alveolar ducts per lung. At
the distal end of each duct, there are two or more alveolar
sacs containing alveoli that number approximately 3 0 0
million i n adults.
The primary purpose of alveoli is to move 02 from
the lungs into the capillaries and tissues. Venules return
oxygen-depleted blood to the pulmonary veins. Carbon
dioxide moves from the pulmonary arteries to the arteri­
oles and then to the capillaries before crossing the alveolar
membranes into the lungs.
The Respiratory Process As previously stated, the med­
ullary center of the brainstem controls involuntary breath­
ing. Inspiration is accomplished by the diaphragm and the
external intercostal muscles and is assisted by the scalenes
and SCMs (sternomastoids or sternocleidomastoids) .
The diaphragm m o v e s downward expanding t h e
chest wall that creates negative pressure in t h e pleural
space, thereby allowing a vacuum effect to pull air into
the lungs. Inspiration continues until pressure inside the
lungs is equivalent to atmospheric pressure. Pulmonary
stretch receptors send inhibitory signals to the inspiratory
394 S E C T I O N VI • N IT R O U S OXI D E-OXYG E N S E DAT I O N
FIGURE 2 1 -3 Anatomy of the lungs and bronchi. The carina
is located at the junction of the trachea and the left and right
bronchi. Foreign obj ects are often found in the carina. It is a
secondary backup for reflex-defensive cough initiation. The right
bronchus is about 2.5 em long and deviates about 25 degrees
from the trachea. The left bronchus is about 5 em long and devi­
ates at about 45 degrees. The right bronchus divides into three
branches that link three upper lobes, two middle lobes, and five
lower lobes. The left bronchus divides into two branches and
links five upper lobes and four lower lobes. Bronchioli are the
smaller subdivisions of the branched bronchial tree, approxi­
mately 1 mm or less in diameter.
center depressing inspiratory muscles causing them to stop
contracting.
Expiration occurs passively as the chest wall and lungs
recoil. The air in the lungs is then pushed out of the lungs.
The volume of each breath, the tidal volume, is the ebb
and flow of respiration.
Tidal volume may also be defined as the amount
of gas inspired into the lungs. It depends largely on the
physical characteristics of the individual. For example,
male lungs are approximately 25 % on average larger than
female lungs. Athletes typically have greater capacities.
Lung diseases can reduce capacity. The average adult tidal
volume at rest is approximately 500 mL. The average res­
piration rate in an adult is approximately 1 2-15 breaths
per minute.
Minute ventilation, also referred to as minute volume
or minute volume flow, is defined as the amount of air
exhaled in one minute and is calculated by multiplying
tidal volume by respiration rate. It is important to use
minute volume flow when determining N20-02 flow rates.
Tidal Volume Respiration Rate = Minute Volume
x
a l s in
� • • • . �: .�� �:. �O�.�� : .1 � � � :�� · · � � :��.
• • • • • • • IIi
Box 21-1 • provides the formula for determining minute
volume flow and a sample calculation.
The flow rate of N20-02 should be equal to the minute
volume, on average 6-7 Lpm based on average tidal volumes
of 500 mL and respiratory rates of 12 per minute in healthy
adults. Pediatric patients exhibit elevated respiratory rates
and lower tidal volumes ( start at 4 Lpm ) , therefore, it is im­
portant to modify minute volumes according to individual
patient needs ( Dionne, Phero, & Becker, 2002).
M aintaining appropriate minute volume is impor­
tant. Too little gas mixture ( N20 + 0 2 ) can make the act
of breathing difficult and produce a suffocating feeling,
whereas too much gas mixture will waste gases and pollute
the environment, exposing personnel to trace gases and
drying patients' eyes.
Gas Exchange Critical gas exchange occurs from alveoli
to capillaries and vice versa through simple diffusion across
partial-pressure gradients. The percentage of each gas de­
termines the partial pressure of each in the mixture. Atmo­
spheric air contains 78.06 % nitrogen ( N2 ) , 21 % oxygen
( 0 2 ) , and 0.04% carbon dioxide ( C0 2 ) at an atmospheric
pressure of 760 mm of mercury at sea level.
G a s e s move from higher to lower pressure. The
amount of gas capable of dissolving in blood depends on
its partial pressure and solubility. N20 and 0 2 have high
partial pressures in the lungs and have been characterized
as freely moving across cell walls into the blood. C02 has a
higher partial pressure in blood than in the lungs and rap­
idly leaves the blood ( see Figure 21-4 •).
Nitrous oxide has poor solubility in blood and rap­
idly leaves the blood when its partial pressure is higher
than that in the surrounding tissues. Poor solubility in the
blood results in a small percentage of N20 being removed
from the inhaled gas in the lungs. A state of equilibrium
is quickly established between the concentration of the
gas in the arterial blood supply and the air in the alveoli.
This property of N20 results in rapid onset of sedation and
rapid elimination of sedative effects when the gas is re­
moved. Once administration is discontinued, N20 rapidly
leaves the blood. This is equally true in the brain and other
organs of the body ( Levering & Wilie, 20 1 1) .
A condition known a s diffusion hypoxia m a y occur
when excess N20 diffuses out of the blood, displacing 0 2
i n the lungs, usually when extraordinary p ercentages of
N20 have been administered ( Jackson & Johnson, 2002).
This can result in a reduction of the 02 blood saturation;
 C HA PT E R 21 • F U N D A M E NTALS FOR T H E A D M I N I STRATI O N OF N ITRO U S OXI D E-OXYG E N S E DATI O N 395

Alveol u s

Cap i l l a ry

FIGURE 21-4 Alveolar Gas Exchange during Nitrous Oxide Delivery. A - Gas exchange
in the alveoli: critical gas exchange occurs from alveoli to capillaries. B - Gases move from
higher to lower pressure: N20 and 02 freely move across cell walls into the blood.

however, with N20 percentages used in dentistry, diffusion
hypoxia does not occur (Jeske et al. , 2004; Quarnstrom
et al., 1991 ) . Dental healthcare providers have been ad­
vised in the past to administer 1 0 0 % 02 to patients at the
conclusion of N20-02 sedation administration in order
to avoid diffusion hypoxia. Considering that the adminis­
tered percentages in dentistry do not reach the higher lev­
els associated with diffusion hypoxia, the administration of
100% 02 at the conclusion of N20 administration appears
to be an unnecessary precaution. Nevertheless, providing
1 0 0 % 02 toward the end of a dental appointment allows
discontinuation while providing a waning placebo influ­
ence. It also allows expired N20 to enter the scavenging
apparatus of the machine, which is sound environmental
practice (B ecker & Rosenberg, 2008) .
Cl i n ical M a n ifestations of Analgesia
a n d Anesthesia
Effects of Nitrous Oxide-Oxygen Sedation
on the Cardiovascular System
Once in the blood, N20 follows the normal course of the
circulatory system. There is no effect on the heart's con­
tractility, output, stroke volume, rate, or rhythm, and blood
flow to other maj o r organs is not significantly affected
(Haas, 1999).
N20-02 has a positive effect on myocardial ischemia
due to its provision of supplemental oxygen and its seda­
tive properties. It tends to dilate the p eripheral vessels
lessening the work needed to move blood. The mixture
of N20 and 02 typically contains 30 % N20 and 70 % O z,
which is more than three times the amount of oxygen in
room air. The increased 02 partial pressure and decreased
workload may help the ischemic heart. By reducing stress
and increasing available 02 in this manner, cardiac pa­
tients are less likely to have adverse reactions during
treatment.
Although blood pressure effects of N20-02 are dose­
related, pressures usually remain within normal limits.
Nitrous oxide can be beneficial in the presence of common
heart conditions such as hypertension, angina pectoris,
and some congenital conditions (Yagiela, Neidle, & Dowd,
1998) .
Effects of Nitrous Oxide-Oxygen Sedation
on the Central Nervous System
Individuals respond to sensory input by what is referred to
as perception, based on past experience. The cerebral cor­
tex receives all sensory input via the thalamus. Nitrous ox­
ide produces a decreased sensory perception that reduces
an individual's ability to react to pain through its effects on
the thalamus and cortex. Memory and mood are affected
to a variable degree depending on the concentration of
N20 . Nitrous oxide often produces mild performance
impairments in memory and patients typically rate their
moods as significantly less alert and calmer during seda­
tion (Thompson et al. , 1999).
Nitrous oxide typically distorts sp atial orientation,
making patients feel heavy or light and floating during its
administration due to its effects on the cerebellum. It also
exerts effects on the brain stem. In general, the brain stem
controls the wakefulness state of the body explaining the
sleepiness that N20 typically produces. The brain stem is
also responsible for movements and sensations related
396 S E C T I O N VI • N IT R O U S OXI D E-OXYG E N S E DAT I O N

to control of the throat, neck, and face, as well as reflex Table 2 1 -2 S u m m a ry of Effects o n Body Syste m s
activities involving breathing and eye movement. Usually
breathing and eye movement are not affected until high Body System Effects at Normal Sedation Levels
levels of N20 are administered ( significantly higher than
levels used in dentistry ) emphasizing the importance of Cardiovascular None to minimal effect on heart's
administering N20 at appropriate levels. contractility, output, stroke volume, rate,
or rhythm and blood flow
The autonomic nervous system ( ANS ) is predomi­
nantly an efferent system transmitting impulses from the
Central nervous Variable degree of amnesia; distorts spatial
CNS to peripheral organ systems. It regulates heart rate, system orientation; produces sleepiness; minimal
force of contraction, the constriction and dilation of blood effect on the autonomic nervous system;
vessels, the contraction and relaxation of smooth muscle in may enhance the CNS depressant effects
various organs, visual accommodation, pupillary size, and of drugs such as barbiturates, tranquilizers,
secretions from exocrine and endocrine glands. The ANS narcotics, and recreational drugs
can increase and decrease activity in these tissues. At nor­
mal levels and in healthy patients, N20-02 has little effect Gastrointestinal Pressure increases can expand air spaces
on the ANS ( Becker & Rosenberg, 2008; Emmanouil & worsening intestinal obstruction
Quack, 2007). May cause nausea
N20-02 sedation can be used for patients with com­
mon nervous system conditions, such as cerebrovascular Middle ear Pressure increases due to expansion of
air spaces
accidents, seizure disorders, and Parkinson's disease. Exag­
gerated reactions or other unexpected consequences may
Ophthalmic May cause expansion of gas bubbles
result when administering N20 to patients with conditions inj ected into eyes after recent retinal
such as autism, mental disorders, and Alzheimer's disease; re-attachment surgery
therefore, medical consultation is advised before admin­
istration. N20-02 sedation may exacerbate the negative Hematopoietic No known effects
aspects of many conditions such as some psychiatric dis­
orders, a history of chemical dependency including alco­ Endocrine No known effects
hol and substance abuse, or being under the influence of
alcohol or drugs at the time of administration. Nitrous Hepatic No known effects
oxide can also enhance the CNS depressant effects of
agents such as barbiturates, tranquilizers, narcotics, and Reproductive Potential for teratogenic toxicity
recreational drugs. It may be contraindicated in these situ­ exists, although it is doubtful that
there is significant risk from a single,
ations. Consultation and careful monitoring are essential
brief exposure; medical consultation
if N20-02 sedation is used ( Emmanouil & Quack, 2007) . recommended before administration
Effects of Nitrous Oxide-Oxygen Sedation
on Other Body Systems
If N20 is administered, it can diffuse into the bubble,
Nitrous oxide can expand air spaces in the body result­ causing expansion and a resultant pressure increase in the
ing in pressure increases in the GI system and should be eye that may result in pain, decreased vision, or blindness.
avoided in patients with intestinal obstructions until re­ Nitrous oxide administration should be postponed until
solved. Nausea is a common side effect of N20-02 seda­ healing is complete ( B erthold, 2002) .
tion, the etiology of which is discussed later in this chapter Nitrous oxide is in FDA Pregnancy Category C and
under Adverse Reactions. is considered a relative contraindication. B ecause of its
Nitrous oxide also increases pressure in the middle ear potential for teratogenic and fetal toxic effects, caution
space and can cause significant damage if middle ear dis­ and medical consultation are strongly advised. Risks and
turbances are present or if there has been recent ear, nose, benefits should always be discussed with patients before
or throat infection blocking the eustachian tube. Compli­ administration ( Little et al. , 20 12).
cations such as hearing loss, tympanic membrane rupture, Nitrous oxide has no known effect o n the hema­
and graft displacement can occur ( Davis, Moore, & Lahiri, topoietic, endocrine, or hep atic systems when used for
1979; Owens, Gustave, & Sclaroff, 1978; Waun, Sweitzer, & dental treatment at typical sedation levels. For a sum­
Hamilton, 1967). Postponing the administration of N20 is mary of the effects of N20-02 sedation on body systems,
recommended until the condition resolves. see Table 21-2 •·
Patients who have had recent ophthalmic surgery,
particularly involving the retina, may have a gas bubble A L L E R G I E S A N D N I T R O U S O X I D E - O XY G E N S E D AT I O N
that was placed in the globe ( bulbus oculi ) of the eye. The There are n o known allergies t o N20 . Allergies t o latex
treatment of detached retina often includes the inj ection may pose a problem if equipment contains latex. Most
of gas to help reposition the retina, allowing it to be re­ companies now m anufacture latex-free tubing, nasal
attached with the assistance of lasers. hoods, and reservoir bags.
 C HA PT E R 21 • F U N D A M E NTALS FOR T H E A D M I N I STRATI O N OF N ITRO U S OXI D E-OXYG E N S E DATI O N
M I N I M U M A LV E O LA R C O N C E N T R AT I O N The concen­
tration at which the effects of an anesthetic gas are pro­
duced is expressed as its minimum alveolar concentration
( MAC ) ( Dionne, Phero, & B ecker, 2002) . MAC repre­
sents the concentration of gas within the alveoli that
renders 50% of patients unresponsive to surgical stimula­
tion. In other words, MAC represents an adequate dose
to achieve general anesthesia for 50% of the population
and is given a MAC value of 1 ( Stoelting & Miller, 2000).
Nitrous oxide is the least potent inhalational anesthetic
and cannot be used to achieve general anesthesia under
normal circumstances. It is important to note, however,
that some patients are hyper-responders. Nitrous oxide
levels considered normal for most patients can result in
general anesthesia for hyper-responders. This highlights
the importance of recognizing symptoms of the various
stages of anesthesia.
Because the MAC of N20 is higher than 1 (1.4) , it can­
not be used as a single-agent general anesthetic and still
supply enough 02 to sustain life (21 % ) ( Stoelting & Miller,
2000) . In other words, in order to achieve a MAC of 1, 104 %
N20 would have to be delivered . This would reduce the
total available oxygen concentration to less than the per­
centage required to sustain life (21 % ) . The higher MAC of
N20 prevents its reliable use as a single general anesthetic
agent; however, it is commonly used in combination with
more potent anesthetic agents as a carrier gas to decrease
the dosage requirements and additional expense when us­
ing higher doses of more potent anesthetic gases.
Many factors reduce the actual inspired nasopharyn­
geal N20 concentration compared with the gas concentra­
tion delivery shown on the flow meters of dental N20-02
sedation equipment. These factors include ill-fitting masks,
mouth breathing, incorrectly calibrated flow meters, and
improperly adjusted scavenging rates. In one study with
adult patients, gas delivery from dental units was reduced
by 3 1 % in the nasal mask and by another 19% on the way
to the nasopharynx ( Klein et al. , 2004).
At typical sedation concentrations in dentistry of
0.3-0.5 MAC (30 % to 50 % ) , N20 produces mild analge­
sic effects that will still require the use of local anesthesia
( Becker & Rosenberg, 2008) .
Nitrous oxide administration has
A D V E R S E REACT I O N S
a significant history of s afety in dentistry most likely
related to its low potency ( MAC =1 .4) and the typi­
cal administration of sub-MAC concentrations in dental
settings ( Morgan, Mikhail, & Murray, 2006; Stoelting &
Miller, 2000) . In fact, no death has been reported follow­
ing the use of N20 in dental offices when appropriate
protocols are followed and N20 machines are properly
functioning.
Many consider N20 to be a mild gas that has only
modest influence on physiologic p arameters ( Morgan,
Mikhail, & Murray, 2006). This opinion seems reasonable
considering that typical doses provided in dental settings
are low. In addition, a recent evaluation of complica­
tions associated with anesthesia administered for dental
397
Table 2 1 -3 S u m m a ry of Adverse Reacti ons to
N20-02 Sedation
Adverse Reactions (Rare i n Occu rrence)
• Dizziness
• Increasingly rigid movements
• Unresponsiveness
Sweating
•
• Nausea and vomiting
• Dilated pupils
treatment reported that N20-02 administration had the
lowest complication rate of all current s e d ation and
analgesia techniques ( Boynes et al. , 20 10).
Although rare, it is important to note that complica­
tions and adverse reactions may occur. The most common
adverse reactions involve excessive dosing. Most of these
patients prob ably received high concentrations and/or
rapid titrations. Signs of excessive concentration include
dizziness, increasingly rigid movements, unresponsiveness,
sweating, and nausea and vomiting, all of which are easily
treatable if they occur. See Table 21-3 • for a summary of
adverse reactions to N20-02 sedation.
Although infrequent, nausea and vomiting are the
primary adverse reactions, as well as the leading causes of
patient dissatisfaction with N20-0 2 administration, espe­
cially during pediatric care ( B ailey et al. , 1990; Nkansah,
Haas, & Saso, 1997) .
The etiology of nausea and vomiting with N20 is mul­
tifactorial. The proposed stimulation of nausea and vomit­
ing by N20 may relate to increased middle ear pressure,
bowel distension and motility, and central nervous system
effects on dop aminergic receptors and opioid peptides
( Muralawa et al., 1995 ; Splinter & Komocar, 1997).
Medical gases are produced using water baths to re­
move impurities but are delivered in a dry state. This can
be problematic for those wearing contact lenses.
When N20-02 is properly titrated and patient behav­
ior is closely monitored throughout procedures, adverse
events are unlikely. Clinicians must continuously observe
for signs of excessive concentrations or adverse reactions.
If adverse reactions occur ( see Table 21-3), N20 concen­
trations should be decreased or discontinued by removing
the mask or nasal hood. In addition to adverse reactions
occurring from properly functioning equipment, there
have been several cases where gases have been switched.
The simple action of disengaging patients from N20-02
equipment following unresponsiveness or unconscious­
ness can prevent adverse outcomes.
Patient Assessment
When considering whether to administer N20-02 s e ­
dation, i t is assumed that examination a n d questioning
have already resulted in a determination that a patient
is able to undergo dental therapy either with or without
some modifications to treatment ( refer to Chapter 1 0 ,
398 S E C T I O N VI • N IT R O U S OXI D E-OXYG E N S E DAT I O N
Apprehensi v e patients
Restl e ss, anxious, or young children
• •
• Long procedures
• •
Hyperacti v e gag reflexes
•
� • • •�e �·p·o�� ���d.i � � l � r. � i �o.r� � r� • • • • • • • • • • • • • • • • •
• •
"Patient Assessment for Local Anesthesia" ) . Indications
and contraindications for N20-02 sedation rely not only
on these previous physical status determinations (see
Appendix 1 0- 1 ) but also on additional determinations
that pertain specifically to N20-0 2 administration.
Indications and Contraindications
As previously mentioned, indications and contraindica­
tions for N20-02 sedation are specific for its delivery
above and beyond previous, thorough overall physical
and mental health assessments that have included advice
from medical professionals when appropriate. Indications
include conditions and situations in which outcomes
can be enhanced by N20-02 sedation delivery or where
outcomes cannot be enhanced, but the risks of adverse re­
actions can be reduced (see Box 21-2 •) . Contraindications
include both relative and absolute categories in which
modifications to treatment or decisions to avoid adminis­
tration may also be permanent or temporary. Some addi­
tional examples of medical and industrial uses of N20 are
included in Boxes 21-3 • and 21-4 •·
CONTRA I N D I CATI O N S F O R N 2 0-0 2 S E DAT I O N As previ­
ously defined in Chapter 10, an absolute contraindica­
tion indicates that a drug may not be safely administered,
whereas a relative contraindication indicates that a drug
may be administered with additional precautions and/or
modifications. A list of absolute and relative contraindica­
tions is provided in Table 21-4 •·
Emergency medicine-to allevi a te pain associ a ted wi t h
heart distress
•
• Obstetrics/gynecology-labor and childbirth
Dermatol o gy-surgical procedures and liposuction
•
Podiatry-some surgical procedures
•
Radiol o gy-to relieve cl a ustrophobia during imaging
•
procedures
•
• Ophthalmology-cataract surgery
• Gastroenterology-for endoscopic examination
• center around the premise that some autistic individuals
Terminal illness-pain control for end-stage disease
•
•
• organizations state that in the presence of vitamin B 1 2
: . . . . . . &. . . . .2008.
Source: C l a rk
. . . . .. ........ ... .. •
B r u n i c k,
. . . . . . . .
Food industry-whipping cream
Auto industry-auto bag explosi v e (in research and
• development)
Motor racing industry-enhances internal combustion
� :• • �����t�� i ��� s.t ?�s: l �c� � �� i :.��n.u;�c��r�n•g• • • • • .
Absolute Contraindications Absolute contraindications
to the use of N20-0 2 sedation include hypoxic-driven, ad­
vanced chronic obstructive pulmonary disease (COPD),
active respiratory infection (URI, TB, influenza, etc.), first
trimester pregnancy, intraocular gas inj ection within 8-12
weeks, severe psychosis (considered a relative contrain­
dication in medicine), latex allergy, if nonlatex N20-0 2
sedation systems are unavailable, recent tympanic mem­
brane grafting, and treatments involving the inj ection of
gases into any body cavity (these require medical consult
before N20-02 administration) .
Relative Contraindications Relative contraindications to
the use of N20-02 sedation include dry air asthma, sub­
stance abuse, alcoholism (including recovered and recover­
ing), claustrophobia, post-traumatic stress disorders, latex
sensitivity (kiwi, banana, or avocado allergy may indicate
a potential latex allergy), current CNS depressant use (in­
cluding over-the-counter [OTC] medications or herbs that
list drowsiness as a side effect) , middle ear problems (such
as blocked eustachian tubes), and patients with colostomy
bags or bowel obstructions (following medical consulta­
tion). If patients are unable to understand the administra­
tion of N20-02 sedation (those with Alzheimer's disease
or mentally compromised), alternative routes of sedation
should be explored.
A generalized hereditary disorder, cystic fibrosis is
associated with widespread dysfunction of the exocrine
glands, accumulation of excessively thick and tenacious
mucous, and abnormal s e cretion of sweat and saliva.
Patients with cystic fibrosis may incur what are known as
emphysematous bullae that have been shown to function­
ally impair pulmonary mechanics, resulting in decreased
e x e r c i s e cap acity and p o s s i b l e r e s p iratory distre s s
(Greenberg, Singhal, & Kaiser, 2003 ) . These patients are
susceptible to the expansive nature of N20 gas, and it is
relatively contraindicated.
Autism is considered by some to be a contraindica­
tion to N20-02 sedation. Although there is currently no
direct evidence of exceptional risk when N20-02 seda­
tion is administered , there is concern among some that
there may be adverse effects. These concerns appear to
have altered vitamin B 1 2 and folate metabolism. Online
discussions and literature written by patient advocate
. deficiency, N20-02 se dation m a y result in neurologic
 C HA PT E R 21
Table 2 1 -4 Contra i n d icat i o n s fo r N20-02 Sedation
Absol ute Contraind ications
• Active respiratory infection (URI, TB, influenza, etc.)
• Advanced COPD (hypoxic driven) (in dentistry; relative in
medicine)
• Intraocular gas inj ection (within 8-12 weeks)
• Latex allergy (exception with non-latex systems)
• Pregnancy (first trimester) *
• Recent tympanic membrane graft
• Severe psychoses (in dentistry; relative in medicine)
• Treatment involving injection or pathology that causes
pockets of gases into a body cavity
*Medical consult recommended.
!Bleomycin (glycopeptide antibiotic used in anticancer treatment) can result in pulmonary fibrosis and impaired lung function.
deterioration. These very serious considerations appear to
be based on theories that have not yet been proven and
do not appear in medical research literature. Further in­
vestigation is warranted before placing definitive labels
on N20-02 use.
Additionally, although rare, exposure to N20 in any
highly susceptible individual may lead to a severe vitamin B12
deficiency such as persons with sickle cell disease ( Orrett &
Hertz, 2012; Jameson et al., 1999; Probasco et al., 2011 ) .
Although pregnancy ( second and third trimesters,
following medical consultation ) is considered a relative
contraindication, maternal pain can be problematic for
the fetus. When patients need to be treated and are ap­
prehensive, N20 can be the safest sedative. Its use in labor
and delivery for anxiety reduction has been advocated for
many years ( Clark & Brunick, 2008 ) .
Table 21-4 provides a summary of absolute and rela­
tive contraindications.
M a n ufactu ring Process
for N itrous Oxide
Nitrous oxide i s manufactured from ammonium nitrate,
the same chemical used to make fertilizers and explo­
sives. Ammonium nitrate is heated to 245-270°C at which
temperature it decomposes to N20 and water in the form
of steam. It is then cooled to room temperature and the
steam condensed, removing most of the water. There are sev­
eral chemical contaminants created during this process that
require scrubbing, including nitrogen dioxide ( N02 ) and ni­
trogen oxide ( NO ) . Once scrubbed, liquefied N20 ( 99.5 %
to 99.9% pure ) is stored at 300 psi at 4°F in insulated tanks
before being sent for distribution to retail customers ( CGA
Associates, 2012 ) . Some safety considerations for N20-0 2
sedation equipment are discussed in Box 21-5 • ·
• F U N D A M E NTALS FOR T H E A D M I N I STRATI O N OF N ITRO U S OXI D E-OXYG E N S E DATI O N 399
Relative Contra indications
• Certain mental/psychological disorders
• Claustrophobia
• Contact lenses
• Current CNS depressant use (includes OTC medications or
herbs causing drowsiness)
• Cystic fibrosis
• Dry air-induced asthma
• Individuals susceptible to Vit B 1 2 deficiency*
• Latex sensitivity
• May be contraindicated for use in patients receiving bleomycin!
• Middle ear problems (e.g., blocked eustachian tubes)
• Post-traumatic stress disorders
• Pregnancy (second or third trimester) *
• Recovering/recovered alcoholic
• Substance abuse
• Use of colostomy bags or bowel obstructions*
A diabatic com p ression: The term refers to a a diabatic
change in gas pressure without significant heat exchange;
in this case, the heat generated both inside and outside of
a tank when val ves are opened quickl y does not have time
to dissipate. The lack of significant heat exchange in adia­
batic compression i s useful in diesel engines, for example,
where compression strokes el evate temperatures that sub­
sequentl y igni te fuel.
I t can be qui t e dangerous when considering N20 or
02 use, however. When gases move rapidly from smaller
to larger volumes, there is little opportuni t y for gener­
ated heat to dissipate. In the case of N20 and 02, when
tank val v es are opened quickly into closed spaces, such
as occurs in lines leading from regulators to piping, they
cause rapid compressions resulting in heat. Once ener­
gized in this manner, gases can ignite nearby flammable
substances such as oils and lubricants. Opening N20
and 02 tanks slowly lowers the risk of dangerous igni-
•
tions of nearby flammable organic substances.
Pressu re variances: Transferring gases from high pres­
sure tanks through a common regulator when hoses are
made of combustible materials can resul t in fi r es. Tanks
should have regulators that lower pressures before gases
enter into fl e xible tubing that l e ads to manifolds or piping
systems.
H ig h-tem p erature ex p osure : If tanks are exposed
to high temperatures (such as from office fires), N20
can degrade into N02 and NO. N02 is a lung irritant
that can result in pulmonary edema and can be fatal
if inhaled in high concentrations (Peterson, 201 2). Any
tanks exposed to high temperatures should be returned
� .t � .s ��� ��� r� . IIi
.
• • • • • • • • • • • • • • • • • • • • • • • • • • • • •
400 S E C T I O N VI • N IT R O U S OXI D E-OXYG E N S E DAT I O N
The U.S. Food and Drug Administration (FDA) estab­
lishes requirements for manufacturing processes and qual­
ity control that must be followed by companies producing
N20 . Compliance is mandatory to assure a high-quality
product that exceeds U. S. Pharmacopeia Specifications.
The U.S. Department of Transportation (D OT) oversees
the packaging and transportation of N20 , considered to
be a hazardous material because of its pressurization. Most
containers are metal tanks that have been imprinted with
critical information such as serial number, inspector num­
ber, and DOT information. Some tanks in circulation may
be as much as 60-70 years old. Unlike heavier older tanks,
newer tanks are made of lighter materials such as aluminum
or fiberglass. State codes for the proper storage of tanks are
influenced by the National Fire Protection Association. In­
dividual states and cities may have additional laws and reg­
ulations regarding storage and use of gases.
H o spitals and m e dical facilities use the m aj ority
of N20 produced in the United States (80% to 85 % ) .
D entistry uses around 1 0 % o f the total. Approximately
83,000 dental offices and clinics in the United States cur­
rently purchase N20 from distributors. The remaining 5 %
o f N20 produced i s used b y industry (CGA Associates,
20 12).
Many variables determine the cost of N20 in den­
tistry, such as the size of the tanks, the quantity ordered,
and the distance from the distributor. These costs vary re­
gionally. Patient fees also vary regionally and are typically
determined by individual dental practices. Many dentists
do not charge for sedation; however, according to a 2008
survey in the United States, the average cost to the patient
for N20 was $ 50.00 (Singhal, 2008) . Some offices charge
per hour of use and some charge per visit, whereas others
incorporate the cost of N20-0 2 sedation into their proce­
dural fees.
Properties of Nitrous Oxide and Oxygen in Tanks
Nitrous oxide is a slightly sweet-smelling, colorless gas at room
temperature, with a boiling point of -88 .SOC ( - 127 .3°F) . It
is stored in tanks primarily as a liquid, with a small gaseous
content above the liquid, and is known to be an oxidizing gas.
The fact that N20 is an oxidizing gas is significant. It requires
clinicians to open both N20 and 02 tank valves slowly in or­
der to dissipate what is known as the heat ofcompression that
may be generated adiabatically as explained in Box 21-5. No
combustible material, such as oil, grease, or lubricants, should
be used on tanks, piping, or regulators located on or stored
near equipment. If these materials enter the orifices of tanks,
piping, or regulators, they may increase the odds of tank igni­
tion. This type of fire will burn fiercely.
In a 20 1 1 incident N20 and 0 2 tanks exploded when
a fire started in a tank storage room. Although an official
cause was not determined (listed in the fire report as ac­
cidental), the damage was significant as demonstrated in
Figure 21-5 •· At a minimum, these photographs illustrate
that N20 and 02 support combustion.
According to the World Meteorological Organization
(20 13), N20 is found in atmospheric air at approximately
323 .2 parts per billion. Its specific gravity is 1.53 (air = 1 )
and its molecular weight i s 44, making i t heavier than both
atmospheric air and 0 2• This characteristic is beneficial
when administering N20-0 2 sedation to pediatric patients.
The nasal hood can be held above the nose to initiate se­
dation until the child becomes more cooperative (this is
referred to as blow by) .
N ITRO U S OXI D E TAN KS Nitrous oxide tanks i n the United
States are painted blue and contain 95 % liquid and 5% va­
por when full. Stored at 70°F gauges will read 750 psi when
full. In pressurized tanks, gaseous portions are always lo­
cated above liquid portions.
Unlike oxygen tanks that decrease in pressure as ox­
ygen is used, N20 tanks maintain a constant pressure of
approximately 745 psi until all the liquid has evaporated,
making residual volume difficult to determine (Dionne,
Phero, & B ecker, 2002) . It is important to monitor tanks
regularly and to have an extra tank available to exchange
when necessary. B ecause of their largely liquid content,
N20 tanks typically last longer than 0 2 tanks.
A size G tank or G-tank holds 1 3 ,834 liters of N20 .
A G-tank of 0 2 holds 5,300 liters. The N20 tanks will last
significantly longer due in part to their liquid content and
the fact that typical administrations deliver only 30% N20 .
OXYG E N TAN KS Comprising approximately 21 % of the
earth's atmosphere, 02 is an odorless, colorless, and taste­
less gas with a boiling point of - 1 83°C. Oxygen's molecu­
lar weight is 32 and its specific gravity is 1.105. It is not
flammable; however, it is similar to N20 in that it supports
combustion.
Oxygen tanks in the United States are painted green
and contain 1 0 0 % gas or vapor. In most of the rest of
the world, the tanks are white. In Canada, they are usu­
ally green with a white top. In Japan, 0 2 is often stored in
black tanks. The amount of pressure on the gauge will read
approximately 2,200 psi when full, and unlike the N20
gauge, the 02 gauge accurately reflects the quantity of 0 2
used. When a tank is half empty, for example, the gauge
will read about 1,100 psi. See Figures 21-5 • and 21-7 •·
S E D AT I O N D E L IV E RY SYST E M S Components of seda­
tion delivery systems include manifolds, copper tubing,
latex or nonlatex hoses, pin index safety systems, regula­
tors, flow meters, reservoir bags, conduction tubing, and
breathing apparatus (see Box 21-6 •) . There are two types
of N20-02 delivery systems for use in dentistry, central
supply and portable machines. Manifolds, copper tubing,
and hoses are required for central supply systems. These
components use what is known as a D iameter-Index
Safety System to help prevent switching gases to the op­
eratory outlets. Pin index safety systems are used only for
portable equipment.
 CHAPTER 2 1 • FUNDAMENTALS FOR THE ADMINISTRATION OF NITROUS OXIDE-OXYGEN SEDATION 401

(A) (C)

IIrY r .-,/ :
AtJ/ .f:'
itlrt
-�.

,.. , ' .
-·

i \: .
. -. i.
_
·

. ·v
� )�·: ..

1 I ·
�...
.· •
.

P: •• I )1,· ;�-�J •
·, ·t.•' ' <. -.,·.
I ;I l.' ::
fLt'i ' : '
:. ·/ . ' I' . .

. I
,(-;q-,._._I '
.

' ... ,_�

�
��.
. -� � ,·

(B) (D)
FIGURE 2 1 -5 Dental Office Oxygen and Nitrous Tank Explosion. A - First response. B - Medical gas tank storage area.
C- Staff work area. D - Patient waiting room.
Source: Courtesy of Richard E. Freier/Spokane Valley Fire Department, Spokane Valley, WA.

CENTRAL SUPPLY DELIVERY SYSTEMS Central supply de­ Figure 21-8 • shows an example of a central supply deliv­
livery systems are used when supplying more than one op­ ery system.
eratory. The initial cost of building a central storage area The two major U.S. manufacturers of N2 0-0 2 sedation
and plumbing is significant; however, long-term costs tend systems are Porter/Matrx and Accutron. Newer models are
to be less when larger tanks are used frequently. The safety equipped with digital displays and other upgrades compared
controls in central supply delivery systems include remote with older models (see Figures 21-9 • and 21-10 •).
shutoff valves (sometimes manifold parts) and pressure In central supply delivery systems, manifolds serve
relief valves (usually gas regulator parts) found on high­ several purposes. They connect multiple tanks, allowing
pressure tanks. These valves reduce the 2,200 psi of a tank full tanks to be accessed once other tanks have been de­
down to atmospheric pressure. If a regulator fails, there is pleted. They also connect the gas supply to central piping
an over-pressure situation. In the case of a fire, the pres­ systems that can supply multiple operatories at the same
sure will rise in the tank. It is better to vent gas than risk a time (see Figure 21-1 1 •). While able to supply up to 10
tank failure that can result in an explosion. rooms at a time, installations for more than 10 rooms at
Central supply delivery units should include scaven­ the same facility may require additional federal and state
ger systems that are effective at eliminating residual gases. regulatory approval and review.
They usually operate via a separate suction system, part Copper tubing does not support combustion and is
of the office suction system. In addition, malfunction and required in central supply delivery systems. In order to
low-tank alarms are often installed along with convenient prevent potentially catastrophic consequences if lines
on and off controls for the equipment. Overall, central sup­ have been crossed, distinct sizes and colors of tubing are
ply delivery systems have more available safety features. installed for each gas (see Figure 21-12 •). Only certified
402 SECTION VI • NITROUS OXIDE-OXYGEN SEDATION

100%full 50%full empty 100%full 50%full 20%fu ll

OXYGEN NITROUS OXIDE

FIG URE 2 1 -6 Oxygen Cylinders and Gauges. FIG URE 2 1 -7 Nitrous Oxide Tanks and Gauges.
Source: Courtesy of Laura Stoddard. Source: Courtesy of Laura Stoddard.

technicians should perform maintenance and repairs on
central supply delivery systems.
In one situation, aging copper pipes and tubing were
replaced with p olytetrafluoroethylene ( PTFE ) prod­
ucts. Increasing the potential for failure, the tanks lacked
regulators and the PTFE tubes were installed directly to
a common regulator. Failure of the PTFE pipes and tub­
ing under high pressure resulted in an explosion and fire
with disastrous results. Even copper piping that is capa­
ble of withstanding high pressures flexes when tanks are
changed, leading to cracks. Although severe incidents are
rare, it is imperative to inspect the equipment and at least
annually perform an inspection and document results. This
will be discussed later in the chapter.
PORTABLE DELIVERY SYSTEMS Portable delivery systems
can be moved from operatory to operatory. They contain
smaller tanks and are perhaps best when sedation is used
infrequently. They can be more expensive to operate if se­
dation is used often because they contain less gas and do
not last as long as the larger tanks used in a central de­
livery system. They also may be harder to monitor when
there is concern of abuse or theft. See Figure 21-13 • for
an example of a portable delivery system.

PIN INDEX SAFETY SYSTEMS Tanks are attached to the

Manifold* yokes of portable stands. Each tank in portable units has
Copper tubing/hoses* its own pattern of holes on the valve stem, known as a pin
Pin index safety system** index safety system, that aligns with pins on the yoke ( see
Regulators Figure 21-14 •). The yoke has pins that correspond to a
Flow meters
pattern of holes on the connectors and fit snugly into the
Reservoir bag
holes of the tank. These arrangements of holes and pins
Conduction tubing
ensure that tanks are correctly attached to the correspond­
Breathing apparatus
ing gas yolks on the stands. Dislodging of pins has allowed

:� � � � ��� ��� : ' ' ' ' ' ' ' ' ' ' ' ' ' ' ' ' ' ' ' ' ' ' ' ' ' •
*Central supply delivery systems. the wrong tank to be placed on the yolk ( N20 tank placed
* ort � i n on an 02 yolk-0 2 tank on the N20 yolk ) resulting in hy­
' poxia, making it critically important to check the assembly
 CHAPTER 2 1
(A)
ALARM PANEL
(B)
FIGURE 2 1 -8 Central Supply Delivery Equipment. A - Nitrous
oxide and oxygen tanks. B - Digital alarm system.
Source: Courtesy of Royann Royer RDH,Accutron.
of the units ( Donaldson, Donaldson, & Quarnstrom, 20 12;
Goebel, 1980).
Regulators are found on both portable and central de­
livery systems. They reduce gas pressures from tanks before
any gas is delivered into the tubing and pipes. Tubing is
color-coded and size-specific for each gas and attaches reg­
ulators to flow meters on these systems. See Figure 21-15 •·
Flow meters are visual indicators of the volume of gas
being delivered, mounted on portable units or attached to
walls of central delivery systems. Calibrated glass tubes
FIGURE 2 1 -9 Central Supply Digital Control Panel.
Source: Courtesy of Porter Instrument Division.
• FUNDAMENTALS FOR THE ADMINISTRATION OF NITROUS OXIDE-OXYGEN SEDATION 403
� �I J I �
, Ill
.
�
.... 1:1!!!
FIGURE 2 1 -1 0 Portable Unit with Digital Control.
Source:
Courtesy of Accutron.
within flow meters are marked with lines corresponding to
total liters of flow per minute. Floating balls inside each
tube ( usually colored green for 02 and blue for N20 ) pro­
vide visual indications of the volumes of the gases deliv­
ered ( see Figure 21-1 6 •). Percentages must be calculated
using flow rates for each gas. The volumes in Lpm should
be measured from the midpoint of each ball. Newer equip­
ment has built-in fail-safe mechanisms that shut off N20
flow whenever 02 pressure falls below preset levels, an
important safety feature.
Reservoir bags provide a volume of gas necessary for
each breath, as high as 20 Lpm over a second or two. When
patients are resting between breaths or exhaling, bags re­
fill from the continuous flow of gas delivered by the ma­
chine. B ags allow additional gas for patients to breathe
when not enough is delivered through hoses and provide
mechanisms for monitoring bre athing and evaluating
404 SECTION VI • NITROUS OXIDE-OXYGEN SEDATION

(A)

(B) FIGURE 2 1 -1 2 Copper Tubing. Copper tubing that does

F I G U RE 2 1 -1 1 Central Supply System Manifolds.

not support combustion is used on central delivery systems.
A- Analog manifold. B - Digital manifold. Source: Courtesy of Royann Royer RDH.

Source: Courtesy of Royann Royer RDH,Accutron.

r,-.

c·'. ( ..

(A)
(B)
FIGURE 2 1 -1 3 Portable Delivery Systems. A - Older open cart. B - Newer closed cart system.
Source: Courtesy of Royann Royer RDH, Courtesy of Accutron.
 CHAPTER 2 1
FIGURE 21-14 Pin Index Safety System. Pin Index Safety Systems
ensure the correct attachment of gas cylinders to delivery units.
Source: Courtesy of Royann Royer RDH.
FIGURE 2 1 -1 5 Regulator. Regulators reduce pressures coming
from cylinders before entering pipes and tubing.
Source: Courtesy of Royann Royer RDH.
• FUNDAMENTALS FOR THE ADMINISTRATION OF NITROUS OXIDE-OXYGEN SEDATION 405
FIGURE 2 1 -1 6 Flow Meter. Flow meters provide visual indica­
tions of the volumes (Lpm) of gases being delivered.
Source: Courtesy of Accutron.
whether more or less gas is needed during administration.
Over-inflated bags indicate that excessive volumes of gas
are being delivered ( see Figure 21-17 •). This wastes gas,
increases excess gas in the operatory, and unnecessarily
increases the expense of sedation. Underinflated bags on
the other hand indicate that insufficient volumes of gas are
being delivered. This can lead to patient discomfort due to
feelings of suffocation, and the sedation is not likely to be
effective at these low levels ( see Figure 21-18 •). If bags
remain underinflated after increasing the flow rates, the
equipment should be checked for leaks ( see Figure 21-19 •).
Silicone rubber or polyethylene conduction tubing
attaches the equipment to the tubing that goes to the nasal
hood ( see Figure 21-20 •). It is corrugated to prevent
kinking and stratification of the two gases. During use it is
important to make sure that nothing is situated on top of
the tubing, potentially blocking the flow of gas and damag­
ing the tubing. After use, both the conduction and nasal
tubing should be soaked and washed according to infec­
tion control policy that is in compliance with OSHA and
local regulations.
The nasal hood is the bre athing apparatus that sits
over the patient ' s nose to facilitate the inhalation of
N20 - 0 2 ( see Figure 21-21 ( A ) and 21-22 •). Nasal hoods
406 SECTION VI • NITROUS OXIDE-OXYGEN SEDATION

FIG URE 2 1 -1 9 Torn Reservoir B ag. A torn or worn reservoir

bag allows leakage of the gasses into room air.
Source: Courtesy of Royann Royer RDH.

FIGURE 21-1 7 Overinflated Reservoir Bag. A ballooned

reservoir bag indicates overinflating due to excessive volumes
of gas being delivered.
Source: Courtesy of Royann Royer RDH.

FIG URE 2 1- 1 8 Underinflated Reservoir B ag. An FIG URE 2 1 -20 Conduction Tubing. Conduction tubing
underinflated reservoir bag indicates that insufficient provides the connection to the tubing feeding the nasal hood.
volumes of gas are being delivered. Source: Courtesy of Royann Royer RDH.
Source: Courtesy of Royann Royer RDH.
 CHAPTER 2 1 • FUNDAMENTALS FOR THE ADMINISTRATION OF NITROUS OXIDE-OXYGEN SEDATION 407

should be placed on the face so the mask fits snuggly
around the nose preventing gas leakage around the mask
and providing comfort for the patient.
There are many types of nasal hoods, but all should
be sterilizable or disposable or have disposable or steril­
izable inserts. For nasal hoods that cannot be sterilized or
(A)
disposed of, disposable inserts that fit inside the hood for
each patient are available; however, some filters have cre­
ated maj or leaks in the past. If a decision is made to use
inserts, only inserts that do not leak should be considered.
Barriers or surface disinfection should be used on devices
that cannot be sterilized, or the devices should be discarded.
It is critical that clinicians consult manufacturers' recom­
mendations before using any chemicals on these devices. It
is also important to understand that most chemical agents
that kill bacteria and viruses are very toxic to lung tissue, so
they must be completely removed before using masks.
Th e bre athing app aratus s h o u l d have s c a v eng­
ing capability to remove excess gas. Scavenging systems
help to eliminate excess gas being exhaled by patients,
therefore limiting environmental exposure to exhaled
N20 . The most commonly used systems consist of two
hoses attached to a nasal hood or a single hose that pro­
vides suction. One hose delivers gas to the patient, while
the other evacuates excess gas being exhaled by the
patient (see Figure 21-21 (B) and 21-22). Most man­
ufacturers have recommendations on scavenging vol­
ume rates. D ental he althcare providers should verify

PORTER PATENTED DOUBLE MASK SCAVENGER DESIGN

source source
To patient From patient From patient Primary

Stage 1 Stage 2 Stage 3 leak area

Inhalation Initial Exhalation Complete Exhalation

e Nitrous oxide e Oxygen e Carbon dioxide

SINGLE MASK DESIGN

To patient From patient From patient Primary

Stage 1 Stage 2 Stage 3 leak area

Inhalation Initial Exhalation Complete Exhalation

(B)
FIGURE 21-2 1 Sterilizable Nasal Hood. A - Porter double mask. B - Comparison of double mask versus single mask systems.
Source: Courtesy of Royann Royer RDH, Porter.
408 SECTION VI • NITROUS OXIDE-OXYGEN SEDATION

F I G U RE 2 1 -2 2 Scavenging Mask and Tubing.

Source: "Example of Airflow of Scavenging Mask." Copyright© by
Porter Instrument. Used by permission of Porter Instrument.

recommended scavenging rates of the manufacturer of

the N20 sedation unit being used. Older delivery systems
without scavenger systems have only a single hose.
CENTRA L SUPPLY DEL IVERY SYSTEMS Scavenging systems
are mandatory for office personnel safety. Those most
commonly used include systems manufactured by Porter/
Matrx ( Parker Hannifin, Hatfield, PA ) and Accutron
( Accutron Inc. , Phoenix, AZ ) . When portable delivery
systems are used, scavengers are attached to high-volume
evacuation systems, as shown in Figure 21-23 •· Central
F I G U RE 2 1 -23 Portable Scavenging System. This specific
system is attached directly to the high-volume evacuator to
capture lost gasses.
Source: Courtesy of Royann Royer.
supply delivery, frequently used in multi-operatory clinics,
has an external suction/exhaust function that vents gas out
of the facility. The appropriate suction/exhaust flow is indi­
cated by a ball in the green area on this Porter equipment
( see Figure 21-24 •).

(A) (B)
F I G U R E 2 1 -24 Central Supply Scavenging System. A - This specific system provides an indicator for
monitoring accurate suction levels. B - Floating ball should be within green band for proper function.
Source: Courtesy of Royann Royer RDH.
 CHAPTER 2 1 • FUNDAMENTALS FOR THE ADMINISTRATION OF NITROUS OXIDE-OXYGEN SEDATION 409

S A FETY MECHANI S M S FOR N20-02 SEDATION There

are at least 12 safety mechanisms available for N20-0 2
sedation equipment. All N20-02 armamentarium should
be maintained and serviced regularly. This ensures safe and
accurate administration and limits long-term personnel
exposure to ambient gases. Clinicians should be aware of the
specific safety mechanisms included in all N20-02 sedation
equipment used in their offices and clinics ( D onaldson,
Donaldson, & Quarnstrom, 2012).

EMPLOYEE SAFETY AND HEALTH GUIDELINES In 1977,

the National Institute for Occupational Safety and Health
( N I O S H ) s e t the maximum exposure limit for N20
concentration to 25 ppm for dental personnel. The most
current NIOSH publication on this guideline (1994) can be
found at www.cdc.gov/niosh.
In 1995, the ADA issued a formal position statement
(A)
that a maximum exposure limit has not been determined.
This statement was a result of a literature review, indicat­
ing that there was no scientific basis for the previously
established exposure limits due to inaccurate studies and
analysis.
The ADA has urged governmental agencies to cre­
ate new evidence -based N20 exposure recommenda­
tions. In October 20 05, the ADA issued a position paper
describing the need to support the expansion of both
basic and clinical research in anxiety and pain control.
It encourages institutions and agencies that fund and
sponsor rese arch to place a high priority on this type
of research, which should include: (1 ) epidemiological
studies that provide data on the number of these proce­ (B)
dures performed and on morbidity and mortality rates,
(2) clinical studies of drug safety and efficacy, (3 ) ba­
sic rese arch on the development of safer and more ef­
fective drugs and techniques, ( 4) studies on improving
patient monitoring, and (5) research on behavioral and
other non-pharmacological approaches to anxiety and
pain control.
When using N20-02 sedation on a routine basis, mon­
itoring of the ambient gases in the air is recommended.
In order to establish a baseline of N20 exposure for clini­
cians, analyzing leaked or trace gases in the environment
is also recommended. Monitoring can identify the need
for improved scavenging and can be useful in revealing
systemic leaks. There are several devices available to de­
tect the presence of trace gases. These include infrared
spectroscopy or spectrophotometry and time-weighted FOFIUSEBY

dosimetry.
Time-weighted dosimetry is an inexpensive method
for m o n itoring individual e x p o s ure to trace g a s. A
b a d g e is worn for a s p e cifi e d p e r i o d of time b efore
being submitted for analysis. This method allows for
continuous m o nitoring and is perhaps e a s i e s t when
N20-0 2 s e dation is used intermittently. An example
o f nitrous oxide monitoring equipment is shown in
Figure 21-25 •·
(C)
FIGURE 2 1 -2 5 Nitrous Oxide Monitoring. A - Clinician is
wearing a monitoring sensor on her right collar. The spectro­
photometry device to her left is analyzing trace gas exposure.
B - Spectrophotometry monitoring device. C - Individual moni­
toring device worn by clinicians.
Source: Courtesy of Royann Royer RDH,Advanced Chemical Sensors Co.
41 0 SECTION VI • NITROUS OXIDE-OXYGEN SEDATION

Principles of Nitrous Oxide Sedation

Nitrous oxide levels and patient responses vary, and pa­
tients may respond differently at subsequent appoint­
c-
m e n t s . E v e n t h o u g h m o s t p at i e n t s r e a c h a d e qu a t e Formula: % NzO = Lpm N20 Total Flow (Lpm 02
s edation levels between 15% a n d 40% N20 , there are + Lpm NzO)
no set concentrations to achieve specific levels of analge­
Example:
3
% NzO ( Lpm NzO c- Lpm 02

: ................. 7..L:�.�:�) .� � �. 7. � .-. :�..•

• 4 •
=

3
sia. In other words, although many patients react as an­
ticipated to these doses with mild sedative and analgesic 4

may react excessively ( hyper-responders ) to lower doses

responses, some of these same patients and other patients

or may barely react to higher doses ( hypo-responders ) at

any particular appointment. This explains the recommen­
dation of performing new titrations at every appointment,

order to achieve appropriate sedation goals ( Jackson &

regardless of previously recorded successful N20 levels, in
Formula: % 02 = Lpm 02 c- Total Flow (Lpm 02
Johnson, 2002).
+ Lpm NzO)
The mechanism by which N20 produces its effect

opioid system ( Dionne, Phero, & B ecker, 20 02). Nitrous

is theorized to involve interaction with the endogenous

oxide stimulates the release of enkephalins ( nociceptive­

regulating pentapeptides, natural painkillers ) that bind

pathways (Zhang et al. , 1999).

to opioid receptors causing reactions of specific analgesic

to enhance the effects of N20-02 ( Clark & Brunick, 2008).

Other non-pharmacological mechanisms can be used
in order to determine the percentage of N20 delivered per
minute, divide the liters of N20 per minute by the total
Box 21-7 • provides some examples.
liters of flow of N20 and 02 per minute. To determine the
percentage of 02 being delivered per minute, divide the li­
Calculating Percentages of Gases
ters of 0 2 being delivered per minute by the total liters of
B efore discussing administration technique, a discussion
flow per minute. An example is provided in Boxes 21-8 •
of percentage calculations when administering N20-0 2
and 21-9 •· For both calculations, the use of total flow in
sedation is critical to proper administration. Rather than
Lpm is used to calculate the percentages.
rely on flow meters, clinicians are advised to calculate
A quick reference chart for determination of N20 and
percentage levels of gases throughout sedation periods in
02 percentages can be found in Appendix 21-1 •·
order to continually determine appropriate dosages for
each individual. This is recommended because percentages
of gases displayed on e quipment may be inaccurate Steps for Administering Nitrous
b e c a u s e of t h e fre q u e n cy o f improperly calibrated Oxide-Oxygen Sedation
machines. Far more important than calculated percentages
are the effects patients are experiencing. Incremental Induction Technique
Similar to local anesthetic drug calculations, calculat­ The following should be included in preoperative N20-0 2
ing the dose of N20 and 02 requires an understanding of procedures:

STEP 1 : PATIENT A SSESSMENT AND INFORMED CONSENT

several factors. The use of total flow in Lpm is used to cal­

tering N20-02 sedation. In healthy patients ( ASA I, II ) ,

culate the percentages of gases administered. For example,
Patient assessment must be completed before adminis­

and medications. Medically compromised patients ( ASA

this usually consists of a review of current medical history

III, IV ) often require consultations with either their pri­

mary care physicians or medical specialists (Jastak, Yagiela,
& D onaldson, 1995). For a summary of ASA values, see
Box 10-2 and Appendix 10-1.
• Music
• • Video eyewear
Informed Consent Patients, parents, guardians, and care­
• Imagery
givers should be informed about sedative agent delivery
• Hypnosis
procedures and consent for sedation should be obtained.
•

:• : � � �� � �� - : • •
Oral premedication (In most states this will require
add t on l t i i
For an example of a consent form for N20-02 sedation,
• • • • . . • • • • • • • • • • • • • • • • • • • • • • see Appendix 21-2 •·
 CHAPTER 2 1 • FUNDAMENTALS FOR THE ADMINISTRATION OF NITROUS OXIDE-OXYGEN SEDATION
Preoperative dietary restrictions should be considered
and communicated to patients, parents, guardians, and
caregivers. The American Academy of Pediatric Dentistry
recommends patients consume little to no food 2 hours be­
fore the planned time of N20-0 2 administration (AAPD,
20 12). Preoperative verbal and written instructions should
be given to patients, parents, guardians, and caregivers.
Baseline vital signs should be obtained unless prohib­
ited by patient behavior. Vital signs should include blood
pressure, heart rate, and respiratory rate. Because it affects
local anesthesia dosing, it is also recommended that weight
be recorded.
STEP 2: PRE-SEDATION PREPARATION
Confirm Function of Armamentarium Assemble all
necessary sedation armamentarium and check for proper
function. Verify that adequate levels of N20 and 02 are
available for the length of appointment planned. Confirm
the availability of an independent 0 2 supply and any other
equipment necessary to deliver oxygen under positive
pressure.
Initiating flow of oxygen Seat the patient in a semi-supine
position. Explain the sedation procedure to the patient.
Establish the air flow volume. As previously mentioned,
tidal volume is the amount of gas inspired into the lungs and
is largely dependent on the physical characteristics of an
individual. The average adult tidal volume is 500 mL based
on an average of 6-7 Lpm. Therefore, start the flow rate at
6 liters of oxygen (100 % ) per minute (see Figure 21-26 •).
Position the nasal hood snugly around the patient's nose to
prevent gas leakage and to prevent excessive dryness of the
patient's eyes. A slide mechanism on the tubes can be used
to tighten the nasal hood. If minor air leaks occur around
nose pieces, despite tightening, 2 x 2 gauze squares can be
placed under them to reduce leakage. Observe the reservoir
bag making certain that it expands and contracts with each
breath, adjusting the flow rate up or down as needed for
optimal expansion and contraction.
C onfirming function of scavenging system While
delivering 100% 0 2> check the scavenging system for
proper function according to manufacturer instructions.
FIGURE 2 1 -26 Flow Tubes. These flow tubes show an initial
flow rate of oxygen of 6 Lpm.
Source: Courtesy of Royann Royer RDH.
41 1
Reconfirm the flow rate by observing that the patient is
breathing normally and reservoir bags are expanding and
contracting with each breath.
STEP 3: INCREMENTAL INDUCTION AND SEDATION MONI­
TORING Incremental induction of N20 may begin by de­
livering 10% N20 for 1 minute. Depending on the type of
equipment, it may be necessary to adjust both 02 and N20
flow levels in order to administer the correct percentage
of N20 . Once the initial flow of 02 has been established,
the Lpm of total gas flow should remain the same through­
out the appointment. It should be adj usted as necessary
so the bag neither over-inflates nor under-inflates as the
appointment proceeds. Example: If the patient's initial
tidal flow is 6 Lpm, the flow of both gases should equal
6 (5.5 liters 02 + 0.5 liters N20) ( s e e Figure 2 1 -27 •).
If an initial tidal flow of 6 Lpm over-inflates the bag, the
tidal flow should be adjusted downward. If the bag under­
inflates, the tidal flow should be adjusted upward.
As induction begins, make sure observable physi­
ological parameters remain normal and patients are able
to respond verbally. It is helpful to remind patients of the
importance of breathing through the nose as much as pos­
sible. B reathing through the mouth not only reduces the
amount of N20 that is available for sedation but also al­
lows N20 to be exhaled into the environment; however,
any time patients seem uncomfortable with their symp­
toms, clinicians can advise them that they may breathe
through their mouths in order to reduce the concentra­
tion of N20 they are inhaling. This is not ideal, but patient
comfort is critically important, especially when relaxation
is the goal. Uncomfortable symptoms should subside
quickly.
B ox 21-10 • provides a summary of the signs to ob­
serve, while Box 21-1 1 • provides guidelines for monitor­
ing patients on N20-0 2 sedation.
It is important to remember that only legally trained
and designated individuals may induce N20-02 sedation.
All designated individuals must be familiar with monitor­
ing techniques and equipment, and once sedation has been
induced, they must continuously monitor patients until
they meet criteria for discharge.
FIGURE 2 1 -27 Flow Tubes. These flow tubes show an initial
flow rate of nitrous oxide of 0.5 Lpm and of oxgen at 5.5 Lpm.
Source: Courtesy of Royann Royer RDH.
41 2 SECTION VI • NITROUS OXIDE-OXYGEN SEDATION
As sedation begins:
• Observable physiologic parameters should remain
• within normal limits.
� • •• � � � ����· · � �� �� � · · �� �� � . � �� ���·•••••••
Eye and swallow reflex should remain normal.
•
• e al un c i hou an
. .
• Oxygenation: Color of mucosa, skin, or blood oxygen
• •
level must be continuously observed and evaluated.
Ventilation: A dentist and/or an appropriately trained
individual can observe chest movement and maintain
verbal communication with a patient. Spoken responses
provide evidence that the patient is conscious and is
continuing with the respiratory process.
• Circulation: Blood pressure and heart rate should be
evaluated preoperatively and postoperatively as neces­
sary and when applicable.
• (2007b),
: � � : �� � : � : � �� •••••••••••••••••••••••••
( 0 )
Source: American Dental Association
.
n t s o og s s
. .
For accurate determination of percentages, the ball on
the flow meter should be centered on the line indicating
tions or equipment gauges ( see Figure 21-28 •) to assess
Lpm. Whether relying on simple mathematical calcula­
flow rates, it is important to restate that the most accurate
determination of appropriate titration results from careful
monitoring of patient signs and symptoms.
F I G U R E 2 1 -2 8 Importance of Monitoring Flow Rates. It
is important to confirm the accuracy of flow tube compared
with equipment gauge readouts . Note while the nitrous oxide
( )
dial set to less than 10%, the actual Lpm shown here by the
flow tubes most accurate is 17%.
Source: Courtesy of Royann Royer RDH.
Common symptoms of sedation include a:
• feeling of warmth
• • sense of relaxation
feeling of heaviness of the extremities
� :•• ��: � . • : � � : �: . � . �� ��� �� ••••••••••••• •
•
i s e f tin i th e r ti
Remind p atients to continue to b r e a t h e d e e p ly
through the n o s e . N ext, incre a s e the flo w of N20 to
20 % for 1 minute while continuing to monitor. At this
point, some patients may begin to feel the effects of the
N20 . This is a good time to describe the common symp­
toms of s e d ation such as a feeling o f warmth and re­
laxation and a sense of heaviness and/or tingling of the
extremities. Box 21-12 • provides a summary of these
sensations.
Next, increase the flow of N20 to 25% for 1 minute.
Continue to monitor and assess symptoms and increase
N20 levels by 5% as needed until desired levels of relax­
ation and sedation are obtained. Most patients reach ap­
Continue to monitor the progression of symptoms ( see
propriate sedation levels between 15% and 40% N20 .
•
American Society of
Bo x 21-13 •). If patients fail to achieve desired levels
of relaxation, instruct them to take three deep breaths
through their noses. It may be necessary to increase total
flow rates to prevent deflating the bags during these deep
breaths. If patients still fail to achieve desired levels, con­
tinue to increase N20 levels by 5% every minute until
mended concentrations are reached ( not to exceed an ab­
the desired symptoms are achieved or maximum recom­
solute maximum of 70% N20 ) . It is important to confirm
that patients are at appropriate levels of sedation through­
out appointments by close observation and appropriate
communication.
Signs of optimal levels of sedation may include:
• • a sense of relaxation and well-being
• •
•
a sense of comfort and awareness of surroundings
an ability to respond rationally and coherently
an ability to acknowledge a reduced sense of anxiety
•
and fear
• a dreamy look and a big smile
• • a tingling or heaviness of extremities
• a slight ringing in the ears; increased hearing range
� .�i•t a� :i: �s•s•h��l•d•r����n •n•o:���� •••••••••••••••• .
 CHAPTER 2 1 • FUNDAMENTALS FOR THE ADMINISTRATION OF NITROUS OXIDE-OXYGEN SEDATION 41 3

port feeling normal ( alert and oriented to place and time ) ,

Once all signs of sedation have resolved and patients re­

they may leave; however, if there is any question about

complete recovery, patients should not be allowed to leave.
• uncontrolled laughter A summary of incremental induction steps 2 through
• sweating 4 is provided in Box 21-15 •, and a more detailed list of all
• nausea steps is provided in Appendix 21-3 •·
•
• marked lethargy, closing mouth frequently
STEP 5: DOCUMENTATION
rate patient record of sedation vary according to j urisdic­
• unresponsiveness, unaware of surroundings, fixed stare The requirements for an accu­
• dysphoria (an emotional state marked by anxiety,
depression, and restlessness) tion. These may include the following: preoperative and
• inability to follow commands postoperative vital signs; initial tidal volume, Lpm of 0 2,
• dilated pupils
Lpm of N20, duration of sedation, any post-sedation find­
•

( Barash, Cullen, & Stoelting, 2001; Stoelting, 2006).

agitated, combative behavior

�: : �� � ��
•

ings or issues, and any adverse reactions and comments

ha l i atio
.li
include accurate accounts in p atient records ( Morgan,
• •. . . • • • • • • • . • • • . • • • • • • • • • . • • • • •

D ocumentation of critical or unusual events should

In cases of excessive sedation, patients may experience Mikhail, & Murray, 20 06). Important details include the
any of a number of signs and symptoms, many of which are specific adverse events that occurred, the time of occur­
listed in B ox 21-14 • and shown in Figure 21-29 •· In re­ rence, and the response to the events. Incomplete, errone­

( Barash, Cullen, & Stoelting, 2001). An example of a pa­

sponse, the level of N20 should be reduced or discontinued ous, and/or illegible documentation can result in liability
until the symptoms have resolved. It is recommended that
masks be removed if excessive sedation symptoms develop. tient record entry format for documenting N20-0 2 seda­
Symptoms will return to normal much faster if masks are tion is provided in Appendix 21-4 •·
removed and patients breathe room air.
Complications and Prevention of Adverse
STEP 4: INITIATING AND MONITORING RECOVERY To be­ Occurrences
gin the process of reversing the effects of sedation, discon­
Nitrous oxide administration in dental practice has a long
tinue the flow of N20 and administer 10 0% 02 for 3-5
history of safety and efficacy. Although complications oc­
minutes. Following this procedure, confirm that vital signs
cur only rarely, it is important to have a sound knowledge
and reflexes have returned to normal. Patients should re ­
and understanding of these events and their management
main seated for an additional few minutes to reduce the
should they occur.
risk of hypotensive episodes. They may sit in operatories
B o th n a u s e a a n d vomiting h av e o c c u r r e d d u r­
or waiting rooms until complete recovery has occurred.
ing N20-02 administration, especially in pe diatric pa­
tients. This is usually associated with an overd o s e , a
rapid incre ase in percentage, or a large initial volume
administered. If a patient becomes sick, N20 should be

Pre-Induction:

• Establish tidal volume: 100% 02 for 2 minutes

Inducing Sedation/Analgesia:

• 10% N20 for 1 minute

•

•
• 20% N20 for 1 minute
• 25% N20 for 1 minute
• Up 5% each minute until level achieved (not to exceed
70% Nz0)

FIG URE 21-29 "Hard Stare. " A fixed "hard stare" is a sign of
Initiating and Monitoring Recovery:

•
. .

: • Administer 100% 02 for 3-5 minutes •

excessive sedation.
Source: Courtesy of Royann Royer RDH. : . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
414 SECTION VI • NITROUS OXIDE-OXYGEN SEDATION
discontinue d and the nasal hood removed . If a p atient
is actively vomiting, make sure his or her head is turned
to the side and use the high-volume dental suction to re­
move vomitus from the mouth.
Some complication reports involve the respiratory
system during the exchange of gases. It should be noted
that N20 may actually have a positive effect on non-dry
air asthmatics because it is nonirritating to mucous mem­
branes and decreases anxiety that often triggers asthmatic
episodes.
Changes in C02 levels in the blood normally initiate
respiration in healthy individuals. This is known as hyper­
carbic drive. The primary stimulus of respiration is driven by
C02 levels that modulate the pH levels of the blood, stimu­
lating breathing. The hypoxic drive mechanism is respiration
stimulated by low 0 2 levels through oxygen sensors in the
carotid and aortic bodies (Mosby's Medical Dictionary, 2012;
Yacoub et al. , 1976) . This is secondary to COrstimulated
respiration and has no effect in healthy individuals.
Patients with severe COPD, on the other hand, who
have lost the ability to respond to C02 levels must rely
on much larger changes in 0 2 levels in order to stimulate
breathing. This puts them at risk if receiving N20-0 2 se­
dation because N20-0 2 depresses hypercarbic drive and
patients may not have enough stimulation for involun­
tary breathing (Becker & Rosenberg, 2008) . Medical con­
sultation is strongly advised before the administration of
N20-0 2 sedation in these situations.
Pneumothorax is an accumulation of air or gas in
the pleural cavity, usually a result of an alveolar rupture
or opening of the pleural space to outside air result­
ing in a collapse of the lung. Postpone treatment with
N20-0 2 sedation until the condition is resolved (Becker &
Rosenberg, 2008) .
Sinus discomfort has been reported by some patients
during N20- 02 administration. Sinus cavities represent
rigid air spaces. N20-02 increases pressure in these areas
potentially causing discomfort. If a patient complains of si­
nus pressure, N20-02 should be discontinued.
The drying effe cts o f respiration during N20-0 2
administration may cause irritation to the cornea or sclera
of the eye, especially if leaks occur around the nosepiece.
Contact lens we arers should remove their contacts to
avoid increased irritation. Patients who report dry and
itching eyes with seasonal allergies may require postpone­
ment of the procedure.
Occupational Risks
Regardless of properly functioning scavenger systems
and appropriate maintenance of equipment, it is impos­
sible to prevent trace amounts from leaking into treatment
rooms during N20-0 2 sedation. Long-term occupational
exposure risk increases when office spaces do not have
adequate ventilation. Incorrect administration of N20-0 2
sedation and poorly maintained equipment contribute to
higher levels of risk.
Chronic occupational exposure may result in detri­
mental effects to dental personnel (Kraj ewski et al. , 2007).
This is a controversial topic because most studies are lim­
ited and long-term data are not readily available; however,
potential side effects may include (CDC, 1994; National
Library of Science, 2014):
•
Reproductive difficulty including the risk of miscar­
riage, with the greatest risk occurring during the first
trimester
•
Megaloblastic anemia related to bone marrow
•
Neurologic disorders leading to sensory and proprio­
ceptive impairment that may be permanent although
they are usually temporary in nature. Chronic ex­
posure (breathing high concentrations, 30% to 50%
N20 , for hours at a time) may cause impaired motor
skills, visual acuity loss, numbness and tingling of the
extremities, weakness and lack of coordination, lack
of strength in the hands, and an electric shock feeling
upon flexion of the neck.
•
Vitamin Bl2-dependent enzyme, methionine syn­
thase interference. Nitrous oxide in high concentra­
tions or long-term exposure may interfere with the
activity of methionine synthase. This enzyme is neces­
sary for DNA synthesis and erythrocyte production.
It is thought that this is an issue for pregnant dental
personnel. The fetus is rapidly growing and cellular
reproduction rates are very high in order to support
rapid fetal growth rate which requires DNA. If vita­
min B12 is blocked, there is no methionine synthase
or DNA production (Yagiela, 1991 ) .
Symptoms are dose- and time-related. The effects o f
short-term exposure are reversible, but long-term, chronic
exposure can have irreversible consequences. It should be
noted that occupational risks or adverse outcomes have
not been reported when sedation is appropriately admin­
istered, adequate ventilation is available, and a scavenger
system is used (Sanders et a!, 2008) .
Chronic N20 abuse can result in the signs and symp­
toms previously listed. Breathing N20 directly from pres­
surized tanks can also cause frostbite to noses, lips, and
intraoral tissues. In extreme circumstances including de­
liberate self-over-sedation, death by hypoxic asphyxia can
occur.
The study of N20-02 sedation and, in particular, its
effects on the body, is an ongoing process. D e spite the
safeguards protecting healthcare workers from chronic oc­
cupational exposure to N20, some exposures are deliber­
ate. Two examples of misuse along with their outcomes can
be found in Box 21-16 •·
ETHICAL AND L EG AL I S SUES M e dical history assess­
ment is critical before sedation of any patient. Patient
consent is recommended although variation exists in the
types of consent processes that are necessary, depending
upon jurisdiction (Baynes, 20 1 1 ) . Evaluation of vital signs
should be obtained before the use of N20-02 sedation.
 CHAPTER 2 1
According to public records, two cases of chronic abuse
and inhaling nitrous oxide before performing treatment
resulted in arrests and state board actions: In 2010, a Hast­
ings, Michigan, dentist's abuse spanned at least two years.
He also allowed his teenage son to inhale nitrous oxide,
and the son then took his friends to "do nitrous". In 20 12,
a Florida dentist's license was subsequently suspended,
adding the following statement: "Due to her chemical
dependence, the dentist does not possess the physical
: � � ? :� � :
• and mental ability and the judgment necessary to practice
�
-
en i t sa � ·
- . . . • • • • • • • • • • • • • • • • • • • • • • • • • •
Contraindications and potential problems must be identi­
fied and protocols established. In some cases, it is advis­
able to consult with a patient's physician before the use of
sedation.
Patient monitoring during sedation is mandatory at
all times. At least one clinician must remain in a treat­
ment room to monitor a patient during N20-0 2 sedation,
and at least one additional, appropriately trained profes­
sional should be nearby and within view. This provides
for improved monitoring and the ability to respond in
the event of an emergency. It also provides a witnessed
defense to any allegations that might arise following the
use of N20-02 sedation. Although controversial, these al­
legations may include those resulting from sexual halluci­
nations. Three elements that are always involved in these
legal cases include treating a patient without an assistant
in the room, high concentrations of N20 , and a failure to
titrate the patient to avoid extension beyond the range of
therapeutic sedation (Malamed & Clark , 2003 ) . Dental
healthcare providers should review individual state and
provincial regulations to make sure staffing, monitoring,
and educational/training requirements for N20 - 0 2 admin­
istration are met or exceeded.
Equipment must be maintaine d on a regular basis.
Recommendations developed by NIOSH provide guide­
lines to assess sedation equipment. The ADA has also
developed a " Safety Checklist for Dental Equipment" to
remind all dental professionals to perform routine safety
checks of equipment (ADA, 2 0 1 2 ) . Appendix 2 1-5 and
21-6 provide additional examples of safety checklists.
Along with medical assessment, patient monitoring,
and equipment maintenance, accurate record keeping is
critical for sedation patients.
STATE AND PROVINCIAL STATUTES States and provinces
have the right to establish rules and regulations for the use
of N20-02 sedation in dental sites. In addition, clinics and
offices frequently develop site-specific standard operating
procedures.
All states and provinces have the right to establish
qu alifications, rules, and regulations for professional
• FUNDAMENTALS FOR THE ADMINISTRATION OF NITROUS OXIDE-OXYGEN SEDATION 41 5
licensure. Each governing body may operate with specific
boards or committees that oversee dental professionals
and the statutes that govern the dental profession, in­
cluding the use of sedation/anesthesia by dental profes­
sionals. Unfortunately, a wide regulatory variation exists
between individual dental boards, especially as it relates
to dental anesthesiology. It is important for all clini­
cians to familiarize themselves with dental statutes and
regulations of the j urisdiction in which they practice, to
complete required training, and to comply with current
regulations and laws.
•
• A review of the rules and regulations for N20 - 0 2 ad­
ministration may be helpful considering its use by dentists
and non-dentist clinicians.
Dentists Most dental schools include didactic and clini­
cal N20 - 0 2 sedation instruction in their pre-doctoral cur­
ricula. Over 80% of recent dental school graduates feel
they were adequately trained in N20 - 0 2 sedation (ADA,
2007a) .
The maj ority of states have rules for dental healthcare
providers administering N20-0 2 sedation to patients. The
ADA recommends that dental healthcare providers have
current certification in basic life support and training in
the administration of N20-02 sedation/analgesia that pro­
vides a thorough understanding of N20 , its properties, and
its effects on patient populations (ADA, 2007a) .
Non-D entist Clinicians The rules and regulations gov­
erning non-dentist clinicians as it relates to N20-02
sedation require a n understanding of the differences be­
tween administering and monitoring N20-02. Administer­
ing N20-02 involves the dispensing, applying, or offering
of N20 analgesia to a dental patient. Monitoring refers
to observing and evaluating patients through clinical ,
electronic, and mechanical means, and by recognizing and
reporting adverse reactions or complications to supervis­
ing dentists. These definitions are also used by a maj ority
of jurisdictions concerning the use of N20-0 2 sedation by
auxiliary personnel in dentistry.
Each state or provincial regulating authority delegates
the level of supervision required during the administration
or monitoring of N20- 0 2 sedation. The maj ority of states
and provinces require direct supervision levels. As of 20 1 1 ,
2 9 states permitted the administration o f N20-02 sedation
by dental hygienists, whereas 17 states allowed monitoring
only (B oynes, 20 1 1 ; American Dental Hygiene Associa­
tion, 20 1 1 ) .
Anesthesia is t h e m o s t closely regulated aspect o f
dentistry, with all states restricting the u s e of deep seda­
tion and/or general anesthesia to dentists with extensive
formal training (Moore et al., 2009) .
Nitrous oxide-oxygen sedation requires a provider
permit in many states and provinces, and all 50 states ad­
dress the use of N20-0 2 sedation in their regulations. In
addition, intravenous sedation requires additional training
beyond the pre-doctoral curriculum.
41 6 SECTION VI • NITROUS OXIDE-OXYGEN SEDATION

Future Development and Alternative: c. Allow recovery and the return of reflexes.
Xenon Anesthesia d. b and c
Xenon is a rare noble gas of the periodic table whose anes­
thetic properties were first noted in 1939. Xenon exerts its
References
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 CHAPTER 2 1 • FUNDAMENTALS FOR THE ADMINISTRATION OF NITROUS OXIDE-OXYGEN SEDATION
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418 SECTION VI • NITROUS OXIDE-OXYGEN SEDATION
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N itro u s Oxid e-Oxyg e n Sed ati o n
Ca l cu l ati o n S u m m a ry Ta b l e

1 50 33 25 20 17 14 13 11 10 9

2 67 50 40 33 29 25 22 20 18 17

3 75* 60 50 43 38 33 30 27 25 23

4 80* 67 57 50 44 40 36 33 31 29

5 83* 71 63 56 50 45 42 38 36 33

6 86* 75* 67 60 55 50 46 43 40 38

7 88* 78* 70 64 58 54 50 47 44 41

8 89* 80* 73 67 62 57 53 50 47 44

9 90* 82* 75* 69 64 60 56 53 50 47

10 91* 83* 77* 71 67 63 59 56 53 50

*Percentage exceeds maximum amount of N20 needed for effective pain/anxiety management in an ambulatory setting and exceeds amounts
able to be delivered by analgesia machines.

Example calculation:

What is the percentage of N20 when administering 4 liters of 02 and 3 1iters of N20?

4 + 3 = 7 liters total flow

3 (liters of N20) ..;. 7 (total Lpm) = 43 % N20

41 9
Sa m p l e N itro u s Oxi d e-Oxyg e n
Sed ati o n Co n sent

Consent for Local Anesthetic and Nitrous Oxide Sedation

Patient Name ------- Date _______

You will be given local anesthesia. LOCAL ANESTHESIA will produce a numb feeling in the area being treated and
only pressure will be felt during treatment. You will be awake and aware of your treatment, but there should be no pain
or significant discomfort.
1. Have a light meal a few hours prior to the procedure.
2. For more extensive procedures you may wish to have someone drive you home.
3. Plan to rest for a few hours after the procedure.

You may choose to add NITR O US OXIDE ANAL GESIA, as a supplement to local anesthesia. Use of Nitrous Oxide
requires that we o btain your consent.
NITROUS OXIDE is also known as "laughing gas." You will be relaxed and somewhat less aware of your surroundings, as
well as less responsive to minor discomfort, and you may or may not recall much of the procedure. Nitrous Oxide is breathed
through a nasal mask and, after a state of relaxation is reached, local anesthesia is administered.
Nitrous Oxide has few lasting effects, and you usually may drive safely after a fairly brief recovery time. However,
for safety precautions, its use does require some preparation on your part. Thus, it is important that you read and un­
derstand the information below and that you prepare by following the instructions carefully. If you are unclear about
anything, please ask your doctor.
1. Recovery time from nitrous oxide is usually very short, but may be prolonged, requiring you to remain in the of­
fice for some time after treatment. Rarely, you may be unable to drive home alone. Thus, it is best to arrange for a
responsible friend or family member to be "on call" for such a possibility.
2. Although not usually required, it may be best to have a responsible adult accompany you to drive you home.
3. You may have a light meal a few hours prior to treatment.
4. You may want to rest for several hours following treatment.

• I understand that the use of Nitrous Oxide, although usually safe and without lasting consequences, may affect me
differently.
• I am prepared to deal with any undesirable side effects of Nitrous Oxide and understand that those possibilities
listed above, as well as others not considered, may occur.
• I agree to the use of Nitrous Oxide analgesia ( "laughing gas" ) to supplement the local anesthesia planned for my
procedure.

0 Patient's or 0 Guardian's Signature: Date:

Guardian's Relationship to Patient:

Clinician Signature: Date

Witness' Signature: Date

420
Ste p s fo r N itro u s Oxi d e-Oxyg en
Sed ati o n I n d u cti o n

Step 1: Patient Assessment and Informed Consent
• Review the patient's medical history, treatment plan,
and individual pain control needs
• Identify alterations, precautions, and contraindica­
tions to care and to use of nitrous oxide-oxygen
sedation
• Take vitals and document in patient record
• Review the intended treatment plan and obtain
informed consent, including nitrous oxide-oxygen
• Administer 20% nitrous oxide for 1 minute
• Explain possible symptoms: warmth, relaxation
'
tingling of limbs
• Administer 25% nitrous oxide for 1 minute
• Continue to suggest symptoms
• Average patient reaches appropriate sedation
between 15% and 40% nitrous oxide
• Continue to increase at 5% intervals until appropri­
ate sedation is achieved or until 50% nitrous oxide is
administered

check for breathing, shallow breathing, loose ma�k

sedation and any other anesthetic agents indicated for
• If no symptoms of sedation are achieved at 50%
care
'
Step 2: Pre-Sedation Preparation kinking of tubing
• Continue at 5% increments until optimum sedation is
• Assemble appropriate armamentarium and confirm
established
proper function of delivery devices
• Do not exceed an absolute maximum of 70% N 0
2
•
M om0 tor throughout appointment for appropriate
Check tubing and reservoir bag for kinks or leaks
•
•

Ad� ust percentage of nitrous oxide as indicated by

Check to make sure unit is on and appropriate
symptoms
levels of oxygen and nitrous oxide are available for
•
length of appointment
patient symptoms
• Confirm availability of an independent oxygen
• Continue to check flow meters and reservoir bag
supply and equipment necessary to deliver oxygen
throughout treatment
under positive pressure.
• Never leave patient unattended; two clinicians
• Seat patient in semi-supine position
should monitor the operatory with patient at all
• Check for correct size of nasal hood
times
• Employ positive, supportive communication
• Explain procedure for sedation and expected Step 4: Initiate and Monitor Recovery
symptoms
• Discontinue the flow of nitrous oxide
• Establish tidal volume
• Administer 100% oxygen for 3-5 minutes
• Initiate 100% oxygen flow ( 6 liters for most adults )
• Take vitals to confirm baseline level
• Place nasal hood and position patient's head for
• Confirm reflexes have returned to normal
comfort
• Have patient remain seated for a few minutes to
• Check to make sure scavenger system is working
reduce the risk of hypotensive episode
properly
• Evaluate patient for complete recovery prior to
• Observe reservoir bag to determine need to increase
dismissal
or decrease tidal volume

� ocum�nt initial tidal volume, pre- and postop

Step 5: Documentation
Step 3: Incremental Induction and Sedation Monitoring
•
• Administer 10% nitrous oxide for 1 minute
vitals: mtrous oxide, and oxygen volumes throughout
• Remind patient to breathe deeply through the nose
appomtment
• Caution patient to limit speech to ensure a
• Document post-sedation oxygenation and any
continuous effect
complications in patient record
• Inform patients that they can breathe through the

mouth to stop effects quickly

421
Sa m p l e Pati e nt Reco rd E ntry fo r N itro u s
Oxid e-Oxyg e n Sedati o n

N20-02 SE DATION R E CO R D

Date: ________ Patient: __________________ Age: _______

ASA Classification: I II III IV

Med Consult Needed: Yes/No If yes, describe results __________________

Treatment Procedure: -------

Procedural Data: ------

Preoperative Postoperative
BP
Pulse
Respiration
N20 Start Time N20 Finish Time
Total Flow (Lpm) Titrated % of N20
Postoperative 02 (in minutes)

Comments:

Clinician Signature: -------

422
Safety Ch eckl i st fo r N itro u s Oxi d e-Oxyg e n
Sed ati o n Eq u i p m e nt
Delivery System and Components
Vi sually in sp e ct the N20-0 2 s e dation d e livery s ys ­
tems an d al l connections before starting anesthetic g a s
administration.
• Ensure that gas cylinders are safely handled and
stored
• Check tank regulators on central supply systems
• Check Diameter-Index Safety System for proper
function
• Check that alarm systems are functioning
• Check portable units for proper function of Pin Index
Safety System
• Do not use any lubricants or oils on equipment
Leak testing of equipment should be performed every
three months with a soap solution to check for bubbles at
pressure connections.
Adapted from ADA Safety Checklist for Dental Equipment and DHHS (NIOSH ) Publication Number 96-107.
Scavenging System and Components
N20 should never be used without properly functioning
scavenging systems.
• Maintain a supply of scavenging masks in a variety
of sizes to assure comfortable and secure fit over
patient's nose
• Perform periodic environmental monitoring for gas
exposure and leaks
• Vent N20 from all scavenging vacuum pumps to the
outside of the building away from fresh air intakes,
windows, and walkways
• Flush N20 from system after procedures by
administering oxygen to the patient for 3-5 minutes
Training
• Conduct regular personnel training, including updates
on nitrous oxide sedation
423
M ed i ca l G as Syste m An n u a l I n s p ecti o n Fo rm

The following checklist assists i n the inspection and maintenance o f medical gas systems per the requirements
of NFPA 99 and manufacturer specifications.

1. Medical gas pipe and manifold labeled with the gas carried and
direction of flow

2. All valves labeled

3. Cylinder manifold change-over signal functional

4. Cylinder reserve/in-use signal functional

5. Warning system components tested

6. Audible visual alarm tested

7. Shut off valve leak tested

8. Connections checked for leaks

9. Med gas room clear of storage

10. Med gas room appropriately labeled

1 1. Gauges (date installed: Reads Correctly Replaced

12. Hoses (date installed: Checked for Leaks Replaced

(Follow manufacturer's recommended replacement schedule if no leaks found)

13. Explain any no answers:

14. List items corrected:

15. List any corrections required:

Inspected by:

Date:

Company:

Modified with permission: MEDICAL GAS SYSTEM ANNUAL INSPECTION FORM (20 14), Spokane Valley Fire Department, Spokane, WA.

424
Introduction
Chapters 1 1-14 include discussions of anatomical factors
relevant to each inj ection technique and assume clinicians
have at least a basic knowledge of head and neck anatomy.
A general discussion of head and neck anatomy, Appen­
dix 1 : Anatomical Review, has been designed to assist in
the identification and review of local anesthetic landmarks
and the anatomic structures in or near the pathways of
intraoral inj ections.
Anatomical Review
The following information is intended only as a review of
head and neck anatomy with an emphasis on local anes­
thetic inj ections. This review assumes that clinicians have
at least a basic knowledge of head and neck anatomy.
Specific discussions relevant to individual inj ection tech­
niques are presented in the following chapters:
Chapter 12- Inj ections for Maxillary Pain Control I
Chapter 13 - Inj ections for Maxillary Pain Control
II - Palatal Approach
Chapter 14 - Inj ections for Mandibular Pain Control
In order to gain the greatest benefit from this section,
it is helpful to refer to a skull as well as a head and neck
anatomy text while referencing it. B efore reviewing the
anatomy of the head and neck, a summary overview of the
tables and figures included in this section is provided.
Overview Summary
Table AR-1: Bones of the skull
Figure AR-1 - Skull - frontal view
Figure AR-2 - Skull - lateral view
Figure AR-3 - Skull - posterior view
Table AR-2: Basilar view of the skull
Figure AR-4 - Skull - basilar view - foramina
Table AR-3: Basilar view of the skull
Figure AR-5 - Skull - basilar view - processes, plates,
arches, fossa
Table AR-4: Intracranial view of the skull
Figure AR-6 - Skull - intracranial view
Table AR-5: Maxillary and palatine bony views
Figure AR-7 - Skull -frontal view -maxilla
Figure AR-8 - Skull - lateral view -maxilla
Figure AR-9 - Skull - palatal view - maxilla and palate
Table AR-6: Mandibular views
Figure AR-lO - Skull - frontal view - mandible
Figure AR-11 - Skull - lateral view - mandible
Figure AR-12 - Skull - medial view - mandible
Table AR-7: Muscles of facial expression
Figure AR-13 - Muscles of facial expression
Table AR-8: Muscles of mastication
Figure AR-14 - Muscles of mastication - lateral view ­
superficial muscles
Figure AR-15 - Muscles of mastication - lateral view -
deep muscles
Table AR-9: Ligaments
Figure AR-16 - Ligaments - medial view
Table AR-10: External carotid artery branches (ECA)
Figure AR-17 -External carotid artery branches
Table AR-11: Venous blood return
Figure AR-18 - Jugular veins
Table AR-12: Ophthalmic division branches of trigeminal
nerve (V1)
Figure AR-19 - Trigeminal - ophthalmic division V1
Table AR-13: Maxillary division branches of trigeminal
nerve (V2 )
Figure AR-20 - Trigeminal - maxillary division V2
Table AR-14: Mandibular division branches of trigeminal
nerve (V3)
Figure AR-21 - Trigeminal - mandibular division V 3
Table AR-15: Facial nerve branches (VII)
Throughout this review, the * symbol designates structures not illustrated
on the associated figure.
Osseous Review
The skull consists of 22 bones (not including the three
small bones within the ear) . Some are paired bilaterally
and others are single. All but one of the skull bones articu­
late with one another by means of sutures composed of
fibrous connective tissue. Sutures initially allow for growth
and expansion of skull bones. Later, after growth has
ceased, they are considered non-moveable except when
subj ected to traumatic force. The only movea ble j oints of
the skull are the temporomandibular j oints, which articu­
late the mandible and the temporal bones.
The skull can be reviewed by identifying bones and
landmarks from all anatomical positions including the in­
tracranial surface. Many of these landmarks are important
to the study of local anesthesia.
A-1
A-2 APPENDIX 1

Table AR-1 Bones of the S ku l l

Cran iu m Face A
(8 bones tota l) (14 bones tota l)
F
Frontal (1) Nasal (2) B
c G
H
Parietal (2) Lacrimal (2)
D
E
Temporal (2) Maxilla (2)

Ethmoid (1) Zygomatic (2)

J

F I G U RE AR-2 Skull - Lateral View A - Frontal ( 1 ) , B - Nasal

Sphenoid (1) Vomer (1)

Occipital (1) Palatal (2) ( 2 ) , C - Lacrimal ( 2 ) , D - Zygomatic ( 1 ) , E - Maxilla ( 2 ) ,

F - Parietal (2) , G - Sphenoid (2),H - Temporal (1),I - Occipital (1),
Inferior nasal concha (2) J - Mandible (1).

Mandible (1)

C ra n i a l a n d Facial Bones A
Cranial bones protect and support the brain, whereas fa­
cial bones form the framework of the face and protect the
underlying viscera. These two general bony features of the B
skull, cranial and facial, will be considered in separate dis­
cussions. Many of the bones can be identified from exter­
nal, basilar, and intracranial views. c

F I G U R E A R- 3 S k ull - P o s t e r i o r View A - P a r i e t a l ( 2 ) ,
B - Occipital (1), C - Temporal (2).

A
Maxilla a n d Mandible
There are numerous anatomical features to review on
maxillary and palatine bones, and on mandibles, relevant
B G to the administration of local anesthesia. The locations of
these features follow anatomic patterns, which are simi­
c
H
lar on different skulls; however, there are occasional and
sometimes significant variations in these patterns. For this
0
reason, when studying anatomy for local anesthesia it can
be useful to view several different skulls, noting similari­
ties and differences among individuals.
E The mandible is the largest and strongest facial bone
because of the density of its cortical plate. Maxillary and
palatine bones typically have thinner cortical plates and
are relatively more porous. The significance of the re­
spective thicknesses of their cortical plates has a bear­
F
ing on local anesthesia. Anesthetic drugs diffuse more
readily through the maxilla compared with the mandible.
Solutions for mandibular anesthesia typically have to be
deposited directly over nerves before they enter bone
FIGURE AR-1 Skull - Frontal View A - Frontal (1 ), B - Sphenoid in order to be reliably effective. Suggested anatomical
(1), C - Ethmoid (1), D -Vomer (1), E - Maxilla (2), F - Mandible, features to locate on skulls are listed in Tables AR-5 •
(1), G - Nasal (2), H - Zygomatic (2), ! - Inferior Nasal Concha (2). through AR-12 •·
 APPENDIX 1 A-3

Table AR-2 Bas i l a r View of the S k u l l

Foramina, Fissures, Canals Structu re/Function/Content

Foramen magnum Nerve: spinal roots of spinal accessory nerve

Artery: vertebral

Other: medulla oblongata

Stylomastoid foramen Nerve: facial

Artery: stylomastoid

Jugular foramen Nerve: glossopharyngeal, vagus, spinal accessory

Artery: meningeal branches

Sinus: inferior petrosal, sigmoid (origin of internal jugular vein)

Carotid canal Nerve: internal carotid plexus

Artery: internal carotid

Foramen lacerum Nerve: none

Artery: none

Other: fibrocartilage in vivo

Foramen spinosum Nerve: meningeal branch of the trigeminal nerve, mandibular division

Artery: middle meningeal

Foramen ovule Nerve: mandibular division of the trigeminal nerve and the lesser petrosal

Artery: accessory meningeal

Vein: emissary

Lesser palatine foramen Nerve: lesser and middle palatine

Artery: lesser and middle palatine

Vein: lesser and middle palatine

Greater palatine foramen Nerve: greater palatine

Artery: greater palatine

Vein: greater palatine

Incisive foramen Nerve: nasopalatine nerve

Artery: sphenopalatine branches

A-4 APPENDIX 1

F I G U R E A R - 4 S k u l l - B a s i l a r V i e w - Fo r a m i n a
A - Pterygomaxillary Fissure, B - Greater Palatine Foramen,
C - Foramen Lacerum, D - Carotid Canal, E - Jugular
G Foramen, F - Foramen Magnum, G - Incisive Foramen,
H - L e s s e r P a l a t i n e For a m e n , ! - Fo r a m e n O v a l e ,
J - Foramen Spinosum, K - Stylomastoid Foramen.

A
8 H

I
c
J
D
E
K

F
H

I
J

Table AR-3 Bas i l a r View of the S k u l l

Processes, Plates,
Arches, Fossae Structures/Function/Content

Styloid process Attachments: stylohyoid, stylomandibular ligaments, styloglossus, stylopharyngeus muscles

Pterygoid process formed by lateral and medial pterygoid plates

Pterygoid fossa Attachments: medial pterygoid, tensor palatini muscles

Hamulus provides support for movement of tendon of tensor veli palatini muscle

Zygomatic arch Attachments: muscles of facial expression

Infratemporal fossa Nerves: mandibular, inferior alveolar, chorda tympani branch of the facial, and lesser
petrosal, and the otic ganglion
Arteries: maxillary, middle meningeal, inferior alveolar, posterior superior alveolar
Veins: pterygoid plexus
Muscles: temporalis, lateral and medial pterygoid

Pterygopalatine fossa Nerves: maxillary nerve division of the trigeminal, posterior superior alveolar, zygomatic,
and pterygopalatine ganglion
Arteries: maxillary, infraorbital, descending palatine
Veins: pterygoid canal, pharyngeal, sphenopalatine posterior superior alveolar,
pharyngeal, descending palatine, infraorbital, sphenopalatine, pterygoid canal,
inferior ophthalmic
 APPENDIX 1 A-5

F I G U R E AR-5 Skull - Basilar View - Processes, Plates, Arches,

Fo s s a A - Pterygopalatine Fo s s a , B - Infratemporal Fo s s a ,
C - Pterygoid Fo ssa, D - Styloid Process, E - Hamulus Pro­
cess, F- Medial Pterygoid Plate, G- Lateral Pterygoid Plate,
H- Pterygoid Process.

A
B E
F
c G
H

Table AR-4 I ntracra n i a l View of the S k u l l

Fissures a n d Foramina Structu res/Function/Content

Foramen magnum Nerve: spinal roots of spinal accessory nerve

Artery: vertebral
Other: medulla oblongata

Jugular foramen Nerve: glossopharyngeal, vagus, spinal accessory

Artery: meningeal branches
Sinus: inferior petrosal, sigmoid (origin of internal jugular vein)

Carotid canal Nerve: internal carotid plexus

Artery: internal carotid

Foramen spinosum Nerve: meningeal branch of the mandibular division of the trigeminal
Artery: middle meningeal

Foramen ovale Nerve: lesser petrosal of the mandibular division of the trigeminal
Artery: accessory meningeal
Vein: emissary

Foram en rotundum Nerve: maxillary division of the trigeminal

Superior orbital fissure Nerve: oculomotor, trochlear, abducens, ophthalmic division of the trigeminal,
ophthalmic (arising from the frontal, lacrimal, and nasociliary nerves)
Vein: ophthalmic
A-6 APPENDIX 1

A
D
E
B
c F

FIGURE AR-7 Skull - Frontal View - Maxilla A - Infraorbital

foramen, B - Canine fossa, C- Canine eminence, D - Zygomatic
process of the maxilla, E- Alveolar process, F- Eminence.

A
FIGURE AR-6 Skull - Intracranial View A - Foramen Ovale, B ­
Foramen Spinosum, C - Jugular Foramen, D - Superior Orbital B ----!;--------+.
c D
Fissure, E - Foramen Rotundum, F - Carotid Canal, G - Foramen
Magnum.

F
Table AR-5 reviews features of maxillary and palatine E
bones viewed from frontal, lateral, and palatal aspects.

M uscle and Ligament Review

F I G U R E AR-8 Skull - Lateral View - M axilla A - Pterygomax­
Selected muscles of facial expression, the muscles of mas­ illary Fissure, B - Zygomatic Process of Maxilla, C - Zygomatic
tication, and two ligaments will be identified in this sec­ Process of Temporal, D - Zygomatic, E - Maxillary Tuberosity,
tion. These muscles and ligaments are important because F- Posterior Superior Alveolar Foramina.

Table AR-5 M axi l l a ry and Palati n e Bony Vi ews

Frontal Lateral Basilar

Alveolar process Zygomatic arch Maxillary bones

Eminence Maxillary tuberosity
• Horizontal plate
• Canine eminence • Posterior superior alveolar foramina • Alveolar process
• Incisive foramen
Canine fossa Inferior temporal fossa
Zygomatic process Pterygopalatine fossa Palatine bones
Infraorbital foramen ( infra-orbital Pterygomaxillary fissure ( maxillary
Greater palatine foramina
nerve, artery, vein ) nerve and maxillary artery )
•

• Lesser palatine foramina

Median palatal suture
Transverse suture
Pterygoid process
• Lateral pterygoid plate
• Medial pterygoid plate
• Pterygoid fossa
 APPENDIX 1 A-7

Table AR-6 M a n d i b u l a r Views

Frontal Lateral I nternal

B ody of mandible Angle of mandible Ramus of mandible

Ramus of the mandible
• Alveolar process and teeth • Lingual
• Mental protuberance • Condylar neck • Mandibular foramen (inferior alveolar
• Mental foramen ( mental nerve, • Condylar head nerve, artery, and vein )
artery, and vein ) • Coronoid process • Pterygoid fovea
• Mandibular notch ( sigmoid notch ) • Retromolar triangle
• External oblique line • Internal oblique line
• Coronoid notch ( anterior border of • Mylohyoid groove
the ramus ) • Mylohyoid line

F
A G
H
B
B c
c D
D
I
E
J A ����....
F I G U R E A R - 9 Skull - Palatal View - M axilla and Palate FIGURE AR-1 0 Skull - Frontal View - Mandible A - Body of
A - Medial Palatine Suture, B - Transverse Palatine Suture, Mandible, B - Alveolar Process, C- Mental Foramen, D - Mental
C - Greater Palatine Foramen, D - Lesser Palatine Foramen, Protuberance.
E - Medial Pterygoid Plate, F - Incisive Foramen, G - Alveolar
Process, H - Horizontal Plate of Maxilla, ! - Pterygoid Palatine
Fossa, J- Lateral Pterygoid Plate.

A
B
c F

G
E
D H

F I G U R E AR-1 1 Skull - Lateral View - Mandible A - Condylar
Head, B - Condylar Neck, C - Mandibular Notch ( sigmoid notch) ,
D - Ramus of the Mandible, E - Angle of Mandible, F- Coronoid
Process, G - Coronoid Notch ( anterior border of the ramus ) ,
H - External Oblique Line.
F I G U R E AR-1 2 Skull - Medial View - Mandible A - Ptery­
goid Fovea, B - Ramus of Mandible, C - Mylohyoid Groove,
D - Mylohyoid Line, E - Retromolar Triangle, F - Internal
Oblique Line, G - Lingula, H - Mandibular Foramen.
A-8 APPENDIX 1

Table AR-7 M uscles of Facial Expression

M uscle Origin Insertion Fu nction

Buccinator Maxillary/mandibular molar Angles o f mouth Chewing; blowing air out

area of alveolar processes; of mouth
pterygomandibular raphe

Depressor anguli oris External oblique line on ramus Angle of mouth Lowers skin tissues of
lower j aw; frowning

Depressor labii inferioris External oblique line on ramus Skin of lower lip Lowers and draws lower
lip laterally

Levator anguli oris Canine fossa below infraorbital Angles of mouth Raises skin tissue from
foramen angles of mouth; smiling

Levator labii superioris Orbit of eye, lower margin Upper lip Raises facial skin above
above infraorbital foramen upper lip

Levator labii superioris Maxillae upper frontal process Upper lip and lateral of Raises upper lip; opens
alaeque nasi nostrils nostrils

Mentalis Mental protuberance Skin of chin Protrudes lower lip; raises

skin of chin

Orbicularis oculi Orbital rim; frontal processes Skin lateral of orbit; circle Closes eyelids; squinting
of maxillae; nasal process of around orbit
frontal

Orbicularis oris Circles mouth Angles of mouth Lips close; lips pucker

Platysma Skin above clavicle and Lower border of mandible Lowers angles of mouth;
shoulder and muscles around mouth raises skin of neck

R isorius Fascia of masseter Orbicularis oris; skin at angle Draws angle of mouth
of mouth laterally

Zygomaticus major Zygomatic bone Angle of mouth Raises angle of mouth;

smiling

Zygomaticus m inor Zygomatic bone Upper lip Raises upper lip

of their locations in or near inj ection pathways and be­
cause of the effects of local anesthetic drugs o n their
function. Muscles themselves are infrequent targets of
anesthesia in dentistry ( see Figures AR- 1 3 • through
AR-16 •) .
Clinicians are encouraged t o identify the origins and
insertions of muscles on skulls and to use skulls with
attached muscles when available ( see Table AR-8 •).
Vascular Review
The vascular system of the head may be defined as the
bl o o d supply to the brain and the extracranial struc­
tures. This vascular network includes arteries, veins, and
capillaries that are mirrored on the right and left sides
of the head. As in other parts of the body, many arteries
and veins share common names, especially those which
 APPENDIX 1 A-9

Levator Labii Superioris External Ca rotid Artery ( ECA)

Aloeque Nasi
Orbicularis Ocu l i
Levator Labii Superioris
Zygomaticus Minor
Zygomaticus Major
Levator Ang u l i Oris
The external carotid is a large, extracranial artery, which
is the most important vessel when considering dental
local anesthesia. The ECA branches from the common
carotid artery at the superior border of thyroid carti­
lage. It travels upward and medial to the internal carotid,
dividing into four maj o r segments, the anterior, medial,
p osterior, and terminal branches. Thes e branches are
listed in Table AR-10 •· Maj or areas of distribution are
included for arteries with significance to dentistry ( see
Figure AR-17 •) .

Venous Dra i nage

Orbicularis Oris
Risorius (cut away)
Depressor Angu l i Oris
Depressor Labii lnferioris
Platysma (cut away)
Mentalis
FIGURE AR-1 3 Muscles of Facial Expression
travel similar pathways and are deeply protected within
tissue. B l o o d vessels are interconnected by what are
known as anastomoses or openings from one vessel into
another.
The venous blood system begins at the capillary networks.
Capillaries connect with small veins or venules. As the vol­
ume of deoxygenated blood accumulates, venules empty
blood into larger veins, which typically follow similar path­
ways on the right and left sides of the head. These path­
ways are more variable compared with arterial pathways
because of the greater degree of anastomosis in veins com­
pared with arteries.
In some areas, networks of veins form what is known
as a venous plexus. The pterygoid plexus is a large venous
plexus located in the infratemporal fossa between the
temporalis and lateral pterygoid muscles. It has two im­
portant functions. It serves as part of the venous network

Table AR-8 M u scles of M astication

M uscle Origin Insertion Function

Buccinator Maxilla, mandible and Angle of mouth Forms anterior portion of

pterygomandibular raphe cheek

Masseter- Anterior 2/3 and inferior Lateral surface angle of Elevates ( closes ) mandible
superficial head border of zygomatic arch mandible

Masseter- Posterior one-third and medial Lateral surface above angle of Elevates ( closes ) mandible
deep head surface of zygomatic arch mandible

Lateral pterygoid- Inferior surface of greater wing Pterygoid fovea under the Lowers ( opens ) mandible;
superior head of sphenoid condyloid process; fibrous lateral movement of mandible;
capsule of TMJ protrusion of mandible

Lateral pterygoid- Lateral surface of Ia teral Pterygoid fovea under the Lowers ( opens) mandible;
inferior head pterygoid plate condyloid process; fibrous lateral movement of mandible;
capsule of TMJ protrusion of mandible

Medial pterygoid Medial surface of lateral Medial surface angle of Elevates ( closes ) mandible
pterygoid plate; pterygoid fossa mandible

Temporalis Temporal fossa Coronoid process of mandible Elevates (closes) mandible;

posterior portion retracts mandible
A-1 0 APPENDI X 1

Tempora l is

Temporalis

Med ia l

Lateral
j Superior
head
pterygoid
-1+-W..-- Buccinator

pterygoid Inferior Orbicularis

head oris

Masseter
Superficial (cut)

F I G U RE AR-1 5 Muscles of Mastication - Lateral View - D eep

head
masseter

FIGURE AR-1 4 Muscles of Mastication - Lateral View ­

Muscles

Superficial Muscles

returning deoxygenated blood to the heart. It also protects Superior pharyngeal

the maxillary artery (which travels inside the plexus in the constructor m uscle
area) by filling or emptying blood as needed, during j aw
movements. Although not a function, the plexus is also im­ Origin of Buccinator � /
Pterygomand ibular
portant in local anesthesia because of the increased risk of muscle "'-...._ raphe
bleeding if it is pierced during inj ection. Lingula Sphenomandibular
Venous blood from the brain or cranial cavity can col­ (at mandibular ligament
lect amid epithelial-lined spaces such as between the end­
Stylomandibular
osteal and meningeal layers of the dura mater. These areas ligament
are called venous sinuses. From sinuses, venous blood
drains into nearby veins. These veins are called emissary
veins, which, unlike most veins in the body, have no valves.
Without valves, blood flow is under greater influence of lo­
cal pressure changes. These changes can cause a two-way FIGURE AR-1 6 Ligaments - Medial View
flow of blood including through veins back into the sinuses.

Table AR-9 Ligaments

Ligament Origin Insertion Fu nction

Pterygomandibular Pterygoid hamulus Posterior of Connects superior pharyngeal constrictor muscle and
raphe mylohyoid line posterior buccinator muscle fibers

Sphenomandibular Spine of sphenoid bone Lingula Limits distension of mandible in an inferior direction
ligament
 APPENDI X 1 A-1 1

Table AR-1 0 External Caroti d Arte ry B ranches (E CA)

Artery Distribution Areas Pathway

Superficial temporal Side of head Posterior to neck of mandible

Parotid gland Superior as a terminal branch of ECA

Anterior branches (3):

• Superior thyroid Thyroid gland Inferior from ECA
Larynx
Some anterior neck muscles

• Lingual Soft tissues under tongue to hyoid bone and Lower posterior border of mandible, forms
tongue multiple branches that travel inferiorly

• Facial Skin and muscles of lips, cheeks, nose,
around eye
Soft palate, palatine muscles, palatine tonsils
Submandibular lymph nodes and salivary glands
Mylohyoid and digastric muscles
Anterior and medial to ramus, superior to
submandibular saliva gland, crosses under
border of mandible, forms multiple branches,
which travel superiorly

Middle branch* Wall of pharynx, soft palate, meninges, posterior Ascends vertically deep in neck between internal
cranial fossa, and many cranial nerves carotid and side of pharynx to undersurface of
• Ascending pharyngeal
base of skull, forms multiple smaller branches

Posterior Posterior scalp Posterior of ECA distal to ramus

branches (2):* Suprahyoid
Sternocleidomastoid muscles
• Occipital

• Posterior auricular Scalp around ear Posterior of ECA

Ear Superior to occipital artery

Terminal branches
Maxillary (MA)
First section

• Deep auricular* TMJ Branches within glandular tissues of parotid

Tympanic membrane behind TMJ
Skin of ear

• Middle meningeal Dura mater Branches in infratemporal fossa

Travels through foramen spinosum

• Inferior alveolar ( IA ) Pulp and periodontium of mandibular molar
and premolar teeth
1. Mylohyoid Floor of mouth, mylohyoid muscle
2. Incisive Pulp and periodontium of mandibular incisor teeth
IA artery travels inferiorly from the MA
between ramus and sphenomandibular
ligament inferior to IA nerve
Branches from IA before it enters mandibular
foramen
IA branches at mental foramen
Internal terminal branch is incisive artery

3. Mental Skin of chin External terminal branch of IA travels through

mental foramen

(Continued)
A-1 2 APPENDI X 1

Table AR-1 0 (Continued)

Artery Distribution Areas Pathway

Maxillary (MA)
Second section
• Deep temporal Temporalis muscle Travels superiorly between temporalis muscle
and pericranium

• Pterygoid branches Medial/lateral pterygoid muscles Variable number of branches supply pterygoid
muscles
Branches inferiorly and superiorly from MA

• Masseteric Masseter muscle Branches between neck of mandible and

sphenomandibular ligament
Travels laterally through mandibular notch

• Buccal Buccinator muscle; skin and mucous Travels forward obliquely between medial
membranes of cheek pterygoid and temporalis to lateral surface of
buccinator muscle

Maxillary (MA)
Third section

• Posterior superior Pulp and periodontium of maxillary posterior Branches before MA enters pterygopalatine
alveolar ( PSA ) teeth fossa
Maxillary sinus Travels along infratemporal surface of maxilla

• Infraorbital ( IO ) Lower eyelid Travels forward in IO groove and canal

Side of nose Exits IO foramen
Upper lip

1. Anterior superior Pulp and periodontium of maxillary anterior Travels inferiorly from IO artery and descends
teeth through alveolar canals
Maxillary sinus

• Sphenopalatine Nasal cavity Travels through sphenopalatine foramen and

enters nasal cavity and forms smaller branches

1. Nasopalatine* Lingual mucosa and gingiva of maxillary Travels along nasal septum and through
anterior teeth incisive foramen

• D escending palatine Hard palatal Travels in palatine canal and divides from
descending palatine to greater and Jesser
palatine arteries

1. Greater pal atine* Gingiva and mucosa of maxillary posterior teeth Travels through greater palatine foramen

2. Lesser palatine* Soft palate Travels through lesser palatine foramen

Palatine tonsils
• Artery of pterygoid Auditory Travels posteriorly into pterygoid canal
canal* Sphenoid sinus tube

*Not illustrated.

If an infection is present, it can spread via the emissary
veins through the sinuses and from there into the brain.
Venous blood from intracranial structures and from
deep structures of the face and neck drain into the internal
jugular vein. The external and anterior jugular veins drain
superficial structures of the head and neck. From these
veins, blood flows into the brachiocephalic veins and then
into the subclavian veins. The right and left subclavians
j oin, forming the superior vena cava, which conducts blood
flow into the right atrium of the heart. See Table AR-1 1 •
and Figure AR-18 •·
 APPENDI X 1 A-1 3

Posterior superior
Superficial temporal artery alveolar artery

Infraorbital artery

Maxi llary artery

Descending
palatine artery

External carotid

Facial artery

Inferior alveolar artery

Lingual artery
Superior thyroid

Deep tem pora l Sphenopalatine

a rteries artery

Superficial -----­ Infraorbital

temporal artery artery

Middle meni ngeal Posterior superior

artery alveolar artery

Anterior su perior
alveolar artery

Inferior alveolar Incisive artery

artery
Mental artery

External carotid Mylohyoid

artery artery Facial artery

FIGURE AR-1 7 External Carotid Artery Branches

A-1 4 APPENDI X 1

Table AR-1 1 Ve nous B l ood Return

Vei n Tributa ries/Collection Areas Pathway

TO EXTERNAL JUGULAR (EJ)

• Retromandibulars Superficial temporal vein Begins within parotid gland

Maxillary vein Travels downward and superficial to ECA
Commonly divides:
Anterior division j oins facial vein
Posterior division flows downward and superficial to ster­
nocleidomastoid muscle

1. Superficial Frontal B egins on side and vortex of skull

temporal Supraorbital Travels downward along temporal bone
Traverses through parotid gland

2. Maxillary External auditory meatus Begins from pterygoid plexus

Tympanic membrane Traverses through parotid gland
Pterygoid plexus Travels backward between sphenomandibular
Middle meningeal ligament and neck of mandible
Posterior superior alveolar
Inferior alveolar

• Posterior auricular Occipital plexus D escends posterior to ear

Superficial temporal plexus Joins posterior part of retromandibular vein

TO INTERNAL JUGULAR (IJ)

• Diploic brain Structures of the brain Posterior to internal carotid artery
Sigmoid sinus of dura mater

• Common facial Frontal region B egins on forehead

1. Supraorbital/ Tissues of orbit Passes downward superficial to frontalis muscle
supratrochlear

2. Angular Supraorbital vein Forms at medial part of eye

Supratrochlear vein Travels lateral of nose
B ecomes anterior facial vein

3. Superior labial Upper lip Anastomoses from upper lip

4. Inferior labial Lower lip Anastomoses from lower lip

5. Submental Chin region Anastomoses with branches of lingual vein and inferior
Submandibular region alveolar vein
Parallels submental artery on superficial of mylohyoid
muscle

6. Lingual Ventral and dorsal surface of tongue Travels with lingual artery
Floor of mouth Deep to hypoglossus muscle
Variable drainage

• Pterygoid plexus Middle meningeal Located in infratemporal fossa near pterygoid muscles,
Anterior superior alveolar around the second and third sections of maxillary artery
Middle superior alveolar Communicates with cavernous sinus, pharyngeal venous
Posterior superior alveolar plexus
Inferior alveolar Anastomoses with deep facial vein, facial vein, and retro­
Greater palatine mandibular vein
Lesser palatine
Sphenopalatine

Anterior
retromandibular vein
Posterior
retromandibular vei n
Posterior auricular vei n
External j u g u lar vei n
�-"""'1��=----=�=---d\-
1!
""'
""--- I nternal j u g u lar vein
FIGURE AR-1 8 Jugular Veins
Nerve Review
The target nerves of most dental local anesthetic inj ections
are branches of the trigeminal nerve. A comprehensive
knowledge of the trigeminal nerve is essential to perform­
ing dental local anesthetic techniques. In addition to target
nerves, branches of the facial nerve are sometimes inad­
vertently anesthetized because of their close approxima­
tion to trigeminal branches within oral and facial tissues.
In all cases, nerve pathways can vary and their variations
can significantly affect the success of anesthesia. In order
to understand typical nerve branch patterns, skulls with at­
tached nerves can be helpful.
Suggested anatomical features to locate on skulls are
listed in the tables in this section.
Trigeminal Nerve
The trigeminal nerves are the largest of the cranial nerves.
Similar innervation patterns are seen on both the right and
left sides of the face. They have afferent or sensory nerve
roots that convey information about touch, temperature,
pain, and proprioception from the scalp, face, oral cavity,
tongue, and teeth, and a smaller efferent or motor nerve
root, which provides innervation mainly to the muscles of
mastication.
Sensory nerves travel to each trigeminal ganglion lo­
cated on the anterior aspect of the petrous portion of the
temporal bone. B eyond the ganglion, sensory nerve fibers
APPENDI X 1 A-1 5
Maxi l lary vein
Pte rygoid
plexus
Anterior
facial vei n
Deep facial vein
� S u perior labial
(extend branches)
!
\' I nferior labial
S u b m e ntal
(extend branch)
Common facial vein
continue into the mid-lateral section of the pons in the
brainstem.
Motor roots of the right and left mandibular divisions
form in the pons and medulla. They travel in separate lo­
cations from sensory nerves, in a lateral and inferior di­
rection to the trigeminal ganglion before exiting the skull
through the foramen ovale and j oining the sensory roots of
the mandibular division.
The three divisions of the trigeminal are the ophthal­
mic (V1), maxillary (V2) , and mandibular (V3) nerves. All
three divisions pass through openings in the sphenoid
bone. The ophthalmic nerve passes through the superior
orbital fissure. The maxillary nerve passes through the fo­
ramen rotundum. The mandibular nerve passes through
the foramen ovate.
Ophth a l m ic Division (V 1 )
The ophthalmic nerve is the first division of the trigemi­
nal nerve. It transmits sensory information through the
superior orbital fissure and travels along the lateral wall
of the cavernous sinus to the anterosuperior aspect of
the trigeminal ganglion. The ophthalmic is the small­
est division of the trigeminal nerve and has three main
branches, the frontal, lacrimal, and nasociliary. Local an­
esthetic inj ection techniques in dentistry do not typically
target these branches. See Table AR- 1 2 • and Figure
AR-19 •·
A-1 6 APPENDI X 1

Table AR-1 2 O p htha l m i c Division Branches of Trigem i n a l Nerve (V1)

Nerve Innervation Pathway

• Frontal Skin of forehead Develops from two smaller nerves

Eyelids Travels along superior of orbit
Skin of nose

• Nasociliary Medial of eyelid Develops from several smaller nerves

Side of nose Travels across optic nerve and then along medial wall of orbit
Parts of eyeball
Mucous membrane of nose
Paranasal sinuses

• Lacrimal Lateral of upper eyelid Travels along lateral superior of orbit

Conjunctiva Receives autonomic nervous fibers from zygomatic branch of maxillary
Lacrimal gland nerve

infraorbital canal, and on the face. In dentistry, maxillary

and palatal inj ection techniques are used to anesthetize
the maxillary nerve and its branches. See Table AR-13 •
and Figure AR-20 •·

Mandibular Division (V3)

FIGURE AR-1 9 Trigeminal - Ophthalmic Division V1
A - Frontal, B - Nasociliary, C - Lacrimal.
Maxi l l a ry Division (V2 )
The maxillary nerve is the second division of the trigemi­
nal nerve. It transmits sensory information in the maxillary
region from the maxillary teeth, periodontium and gingiva,
and from the maxillary sinuses, nasal cavity, palate, naso­
pharynx, a portion of the dura mater, and the skin cover­
ing the maxillae. The maxillary nerve passes through the
foramen rotundum in the sphenoid bone to the mid-ante­
rior aspect of the trigeminal ganglion. The maxillary nerve
branches in four areas, the cranium, pterygopalatine fossa,
The mandibular nerve is the third a nd largest division
of the trigeminal nerve and the only division to con­
tain a motor or an efferent root. The larger sensory or
afferent root transmits information from half the man­
dibular teeth, their associated periodontium, the mucous
membranes of the cheek, the anterior two-thirds of the
tongue, mastoid cells, lateral scalp, the skin anterior to
ear, the lower cheek, lower lip and chin, parotid gland,
the temporomandibular j oint, and the remaining bone of
the mandible on one side.
Muscles innervated by the efferent components in­
clude the temporalis, masseter, medial and lateral ptery­
goid, tensor veli palatini, and the tensor tympani.
The nerves of the mandibular division branch in three
areas, including the undivided trigeminal nerve and the
anterior and posterior division. In dentistry, mandibu­
lar inj ection techniques are used to anesthetize several
branches of the mandibular nerve. See Table AR-14 • and
Figure AR-21 •·
Facia l Nerve (VI I )
Local anesthetic techniques in dentistry have been devel­
oped to anesthetize branches of the trigeminal nerve. Some
extent of facial nerve anesthesia is unavoidable at times
when using these techniques. Like the trigeminal nerve, fa­
cial nerves have consistent patterns of innervation with fre­
quent variations on the right and left sides of the face. Facial
nerves have efferent, parasympathetic, and afferent roots.

Table AR-1 3 Maxi l l a ry Division Branches of Tri g e m i n a l N e rve (V2)
Nerve
• Middle meningeal nerve
• Zygomatic
1. Zygomaticofacial
2. Zygomaticotemporal
• Nasopalatine ( NP )
• Palatine
1. Greater palatine
2. Lesser palatine
• Posterior superior
alveolar ( PSA )
• Infraorbital
1. Middle superior
alveolar ( MSA )
2. Anterior superior
alveolar (ASA )
• Superior labial
• External nasal
• Inferior palpebral
Innervation
CRANIAL BRANCHES
Dura mater
PTERYGOID FOSSA BRANCHES
Side of forehead skin
Upper cheek skin
Gingival, mucosal, and osseous tissue from
central incisor to canine
Palatal gingival, mucosal, and osseous tissue
from premolars to posterior of hard palate
Palatal mucosa of soft palate
Dental pulp, facial gingiva, periodontal ligament,
alveolar bone of maxillary first, second, and
third molars, except mesiobuccal root of first
molar
INFRAORBITAL CANAL BRANCHES
D ental pulp, facial gingiva, periodontal liga­
ment, and alveolar bone of maxillary teeth,
including incisors, canine, first and second pre­
molars, and mesiobuccal root of first molar in
some individuals
Dental pulp, facial gingiva, periodontal liga­
ment, and alveolar bone of maxillary first and
second premolars and mesiobuccal root of
first molar in some individuals
Dental pulps, facial gingiva, periodontal ligament,
and alveolar bone of maxillary central incisor
through canine
TERMINAL FACIAL BRANCHES
Upper lip skin and mucous membranes
Lateral of nose skin
Lower eyelid skin
APPENDI X 1 A-1 7
Pathway
Formed from convergence of small nerves from
dura mater
Join maxillary nerve near trigeminal ganglion
Travels with middle meningeal artery
Travels through inferior orbital fissure
Travels through inferior orbital fissure
Travels through incisive foramen and incisive
canal
Along nasal septum to roof of nasal cavity
Travels through greater palatine foramen on
hard palate of maxilla
Travels through lesser palatine foramen to pala­
tine canal
Commonly divides:
External branch travels along surface of poste­
rior maxilla
Internal branch travels through PSA foramina
on tuberosity of maxilla
Formed by the convergence of terminal facial
branches, MSA and ASA nerves
Travels through the infraorbital canal
Travels from dental plexus
Variable innervation or MSA
May be absent
Travels from dental plexus through
anterior of maxillary sinus and
infraorbital foramen
Travels from upper lip and to infraorbital
foramen
Travels from lateral side on nose to
infraorbital foramen
Travels from lateral side on nose to
infraorbital foramen
A-1 8 APPENDI X 1

FIGURE AR-20 Trigeminal- Maxillary Division V2 A- Zygomatic,

B - Pterygopalatine Ganglion, C - Greater Palatine, D - Lesser
Palatine, E - Posterior Superior Alveolar, F- Infraorbital,
G - Inferior Palpebral, H - External Nasal, ! - Superior Labial,
J- Middle Superior Alveolar, K- Anterior Superior Alveolar,
L- Nasopalatine, M- Maxillary Dental Plexus.

Table AR-1 4 M a n d i b u l a r Division Branches of Trigem i n a l Nerve (V3)

Nerve Innervation Pathway

UNDIVIDED NERVE

• Nervus spinosus Dura mater Formed from convergence of nerves from dura
mater
Enters skull through foramen spinosum

ANTERIOR DIVISION

• Masseteric Masseter muscle Travels laterally superior to lateral pterygoid

Small branch to TMJ muscle
Crosses mandibular notch with masseteric
artery
Anterior to TMJ

• Temporal Temporalis muscle Travels superior to lateral pterygoid muscle

1. Anterior temporal between skull and temporalis muscle
2. Posterior deep temporal

• Buccal Skin and mucous membrane covering buc­ Travels anteriorly between heads of lateral
cinator muscle pterygoid muscle and along inferior part of
Gingiva mandibular molars temporalis muscle to anterior of masseter
muscle
Crosses anterior border of ramus and enters
cheek
Does not innervate buccinator muscle

• Lateral pterygoid Lateral pterygoid muscle Travels into deep surface of muscle

POSTERIOR DIVISION

• Auriculotemporal Skin of temporal area Travels posteriorly and inferior to lateral pter­
ygoid and to medial side of ramus, superiorly
deep to parotid gland, over zygomatic arch
and branches to superficial temporal nerves
 APPENDI X 1 A-1 9

Nerve Innervation Pathway

• Lingual Mucous membrane and gingival of lingual Descends between medial pterygoid muscle
side of mandibular teeth and ramus
Anterior two-thirds of tongue and floor of Crosses ramus and travels anteromedially to
mouth inferior alveolar nerve

• Inferior alveolar ( IA )
Dental pulp, facial gingiva, periodontal
ligament and alveolar bone of mandibular
teeth except for facial gingiva of mandibu­
lar molars
Travels medial to lateral pterygoid muscle
through pterygomandibular space between
sphenomandibular ligament and medial surface
of ramus
Enters mandibular foramen and travels in man­
dibular canal

1 . Mylohyoid Mylohyoid muscle Branches before IA enters mandibular foramen

Anterior belly of digastric muscle Descends in mylohyoid groove deep on medial
surface of body of mandible

2. Mental Skin of chin Travels through mental foramen as a terminal

Lower lip skin and mucous membrane branch of IA nerve

3. Incisive Dental pulp, facial gingiva, periodontal Travels as a terminal branch of IA nerve
ligament and alveolar bone of mandibular
premolar and anterior teeth

The facial efferent root forms in the facial nerve nu­

cleus in the pons. It exits between the pons and medulla
on the ventral surface and travels to the petrous portions
of the temporal bone, into the auditory meatus. It then
follows a winding course through the facial canal. The
facial nerve exits the skull through the stylomastoid fo­
ramen and travels within the parotid gland, dividing into
five maj or branches on each side of the face.
The nervus intermedius of the facial nerve carries
both parasympathetic fibers and afferent fibers. It is called
the nervus intermedius because it arises between the ef­
ferent facial nerve and the vestibulocochlear nerve (VIII)
in the pons. It travels alongside the efferent root to the
petrous portion of the temporal bone and through the in­
ternal auditory meatus. At the facial canal, the nervus in­
termedius unites with the efferent root at the geniculate
ganglion.
Within the facial canal, three branches divide from
the facial nerve, the greater petrosal, the nerve to stape­
dius, and the chorda tympani. Distal to the stylomastoid F I G U R E A R - 2 1 Tr i g e m i n a l - M an d i b u l a r D iv i s i o n V3
foramen, the facial nerve divides into a posterior auricular A - Mandibular Division, B- Nervus spinosus, C- Auriculotemporal,
branch, a branch to the posterior belly of digastric and the D - Inferior Alveolar, E - Submandibular Ganglion,
stylohyoid muscles, and to the muscles of facial expression. F - Masseteric, G - Mylohyoid, H - Temporals, I - Pterygoids,
The muscles of facial expression include temporal, zygo­ J - B u c c a l , K - L i n g u a l , L - M an d i b u l a r D e n t a l P l e x u s ,
matic, buccal, marginal mandibular, and cervical muscles. M - Incisive, N - Mental Buccal, K - Lingual, L - Mandibular
See Table AR-15. Dental Plexus, M- Incisive, N- Mental.
A-20 APPENDI X 1

Table AR-1 5 Facial Nerve B ra n ches (VII)

Nerve Innervation Pathway

BRANCHES IN FACIAL CANAL

• Greater petrosal Parasympathetic to lacrimal gland From geniculate ganglion, travels to anterior
Special afferent taste to palate surface of petrous temporal bone, and to
pterygoid ganglion
Joins with branches of maxillary nerve

• Stapedius Motor to stapedius muscle in middle ear Travels through small canal in pyramidal
eminence to small stapedius muscle

• Chorda tympani Parasympathetic to submandibular and Travels posterior to anterior across the
sublingual glands tympanic membrane in middle ear, between
Special afferent taste fibers for anterior malleus and incus; through petro-tympanic
two-thirds of tongue fissure into infratemporal fossa
Joins with lingual nerve and travels to
submandibular ganglion
Fibers innervate glands
Extend to anterior two-thirds of tongue with
lingual nerve

BRANCHES DISTAL TO STYLOMASTOID FORAMEN

• Posterior auricular Motor to occipital belly of epicranial Travels superiorly behind ear in front of
muscle mastoid process
Posterior of ear and scalp

• Posterior belly of digastric and Motor to belly of posterior digastric and Branches form near posterior of muscles
stylohyoid stylohyoid muscles under mandible

• Facial expression
1. Temporal Motor to frontal belly of epicranial, Branches from parotid plexus and distributes
superior part of orbicularis oculi, and superficially to muscles innervated
corrugator supercilii muscle

2. Zygomatic Motor to muscles at lateral angle of Travels across zygomatic bone to lateral of
orbit, inferior part of orbicularis oculi orbit
and zygomatic major and minor muscles Joins fibers of maxillary nerve

3. Buccal Motor to buccinator, risorius, orbicularis Travels under skin superficially to muscles
oris muscles Joins fibers of ophthalmic and infraorbital
Upper lip, small muscles of nose nerves

4. Marginal mandibular Motor to lower orbicularis oris and Travels anteriorly under platysma and triangularis
mentalis muscles muscles
Lower lip and chin Joins fibers of mental branch on IA nerve

5. Cervical Motor to platysma muscle Travels below mandible

Norton, N. (2007). Netter's head and neck anatomy for dentistry.

Baker, E. W. (20 10). Head and neck anatomy for dental medicine.
New York: Thieme.
Malamed, S. F. (2004). Handbook of local anesthesia (5th ed.).
St. Louis: Elsevier Mosby.
Malamed, S. F. (20 1 3 ) . Handbook of local anesthesia (6th ed.).
St. Louis: Elsevier Mosby.
Netter, F. H. (2003). Atlas of human anatomy (4th ed.). Philadelphia:
Saunders Elsevier.
Philadelphia: Saunders Elsevier.
Pansky, B., & Gest, T. R. (20 14). Lippincott's concise illustrated
anatomy (Vol. 3). B altimore: Lippincott Williams & Wilkins.
Rohen, J. W., & Yokochi, C. (1993). Color atlas of anatomy
(3rd ed.). New York: Igaku-shoin Medical Publishers, Inc.
Structure of the Human Body. Retrieved November 12, 2008,
from www.meddean.luc.edu/Lumen/meded/grossanatomy
Chapter 1 -Perspectives on Local
Anesthesia for Dental Professionals
These questions are provided to generate discussion.
• Identify a variety of local anesthesia providers in
North America.
• Identify and discuss the importance of the funda­
mentals of pain management.
• Identify and discuss the responsibilities of local anes­
thesia providers.
Chapter 2-Fundamentals of Pain
M anagement
Question 1 : Which statement best describes pain as a pro­
tective response?
Answer 1 : C - Pain is a rapid, reflexive, subconscious
reaction.
Question 2: Which of these groups of variables does not
affect the experience of pain?
Answer 2: D - All of these affect individual pain experi­
ences except body weight and height.
Question 3 : Which one of the following statements regard­
ing nociception is true?
Answer 3: A - Nociception is polymodal. This means
that it can detect inj ury from chemical, mechanical,
and thermal stimuli even though all are registered
as pain.
Question 4: Which one of the following is an example of
neuropathic pain?
Answer 4: D - Neuropathic pain is caused by nerve tissue
injury or dysfunction of the sensory nerves in the cen­
tral or peripheral nervous systems. Trigeminal neural­
gia is the only example of this.
Question 5: Which one of the following will help patients
cope with anxiety and fear?
Answer 5: D - Prepare, rehears e , empower, and praise
patients to reduce anxiety and fear. The PREP strat­
egy can build trust and provide reassurance. Clinicians
may find the use of these stress-reducing techniques
helpful for themselves as well.
Question 6: In the process of debriefing, which one of the
following is not useful when managing fearful patients?
Answer 6: D -This response does not include patient par­
ticipation in decision making.
C hapter 3-The Neuroanatomy and
Neurophysiology of Pain Control
Question 1 : Which of the following statements most
accurately describe(s) the maj or differences between
sensory and motor neurons?
Answer 1 : D - All of the above accurately describe the
differences between sensory and motor neurons.
Question 2: Which of the following sequences best describes
the events in a successful impulse generation?
Answer 2 : A - Stimulation slowly depolarizes. In a suc­
cessful impulse generation, the firing threshold is
reached and rapid depolarization occurs followed by
recovery to the resting state.
Question 3: How are Schwann cells and nodes of Ranvier
related?
Answer 3: C - Gaps between cells on nerve membranes
are called nodes of Ranvier.
Question 4: Which fiber types are responsible for providing
sensory information from dental and periodontal tissues?
Answer 4: D - "A" delta and "C" fibers.
Question 5: Which of the fibers in question #4 are myelinated?
Answer 5: C - "A delta" fibers are lightly myelinated; "C"
fibers are nonmyelinated.
Question 6: What are three divisions of the dental plexus?
Answer 6: C - Interdental, interradicular, and dental.
Chapter 4-Pharmacology Basics
Question 1 : Elimination half-life refers to which one of the
following?
Answer 1: C - Half-life refers to the time it takes for 50%
of a drug to be removed from the systemic circulation.
Question 2 : Ester local anesthetics are metabolized in
which one of the following pathways?
Answer 2: B- Esters are metabolized in the blood via
plasma cholinesterase.
A-21
A-22 APPENDI X 2
Question 3 : CNS toxicity occurs because of:
Answer 3: A - CNS toxicity is due to conduction blockade of
vital functions within the CNS due to the normal func­
tioning of nerve cells in response to local anesthetic drugs.
Question 4: CVS toxicity occurs because of:
Answer 4: C - Decreased myocardial contractility and hy­
potension due to vasodilation, if they occur, will fur­
ther worsen an already developing CNS depression.
Some initial heart rate elevation and hypertension
may occur, however, in early overdosing.
Question 5: Which portion of the anesthetic molecule is
responsible for binding to the receptor site inside the
nerve membrane thereby preventing depolarization?
Answer 5 : D - Only the cation can bind to the specific re­
ceptor sites in nerve membranes to prevent impulse
generation and conduction.
Question 6: Which part of a local anesthetic molecule deter­
mines the classification of the drug as an ester or amide?
Answer 6: C - Local anesthetic drugs are classified accord­
ing to their intermediate chains as esters or amides.
Except for its largely nonhepatic, ester-like metabolic
pathways and its therefore shorter elimination half­
life, articaine cannot be mistaken for an ester.
Question 7: Which of the following is not a systemic reac­
tion to an overdose of a local anesthetic agent?
Answer 7: A - An overdose of local anesthetic drugs will
result in depression of the CNS. The initial excitatory
phase is actually due to depression of inhibitory actions
of the CNS.
Chapter 5-Dental Local Anesthetic
Drugs
Question 1 : The definition of the maximum recommended
dose ( MRD ) of a drug fits best which one of the fol­
lowing definitions?
Answer 1: D - The MRD of a drug is an established safe
guideline for administration.
Question 2: Which one of the following best describes ar­
ticaine's metabolism?
Answer 2: B- Articaine is primarily metabolized via
plasma cholinesterase. Its metabolism is not similar to
prilocaine's. It is metabolized only one about 5% to
10% in the liver. Very little is excreted unchanged.
Question 3 : You are treating a patient with significant car­
diovascular compromise who suffers from significant
liver damage. Which one of the following drugs would
be most appropriate for this p atient when you are
anesthetizing the maxillary right quadrant?
Answer 3: C - 4 % articaine , 1 :200,000, addresses both
significant CVS and hepatic compromise. The other
three drugs are metabolized in the liver, including 3 %
mepivacaine , which otherwise would b e a n excellent
choice in CVS compromise. At 1:200,000 epinephrine,
articaine is the best overall selection.
Question 4: A periodontist requires hemostasis on palatal
tissues in the maxillary left quadrant before elevat­
ing a surgical flap. Which one of the following drugs
would furnish the most vigorous hemostasis?
Answer 4: C - The local anesthetic drugs are irrelevant to
hemostasis. Epinephrine provides the most vigorous
hemostasis. Its highest concentration is found in the
1 :50,000 dilution.
Question 5: Which characteristic of a local anesthetic
d r u g d e t e r m i n e s how w e l l i t w o r k s w i t h o u t a
vasoconstrictor?
Answer 5: B- Vasoactivity. Drugs that are weak vasodila­
tors will remain in the area of deposition longer. Vig­
orous vasodilators enhance their own uptake into the
systemic circulation, and therefore, vasoconstrictors
must accompany their use.
Question 6: If a patient is taking a tricyclic antidepressant
and a beta-blocker, which one of the following drugs
would be most appropriate to administer?
Answer 6: C - Tricyclic antidepressants require care with
vasoconstrictors, and levonordefrin, especially, should
not be used because of the risk of serious elevations
of BP. Levonordefrin is safer to use in the presence of
beta-blockers compared with epinephrine. There are
no issues with mepivacaine plain because there are no
contraindications to the anesthetic drugs themselves.
Question 7: Methemoglobinemia is a life-threatening con­
dition that may be precipitated by which one of the
following drugs?
Answer 7: C - Prilocaine.
Question 8: Arrange the inj ectable local anesthetic drugs
in descending order of overall CNS and CVS toxicity.
Answer 8: B- Considering overall toxicity to the CNS and
CVS, prilocaine is the least toxic, approximately seven
times less toxic compared with bupivacaine. Articaine
is less toxic than lidocaine and mepivacaine overall is
more toxic than lidocaine, although it is not thought to
be in doses used in dentistry.
C hapter 6-Vasoconstrictors
in Dentistry
Question 1 : Which one of the following vasoconstrictors is
most useful in providing hemostasis?
Answer 1 : B - Epinephrine provides the most vigorous
hemostasis of this group.
Question 2: A patient has significant cardiovascular dis­
ease and requires a restorative procedure on tooth
#5 . Retraction cord and hemostasis are needed in
order to keep the restorative site dry. Which one of
the following drugs would be most indicated in this
situation?
Answer 2: A - Dilutions of 1 :200,000 epinephrine contain
the least 'vasoconstrictor' and are indicated because
they are the s afest and yet provide hemostasis. If

hemostasis were not needed, plain drugs would work
well in shorter treatment times.
Question 3 : Which one of the following statements is true?
Answer 3 : C - Levonordefrin provides less cardiac stimu­
lation compared with epinephrine.
Question 4: Epinephrine's metabolism is relatively rapid
after local anesthesia administration.
Answer 4: A - Compared with the local anesthetic drug's
metabolism, epinephrine ' s metabolism is generally
much more rapid.
Question 5: Metabolic enzymes for epinephrine include
which of the following?
Answer 5: A - Epinephrine is metabolized by COMT and
MAO.
Question 6: A diabetic patient requires periodontal ther­
apy on the upper and lower right quadrants . She is
well-controlled and otherwise healthy. Which one of
the following represents the safest and most effective
local anesthesia regimen?
Answer 6: B - Epinephrine can raise blood sugar levels.
The lowest quantity of epinephrine is found in combi­
nation " B " where half of the administered volume has
no epinephrine. The lowest amount of vasoconstric­
tor should always be used in all individuals. B ecause
this patient is a well-controlled diabetic and otherwise
healthy, no special precautions are necessary and the
default principle applies. Use the least amount of drug
necessary.
Chapter 7-Dose Calculations for
Local Anesthetic Solutions
Question 1 : All of the following are correct when consid­
ering MRDs, except:
Answer 1 : C - The absolute maximum for lidocaine is
500 mg ( 3.2 mg/lb, 7.0 mg/kg )
Question 2: Relevant information and mathematical oper­
ations required to calculate drug doses for local anes­
thetics and vasoconstrictors include all but which one
of the following?
Answer 2: D- Local anesthetic toxicity is weight related,
but height is not a relevant factor.
Question 3: Which one of the following is not related to
the MRD for 2% lidocaine, 1 : 1 00,000 epinephrine?
Answer 3: B- This is correct for epinephrine alone but is too
much for lidocaine, the limiting drug in this situation.
Question 4: What is the MRD for vasoconstrictors when
administering 2% lidocaine, 1 : 1 00,000 epinephrine, to
a healthy individual?
Answer 4: C - 0. 2 mg is the MRD for epinephrine in a
healthy individual.
Question 5: An individual has received 4 cartridges of
2 % lidocaine , 1 : 1 00 , 0 0 0 epinephrin e , and is n o t
APPENDI X 2 A-23
profoundly anesthetized. How many cartridges of 4 %
articaine, 1 :200,000 epinephrine, may be administered
if the individual weighs 160 lbs?
Answer 5 : C - 4 cartridges of 2% lidocaine = 144 mg. The
absolute maximum is 500 mg for lidocaine or 3.2 mg/
lb x 150 or more pounds = 480 mg. 480 mg - 144 mg
= 336 mg. 336 mg/72 mg per cartridge of 4% artic­
aine = 4.5 cartridges ( rounded down to nearest half
cartridge ) .
Question 6: How many cartridges of 4 % articaine, 1 :200,000
epinephrine, may be administered for an individual with
significant cardiovascular compromise?
Answer 6 : D - The m aximum for epinephrine in sig­
nificant cardiovascular compromise is 0.04 mg. Each
cartridge of a dilution of 1 :200,000 epinephrine con­
tains 0.009 mg of epinephrine. 0.04 mg/0.009 mg per
cartridge of 4% articaine, 1 :200,000 epinephrine = 4
cartridges.
Question 7: Which one of the following accurately de­
scribes available formulations?
Answer 7: C - Available formulations of 2% lidocaine in­
clude 1 : 1 00,000 epinephrine and 1 :50,000 epinephrine.
Question 8: The maximum dose per weight of 4% artic­
aine, 1 : 1 00,000 epinephrine, for children is:
Answer 8: D - The maximum dose per pound of 4% artic­
aine is 3.2 mg/lb for all individuals.
Question 9: 0 . 5 % bupivacaine , 1 : 200,000 epinephrine ,
contains how many milligrams o f anesthetic drug per
cartridge?
Answer 9 : A - By definition, a 1 % drug contains 10 mg
per milliliter. There are therefore 18 mg in a 1 .8 mL
cartridge. 0.5 % drugs contain half this amount or 5 mg
per milliliter. In 1 . 8 mL of a 0.5 % drug, there is 5 mg
in the first milliliter and 5 mg x 0.8 4 mg in the addi­
=
tional 0.8 mL. 5 mg + 4 mg = 9 mg/cartridge of a 0.5 %
drug.
Chapter 8-Topical Anesthetics
Question 1 : Eutectic mixtures have which of the following
characteristics?
Answer 1 : D - The term eutectic refers to a substance that
has a lower melting point than any of its ingredients.
Eutectic topicals not only have lower melting points
to facilitate penetration through tissue barriers but
they are formulated primarily in the base form so that
they can provide anesthesia more rapidly.
Question 2: Which of the following lists is most accurate
when describing topical anesthetic uses?
Answer 2: D - All of the above.
Question 3: Which one of the following statements is in­
correct regarding maximum recommended doses of
topical anesthetics?
Answer 3 : C - Metered sprays are generally easier to
track. Unmetered sprays are not.
A-24 APPENDI X 2
Question 4: Generous quantities of topical and inj ected
anesthesia have been administered when the patient
begins to shake and appears agitated and anxious. Is
there reason for concern?
Answer 4: A - Tremors and agitation may be early signs
of CNS depression. They are also reactions that occur
in response to the stress of dental appointments. It is
important to remain alert to the development of fur­
ther signs and symptoms of CNS depression.
Question 5: Topical anesthetic mixtures may be of benefit
in all but which one of the following ways?
Answer 5: D - Adding additional drugs does not decrease
the potential for adverse reactions; it generally in­
creases the potential.
Question 6: All of the following statements are true re­
garding compounded drugs, except:
Answer 6: B - Compounded drugs, including compounded
topicals, may be used only by individuals for whom
they were prescribed.
Question 7: The predominantly base form of lidocaine
topical anesthetic is safer than the predominantly hy­
drochloride salt.
Answer 7: A - True. The base form has less ability to be
absorbed systemically.
Question 8: Dyclonine hydrochloride is an excellent and
very durable topical anesthetic and belongs to which
one of the following classes of anesthetic?
Answer 8: B - Dyclonine has a ketone linkage as opposed
to amide or ester.
C hapter 9-Local Anesthetic Delivery
Devices
Question 1 : Which one of the following statements is
correct?
Answer 1: D - Negative pressure is developed in both sy­
ringes although the mechanism for creating the pres­
sure is different for each.
Question 2: Which one of the following is correct when
addressing OSHA requirements for medical device
safety in dentistry?
Answer 2: D - It is permissible to bend uncontaminated
needles according to OSHA. Two hands are never al­
lowed unless one is holding a hemostat or cotton pli­
ers to hold the cap. Contaminated needles may never
be bent.
Question 3 : In comp aring a 2 5 -gauge n e e d l e with a
30-gauge needle, the 25-gauge needle:
Answer 3: D - 25 -gauge n e e d l e s have larger lumens
and are thought to have greater ease of aspiration;
30-gauge needles have the greatest risk for breakage;
studies demonstrate that patients cannot perceive the
difference between the various needle gauges ; and
because of the ease of aspiration, 25-gauge needles
are beneficial in highly vascular areas.
Question 4: Long needles are approximately _____
long
Answer 4: B - Long needles average -32 mm (Ph inches),
with some noted to be as long as 40 mm.
Question 5: When a stopper is extruded, what has likely
caused the problem?
Answer 5: B - Freezing during shipping or handling causes
expansion of the solution that dislodges the stopper.
Question 6: During an infiltration inj ection, you give the
patient three stopper-widths of local anesthetic. How
much solution have you inj ected into the patient?
Answer 6: D - Each stopper's width displaces 0.2 mL of
solutions; therefore, three stoppers would displace
0.6 mL.
Question 7: What substance is used as the preservative for
epinephrine in local anesthetic cartridges?
Answer 7: A - Sodium bisulfite and methylparaben are
preservatives; however, because of the high incidence
of allergy to methylparaben, it is no longer used in lo­
cal anesthetic agents.
C hapter 1 0-Patient Assessment for
Local Anesthesia
Question 1 : The delivery of local anesthesia requires
both medical and technical skills. Which one of the
following is not one of the six elements of the ASA
Medical Components of Care associated with regional
anesthesia?
Answer 1: B - Although useful for planning a course of
anesthesia, tooth charting is not one of the ASA Med­
ical Components of Care.
Question 2: The ASA (American Society of Anesthesiolo­
gists) Physical Status Classification System categorizes
patients based on their overall health. Classification
P3 describes which one of the following?
Answer 2: B - ASA Classification P3 is defined as "Severe
Systemic Disease."
Question 3 : Which of the following is not considered a
main tool for patient assessment when planning for lo­
cal anesthesia?
Answer 3: C - Although important when monitoring total
doses of drug delivered, this is not considered a main
tool for patient assessment.
Question 4 : Which one of the following drugs is an ab­
solute contraindication for patients with poorly con­
trolled or uncontrolled hyperthyroidism?
Answer 4: C -Epinephrine and Felypressin are both vaso­
constrictors; however, Felypressin has no adrenergic
effects and is therefore safe to use for patients with
hyperthyroidism.

Question 5: Your patient has identified or you suspect that
your p atient has used methamphetamines approxi­
mately 20 hours ago. Which of the following would be
the most appropriate action when considering the use
of local anesthetics?
Answer 5: C - Administration of vasoconstrictors may
result in hypertensive crisis, stroke, or myocardial in­
farction. It is recommended that you not administer
local anesthetics with vasoconstrictors for a minimum
of 24 hours after methamphetamine use.
Question 6: For which one of the following medical condi­
tions is it unnecessary to obtain a medical consultation
from the patient's physician before dental treatment?
Answer 6: B - Myocardial infarction within 3 weeks is an
absolute contraindication to care.
Chapter 1 1 -Fundamentals for
Administration of Local Anesthetic
Agents
Question 1 : A technique which deposits anesthetic solu­
tion near larger terminal nerve branches for treatment
near the site of an inj ection is called:
Answer 1: C - A field block inj ection deposits local anes­
thetic solution near larger terminal nerve branches for
treatment near the site of inj ection.
Question 2: Which one of the following describes the tar­
get site for local anesthetic solutions?
Answer 2: B - The deposition site is the anatomical loca­
tion where drugs are deposited.
Question 3 : The first step in the administration of local an­
esthetic solutions is to:
Answer 3 : C- Thorough patient assessment is critical to
safe local anesthetic administration. Patient assess­
ment must precede all other steps.
Question 4: A primary benefit of orienting needle bevels
toward bone during inj ections is that it:
Answer 4: A - Orienting the bevel toward bone reduces
discomfort and trauma to periosteum when bone is
contacted. In the event of inadvertent contact, the nee­
dle tends to glance off the bone rather than pierce the
periosteum. Although reducing discomfort is important
(Answer D ) , many other aspects of inj ections which
decrease discomfort have nothing to do with bevel ori­
entation. Option A is the better answer because bevel
orientation specifically reduces trauma to the perios­
teum in addition to providing for more comfort.
Question 5: Which one of the following is the most appro­
priate local anesthesia chart entry?
Answer 5: D - This is the only sample that has all compo­
nents: date, drug(s), total drug volume(s), inj ection(s)
or sites, results of aspiration test(s) , a notation on ad­
verse events, and clinician signature.
APPENDI X 2 A-2 5
Q uestion 6 : When is it safe to deposit local anesthetic
solution?
Answer 6: D - It is s afe to deposit the anesthetic solu­
tion once a negative aspiration is confirmed, includ­
ing when there is no preceding positive aspiration;
when previous positive aspiration does not obscure
subsequent aspirations; and only when the clinician
essentially starts fresh with a new cartridge and new
aspiration, not after a positive aspiration that obscures
the results.
Question 7: The most important safety step(s) during a lo­
cal anesthetic injection is( are):
Answer 7 : D - It is not only critical to determine if a
needle lumen lies within a vessel before deposition
but also critical to administer drugs slowly in case the
needle lumen lies within the vessel despite negative
aspiration test results.
Question 8: Upon completion of an inj ection, the most im­
portant su bsequent step is to:
Answer 8: C - Make the needle safe with a one-handed
technique . This optimizes safety for all personnel.
Once this has been done, attend to the patient.
Chapter 1 2-lnjections for M axillary
Pain Control I
Question 1 : Which one of the following statements best
describes the needle pathway for an infiltration inj ec­
tion technique?
Answer 1: A- A is the correct choice . B is incorrect be­
cause the needle is not oriented distal to the long axis
of the tooth. C is incorrect because the needle does
not pass through bone. D is incorrect because the mu­
cosa and connective tissue in this area are not typi­
cally thickened.
Question 2: When infiltration inj ections are unsuccessful,
it may be helpful to:
Answer 2 : B - This is the correct answer. Visualization,
p alpation, and reassessment of available landmarks
are most useful. A is incorrect in most instances unless
the wrong size was used in the first place, such as an
ultrashort needle. C is incorrect because contact with
bone results in pain and trauma, not increased suc­
cess. D is incorrect because the patient is not the one
responsible for the inj ection parameters.
Question 3: The middle superior alveolar nerve is absent
in approximately 28% to 50% of individuals.
Answer 3: B - The MSA nerve is present in somewhere
between 28% and 50% of individuals.
Question 4: In a typical adult patient, the infraorbital fora­
men is approximately 8-10 mm below the infraorbital
ridge.
Answer 4: A - This range is considered normal for the av­
erage adult.
A-26 APPENDI X 2
Question 5: Which one of the following provides the most
accurate description of the field of anesthesia in a PSA
inj ection?
Answer 5: D - This is the only accurate description. A,
B, and C are incorrect. The premolars are not anes­
thetized by a PSA inj ection nor are the mandibular
molars or the maxillary teeth to the midline.
Question 6: Which one of the following is most likely to
increase the risk of hematoma following a PSA nerve
block?
Answer 6: A - Overinsertion of needles increases the risk
of hematoma formation in PSA blocks. This can oc­
cur both by deeper insertion into the pterygopalatine
fossa or by location too posteriorly initially.
Chapter 1 3-lnjections for M axillary
Pain Control 1 1-Palatal Approach
Question 1 : Which one of the following statements best
describes the deposition site for a nasopalatine nerve
block?
Answer 1: B - This is correct compared with A because al­
though deposition is at the incisive foramen, the nee­
dle is not advanced into the nasopalatine canal. C is
incorrect because the nasopalatine nerve block is not
performed at the anterior palatine foramen. D does
not describe a location at the incisive foramen.
Question 2: The most common cause of failure for palatal
inj ection techniques is:
Answer 2: D - This is the correct answer. B oth failure to
deposit the solution close to the bone or foramen and
insufficient volumes deposited reduce the amount of
drug that diffuses through the bone to the nerves.
Question 3 : The AMSA technique can provide anesthe­
sia for areas traditionally anesthetized by which one of
the following groups of injections?
Answer 3: B - This is the best answer. The AMSA tech­
nique provides anesthesia for structures traditionally
anesthetized by the ASA, MSA, NP, and GP injections.
Question 4: Which one of the following statements is true
of NP nerve blocks?
Answer 4: D - This is the best answer. The aspiration rate
is similar to other palatal techniques. NP blocks do
not provide more durable anesthesia compared with
other palatal techniques. When performed as recom­
mended, they provide bilateral anesthesia.
Question 5: Which one of the following is an important
consideration in all palatal LA procedures?
Answer 5 : B- This is the best answer. Applying topical
for 1-2 minutes is typical of many inj ections. Using
patch topicals in the palate is helpful but not neces­
sary. Slow deposition of solution is important to avoid
damage to tissue, which has difficulty accommodat­
ing the volumes of solution necessary in many palatal
techniques. Pain is reduced with slow administration
and safety is enhanced.
Question 6: AMSA nerve blocks provide bilateral anes­
thesia of palatal tissues at least 20 % of the time.
Answer 6 : B - Solution in AMSA blocks does not cross
the midline and provides same-side anesthesia only.
C hapter 1 4-lnjections for M andibular
Pain Control
Question 1 : The rate of positive aspiration in the inferior
alveolar nerve block is the highest of all techniques
and approximates which one of the following?
Answer 1: C- The rate of positive aspiration in alveolar
nerve blocks is 1 0 % to 1 5 % . This is the highest rate of
all techniques described in this text. In practical terms,
this means anticipating a positive aspiration in 1 to 2
out of every 10 inferior alveolar blocks.
Question 2 : Which one of the following techniques is
an alternative to ne arly all mandibular anesthetic
techniques?
Answer 2: C- The periodontal ligament inj ection (PDL) ,
although providing only limited areas of anesthesia, is
an alternative to nearly all other techniques, mandibu­
lar and maxillary.
Question 3: Which one of the following result(s) in pulpal
anesthesia?
Answer 3: D -Neither the buccal nor the mental nerve blocks
provide pulpal anesthesia to the mandibular teeth.
Question 4: When administering a Gow-Gates mandibular
nerve block, all of the following are essential, except:
Answer 4: D - Even though there are both extraoral and
intraoral landmarks for the Gow-Gates nerve block, it
is not necessary to remove j ewelry before administer­
ing it.
Question 5: Palpating anatomy before all mandibular an­
esthetic procedures is:
Answer 5: B - Palpating anatomy is essential to some
techniques and not very helpful in others. While the
statement that it is an unnecessary step is obviously
false, palpation is not even possible in lingual nerve
blocks, for example.
Question 6: Which one of the following is the correct
order, from inferior to superior location, of the man­
dibular techniques listed in relation to the pterygo­
mandibular space.
Answer 6: B - The correct order from inferior location to
superior location in the pterygomandibular space is
lA, Akinosi, Gow-Gates.

Chapter 1 5-Supplemental
Techniques and Adjunctive Strategies
Question 1 : The rate of deposition of local anesthetic
drugs in intraosseous, intrapulpal, and PDL inj ections
is best represented by which one of the following?
Answer 1: C - The rate of deposition of solution in each
of these techniques is slow (0.2 mL over 20 seconds).
Question 2: Which one of the following techniques does
not typically provide reliable pulpal anesthesia?
Answer 2: C - The intraseptal technique does not provide
reliable or durable pulpal anesthesia.
Question 3: Which one of the following is not recommended
as an anesthetic approach in irreversible pulpitis?
Answer 3 : C - A 5 % concentration of lidocaine may be
effective in this situation, but it is also unavailable in
dental cartridges and is two-and-one-half times more
toxic that 2% lidocaine solutions.
Question 4: What is the approximate success rate of infe­
rior alveolar nerve blocks according to Wong, in pulp­
ally involved teeth?
Answer 4: C - 30 % .
Question 5 : Which one of the following statements is true
regarding PDL injections?
Answer 5: D - Solution diffuses through the alveolus; there­
fore, the PDL is an intraosseous technique. The orienta­
tion of the bevel is irrelevant to success, and the technique
is very useful as a supplementary technique when other
techniques have failed to provide profound anesthesia.
Chapter 1 6-Troubleshooting
Inadeq uate Anesthesia
Question 1: Inadequate anesthesia may typically be caused
by all of the following, except:
Answer 1: C - Manufacturing processes are well-regulated
and rarely, not typically, may be the cause of inade­
quate anesthesia. On the contrary, product recalls are
more typical when atypical errors occur during manu­
facturing processes.
Question 2: Infiltration (supraperiosteal) anesthesia over
the apex of #9 has failed to achieve adequate an­
esthesia. Which one of the following is not a likely
possibility?
Answer 2: D - Inflammation with no signs or symptoms is
unlikely to inhibit anesthesia.
Question 3: The relative acidity of tissues into which anes­
thetic drugs are inj ected is related to the efficacy of a
drug in the following manner:
Answer 3: B - Increases in cationic concentrations de­
crease the rate of success.
APPENDI X 2 A-27
Question 4: Possible successful approaches when an infe­
rior alveolar nerve block fails to provide complete and
profound pulpal anesthesia are:
Answer 4: D - PDL inj ections, mylohyoid nerve blocks,
and Gow-Gates blocks are all useful supplements
when inferior alveolar nerve blocks fail to provide ad­
equate pulpal anesthesia.
Question 5: Two inj ections of 2 % lidocaine, 1 : 1 00,000
epinephrine (total lidocaine = 72 mg) , have failed to
provide adequate anesthesia. Useful supplemental al­
ternatives, regardless of the location or technique, in­
clude all of the following, except:
Answer 5 : C - Mylohyoid blocks are useful only in the
mandible.
Question 6: By which of the following mechanisms do in­
traosseous techniques work?
Answer 6: D - Intraosseously administered s o lutions
s lowly diffu s e through a l v e o l a r bone t o d e n t a l
plexuses.
Question 7 : Where is the deposition site for the Gow­
Gates nerve block located relative to the inferior al­
veolar nerve block?
Answer 7: B - The Gow-Gates is located at a higher level
than the Vazirani-Akinosi block which is higher than
the IA block.
Question 8: Some nerve blocks require far greater vol­
umes of solution compared with others.
Answer 8 : A- The statement is true. For example, the
minimum volume of solution for a Gow-Gates nerve
block is 1 . 8 mL, which is nine times typical volumes
for one site of a PDL inj ection, or 0.2 mL.
Chapter 1 7-Local Anesthesia
Complications and M anagement
Question 1 : A clinician is administering an IA nerve block
before therapy when the p atient suddenly j erks and
the needle breaks. The embedded portion is not vis­
ible. What should the clinician do?
Answer 1 : D - Some embedded needles are retained in
tissue after evaluation. Evaluation by an oral surgeon
may result in a decision to retain the needle versus
the greater damage that might occur with attempted
removal. Even though needle fragments are typically
removed today, referring for removal may make the
patient believe that either the referring clinician or the
surgeon is acting inappropriately if the decision is made
to retain the embedded fragment. Refer for evaluation.
Que stion 2: A second cartridg e of 2 % lidocaine has
been administ e r e d for an I A nerve b l o c k w hen
the 1 60-lb patient becomes anxious a nd states that
she d o e s n ' t fe e l well, even a little nauseous. S h e
A-28 APPENDI X 2
becomes less anxious as she becomes increasingly
fatigued, her speech becomes slurred, and she re­
ports a numb feeling all around her mouth. Which
one of the following statements best describes these
observations?
Answer 2 : C - Two cartridges is not an overdose in a
healthy 1 60-lb adult unless intravascularly adminis­
tered or the patient is a hyper-responder. The progres­
sion of signs and symptoms to slurring of speech and
perioral numbness is not consistent with anxiety. As­
suming the patient has no history of hyper-response,
the likely mechanism for overdose is intravascular
administration.
Question 3 : Allergies to topical anesthetic drugs that cause
mucosal signs and symptoms hours to days after expo­
sure are explained best by which one of the following
reactions?
Answer 3: A - Reactions with signs and symptoms occur­
ring many hours to days after contact with a drug are
characterized as delayed sensitivities.
Question 4: A patient calls several days after an lA block
and reports that numbness is still present along with
some annoying, occasional sharp pains. Which of the
following terms best describes what is occurring?
Answer 4: C - These symptoms are consistent with pares­
thesia (prolonged numbness) and dysesthesia (sharp
pains).
Question 5 : Which of the following responses is most ap­
propriate after rapid tissue swelling is noticed after a
PSA block?
Answer 5: C - Place pressure over the area as quickly as
possible and then apply ice , when available. Advise
the patient regarding the development of discolor­
ation. Instruct the patient to apply ice intermittently
for the next 6 hours and to avoid aspirin for pain.
Advise the patient to notify you immediately of any
change, especially the development of signs and symp­
toms of infection or limited j aw opening.
Question 6: Of the following possible adverse reactions,
which one occurs most frequently?
Answer 6: C - Of the three, overdose is the most frequent
systemic complication.
Question 7: Considering all of the following measures for
preventing overdose, which one is most important?
Answer 7: B - Slow administration is the most impor­
tant safety factor in local anesthetic drug administra­
tion and incre a s e s the s afety m argins of all the
other preventive strategies mentioned. Aspiration
is critical but not always completely reliable. Cal­
culating appropriate maximum doses is also critical
but hyper-responders may react adversely to doses
which are carefully calculated and considered to be
appropriate. Reassurance does not even address this
issue.
C hapter 1 8-lnsights for Fearful
Patients
Question 1 : There is a new patient in the chair. During
appropriate introductions including handshaking, it
is noticed that the patient's hands are clammy and he
has perspiration on his upper lip. He appears very stiff
and responds with a brief yes or no to attempts to en­
gage him in conversation. When deciding whether or
not he is apprehensive about the dental treatment he
is scheduled to receive, the most appropriate strategy
would be to:
Answer 1 : C - Check out and confirm the observations
about possible concerns regarding dental treatment
by asking a few simple questions: "When was your last
dental visit?" "How did it go?" "Do you have any con­
cerns about receiving treatment today?" Patients want
to know that their care provider is concerned about
them. If the patient is fearful, this may affect their abil­
ity to receive an inj ection and whether or not the an­
esthetic is effective. Obtaining this information before
treatment allows clinicians to develop plans, which ad­
dress problems methodically and to increase the likeli­
hood of success. This patient is also reassured that he
is in the hands of a caring and competent professional.
Question 2: Establishing trust in the patient-clinician rela­
tionship is especially important for fearful dental pa­
tients because they need to learn:
Answer 2: B - Fearful patients need to learn how to be
assertive and express their concerns. They need to
ask questions about their worries, including comfort
during treatment. Good communication empowers
fearful patients with a sense of control, whereas poor
communication can lead to anger and aggressive be­
havior rather than helpful assertive behavior. When
trust is developed in this manner, it is helpful to both
the patient and the clinician.
Question 3: Providing patients with information is an im­
portant means of increasing their sense of control in
the dental environment. When providing information
to a fearful patient about an aversive procedure:
Answer 3: D - When the procedure is described in simple
steps, the fearful patient will not be overwhelmed by
the prospect of treatment and will not be startled by
each new aspect of the treatment process. It is impor­
tant not to surprise fearful patients and to let them
know what sensations are normal, especially when ad­
ministering local anesthesia.
Question 4: It is important to have the skills and confi­
dence necessary to teach anxious and fearful patients
how to relax in the dental chair. When a patient learns
the physical relaxation skills of deep breathing and
muscle relaxation:
Answer 4: D -The physical relaxation skills of deep breath­
ing and muscle relaxation are easily taught and quickly

learned by dental patients. Additionally, the clinician
can directly observe whether or not the patient is ac­
tively using the skills and whether or not the patient
needs coaching. Anxiety leads to muscle tension and
shallow breathing, both of which increase the patient's
sense of physical discomfort. Muscle relaxation and
deep breathing counteract these, and patients appreci­
ate having a technique that can be used to gain relief
from the symptoms of anxiety. These techniques re­
duce mental stress as it is not possible to be physically
relaxed and psychologically anxious at the same time,
and the active focus on implementing relaxation tech­
niques displaces the fearful conjectures. The clinician
benefits from the patient's ability to use these skills
because a tense and anxious patient has a lower pain
threshold, is more easily hurt and startled, and cannot
distinguish between anticipated pain and the actual
experience of pain both during the administration of
local anesthetic and when assessing if the patient is ad­
equately anesthetized to proceed with treatment.
Question 5: Patients who are fearful of dental injections
can benefit from having the opportunity to rehearse
the procedure before receiving the actual inj ection.
The obj ective of the rehearsal is to:
Answer 5: B - A rehearsal provides the patient with the
opportunity to practice the relaxation skills learned
while the clinician simulates the steps involved in ad­
ministering local anesthetic. Patients gain knowledge
about their role and what is involved in the actual pro­
cedure without the pressure to accomplish treatment.
Question 6: Some patients will report a history of receiv­
ing dental care without being adequately anesthetized.
They may not be anxious about the inj ection proce­
dure, but will be reluctant to proceed with treatment
after the administration of local anesthetics. Despite
soft-tissue signs and symptoms of anesthesia, they
do not believe the teeth are num b . The next step for
these patients should be to:
Answer 6: A - Inform the patient of the technique to ver­
ify that the tooth is anesthetized before proceeding
with treatment. The EPT is very useful for this pur­
pose, and patients are receptive to the idea of a de­
vice that makes the determination obj ectively rather
than relying on subj ective responses that have not
been reliable in the past. If there is no EPT avail­
able, an ultrasonic instrument can be used along with
time structuring technique (counting to " 1 , " then "2,"
and "5") to verify profound anesthesia for the patient.
Chapter 1 9-lnsights from Pediatric
Dentistry
Question 1 : Why is it generally more critical to consider
toxicity of local anesthetics in pediatric patients than
in adults?
APPENDI X 2 A-29
Answer 1: B - Although elements of A, C, and D may be
true, the key issue is the greatly reduced body weights of
children. There is a higher possibility of overdosing when
clinicians are accustomed to treating adults and giving a
"standard dose" of the anesthetic solutions. These "stan­
dard" adult doses may well be too much for children.
Question 2: How does excellent anesthesia serve as a man­
agement tool for children?
Answer 2: D - Much of the success of any pediatric den­
tal appointment has to do with comfort and efficiency.
When profound anesthesia has been obtained, all pro­
cedures will be more comfortable for the child and it
becomes possible to accomplish more at each visit.
Question 3: In which of the following ways do anatomic
variations affect the choice of inj ection techniques for
children?
Answer 3: A- For primary teeth, penetrations generally do
not need to be as deep as for permanent teeth. Cortical
plates are thinner in children, and the inferior alveolar
foramen is more inferior compared with adults.
Question 4: Which of the following describe s ways in
which an assistant can play a vital role in the success­
ful administration of local anesthetics to children.
Answer 4: C - The primary focus of an assistant during in­
jection procedures must be the safety of the child. The
clinician administering the inj ection cannot control
gross body movements of the child while inj ecting.
The assistant must respond to any quick and unex­
pected movements that occur in order to ensure the
safety of the child.
Question 5: Which of the following are benefits of using
age- appropriate terminology and specific positive
feedback during the successful anesthetic administra­
tion in pediatric patients?
Answer 5: D - There are few management techniques as
profoundly effective for children as helping them to
understand what is happening to them and around
them. It is universally accepted that people are most
fearful of what they don't know. By helping children
understand and develop favorable pictures of proce­
dures, positive responses are far more likely to result.
Question 6: Which of the following is true when consider­
ing inj ection techniques in children?
Answer 6: B - The inferior alveolar foramen is typically
more inferior in children than in adults. Mandibular
infiltrations frequently work well, and short needles
are often preferred in children.
Question 7: When children traumatize soft tissues im­
mediately following inj ection s , what is the b e s t
management?
Answer 7: A - Cold packs minimize circulation and de­
crease initial swelling. Eight to twelve hours later, once
the swelling has stopped, warm packs are appropriate
A-30 APPENDI X 2
because they increase circulation and promote heal­
ing. Antibiotics are rarely indicated.
Chapter 20-lnsights from Specialties:
Oral Surgery, Periodontics, and
Endodontics
Question 1 : Which one of the following methods of adjust­
ing doses of local anesthetic drugs for children is rec­
ommended in this chapter?
Answer 1: A - Clark's rule is suggested in this chapter as
the most practical method for altering doses for chil­
dren based on weight. Young's rule bases the calcula­
tion on age. The Rule of Inference is a legal principle
and Heuristic rules apply to common sense.
Question 2: Specific challenges in oral and maxillofacial
local anesthesia include all of the following, except:
Answer 2: D - All of the above. Management of patients
with diverse ages and medical backgrounds, manage­
ment of oral infections, limiting the potential for nee­
dle tract infections, and achieving adequate anesthesia
in the presence of these infections are all specific chal­
lenges in oral and maxillofacial surgery.
Question 3: Which one of the following is not a local anes­
thesia consideration in oral and maxillofacial surgery
when treating an infected patient?
Answer 3: C - Local anesthetics with higher pHs should
be used in the presence of infection.
Question 4: Which one of the following is not an adverse
event following local anesthetic inj ections?
Answer 4: B -Numbness is not an adverse event. The vast
maj ority of inj ections do not result in infections when
sterile needles are used, but when they occur, infec­
tions are undesired or adverse. Postoperative soreness
is common after inj ections but also adverse . Trismus
is also relatively common and not desired (adverse).
Question 5: Which one of the following is not an option for
treatment of patients with true local anesthetic allergies?
Answer 5: D - A, B, and C are alternate options when pa­
tients are allergic to all local anesthetic drugs. D is a
preservative in fruit juices.
Question 6: Systemic complications related to inferior al­
veolar blocks include all of the following, except:
Answer 6: A - Hematomas are localized, not systemic re­
actions to the tearing of blood vessels.
C hapter 2 1 -Fundamentals for
the Administration of Nitrous
Oxide-Oxygen Sedation
Question 1 : The reservoir bag monitors which of the
following?
Answer 1: D - Depth of respiration and the need to adj ust
the Lpm can be monitored by observing the reser­
voir bag. The bag allows additional gas for patients
to breathe when not enough is delivered through
the hoses and provides a mechanism for monitoring
breathing and evaluating whether more or less gas is
needed during administration.
Question 2: Nitrous oxide sedation may be contraindicated
in patients with which of the following conditions?
Answer 2: D - Recovered alcoholics may relapse if seda­
tion is administered, patients with COPD may have
respiratory issues that are further compromised, and
those with cystic fibrosis may incur what are known as
emphysematous bullae.
Question 3: Which of the following reactions would indi­
cate that a patient is being over-sedated?
Answer 3: C - Unresponsiveness would be a definite sign
of over-sedation.
Question 4: The effects of adequate sedation may include
which of the following?
Answer 4: D - Relief of anxiety, heaviness of the legs, and
a warm flushed feeling are all subj ective signs of ad­
equate sedation.
Question 5: Most patients will achieve the desired level of
sedation at what percentage of nitrous oxide?
Answer 5: C - Most individuals will achieve a desired
level of sedation at 1 5 % to 40% nitrous oxide, while
some will be hypo-responders (requiring higher con­
centrations) and hyper-responders (requiring lower
concentrations).
Question 6: Oxygen is delivered for 3-5 minutes after den­
tal sedation in order to:
Answer 6: C - Nitrous oxide concentrations used in den­
tistry do not cause diffusion hypoxia; oxygen d e ­
livery is provided to eliminate nitrous oxide from
hoses and to allow time for recovery and the return
of reflexes.
A American Society of Anesthesiologists (ASA) Physical
Aberrant innervation unexpected variations in anatomic
patterns of innervation
Absolute contraindications situations in which local
anesthetic or vasoconstrictor drugs or nitrous oxide­
oxygen sedation cannot be administered safely
Absolute refractory period during which the generation
of new impulses along previously fired sections of nerve
membranes is physiologically impossible
A b s o r p t i o n p a s s a g e of a d r u g f r o m i t s s i t e o f
administration to the bloodstream
Accessory innervation expected variations in anatomic
patterns of innervation
Action potential refers to the electronic signal generated
and conducted to the CNS and from the CNS to effector
organs, cells, and tissues in response to stimulation
Acute pain pain of relatively short duration from seconds
to no longer than about 6 months
Adrenergic having effects similar to epinephrine
Adrenergic receptors receptors that respond to
catecholamines such a s epinephrine and norepinephrine
Adverse drug events or reactions (ADR) undesired
effects that occur in response to the pharmacologic
actions of a drug, including the events surrounding the
administration of the drug and described in terms of
their local or systemic effects or as complications
Adverse events see Adverse drug events or reactions
Age-appropriate terminology language that is consistent
with a child's level of comprehension and maturity
Ageusia loss of the ability to perceive sweet, sour, bitter, or
salty substances due to chorda tympani injury, otherwise
referred to as altered taste sensations or perversions
Alternative medicine refers to the use of complementary
a n d a l t e r n a t i v e m e d i c i n e ( C A M ) in p l a c e o f
conventional medicine
Alveolar ducts fin e air p as s a g e s at the e nd s of the
respiratory bronchioles
Alveolar sacs see Alveoli
Alveoli tiny air sacs located at the end of each air duct
in the lungs where the exchange of oxygen and carbon
dioxide occurs
Ambient gases mixture of elements present in the air in a
particular environment
American S o ciety of Anesthesiologists e ducational
research and scientific association of physicians
Status Classification System see ASA Physical Status
Classification System
Amide class of local anesthetic drugs in which an aromatic
component is linked to a secondary or tertiary amine by
an amide
Analgesia loss of the sense of pain while conscious
Anesthetic inadequacy lack of sufficient numbness to
provide comfortable therapy related to clinician- or
patient-dependent factors
Angioedema localized swelling brought about by the
rapid subcutaneous release of histamine after topical or
occasionally inj ectable local anesthetic administration;
despite the association with local anesthetics, on many
occasions there is no identifiable antigen
Anterior middle superior alveolar ( A M S A ) nerve
block provides p ain management for the incisors,
canine, and premolars on the side anesthetized as well as
palatal tissue from the midline through the molars and
the buccal periodontium of the pulpally affected teeth
Anterior superior alveolar (ASA) nerve block provides
pain management for the pulps of the maxillary central
incisor through the canine on the inj ected side and their
facial periodontium
Anxiety emotional response to a threat or danger that is
not immediately present or is unclear
Apoptotic programed biochemical events leading to cell
death in multicellular organisms
Armamentarium ( l o c al anesthetic) a l l e quip m e n t ,
materials, and devices used during the delivery o f local
anesthetic agents
Articaine intermediate- acting amide local anesthetic
drug noted for its fast onset and highly lipophilic
characteristics
ASA physical status classification medical components
o f care a s d e fin e d by the A m e r i c a n S o ci e t y of
Anesthesiologists
Aspiration test determines whether or not the tip of
a n e e d l e is e m b e d d e d within a b l o o d v e s s e l ; it is
accomplished by applying gentle, brief back pressure
on the upper inside surface of the thumb-ring and
observing for the absence or entry of blood into the
cartridge
Atypical plasma cholinesterase form of cholinesterase that
results from a genetic, autosomal recessive condition in
which there is an impaired ability to metabolize ester
local anesthetics
G-1
G-2 GLOSSARY
Axolemmas bilayere d , p h o s p h o lipid membranes o f
neurons, also known a s neurolemmas
Axon processes or fibers of individual nerve cells that
transmit signals to and from the central nervous system
Axoplasm cytoplasm or intracellular environment of a
nerve cell
B for the buccal soft tissue along the molar teeth in the
Backflow term applied when solution is inj ected under
pressure into tissues but the tissue resistance is so great
it forces solution to flow backward into the oral cavity;
this occurs primarily in buccal nerve blocks and in the
palate as well as in intraosseous inj ections such as the
PDL where solution can backflow through the sulcus
into the mouth rather than diffuse through alveolar
bone
Behavioral control allows patient to take actions to lessen,
shorten, or terminate stressful situations
Behavioral guidelines coaching instructions for parents
and guardians present during treatment of children;
includes use of calm, neutral facial and body postures,
gentle touches, gentle hand holding, and silent
observation
Behavioral indicators of fear overt behaviors such as
pacing in the waiting room, fidgeting, wringing hands,
gripping arms of chairs, or opposite responses such as
quiet, nonresponsive postures
Benzocaine ester topical anesthetic that exists almost
entirely in the base form
Bevel diagonal cut that makes the point of a needle
Bilateral mandibular blocks technique that decreases risk
of postoperative incidence of lip biting in children
H i - rotational insertion n e e d l e insertion technique
described for the Wand® handpiece system (STA Single
Tooth Anesthesia System® Instrument and CompuDent
Instruments ™ ) that reduces forces generated when
needles are moved through tissues, which result in
needle deflection
Biofeedback method through which patients can modify
their physiological responses to pain and anxiety; allows
patients to exert at least some voluntary control over
involuntary responses
Biotransformation process whereby local anesthetic drugs
are broken down to less toxic or nontoxic metabolites
before being excreted
Biphasic occurring in two relatively distinct phases
Blanching visible indicator of the diffusion of anesthetic
solution through tissues due to decreased blood flow,
which is more pronounced when vasoconstrictors are
used; blanching may be described as pale pink to white in
color with visibly less color compared with adjacent tissues
Breech-loading syringe with a large side opening for
easing insertion of the local anesthetic cartridge
Bronchioli subdivision of the bronchi having cuboidal
shaped epithelial cells 1 mm or less in diameter
Buccal infiltration with articaine supraperiosteal inj ection
over the buccal roots of mandibular posterior teeth to
provide primary or supplemental pulpal anesthesia of
the teeth
Buccal ( B) nerve block provides p ain management
mandibular region
Bupivacaine long-acting amide local anesthetic drug
Butamben ester topical anesthetic used in combination
with other topicals, in dentistry
c
C an c e l l o u s b o n e s y n o n ym o u s w i t h s p o n gy b o n e ,
compressible bone underlying the cortical plates o f the
maxilla and mandible
Cardiac dose safe limit of vasoconstrictor drugs for a
patient with ischemic heart disease
Carina located at the junction of the trachea and the left
and right bronchi
Carpule glass cylinder holding local anesthetic drugs and
other contents in solution for injection into oral tissues; a
trademark term of Cook-Waite Laboratories for cartridge
Cartridge non trademark synonym for carpule
Cartridge-type syringe syringe with a large side opening
for easing insertion of the local anesthetic cartridge
Cartridge volume guaranteed volume of solution in a
cartridge
Catecholamine chemical compound consisting of a catechol
and an amine component that has a sympathomimetic
action (stimulates adrenergic receptors)
Cation any p o sitively charged i o n ; s p e cifically the
positively charged local anesthetic ionic molecule that
exists in aqueous solutions of local anesthetic drugs
CCLAD-controlled low pressures pressures generated by
computer-regulated drug delivery systems that precisely
control defined fluid pressures and fluid volumes over
time. Fluid pressures are controlled below a prescribed
maximum pressure limit to minimize tissue damage and
subj ective pain response.
C ell body p art o f a neuron that provides metabolic
support and, in the case of motor neurons, also conducts
impulses
Cerebrovascular accident (CVA) rapid loss of brain
function due to a disruption of blood supply that results
in permanent impairment due to blockage or rupture of
an artery to the brain
Cholinesterase enzyme responsible for breaking down
esters and articain e ; manufactured primarily but
not exclusively in the liver, cholinesterase is widely
distributed; also referred to as plasma cholinesterase

Chronic Obstructive Pulmonary Disease (COPD) lung
d i s e a s e s t h a t i m p e d e airflow, m a k i n g b r e athing
difficult
Chronic pain pain that lasts for more than 6 months, with
or without an identifiable cause
Clark's rule method for calculating and confirming safe
local anesthetic doses in children based upon weight
C o gnitive control mental maneuvers through which
patients can lessen their fearful, negative thoughts and
their reactions to these thoughts
Cognitive distraction practice of distraction that actively
shifts a patient's focus away from a stressful situation to
a less-stressful point of focus
Complementary and alternative medicine (CAM) " a
group of diverse me dical and he alth care systems,
practices, and products that are not generally considered
part of conventional medicine," as defined by the U.S.
National Institutes of Health
C o m p l e m e n t a r y m e d i c i n e r e f e r s to t h e u s e of a
nonmainstream approach together with conventional
medicine
Complications see Adverse drug events or reactions
Compounded drugs drugs formulated by compounding
pharmacies
Computer-controlled local anesthetic delivery (CCLAD)
computer-driven arrangement of software, hardware, and
injection devices used to administer anesthetic injections
in which the rate of delivery and fluid pressures are
predetermined by a software-driven motor
Concentration gradient term referring to the relative
amounts of substances on differing sides of membranes
(in local anesthesia, neural membranes)
Concomitant drug that has been administered while other
drugs are still in effect
Conduction blockade inability of impulses to pass through
certain segments of nerve membranes, which occurs
when local anesthetic drugs have been administered
C o nduction tubing c o r r u g a t e d s i l i c o ne , r u b b e r , o r
p o lyethylene tubing t h a t attach e s t o the nitrous
machine that leads to the nasal hood
C ontraindications: absolute, relative, permanent, or
temporary Absolute - local anesthetics may not be
administered ; this may be temporary or permanent.
Rel ative - local anesthetics m ay b e administered
but only with modification; this may be temporary or
permanent.
Control power to influence or direct behavior or the
course of events
Copper tubing utilized in central supply nitrous oxide­
oxygen delivery systems because it does not support
combustion
Core bundle fascicule located in the central region of a
nerve
GLOSSARY G-3
Coronoid notch landmark for lA inj ections; concavity
on the anterior border of the ramus of the mandible
used to identify a height of penetration that allows for
advancement of the needle to a site directly above the
mandibular foramen
Cortical plate dense layer of bone surrounding the spongy
underlying bone; the cortical plate in the mandible
is generally more dense than the cortical plate of
the maxilla and more difficult to penetrate during
intraosseous inj ections
Cricoid cartilage strong ring-shaped connective tissue
surrounding the trachea
Cricothyrotomy emergency procedure used to create
respiration access between the thyroid and cricoid
cartilages when upper airways are occluded
Cross-innervation overlap of terminal nerve fibers of the
contralateral side
Cumulative trauma effects of nonergonomic positions
during procedures can become significant over a period
of time
C y s t i c fib r o s i s g e n e tic d i s e a s e c a u s i n g functi o n a l
impairment of pulmonary mech anics a n d p o ssible
respiratory distress
D
Debriefing post-treatment discussion of an appointment
experience
Deep breathing coping response to overcome fe ar of
needles and inj ections
D e e p s e d a t i o n d r u g - i n d u c e d s t a t e of d e p r e s s e d
consciousness accompanied b y p artial or complete
loss of protective reflexes, including the inability to
continually maintain an airway independently and/or to
respond purposefully to physical stimulation or verbal
command; general anesthesia
Dendritic zone zone of a sensory nerve where stimulation
occurs
Dental anxiety scale (DAS) method for measuring dental
anxiety and fear
Dental fears questionnaire method for measuring dental
anxiety and fear
D e ntal l o cal a n e s t h e s i a p r o v i d e r s i n c l u d e d e n t a l
hygienists and i n some states and provinces, mid-level
and/or expanded function providers who are allowed to
administer local anesthesia for effective pain control of
the oral cavity
Dental neural plexus see Dental plexus
Dental plexus network of nerves surrounding teeth that
innervate the pulp and their supporting structures
Depolarize to transform an area of nerve membrane from
an excitable to a less excitable or nonexcitable state
Deposition site any site at which local anesthetic solution
is injected; target site for the blockade of a specific nerve
G-4 GLOSSARY
Devices (medical, local anesthetic) syringes, cartridges,
needles, and recapping and disposal items
Diaphragm semipermeable barrier that is centered in the
cap of an anesthetic cartridge, commonly made of latex
rubber or, increasingly, of nonlatex rubber
Diffusion hyp oxia brief decrease in alveolar oxygen
tension
Dilution ratio ratio of vasoconstrictor drug to volume of
solution, expressed in mg/mL (e.g., one gram in one
hundred thousand milliliters is expressed as 1 : 100,000)
Dissociation constant e quilibrium constant o f local
a n e s th e t i c drugs i n s o l u t i o n , d e s crib e d b y the
Henderson-Hasselbalch equation, and optimized by
adjustments to the pH of a solution
Distribution transfer of drugs from circulation to the
tissues and organs in the body
Diurnal body rhythms variable response to drugs during
different times of a day
Drug concentration concentration of local anesthetic in a
cartridge, expressed in percentages (e.g. , 0.5 % , 2 % , 3 % ,
and 4 % )
Drug percentages expression of the relative amount o f
drug i n a cartridge (a 4 % drug, e . g . , contains twice a s
much drug per volume a s a 2 % drug)
Drug ratio drug dilution
Durable blockade impulse extinction on larger, more
heavily myelinated nerves requiring greater volumes of
local anesthetic drug
Dyclonine hydrochloride topical anesthetic with a ketone
linkage, as opposed to amide or ester linkage
Dynamic Pressure Sensing® (DPS) patented process that
allows for real-time audible feedback of fluid pressures
during inj ections with the STA Single Tooth Anesthesia
System® Instrument
Dysesthesia sensation of pain from non-noxious stimuli
that may follow local anesthetic procedure s ; one of
several possible results following nerve damage
E
Electric pulp tester device designed to test the vitality of
teeth by using an electric current
Electrical potential difference in the electrical charge
across a membrane
Elimination process through which drugs or fractions
of drugs and metabolites are removed from the body,
primarily via the kidneys
Elimination half-life time it takes to eliminate 50 percent
of a local anesthetic drug from the blood
Embedded needles needles or needle fragments that have
broken off and are buried in tissues
End cap aluminum cover that fits tightly around the end
of a cartridge and holds the diaphragm in place
Endoneurium anatomic structure that separates individual
nerve fibers and insulates their electrical activity
Engineering controls (EC) controls (e.g. , sharps disposal
containers, s elf- she athing needles, and devices for
the prevention of needlestick inj uries) that isolate or
remove bloodborne pathogens from the workplace
Epinephrine naturally occurring neurotransmitter
Epineural sheath outer covering of the epineurium
Epineurium loose connective tissue layer that surrounds
the fasciculi, their associated supporting connective
tissue including blood vessels and lymphatics, and the
perineuria
Epiglottis elastic cartilage flap attached to the entrance of
the larynx
Ester class of local anesthetic drugs in which an aromatic
component is linked to a secondary or tertiary amine by
an ester
Eutectic mixture mixtures of local anesthetic drugs used
as topical that contain higher concentrations of base
molecules formulated as homogeneous creams, which
provide increased depths of anesthesia, faster onset
on skin, and greater depth of penetration on mucosa
compared with non-eutectic topicals
Expiration passive outward flow of air from the lungs as
the chest wall and lungs recoil
Extracellular outer environment of nerves beyond their
membranes and associated Schwann cells
F
False negative aspiration seemingly negative aspiration
where a location of the needle tip within a vessel has
been concealed by suction of the vessel wall over the
lumen of the needle during aspiration
Fascial planes superficial fascia and deep cervical fascia
dividing the neck into several compartments that are
potential b arriers to the unrestricted flow of local
anesthetic drugs that can deflect solutions away from
intended target sites
Fasciculi bundles of nerve fibers
Fear emotional response to an immediate threat or danger
Felypressin synthetic hormone with vasoconstrictive
properties
Fi e l d b l o ck inj e c t i o n t e c h n i q u e i n d i c a t e d w h e n
procedures are confined t o one o r two teeth o r t o tissues
in a limited area; commonly referred to as infiltration
Fight or flight response neurotransmitter-mediated
mechanism resulting in increased heart rate and blood
pressure, dilation of the pupils and of the bronchial
and skeletal muscle vasculature, and constriction of
mesenteric vessels
Finger grip part of a syringe for controlling aspiration and
rate of delivery

Firing threshold point at which a sufficient change in
electrical potential has occurred to generate a nerve
impulse
Flow meters visual indicators of the volume of gas being
delivered, mounted on the portable units or attached to
the walls of central delivery systems
Fluid dynamics complex interaction of variables related
to the movement and control of fluids during inj ection.
These variables include, but are not limited to, fluid
flow rate, fluid pressure, fluid volume, tissue density,
tissue compliance, tissue pressure gradients.
Fluid flow rate rate at which a fluid is moved into tissues,
typically measured as mL/sec
Fluid pressure pressure of a fluid during movement into
tissues, typically measured as psi or mmHG
Focusing attention technique to prevent anticip atory
anxieties or thoughts of what might happen during
treatment
Functional capacity assessment tool to identify when a
medical risk is the greatest
Fu n d a m e n t a l s of p a i n m a n a g e m e n t c o n d u c t i n g
comprehensive assessment, recognizing and responding
to p a t i e n t f a c t o r s , i n t e g r a t i n g e v i d e n c e - b a s e d
knowledge; understanding relevant drugs, their effects,
indications, and contraindications; and developing
clinical decision-making skills and mastering a wide
variety of techniques and appropriate modifications
G hub and needle shaft) ; also known as needle hubbing
Ganglia group of nerve cell bodies outside the CNS
Gas exchange occurs from alveoli to capillaries and vice
versa through simple diffusion across partial-pressure
gradients
Gate control theory n e r v e imp u l s e s g e n e r a t e d by
more painful an d subsequent stimuli, such as needle
penetrations, that can be blocked within the spinal
nervous system
Gauge diameter of the lumen of a needle; historically, this
is based on the number of lead balls, each of which just
barely fits inside a shotgun barrel, that add up to a pound;
a greater number of balls is required to add up to a pound
from a smaller barrel lumen - hence higher gauges such
as 30-gauge needles are smaller than 27 and 25 gauge
General anesthesia drug-induced loss of consciousness
during which patients are incapable of being aroused,
even with p ainful stimulati o n; ability to maintain
ventilatory function often impaired
Gow-Gates ( G G ) nerve block true mandibular block
that provides pain management for multiple teeth and
typically all of their supporting periodontium in one
mandibular quadrant
Graduated exposure treatment rehearsal to introduce
new procedures, similar to tell-show-do technique
GLOSSARY G-5
G r e a t e r palatine ( G P ) nerve b l o ck p r o v i d e s p a i n
management for palatal soft and osseous tissues distal
to the canine in one quadrant
Guided imagery method to replace negative thoughts
with mental images of pleasant scenes or scenarios to
establish cognitive control over fearful situations
Guided visualization see Guided imagery
H
Harpoon part of a syringe that engages the stopper in order
to aspirate and to advance the stopper in the cartridge
causing solution to flow from the tip of the needle
Harpoon-type aspirating syringe syringe designed with a
harpoon-shaped end attached to the piston that embeds
into the rubber stopper to permit an aspiration test
Hematoma pool of vascular contents formed from the
leaking of blood into surrounding tissues; usually occurs
after inadvertent nicks of blood vessels during injections
Hemostasis in local anesthesia, halting the flow of blood
using vasoconstrictors
Henderson-Hasselbalch equation expression of pH as a
function of the concentrations of weak acids and bases
in solution
Hub point at which the shaft of a needle j oins and secures
the needle to the syringe adaptor
Rubbing maneuver that describes the practice of inserting
the needle to its entire length (to the j unction of the
Hydrophilic having a tendency to interact with or be
dissolved by water; water loving
Hypercarbic drive primary stimulus of respiration driven
by pH level of the blood modulated by the presence of
C0 2 in healthy individuals
Hyperesthesia increased sensitivity to stimuli following
nerve injury
Hyper-responders individuals who respond with adverse
systemic signs and symptoms when less-than-maximum­
recommended doses of local anesthetics have been
administered
Hypersensitivity allergy
Hypervolemic abnormal increase in blood volume where
there is too much fluid in the blood; opposite condition
is hypovolemia, which is too little fluid volume in the
blood
Hypogeusia relative loss of the ability to perceive sweet,
sour, bitter, or salty substances due to chorda tympani
injury, otherwise referred to as altered taste sensations
or perversions
Hypo-responders individuals who respond with adverse
systemic signs and symptoms only after greater-than­
maximum-recommended doses of local anesthetics
have been administered
G-6 GLOSSARY
Hypoxic drive secondary stimulus of respiration driven by
low 02 levels through oxygen sensors in the carotid and
aortic bodies in individuals with severe COPD
Idiosyncratic adverse events that have no known etiology
Impulse extinction interruption of impulse propagation
along p articular areas o f nerve membranes (local
anesthesia induces impulse extinction)
Impulses signals generated and conducted along nerve
membranes that provide the CNS with awareness of
tissue stimulation or damage or that initiate reactions
from effector organs and tissues in response to the
stimulation or damage
Incisive (I) nerve block provides pain management for
the buccal mucous membrane and skin of the lower lip
and chin, and the pulps and periodontium of the teeth
anterior to the mental foramen, to the midline ; also
referred to as the mental incisive nerve block (MI)
Infe r i o r alveolar ( l A ) nerve b l o c k p r o v i d e s p a i n
management for mandibular teeth i n one quadrant and
much of their supporting periodontium
I n fi l t r a t i o n inj e c t i o n t e c h n i q u e i n d i c a t e d w h e n
procedures are confine d to o n e o r two teeth or t o
tissues in a limited area; see Field block
Informational control simple sensory description of what
a patient can expect of an imminent aversive procedure
Informed consent legal principle that involves a higher
burden of consent than merely agreeing to treatment;
the patient must be informed as to the specific risks and
rewards of procedures and therapy
Infraorbital (10) nerve block provides pain management
of anterior and premolar teeth in one quadrant and their
buccal periodontium as well as the upper lip, lateral nose,
and the lower eyelid on the same side as the injection
Intranasal anesthesia nasal delivery of local anesthetic
drugs
Inspiration inflow of air to the lungs accomplished by the
movement of the diaphragm and the external intercostal
muscles that expand the chest wall creating a negative
pressure in the pleural space, thereby allowing a vacuum
effect to pull air into the lungs
Inte grative m e dicine combines treatments from
c o n v e n t i o n a l m e d i c i ne a n d c o m p l e m e n tary a n d
alternative m edicine f o r which there is some high­
quality evidence of safety and effectiveness
Intermediate chain hydrocarbon linkage between the
working ends of local anesthetic molecules, which also
determines the pathway of metabolism of the drugs
Internal oblique ridge inferior alveolar nerve block
landmark defining the lateral extent of the area into
which penetration is made, which when accurately
identified, can prevent premature contact of the tip of
the needle with the bone of the mandible
Interpapillary inj ection deposition of small volumes of
local anesthetic while penetrating from the buccal
aspect to the lingual aspect of a papilla; an infiltration
technique
Intracellular environment within cell membranes, in this
case, nerve cell membranes
IntraFiow device used for intraosseous inj ection that
forms a guide sleeve that remains in place after bony
perforation, which allows for ease of needle penetration
Intraligamentary injection technique that deposits a drug
solution in an area surrounded by ligaments, tooth roots,
and bone, also referred to as peridental; see Periodontal
ligament injection (PDL)
I n t r a o s s e o u s a n y inj e c t i o n t e c h n i q u e in w h i c h
perforation or penetration into bone or periodontal
ligament is necessary in order to achieve anesthesia;
solution diffuses through bone in order to reach target
nerves
Intraosseous injection see Intraosseous
lntrapulpal inj ection technique that provides anesthesia
for pulpally involved teeth when other techniques have
failed
Intraseptal inj ec tio n t e chnique tha t p r o v i d e s p ain
management for the periodontium lingual to a tooth;
p articularly u s e fu l w h e n p al a t a l t i s s u e s r e q uire
anesthesia and clinicians and/or patients wish to avoid
palatal inj ections
Intravascular administration depositing local anesthesia
solution within a blood vessel
Ion channels pathways within nerve membranes through
which charged atoms can pass
Isoenzyme system hep atic system where the primary
metabolism of amides occurs, also known as the p450
isoenzyme system
J
Jet inj e ction device that uses narrow bursts of air to
penetrate mucosa without needles
L
Laryngopharynx lowermost part of the pharynx from the
epiglottis to the cricoid cartilage
Larynx important regulator of respiration between the
pharynx and the trachea containing walls of cartilage,
muscles, and vocal cords
Left bronchus branch of the bronchi about 5 em long and
deviates at about 45 degrees from the trachea, divides
into two branches, and links five upper lobes and four
lower lobes
Levonordefrin synthetic catecholamine used in some
solutions of local anesthetic drugs
Lidocaine intermediate- acting amide local anesthetic
drug

Limiting drug drug that determines the maximum amount
that may be administered when considering more than
one type of local anesthetic drug to be administered
during an appointment
Lingual (L) nerve block provides pain management for
the lingual soft tissues of the mandible
Lipophilic h aving a tendency to interact with or b e
dissolved b y lipids; lipid o r fat loving
Local anesthesia temporary loss of sensation in a specific,
usually small area of the body
Local anesthetic drug any drug that renders nerve tissues
insensitive to stimulation by preventing the generation
and conduction of nerve impulses
Local infiltration see Infiltration inj ection
Lumen inner space of a hollow needle, otherwise known
as the opening
M Methamphetamines highly addictive stimulant drugs,
Mandibular infiltration inj ection technique that allows
diffusion of anesthetic solution through thinner cortical
plates with less dense bone; more frequently used in
children
Mandibular infiltration with articaine s e e B u c c a l
infiltration with articaine
Manifold device that connects multiple cylinders together,
controls flow of gases, and connects the gas supply to a
central piping system
Mantle bundle fascicule located in the outer region of a
nerve
Manual syringe uncontrolled high pressures pressures
g e n e r a t e d b y m a n u a l d e n t a l s y r in g e s w h e n t h e
force applied to mechanical plungers is subj ectively
controlled by the operator's hand. Fluid pressures and
flow rates manually produced by mechanical systems
are in response to the back-pressure and resistance
encountered by entry of a fluid into tissues. Fluid
pressures and flow rates cannot be precisely defined or
precisely controlled during fluid movement.
Maxillary (MNB) nerve block provides hemimaxillary
pain management; also referred to as second division or
V2 nerve block
Maximum exposure limit set in 1977 by the National
Institute for Occupational Safety and Health (NIOSH)
for nitrous oxide concentration to 25 ppm for dental
personnel
Maximum recommended dose (MRD) individualized
l a r g e s t d o s e o f a n e s t h e ti c d r u g that s h o u l d be
administered at o n e time, n o t n e c e s s arily at one
appointment (re- administration may b e possible in
the same appointment depending on the elimination
half-life of the drug administered and the length of the
appointment)
Medical devices see Devices (medical, local anesthetic)
GLOSSARY G-7
Medulla oblongata lower half of the brainstem that is
continuous with the spinal cord; it drives involuntary
respiration
Megaloblastic anemia blood disorder related to bone
marrow changes
Membrane expansion theory observed phenomenon
through which approximately 10% of a local anesthetic
drug's effect on nerve membranes may be explained
Mental incisive (MI) nerve block see Incisive nerve block
Mental (M) nerve block provides pain management for the
buccal soft tissues in the mandible, anterior to the mental
foramen
Mepivacaine short- to intermediate-acting local anesthetic
that is a weak vasodilator
Metabolic equivalent of task (MET) measure equivalent
to the aerobic demand of various physical activities,
also referred to as metabolic equivalent
Metabolism see Biotransformation
avoid administration of vasoconstrictors for a minimum
of 24 hours after methamphetamine use
Methemoglobinemia condition induced by drugs and other
substances, including prilocaine, benzocaine, and articaine,
which can result in a life-threatening depletion of oxygen
in the tissues
Middle superior alveolar (MSA) nerve block provides
anesthesia to structures innervated by the MSA nerve,
when present, and its terminal branches, to include the
pulps of the maxillary first and second premolars and
their facial periodontium
Milligram metric measure of weight used to calculate
and record recommended doses of drugs and doses
delivered
Milliliter metric measure of volume used to calculate
and record recommended doses of drugs and doses
delivered
Minimal sedation drug-induced minimally depressed level of
consciousness in which a patient is able to independently
and continuously maintain an airway and respond
normally to tactile stimulation and verbal commands
Minimum alveolar concentration concentration at which
the effects of anesthetic gases are produced
Minute volume also referred to as minute ventilation or
minute volume flow, is the amount of air exhaled in one
minute and is calculated by multiplying tidal volume by
respiration rate.
Moderate sedation drug-induced depression of
consciousness during which p atients can respond
purposefully to verbal commands, either alone or
accompanied by light tactile stimulation
Motor nerves transmit impulses from the CNS to effector
cells, tissues, and organs
Motor neurons nerve cells that carry impulses away from
the CNS to effector cells, tissues, and organs
G-8 GLOSSARY
Muco gingival j unction of t he fre e muco s a and t h e
attached gingiva in maxillary molar regions, a landmark
for Vazirani-Akinosi nerve blocks
Muscle relaxation progressive coping skill for fearful
patients in which different muscle groups are tensed
and relaxed throughout the body
Myelinated refers to nerves that are enclosed by multiple
layers of Schwann cells
Mylohyoid nerve block provides pain management for
supplemental p ain management during procedures
involving mandibular molars when IA blocks fail to
provide profound anesthesia
N
Nasal hood breathing apparatus that sits over the patient's
nose to facilitate the inhalation of N20/02
Nasopalatine (NP) nerve block provides pain management
for palatal soft and osseous tissue in the anterior third of
the palate, approximately from canine to canine
Nasopharynx uppermost part of the pharynx that extends
from the lower skull to the soft palate
Needle device that penetrates tissues and through which
local anesthetic solution flows into them
Needle adaptor threaded surface at the end of the barrel
onto which needles are screwed
Needle cap plastic cover that protects the needle from
contamination before and after use
Needle pathway route a needle travels as it advances to a
target site
Needle tract infection infection that has been spread
along a needle pathway
Negative aspiration absence of visible blood in a cartridge
following an aspiration test
Nerve block see Nerve block inj ection
Nerve block inj e ction deposition ne ar a maj or nerve
trunk at a greater distance from the area of treatment,
which provides wider areas of anesthesia
Nerve fibers axons and their associated Schwann cells
Neurolemma outer membrane of a neuron, also known as
an axolemma
Neurons nerve cells; basic units of nerves
Neurop athic pain pain due to inj ury or dysfunction
of sensory nerves in the CNS ; can occur in CNS or
peripheral nerves
Neutral base form of a local anesthetic molecule in which
there is no ionic charge
Nitrous oxide colorless, sweet-tasting gas used as a mild
anesthetic for dental and medical procedures
Nitrous oxide abuse deliberate inappropriate us e of
nitrous oxide to obtain mood-altering effects
Nociception detection of tissue injury
Nociceptive pain pain due to tissue injury
Nociceptors sensory receptors that detect injury
Nodes of Ranvier spaces between adj acent S chwann
cells where nerve membranes can be exposed to local
anesthetic drugs in myelinated nerves
Norepinephrine naturally o ccurring a d r e n e rgic
neurotransmitter
Novocaine amide local anesthetic drug that is virtually
worthle s s in d e n t i s try without the a dditio n of a
vasoconstrictor
0
Occult hematoma clinically undetected hematoma
Occupational exposure long-term exposure risk related
to the presence of nitrous oxide gas in room air due to
inadequate ventilation, incorrect administration of nitrous
oxide sedation, and/or poorly maintained equipment
Onset® buffering system for dental local anesthesia
cartridges
O r aVe r s e ® p h a r m a c e u t i c a l a g e n t ( p h e n t o l a m i n e
m e sylate) available f o r t h e reversal o f soft-tissue
anesthesia
Oropharynx mid portion of the pharynx, contains the
tonsils, eustachian tubes, and opening of the mouth,
continuous structure from the oral cavity to the soft
palate and epiglottis
Overdose administrations of drugs that result in signs and
symptoms of CNS and CVS depression
O xy g e n o d o r l e s s , c o l o r l e s s , a n d t a s t e l e s s g a s , n o t
flammable; however, i t supports combustion
p
P450 isoenzyme system see Isoenzyme system
Pain unpleasant feeling or sensation usually associated
with actual or potential tissue damage
Pain disorders a s s o ciated with psychogenic factors
related to mental or emotional problems that affect the
experience of pain
Pain m a n a g e m e n t p r o p e r a d m i n i s t r a t i o n of l o c a l
anesthetic that allows fearful p atients t h e ability t o
cope with and tolerate treatment
Pain threshold point at which a stimulus first produces a
sensation of pain
Pain tolerance individual's reaction to painful stimuli
Palatal -anterior s u p e r i o r alveolar ( P - A S A ) nerve
block provides pain management for maxillary anterior
sextants, including the palatal and facial periodontium
of affected teeth; also known as the palatal approach
anterior superior alveolar nerve block
Parent guidelines guidelines for parents and guardians
accompanying children to dental appointments that
include everything from learning to be silent observers
to awareness of the importance of facial expressions
and body postures to successful appointments

Pare s t h e s i a l i n g e r i n g p a i n , n u m b n e s s , i n c r e a s e d
sensitivity, o r taste alterations resulting from nerve
injury associated with local anesthetic injections
Penetrating end part of the needle shaft opposite the tip
of the needle that pierces through the center of the
diaphragm of the local anesthetic cartridge; also known
as the cartridge penetrating end
Penetration site specific location where a needle first
pierces mucosa
Peridental see Periodontal ligament inj ection (PDL) and
Intraligamentary inj ections
Perilemma inner layer of the perineurium
Perineurium bundles individual nerve fibers into fasciculi
Periodontal ligament inj e ction ( P D L ) intra o s s e o u s
inj ection technique for single teeth, for supplemental
anesthesia of individual teeth when other techniques
have failed to provide profound anesthesia, when
widespread anesthesia is contraindicated, and when
total doses need to be minimized; also known as the
intraligamentary or peridental technique
Pharmacodynamics part of the pharmacology of a drug
that refers to the actions of the drug on the body
Pharmacokinetics part of the pharmacology of a drug that
refers to the management and disposition of the drug
by the body
Pharynx muscular pass ageway 1 2 to 14 em long that
i s d ivi d e d into t h r e e r e g i o n s , the n a s o p h ar y n x ,
oropharynx, and laryngopharynx
Phenylephrine weak, noncatecholamine vasoconstrictor
Phobia described in the American Psychiatric Association's
Diagnostic and Statistical Manual of Mental Disorders
as a persistent, irrational fear of a specific obj ect or
situation that results in a compelling desire to either
avoid the situation or endure it with dread
Physical tolerance ability to tolerate the actual mechanics
of procedures, such as keeping the mouth open or
sitting for extended procedures
Physiolo gical indicators of fear include perspiration,
changes in respiration, shallow breathing, incre ased
heart rate and blood pressure, or holding breath during
inj ections
Pin index safety system ensures that tanks are correctly
attached to the corresponding nitrous oxide or oxygen
gas yolks on the stands; used with portable nitrous
oxide-oxygen delivery systems only
Piriform recess deep cavity found on either side of the
larynx that directs food around it
Piston part of the syringe that engages the harpoon in
the cartridge stopper to deposit solution and facilitate
aspiration tests
pKa dissociation constant of a drug that relays relative
onset time information; see Dissociation constant
Pneumothorax accumulation of air or gas in the pleural
cavity, usually a result of an alveolar rupture or opening
GLOSSARY G-9
of the plural space to the outside air resulting in the
collapse of the lung
Polarized potential across a nerve membrane whenever it
is not at 0 mV
Polymodal p ain receptors that respond to all types of
stimuli
Positive aspiration presence of visible blood in a cartridge
following an aspiration test
Positive coping statement method by which patients can
establish cognitive control during treatment situations;
reaffirms that all is going well during procedures by use
of simple statements
Positive feedback behavioral management technique that
emphasizes specific aspects of procedures that are going
well, such as thanking a child for opening wide
Postanesthetic trauma self-injury caused by lip, tongue, or
cheek biting, which occurs due to lack of sensation of
anesthetized tissues
Posterior superior alveolar (PSA) nerve block provides
anesthesia for p ain management of multiple molar
teeth in one quadrant and their buccal periodontium
Pre-anesthesia anesthesia that is already in effect from
previous inj ections in an area , or a two-step topical
method that includes an initial 1-minute application of
topical followed by 1 minute of pressure anesthesia
Premature contact contact m a d e with b o n e b efore
reaching an optimum deposition site
PREP acronym for one of a number of strategies that
help p atients cope with fear and anxiety in order
to build trust and provide reassurance, specifically:
Prepare, Rehearse, Empower, and Praise
Pressure anesthesia technique used to enhance patient
comfort during palatal needle penetration through
the use of pressure applied with either cotton swab or
blunt-ended instrument handle to cause blanching,
before penetration
Prilocaine intermediate-acting amide local anesthetic drug
Procaine once-popular ester local anesthetic drug now
rarely used in dentistry and no longer available in
dental cartridges; see Novocaine
P r o g r e s s ive m u s c l e r e l a x a t i o n ( P M R ) r e l a x a t i o n
technique learned b y tensing and then relaxing different
muscle groups throughout the body
Propagation process of sequential impulse generation
along nerve membranes to processing areas in the CNS
or to effector cells, organs, and tissues
Prote ctive response physiologic reaction to prevent
bodily harm
P s e u d o ch o l i n e s t e r a s e e n z y m e r e s p o n s i b l e for t h e
metabolism o f ester local anesthetic drugs
Psychogenic factors aspects not attributable to specific
injuries or pathology when discussing pain disorders
Psychological tolerance ability to tolerate the mental
demands of procedures, such as the anticipation of pain
G-1 0 GLOSSARY
Pterygomandibular raphe me dial extent of the area
into which penetration is made for inferior alveolar
inj ections
R to a decrease in the length of membrane along which
Rapid depolarization event that occurs along a nerve
membrane, after the firing threshold has been attained,
where su fficient p o tential has b e e n p r o v i d e d to
generate a nerve impulse
R e fr a c t o r y s t a t e s t a t e fo l l o w i n g a n e r v e imp u l s e
generation i n which a subsequent impulse generation is
either temporarily impossible or more difficult
Regulator reduces gas pressures from tanks before gas
is delivered into the tubing and pipes; located on both
portable and central nitrous oxide-oxygen delivery systems
Rehearsals practicing coping skills while simulating the
steps involved in actual dental procedures, at the same
time relieving everyone of the burden of having to
accomplish any treatment
Relative contraindications contraindications to local
anesthetic delivery that allow procedures to proceed
but only after appropriate modifications
Relative refractory state p e r i o d in which a p artial
attainment of the resting state has occurred and during
which a larger stimulus is required in order to achieve
a successful firing along previously fired segments of
nerve membranes
Relaxation response restful state that modifies physical
and emotional responses to stress
Repolarization reversal of ion concentrations in the
recovery phase when the nerve has attained a potential
of approximately +40 mV
Rescue injection inj ection of local anesthetic administered
whenever an initial inj ection fails to provide profound
anesthesia
Reservoir bag provides a volume of gas necessary for
each breath, as high as 20 Lpm over 1 to 2 seconds
Respiratory system includes the organs involved in the
exchange of oxygen and carbon dioxide gases across
pulmonary/capillary membranes during respiration
Resting state state in which a nerve is receiving little to no
stimulation
Retrospective control see Debriefing
Reversible ischemic neurologic deficit (RIND) disruption
of blood supply within the brain that lasts from 24 to 72
hours, differentiating it from a TIA
Right bronchus branch of the bronchi about 2.5 em long
and deviates about 25 degrees from the trachea, divides
into three branches that link three upper lobes, two
middle lobes, and five lower lobes
Risk assessment making a determination of a patient's
ability to withstand local anesthetic procedures before
initiating them
s
S altatory conduction process whereby impuls e s are
more rapidly conducted along myelinated nerves due
impulses must be generated in order to reach their
destinations
Scavenging systems help to eliminate excess gas being
exhaled by p atients, thereby limiting the clinician's
environmental exposure to exhaled nitrous oxide
Schwann cells connective tissue cells that protect neurons
in the peripheral nervous system
S chwann cell sheaths S ch w a n n c e l l s , d e scrib e d a s
enclosing neurons
S c o o p t e chnique recapping t e chnique for n e e d l e s ;
requires a clinician to slide a n uncapped needle into
a needle cap (she ath) while the cap is lying on an
instrument tray or table
Second division nerve block see Maxillary nerve block
Sedation induction of a relaxed state to alleviate anxiety
and discomfort
Self-aspirating syringe syringe designed to perform an
aspiration test when brief, gentle pressure is applied,
then released against the thumb disk located on the
piston above the finger grips of the syringe
Self-report principal method for obtaining information
about a patient; techniques may include questionnaires
and interviews
Sensory modality ability of a stimulus to be detected by a
specific receptor
Sensory nerves nerves that relay information to the CNS
regarding tissue injury and stimulation
Sensory neurons nerve cells that carry incoming impulses
from the body to the CNS for processing
Shaft flexible, hollow, stainless steel cylinder with a sharp
tip and bevel on one end and a cartridge-penetrating
portion on the other; also referred to as a shank
Shank see Shaft
Slow depolarization initial depolarization or electrical
activity along a nerve membrane during which there
is insufficient d e p o l arization to generate a nerve
impulse
S o dium ion pumps active pumps that enhance the
movement of sodium ions both into and out of sodium
channels
Somatic pain nociceptive pain that occurs on superficial
structures such as skin and muscles caused by traumatic
injuries
Specific positive feedback positive feedback for specific
desirable behaviors
Specific protein receptor site areas in ion channels of
nerve membranes in which local anesthetic molecules
are bound

Specific protein receptor theory theory that explains
the binding of local anesthetic molecules in nerve
membranes and the majority of their behavior
Spongy bone compressible bone underlying the cortical
plates of the maxilla and mandible
Stabident device used for intraosseous inj ections that
forms a guide sleeve which allows for ease of needle
penetration
Stopper silicone rubber portion of a cartridge that when
engaged by a syringe harpoon is advanced by the piston
to deposit solution, also referred to as a bung
Stress reduction protocols (SRP) protocols aimed at
preventing psychogenically generated adverse events
Success variably defined provision of profound anesthesia
Supportive communication communication that begins
during the pre-inj ection period aimed at providing
reassurance and trust
Supraperiosteal injection see Field block injection
Sympathetic nervous system part of the nervous system
associated with so-called fight or flight reactions
Sympathomimetic drugs that mimic naturally occurring
a d r e n e rgics, inc l ud i ng b o t h c a t e c h o l a m i n e s a n d
noncatecholamines
Synapses areas of connection of nerve cells; also referred
to as junctions
Syringe adaptor plastic or aluminum hub through which
the needle shaft passes
Syringe barrel part of a syringe designed to hold glass
cartridges of local anesthetic solutions
Syringes medical devices that come in a variety of designs
for delivering local anesthetic drugs
Systematic desensitization process of decreasing fear or
anxiety by gradual exposure to the thing that is feared
while using relaxation techniques
T organized collagen fibers. Examples are subcutaneous
Tachyphylaxis synonymous with rapid drug tolerance, the
need for increasing doses in order to achieve similar
therapeutic effects
Terminal arborization tree-like zones of neurons where
impulses are transmitted to other nerves or nuclei of
the CNS
Tetracaine ester anesthetic used only in topical form in
dentistry
Thumb ring p art of a syringe that accommo d ates the
clinician's thumb in order to advance or retract pistons
Thyroid cartilage largest, shield-shaped cartilage of the
larynx forming the laryngeal prominence; commonly
called the Adam's apple
Thyrotoxic crisis acute, life-threatening state induced by
excessive release of thyroid hormones, thyroid storm
GLOSSARY G-1 1
Thyrotoxicosis excess of thyroid hormone in the body;
hyperthyroidism
Tidal volume amount of gas inspired into the lungs
Time structuring process whereby patients are informed
o f the time it will take to administer a p articular
inj ection
Tim e - weighted d o simetry i n e x p e n sive m e t h o d for
monitoring an individual's exposure to trace gas
Topical anesthetic techniques modifications for children
include allowing them to choose the flavor of topical, or
the use of a topical patch
Trace gases detectable presence of typically low levels of
elemental gases such as nitrous oxide in an enclosed
environment
Trachea muscular breathing passageway contiguous with
the larynx that divides into two bronchi, commonly
called the windpipe
Transient ischemic attack (TIA) disruption of the blood
supply within the brain that lasts only minutes to 24
hours with symptoms resolving within a day despite
the fact that brain injury may have occurred; frequently
referred to as mini-stroke
Treatment modifications modifications made to planned
local anesthetic procedures after p erforming risk
assessments and after consulting the ASA Physical
Status Classification System
Trigger words words and terms that are n o t e asily
accepted by young patients, such as shot and needle
Trismus motor disturbance of the trigeminal nerve or,
more simply, an inability to open the mouth
Troubleshooting strat egies ability to m a ke critical
assessment of inadequate anesthesia and determine
resolutions
Type 1 - low-density tissue tissues comprised of a loosely
organized connective tissue matrix interposed with
adipose tissue, intercellular fluids, and small volumes of
connective tissues of the maxillary buccal mucosa and
infra-temporal fossa.
Typ e 2 - moderate-density tissue tissues compri s e d
of a combination o f densely p a c k e d collagen fib er
bundles interposed with a small amount of glandular
tissues and adipose tissue. Relatively small amounts
of intercellular fluids are found in these tissues. A
moderate degree of collagen organization is found in
tissues of this type. Examples are the attached palatal
gingiva, attached gingival tissues, and muscle tissues of
the oral cavity.
Type 3 - high-density tissue tissues comprised of densely,
highly organized collagen fiber matrices with minimal
amounts of intercellular fluids. The s e tissues are
typically bound to periosteum. Examples include the
periodontal ligament and muscle tendons.
G-1 2 GLOSSARY
u Vocal distraction behavioral management technique that
Unmyelinated (nonmyelinated) nerves that have only a
thin layer of myelin protecting them
v
V2 nerve block see Maxillary nerve block
Vasoconstrictors adrenergic drugs that are combined with
local anesthetic drugs in order to increase their efficacy
and safety
Vasopressor see Vasoconstrictors
Vazirani-Akinosi (Akinosi) nerve block provides pain
management for the mandibular teeth in a single
quadrant, especially when the ability to open the j aw is
limited, either due to physiologic, pathologic, or phobic
circumstances ; also known as Vazirani-Akinosi (VA)
nerve block
Visceral pain nociceptive p ain that occurs in internal
body cavities and is caused by compression, expansion,
stretching, and infiltration of structures
Visualization cognitive strategy to help patients reduce
stress; especially beneficial in dentistry to manage fears,
particularly fear of needles; see Guided visualization
and Guided imagery
keeps children focused on the clinician's voice rather
than on the dental procedure
w
Window part of a syringe that makes the cartridge
available for inspection throughout injection procedures
to assure accurate aspirations and to monitor the
volume and speed of administration
Work practice controls ( W P C ) controls, including
techniques to prevent needlestick inj uries that reduce
the likelihood of exposure by altering the manner in
which a task is performed (e.g., prohibiting recapping of
needles by a two-handed technique)
X
X-Tip device u s e d for intrao s s e o u s inj ections that
forms a guide sleeve, which allows for ease of needle
penetration
y
Young's rule method for calculating safe doses of local
anesthetics in children based upon age, regardless of
weight
A American Academy of Pediatric
Aberrant innervations, 325-326
Absolute contraindications, 178, 398, 399
Absolute refractory state, 24
Absorption, 37
and distribution, 41
systemic, 28, 33, 41, 105, 1 1 1
o f vasoconstrictors, 85
Accessory innervations, 325-326
Accutron, 40 1 , 408
Acetaminophen, methemoglobinemia
and, 179
Action potentials, 21
Acute pain, 6
A delta fibers (AS) , 19
Adiabatic compression, 399
Adjunctive strategies, 313
Administration
of local anesthesia, 196-210, 212
of topical anesthetics, 1 17-1 19
Adrenaline, 79, 85. See also Epinephrine
Adrenergic receptors, 79
mixed-acting drugs and, 80
sympathomimetic drug influence on, 80
types of, 80
vasoconstrictor toxicity and, 84
Adrenergic vasoconstrictors, 80, 85
Adverse drug events (ADR), 181
Adverse events, 8 1 , 332
in vasoconstrictor overdose, 84
Adverse reactions, 332, 397
A fibers, 19
Age-appropriate terminology, 370
Ageusia, 339
Air bubbles, in drug cartridges, 142, 142
Airway compromise, 384
Akinosi technique, 292
Allergic response, vs. vasoconstrictor
overdose, 85
Allergies, 181, 345, 348-349, 384
benzocaine, 108
epinephrine-related, 85
latex, 140
local anesthetic, 384
and nitrous oxide-oxygen sedation, 396
Alpha ( a ) receptors, 80
Alternative medicine, 171
Alveolar ducts, 393
Alzheimer's disease, local anesthesia
and, 181
Ambient gases, 409
American Academy of Allergy, 140
D entistry (AAPD) , 46, 95
American Association of Orthopedic
Surgeons (AAOS), 181
American Cancer Society (ACS) , 199
American Dental Association (ADA), 79,
81-82, 141 , 181 , 391, 409, 415
criteria for Local Anesthetics Color
Coding, 141 , 142
American Heart Association (AHA), 8 1 ,
179, 180
American Society of Anesthesiologists
(ASA), 170, 172
Physical Status Classification System,
170-17 1 , 187-188
Amides, 35
biotransformation of, 41
chemical formulas of, 36
identification of, 37
Amitriptyline, 383
AMSA nerve blocks. See Anterior middle
superior alveolar (AMSA) nerve
blocks
Anaej ect, 130
Analgesia, 397
Analyses of variance (ANOVA), 321
Anaphylaxis, 81, 182, 350
Anatomic variations, 274, 324-327
Anesthesia, testing effectiveness of,
364-365
Angioedema, 349
ANS (autonomic nervous system) , 396
Anterior mandible, 27
Anterior middle superior alveolar
(AMSA) nerve blocks, 254-260, 385
anatomical factors, 256
confirming anesthesia, 258-259
deposition rate and blanching for, 258
field of anesthesia, 255
injection failure, common causes of, 259
technique factors, 256
technique modifications and
alternatives, 260
technique steps, 256-258
troubleshooting, 259-260
Anterior superior alveolar (ASA) nerve
blocks, 223-225, 326-327
anatomical factors, 223
complications, 225
confirming anesthesia, 224
field of anesthesia, 223
injection failure, common causes of, 224
technique factors, 223-224
technique modifications and
alternatives, 225
technique steps, 224
troubleshooting, 224-225
Antibiotic premedications, 174
Anticoagulants, 334
Anticonvulsants, local anesthesia
and, 192
Antipsychotics, local anesthesia
and, 192
Anxiety
defined, 359-360
fear and, 9, 382-383
PREP strategy and, 9
recognizing, 360-361
Anxiolytics, local anesthesia and, 192
Armamentarium, 382, 411
asembling appropriate, 199-200
defined, 129
for dental local anesthesia, 129-151
Articaine, 28, 34-35, 39, 41-42, 48, 55-57
background, 55
dentistry, effective concentrations in, 55
duration of action, 48, 55
in endodontics, 386
FDA pregnancy rating for, 54
half-life value, 42, 54
IA nerve blocks and, 340
mandibular infiltrations with, 276
for pediatric patients, 372, 374
pH Value, 53
pKa of, 39, 52-53
relative potency, 56
relative toxicity, 56-57
ASA nerve blocks. See Anterior superior
alveolar (ASA) nerve blocks
ASA Physical Status Classification
System (ADA), 170-17 1 , 187-188
Aspirating syringes, 130
harpoon-type, 130
self, 130, 133
Aspiration, 203-205
false negative, 204, 205
negative, 204
positive, 204-205 , 206
test, 203
Asthma, 176
AstraZeneca, 1 14, 1 16, 1 17
Atypical plasma cholinesterase, 178, 350
Autonomic nervous system (ANS), 396
Axolemma, 18
1-1
1-2 I N DEX
Axons, 16
anatomy of myelinated, 18
nerve, 16
Axoplasm, 21. See also Intracellular
environment, of a nerve
B pKa, 39, 52, 53, 66
Backflow, 300
Bar Code Label Requirements for
Human Drug Products and
Biological Products, 141
Baseline vital signs, 4 1 1
Base molecules, neutral, 38-39
BeeGentle, 107
Behavioral control, 362
B ehavioral guidelines, 371
B ehavioral indicators of fear, 360-361
Behavioral management techniques,
375-376
Benzocaine, 106-109
biotransformation of, 41-42
pKa of, 52
pregnancy category of, 68
B enzocaine, butamben, and tetracaine
(combination) , 1 1 3
B enzodiazepines, 382-383
Beta-blockers, 182
Beta ({3) receptors, 80
B evel, 136, 136
Bifid IA nerves, 274
Bilateral mandibular blocks, 377
Bilayered phospholipid membranes, 16
Biofeedback, 364
Biotransformation, 33
of bupivacaine, 65
and elimination, 41
of vasoconstrictors, 84-85
Biphasic CNS depression, 40
Hi-rotational insertion, 165
Blanching, 251, 258, 259, 302
Blocadren, 193
Blow by, defined, 400
BNBs (Buccal nerve blocks) , 282-283 ,
296
Braun, Heinrich, 33
Breech-loading, cartridge-type syringe,
130, 134
Broken needles, 336-337
prevention of, 336
response and management of, 336-337
Bronchioli, 393, 394
Buccal nerve blocks (BNBs), 282-283,
296
Bupivacaine
background, 64
biotransformation of, 41
CVS effects, 40
dentistry, formulations for use in, 64
duration of action, 64
excretion, 66
FDA pregnancy rating for, 54
half-life, 42, 53, 54, 66
metabolism, 65
MRD, 65
onset of action, 66
in oral and maxillofacial surgery, 382
overdose, 346
pH, 53, 66
relative potency, 65
relative toxicity, 65
safety in lactation, 66
special postoperative considerations
for, 65
topical applications, 66
vasoactivity, 66
Butamben, 1 12
effective concentrations in dentistry,
113
examples o f topical anesthetic
products containing, 1 1 3
excretion, 125
onset of action, 1 1 3 , 125
pregnancy category, 1 1 3 , 125
c cholinesterase
CAO Group, 107
Cap leakage, 142
Carcinogenicity, lidocaine and, 51
Cardiac dose, 94
of vasoconstrictors by drug ratio, 95
Cardiovascular accident (CVA), local
anesthesia and, 180
Cardiovascular collapse reversal, 347
Cardiovascular disease
and hyperthyroidism, 179
local anesthesia and, 190
MET ratings for, 175
Cardiovascular system (CVS)
effect of local anesthesia on, 40-41
effects of nitrous oxide-oxygen
sedation on, 395
overdoses and, 346, 348
selected {3 and {3 adrenergic effects on,
81
Carestream Health Inc. , 46, 52, 130
CARL (Computer Assisted Relaxation
Learning) program, 366
Carpule, 140
Cartridges, converting milligrams to, 9 1 ,
94
Cartridge volume, 90
Catecholamine, 79
Catecholamine-0-methyltransferase
(COMT) , 83, 85
Cations, 16, 38, 39
Cell bodies, 16
Center for Drug Evaluation and
Research (FDA), 46
Centers for Disease Control and
Prevention (CDC), 138, 200
Central nervous system (CNS)
depression of, 176, 177
effect of local anesthesia on, 40
effects of nitrous oxide-oxygen
sedation on, 395-396
overdoses and, 347-348
Central supply delivery systems, 40 1-402,
408
Cepacol, 1 09, 1 1 0
Cervical nerve innervation, 274
Cetacaine, 1 1 3
Cetylite Industries Inc. , 1 1 3
C fibers, 1 9
Cheek bite, 372
Chemical barriers, to local anesthesia,
322-324
Child Henke-Ject Intraligamental
Syringe®, 305
Children
drug doses for, 95-96
inj ection technique variations for,
376-380
OTC teething medications, 108
special considerations for obesity in, 371
topical anesthetics, use of, 374
Cholinesterase, 41. See also Plasma
Chronic obstructive pulmonary disease
(COPD), 398
Chronic pain, 6
Clark's Rule, 95
Clinical examinations, for patient
assessment, 172-173
Clinician judgment, 322
Clotting disorders, 174
Cocaine, 33, 182-183, 383, 384
Cognitive control, 361
Color coding
cartridge labeling and, 141
of drug cartridge, 141 , 142
Comfort Control Syringe (CCS), 147-148
Complementary and alternative medicine
(CAM), 171
Complementary medicine, 171
Complications
defined, 332
local, 333-345
systemic, 345-351
Compounded drugs, 105
CompuDent/Wand Instrument, 147-150,
148, 149
Computer-controlled local anesthetic
delivery (CCLAD ) , 130, 147, 303
benefits for PDL injections, 163
comfort control, 147
device features, 163-164
explained, 147
fluid dynamics and anatomical
location, implications of, 162
history of, 161-162
manual syringes vs., 162-163
for NP nerve blocks, 164
for P-ASA nerve blocks, 166
for PDLs, 300
technique considerations, 165-167
 INDEX 1-3

COMT (catecholamine-0- Dentsply International, 130 Direct negative experience, 360

methyltransferase ) , 83, 85 Dentsply Maillefer, 146 Dissociation constant, 39
Concentration gradient, 25 D entsply Pharmaceuticals, 106, 1 14, 179 Distribution, 37, 41
Concomitant, 172 Dentsply/Professional, 147 Diurnal body rhythm, 321
Conduction tubing, 405 , 406 Depolarization Division 2 nerve block, 232. See also
Congestive heart failure (CHF) , 176 rapid, 23-25 Posterior superior alveolar (PSA)
Contraindications and repolarization, 26 nerve blocks
to local anesthesia, 178-183 slow, 23, 24 Dopamine, 79-80
for nitrous oxide-oxygen sedation, D eposition site Dose calculations
398-399 AMSA nerve blocks, 256, 257 additional doses of different drugs,
Control ASA nerve blocks, 223 , 224 91-92
behavioral, 362 BNBs, 282 additional doses of same drugs, 91
cognitive, 361 errors, 222 for children, 95-96
defined, 361 explained, 198, 219, 248 factors required for, 89-90
informational, 361 GGs (or GGMNBs), 289, 293 for local anesthetics, 89-92
restrospective, 362 GP nerve blocks, 261 , 261 for vasoconstrictors, 92-95
Cook, Harvey, 130, 197 IA nerve blocks, 271 , 272 Drug cartridges
Cook Laboratories, 130 INBs, 287 air bubbles in, 142
Cook-Waite Laboratories, 130, 140, 197 for infiltrations inj ections, 220 anatomy of, 140
COPD (chronic obstructive pulmonary intra osseous inj ections, 307 cap leakage, 142
disease), 398 intrapupal technique, 3 1 1 , 312 contents of, 140-141
Copper tubing, 401-402 intraseptal technique, 310 defined, 140
Core bundles, 20, 21 IO nerve blocks, 229, 230 disposal of, 144-145
Corgard, 170, 182 LNBs, 280 handling, storage, and expiration, 143
Coronoid notch, 269, 270, 270 mandibular infiltrations with articaine, integrity of, 141-142
Cortical plates, 305 276 labeling and color coding of, 141
Creams, 1 05-106, 1 09 maxillary nerve blocks, 238, 239, 240 quality of, 322
Cross-innervation, 225 MNBs, 284 warming, 376
Cumulative effect, 209 MSA nerve blocks, 226, 226 Drug concentration, 90
Cumulative trauma disorders (CTDs), mylohyoid nerve blocks, 278 Drug dosages, pediatric, 371 , 382
207 NP nerve blocks, 249, 249 Drug percentage, 90
Cystic fibrosis, 398 P-ASA nerve blocks, 253, 253 Drug tolerance, 324, 326
PSA nerve blocks, 233, 233 Drug volumes, for IA nerve blocks, 273
D rate of delivery, 205-206 Durable blockade, 27
Debriefing, 9, 362 VA nerve blocks, 282 Duran est, 48
Deep breathing, 363 Desensitization, 363 Duration of action
Deep sedation, 391 Device evaluation form, sample, 154-155 of articaine, 55, 57
Delivery devices D evices of benzocaine, 108
CCLADs, 147 CCLADs, 147 of benzocaine, butamben, and
Comfort Control Syringe (CCS), 147, Comfort Control Syringe (CCS), tetracaine combination, 1 1 3
147-148 147-148 of bupivacaine, 6 4 , 65
drug cartridges, 140-145 defined, 129 of dyclonine hydrochloride, 1 1 0
for intraosseous inj ections, 146-147, intraosseous inj ection, 146-147 o f lidocaine, 4 8 , 1 1 1
146-147 j et injection, 1 18-1 19, 150, 151 o f lidocaine/prilocaine mixture, 1 15,
introduction, 129 latex allergies and local anesthesia, 140 1 17
j et injectors, 150 medical, 129 of lidocaine topical, 1 1 1
needles, 135-140 needle recapping, 138 o f mepivacaine, 59, 60
for periodontal ligament inj ections, 146 for pain control in dentistry, 130 of prilocaine, 61, 63
response to needlesticks, 145 safety syringes, 150-15 1 of procaine, 66-67
syringes, 131-134 Diabetes, local anesthesia and, 190 of tetracaine, 1 1 2
Dementia, local anesthesia and, 181-182 Diabetics Dyclone, 1 1 0
Demyelination, 18 brittle, 83 Dyclonine hydrochloride, 1 1 0
Dendritic zones, 16 metabolic issues, 177 duration o f action, 1 1 0
Dental Anxiety Scale (DAS) , 172 uncontrolled, 52 excretion, 1 1 0
Dental fears questionnaires, 171 Diagnostic and Statistical Manual of lactation, 1 1 0
Dental history, for patient assessment, Mental Disorders, 360 metabolism, 1 1 0
171-172 Diameter-Index Safety System, 400 MRD for, 1 1 0
Dental Hi Tech, 130 Diaphragm, of drug cartridge, 140 onset o f action, 1 1 0
Dental hygienists, 3 Diazepam, 383 pregnancy category, 1 1 0
Dental local anesthesia providers, 3 Diffusion hypoxia, 394 toxicity, 1 1 0
Dental neural plexus, 20, 21 Dilution ratios, 81, 92, 93 Dynamic Pressure Sensing Technology®
Dental plexus, 20, 219, 256, 305 Direct-acting drugs, 79 Instruments, 147
1-4 I N DEX
Dysesthesia, 339
Dysrhythmic effects, 383
E of lidocaine/prilocaine mixture, 1 16,
Ectopic IA nerves, 274
Electrical potential, 21, 22-23
Electric (electronic) pulp tester (EPT) ,
364-365
Elimination half-life, 42
of articaine, 42, 54, 58
of bupivacaine, 42, 54, 66
of lidocaine, 42, 53-54
of mepivacaine, 42, 54, 61
of prilocaine, 42, 54, 63
of procaine, 54, 68
Embedded needles, 337
EMLA (Eutectic Mixture of Local
Anesthetics) , 1 16
End cap, of drug cartridge, 140
Endocarditis, 181
Endodontics, 385-387
intraosseous inj ections in, 386
intra osseous technique, 386-387
intrapulpal inj ections in, 387
managing fear in, 386
topical anesthetics in, 386
use of anesthetics in, 386
Endoneurium, 19
Engineering Controls (EC), 138, 139
Ephedrine, 79-80
Epinephrine, 33, 46, 81-83 . See also
Adrenaline
allergies to, 345
diabetics and, 83
halothane and, 383
history of, 81-82
hyperthyroidism and, 177
insulin and, 83
lidocaine with, 46-48
maximum safe doses for, 82, 93
as vasoconstrictor, 79-80
Epineural sheath, 19
Epineurium, 19
Ergonomic position, 207-208
Ergonomics, for inj ection administration,
207-210
Esters, 35
biotransformation of, 41-42
easy identification of, 37
metabolization of, 1 1 3
Etidocaine, 48
Eutectic mixtures, 1 1 3-117
lidocaine and prilocaine eutectic
mixtures, 1 16-1 17
lidocaine and prilocaine periodontal
eutectic mixture, 1 14-1 16
Excretion
of articaine, 57, 58, 74
of benzocaine, 108, 121
of benzocaine, butamben, and
tetracaine combination, 1 1 3
o f bupivacaine, 6 5 , 6 6 , 77
of butamben, 125 Gels, 105-108
of dyclonine, 1 10, 122 General anesthesia, 28, 391
of lidocaine, 48, 5 1 , 73, 1 1 1 , 123 Generalized anaphylaxis, 350
Glaucoma, local anesthesia and, 190
1 17 Glucocorticoids, local anesthesia and, 192
of mepivacaine, 60, 75 Gow-Gates Mandibular nerve blocks
of prilocaine, 63, 76 (GGs or GGNMBs), 165, 209,
of procaine, 67 288-292, 297
of tetracaine, 1 12, 124 GP nerve blocks. See Greater palatine
Excretory system, patient assessment (GP) nerve blocks
and, 178 Graduated exposure, 364
Extracellular environment, of a nerve, Greater palatine (GP) nerve blocks,
21 , 22 260-262
anatomical factors, 260
complications, 262
F
confirming anesthesia, 261-262
Facial nerve paralysis, 342-343
field of anesthesia, 260
prevention of, 342
inj ection failure, common causes of,
response to, 342
262
False negative aspirations, 204, 205
technique factors, 261
Fasciculi, 19
technique modifications and
Fear
alternatives, 262
behavioral indicators of, 360-361
technique steps, 261
defined, 359
troubleshooting, 262
development of, 360
Guided imagery, 361-362
physiological indicators of, 361
Guided visualization. See Guided
recognizing, 360-361
imagery
Fearful patients
development of fear, 360
H
foundations of treatment, 361-363
Halothane, 383
introduction, 359
Halsted, William, 33, 197
practical applications, 363-366
Harpoon, 132, 134
recognizing fear and anxiety, 360-361
Harpoon type aspirating syringe, 130
terminology, 359-360
Heat of compression, 400
Fears patients, defined, 359
Hematomas, 223
Federal Food Drug and Cosmetic
case management, 352-353
(FD&C) Act, 129
described, 333
Felypressin, 86
formation case, 334
Field block injections, 197-198
management of, 335
Fight or flight response, 8, 359
occult, 333
Finger grips, 132, 132, 134
prevention of, 334-335
Firing threshold, 23
Hemophilia, 174
rapid depolarization and, 23-25
Hemostasis, 385
slow depolarization and, 23
Henderson-Hasselbalch equation, 39
Flow meters, 403 , 405
Henry Schein, 35
Fluid dynamics, 162
Hepatic disease, local anesthesia and, 191
Fluid flow rate, 162
Herpetic lesions, 343
Fluid pressure, 162
Herpetiform aphthous ulcerations,
Fluothane, 383
343, 343
Focusing attention, 362
Histamine H2 Receptor Blockers, local
Food and Drug Administration (FDA),
anesthesia and, 193
46, 400
Hives, 349
Freud, Sigmund, 33
Rubbing, 336
Fulcrum positions, 213
Hubs, of needles, 136, 138
Functional capacity, 175
Hydrophilic ends, 16
Hypercarbic drive, 414
G Hyperesthesia, 339
Ganglia, 16 Hyper-responders, 345
Gas exchange in alveoli, 394-395, 395 Hyper-response, 85
Gate Control Theory of Pain Perception, Hypersensitivity, 85, 348
250 Hypertension, local anesthesia and,
Gauge, 135 180-18 1 , 190

Hyperthermia, local anesthesia
and, 191
Hyperthyroidism, 177
cardiovascular disease and, 179
local anesthesia and, 190
Hypodermic syringes, 130
Hypogeusia, 339
Hypo-responders, 345
Hypothyroidism, local anesthesia and,
177, 190
Hypoxic drive, 414
lA nerve blocks, 268-280, 294, 296, 30 1 ,
327, 340, 342-343, 384-385
Idiosyncratic events, 350
Imipramine, 383
Immunology Task Force on Allergic
Reactions to Latex, 140
Impulse extinction, 27
Impulses, 16
Inadequate anesthesia
administration-related factors, 321-322
anatomic variations, 324-327
chemical barriers, 322-324
defining success, 321
described, 320
inflammation, 323, 327
intravascular inj ections, 327
introduction, 320-321
physical barriers, 322-324
psychological barriers, 322
reassessment of technique for,
365-366
suggested reading on, 320
Incisive nerve blocks (INBs), 248,
286-288, 296. See also
Nasopalatine (NP) nerve blocks
Incremental induction technique,
410-41 3
Inderal, 182, 193
Indirect-acting drugs, 79
Infection control guidelines, 153
Infections, 344-345 , 383-384
Infective endocarditis (IE), 181
Inferior alveolar nerve, 27, 55, 57
Inferior alveolar nerve block, 165-166
Inferior alveolar (IA) nerve block, 165-
166, 209, 268-280, 294, 296, 3 0 1 , 327,
340, 342-343, 384-385
Infiltration inj ections, 197. See also
Inj ections
field of anesthesia for, 220
height of penetration for, 220
penetration site for, 220
Infiltrations, 197
buccal, 198
field block and, 197
local, 197
mandibular, 198
vs. nerve blocks, 198
Inflammation, 38, 323, 327, 383-384
Informational control, 361
Informed consent, 199, 410
Infraorbital (IO) nerve blocks,
228-232
anatomical factors, 229
vs. ASA Nerve Blocks, 228
complications, 232
confirming anesthesia, 230
field of anesthesia, 228-229
inj ection failure, common causes of,
231
technique factors, 229
technique modifications and
alternatives, 232
technique steps, 230
troubleshooting, 23 1-232
Inj ection procedure
BNBs, 282
GGs (or GGMNBs), 290-291
for IA nerve blocks, 271
INBs, 288
for intra osseous technique, 308
for intrapulpal technique, 312
for intraseptal technique, 310
LNBs, 281
mandibular infiltrations with articaine,
276
MNBs, 284-285
mylohyoid nerve blocks, 278
for PDL inj ections, 303
VA nerve blocks, 293
Inj ections
benefits of CCLAD for PDL, 163
completion of, 206
definitions, 197
ergonomics for, 207-210
failure causes, 304, 309
field block, 197-198
guidelines, 198-207
infiltration, 197
initiating, 202-203
intraosseous, 327
intravascular, 327
management techniques for pediatric
dental, 375, 375
mandibular, 267-298
maxillary, 218-242
nerve block, 198
pain on, 335-336
palatal, 247-262
preparing site for, 201-202
steps for, 198-207
terminology, 197-198
Inj ection techniques, 148, 197
Inspiration, 393
Insulin, epinephrine and, 83
Integrative medicine, 171
Intermediate chains, 35
Internal oblique ridge, 270, 270
International Association for the Study
of Pain (IASP), 5, 360
Interpapillary injections, 252, 385
INDEX 1-5
Intracellular environment, of a nerve, 21.
See also Axoplasm
IntraFiow device, 146, 147, 386
Intraligamentary technique, 300
Intralipid, 347
Intranasal anesthesia, 241
Intraoral paresthesia, 176
Intraosseous inj ection devices, 146-147,
146-147
Intraosseous injections, 327, 386
Intra osseous techniques, 305-309
Intrapulpal inj ections, in
endodontics, 387
Intrapulpal technique, 3 1 1-3 12
Intraseptal technique, 309-3 1 1
Intravascular administration, 130
Intravascular inj ections, 327. See also
Inj ections
Ion channels, 21-22
IO nerve blocks. See Infraorbital (IO)
nerve blocks
Isoproterenol, 79-80
J
J. Morita, Nashika Line, 130
Jet inj ection devices, 1 18, 150, 151
Journal of the American Dental
Association, 314
Journal of the Canadian Dental
Association, 82
K
Keystone Industries, 1 1 9
Kidney dysfunction, local anesthesia
and, 179
Kodak Dental Systems, 130
Koller, Carl, 33
Kovacaine Mist™, 241-242
L
Labeling, of drug cartridge, 141
Lactation
articaine and, 57, 58, 74
of benzocaine, butamben, and
tetracaine combination, 1 1 3
benzocaine and, 109
bupivacaine and, 65, 66, 77
of dyclonine, 1 1 0
lidocaine and, 4 8 , 5 5 , 7 3 , 1 1 1
o f lidocaine/prilocaine mixture,
1 16, 1 17
lidocaine topical and, 1
mepivacaine and, 60, 6 1 , 75
prilocaine and, 63, 64, 76
procaine and, 68
tetracaine and, 1 1 2
Larynx, 392-393, 393
Latex allergies, 140, 384
Lesions, 343-344
Levonordefrin, 59, 79, 83-84, 383, 385
maximum safe doses for, 93
1-6 I N DEX
Lidocaine, 46-55, 1 10-1 1 1
background, 46
biotransformation of, 41
concerns regarding carcinogenicity
and, 5 1
dentistry, formulations for use in,
46-48
duration of action, 48, 1 1 1
i n endodontics, 386
excretion, 5 1 , 1 1 1
FDA-approved maximum doses of, 89
half-life value, 42, 53, 54
maximum recommended dose (MRD),
48-49, 1 1 1
metabolism, 50-5 1 , 1 1 1
onset o f action, 5 3 , 1 1 1
i n oral and maxillofacial surgery, 382
overdose of, 346
for pediatric patients, 371-372
pH, 52-53
pKa, 39, 52-53
pregnancy category, 53-55, 1 1 1
relative potency, 49-50
relative toxicity, 50
safety during lactation, 55
topical preparations, 53
vasoactivity, 51
Lidocaine/prilocaine mixture, 1 14-1 17
Limiting drug, 93-94
Lingual nerve anesthesia, 269
Lingual nerve blocks (LNBs), 280-282
Lingual nerves, 384
Lip bite, 337, 338, 372
Lipid membranes, 16
Lipophilic ends, 16
Liquid rinses, 106
Liver dysfunction, local anesthesia and,
179
LNBs (Lingual nerve blocks) , 280-282
Local adverse reactions, to topical
anesthetics, 1 17
Local anesthesia, 34
administration of, 198-207
armamentarium for dental, 129-151
cardiovascular system, systemic effects
of, 173-176
cartridge volume, 90
contraindications to, 178-183
defined, 28
desirable properties of, 34-35
documentation of, 206-207
effect on CNS, 40
effect on CVS, 40
excretory system, systemic effects of,
178
future developments in topical, 1 19
history of, 28
inflammation and, 38
in inflammation and infection, 383-384
inj ectable, 35
introduction to, 28
ionic basis of, 38
mepivacaine as, 325 GGs (or GGMNBs), 288-292
metabolic systems, systemic effects of, IA nerve blocks, 268-280
176-177 INBs, 286-288
nervous system, systemic effects of, 176 introduction, 268
for obese children, 371 LNBs, 280-282
in oral and maxillofacial surgery, 382 MNBs, 283-286
pharmacodynamics of, 36-42 techniques, 268
pharmacokinetics of, 36-42 VA nerve blocks, 292-294
pKa and pH, 39, 53 Mandibular molars, 198
primary benefit of, 34 Manifolds, 399
respiratory system, systemic effects of, Mantle bundles, 20
176 distribution of, 27
reversal, 373-374 local anesthesia, significance of, 27
routes of delivery, 34 Maxillary inj ections. See also
scope of practice, 3 Inj ections
significance of core and mantle ASA nerve blocks, 223-225
bundles on, 27 future perspectives, 241-242
steps in the administration of, 198-207, infiltrations, 219-223
212 introduction, 219
toxicity and, 382 IO nerve blocks, 228-232
vasoactivity of, 39 maxillary nerve block, 236-241
workings of, 28 MSA nerve blocks, 225-228
Local anesthesia, contraindications to PSA nerve blocks, 232-236
absolute contraindications, 178 techniques, 219
allergies, 181 Maxillary nerve block, 236-241
beta-blockers, 182 anatomical factors, 238
cardiovascular disease and confirming anesthesia, 240
hyperthyroidism, 179 facial approach to, 239-240
cerebrovascular events, 180 field of anesthesia, 237-238
cocaine, 182-183 inj ection procedure, 240
dementia-related diseases, 181-182 palatal approach to, 238
hypertension, 180 technique factors, 238
liver or kidney dysfunction, 179 technique steps, 238-239, 240
medical compromise, examples of, Maxillary plexus, 256
178-179 Maximum exposure limit for nitrous
methamphetamine, 183 oxide, 409
myocardial infarction, 180 Maximum recommended doses (MRD), 42
pharmacological compromise, of articaine, 56, 57, 74
examples of, 182 of benzocaine, 108, 121
pregnancy, 181 of benzocaine, butamben, and
premedication, considerations for, tetracaine combination, 1 1 3
180-181 o f bupivacaine, 65, 77
psychological compromise, examples of butamben, 125
of, 183 of dyclonine, 1 10, 122
relative contraindications, 178 elimination half-life and, 42
Local infiltrations, 197 of lidocaine, 48-49, 73, 1 1 1 , 123
Lorna linda inferior alveolar nerve block of lidocaine/prilocaine mixture, 1 15,
technique, 279 116
Lorazepam, 383 local anesthesia and vasoconstrictor
Ludwig's angina, 384 reference, 1 0 1
Lumen, 136 for local anesthetics, 4 8 , 8 9 , 94
of mepivacaine, 60, 75
M of prilocaine, 62, 63, 76
Madaj et, 150 of procaine, 67
MadaJet XL, 1 19 of tetracaine, 1 12, 124
MADA Medical Equipment for topical anesthetics, 1
International, 150 for vasoconstrictor drugs,
MADA Medical Products Inc. , 1 1 9 92-93, 94
Mandibular infiltrations, 377-378 Medical conditions
with articaine, 276 local anesthesia modifications for, 173 ,
Mandibular inj ections 190
BNBs, 282-283 undiagnosed and undisclosed, 173
 INDEX 1-7

Medical consultation, for patient explained, 179-180, 350-351 injection failure, common causes of, 251
assessment, 173 local anesthesia and, 178-179 technique factors, 249
Medical devices, 129 patient education, 179 technique modifications and
Medical history, for patient assessment, prilocaine and, 6 1 , 63 alternatives, 252
171-172 signs and symptoms of, 108, 179 technique steps, 249-251
Membrane expansion theory, 37-38 topical anesthetics and, 1 17-1 18 troubleshooting, 251-252
Mental nerve blocks (MNBs), 283-286, treatment, 179 National Institute for Occupational
296 Methoxamine, 79-80 Safety and Health (NIOSH), 409
Mepivacaine, 58-61 Midazolam, 383 National Institutes of Health (NIH), 171
AAPD maximum recommended Middle superior alveolar (MSA) nerve Needle adaptor, 132, 134
doses, 96 blocks, 225-228, 326 Needle bevel, 165
background, 58-59 anatomical factors, 225 Needle caps, 138
biotransformation of, 41 complications, 227-228 Needle pathways
dentistry, formulations for use in, 59 confirming anesthesia, 227 AMSA nerve blocks, 256
duration of action, 48, 59-60 field of anesthesia, 225 ASA nerve blocks, 223
excretion, 60 inj ection failure, common causes of, backward, 240
FDA-approved maximum doses of, 89 227 BNBs, 282
half-life, 42, 54, 61 technique factors, 226 considerations, 198
lactation, safety during, 61 technique modifications and downward, 240
metabolism, 60 alternatives, 227 explained, 198, 219, 248
MRD, 60 technique steps, 226-227 GGs (or GGMNBs), 289
onset of action, 61 troubleshooting, 227 GP nerve blocks, 261
for pediatric patients, 371 Milestone Scientific Inc. , 130, 147-148, IA nerve blocks, 270-271
pH value, 53, 61 151, 162 INBs, 287
pKa of, 39, 52, 60 Milligrams, converting to cartridges, for infiltrations inj ections,
pregnancy category, 61 91, 94 198, 219-220
relative potency, 60 Miltex Inc., 146 intraosseous inj ections, 306-307
relative toxicity, 60 Minimal sedation, 391-392 intrapupal technique, 3 1 1
topical preparations, 61 Minimum alveolar concentration, 397 intraseptal technique, 310
used as local anesthetic, 325 Minute ventilation. See Minute volume inward, 240
vasoactivity, 60 Minute volume, 394 IO nerve blocks, 229
Mesiobuccal roots, 226 Mixed-acting drugs, 80 LNBs, 280
Metabolic equivalent of task (MET), 175 Mizzy/Keystone Products, 150 mandibular infiltrations with
Metabolic systems, patient assessment Moderate sedation, 391 articaine, 276
and, 176-177 Modernization Act (1997) , 1 05 maxillary nerve blocks, 238, 239-240
Metabolism, 37 Monitoring, patient, 415 MNBs, 284
Metabolites, 41 Monoamine oxidase (MAO ) , 85 MSA nerve blocks, 226
Metabolization Mononeuropathy, 8 mylohyoid nerve blocks, 278
of articaine, 57, 74 Morbidity, 332 NP nerve blocks, 249
of benzocaine, 108, 121 Mortality, 332 P-ASA nerve blocks, 253, 253
of benzocaine, butamben, and Motor nerves, 28 PDL inj ections, 302
tetracaine combination, 1 13 MSA nerve blocks. See Middle superior PSA nerve blocks, 233
of bupivacaine, 65, 77 alveolar (MSA) nerve blocks upward, 240
of butamben, 125 Mucosal lesions, 343-344 VA nerve blocks, 292
of dyclonine, 1 10, 122 Multilingual health history forms, 172 Needles
of levonordefrin, 84 Musculoskeletal disorders (MSDs), 207 anatomy of, 135-136, 136
of lidocaine, 48, 50-5 1 , 73, 1 1 1 , 123 Myasthenia gravis, local anesthesia and, bending, 303, 337
of lidocaine/prilocaine mixture, 1 16, 190 bevels, 321-322
1 17 Myelinated nerves, 18-19 broken, 336-337
of mepivacaine, 60, 75 Mylohyoid nerve blocks, 275, 278 deflection, 137, 322
of prilocaine, 63, 76 Myocardial infarction, 180 dental local anesthetic, 135
of procaine, 67 Myocardial infarction, local anesthesia disposal of, 139, 144-145
of tetracaine, 112, 124 and, 180 embedded, 337
Metaraminol, 80 gauges of, 135, 137, 137-138
Metered sprays, 1 05-106 N hub of, 136
Methamphetamine, local anesthesia Nadolol, 182, 193 introduction, 135
and, 183 Nasal hood, 405, 407, 407 lengths of, 137, 137
Methemoglobinemia, 50, 178-179 Nasopalatine (NP) nerve blocks, 248-252 phobia, 351
acetaminophen and, 179 anatomical factors, 248-249 recapping, l38, 158-160
benzocaine and, 107-108 complications, 252 safety for patients and clinicians,
children and, 108 confirming anesthesia, 251 138-140
drug-induced, 179 field of anesthesia, 248, 248 syringe adaptor of, 136
1-8 I N DEX
Needle selection
BNBs, 282
GGs (or GGMNBs), 290
for lA nerve blocks, 271 , 273
INBs, 288
for intraosseous inj ections, 307
for intrapulpal technique, 312
for intraseptal technique, 309
LNBs, 281
mandibular infiltrations with articaine,
276
mylohyoid nerve blocks, 278
for PDL inj ections, 303
VA nerve blocks, 293
Needlesticks, 145
Needlestick safety, 273
Needle tract infections, 382, 383
Negative aspiration, 204
Nerve block anesthesia, 58, 63
Nerve block inj ections, 198
Nerve blocks. See also specific types
anterior middle superior alveolar
(AMSA), 254-260, 385
anterior superior alveolar (ASA),
223-225 , 326-327
buccal, 282-283, 296
case management on, 328
Gow-Gates Mandibular nerve blocks,
288-292, 297
greater palatine (GP), 260-262
incisive, 286-288
inferior alveolar (lA), 165-166,
268-280, 294, 296, 327, 340, 342-343,
384-385
vs. infiltrations, 198
infraorbital (10), 228-232
lingual, 280-282
maxillary, 236-241
mental, 283-286, 296
middle superior alveolar (MSA),
225-228, 326
mylohyoid, 278
nasopalatine (NP) , 248-252
palatal anterior superior alveolar
(P-ASA) , 252-254
posterior superior alveolar (PSA),
232-236, 326
Vazirani-Akinosi (VA), 292-294, 343
Nerve fibers, 18
types of, 19
Nerve impulses
generation and conduction of, 21-26
local anesthetics on, 26-27
saltatory conduction and, 19
successful generation of, 30
Nerve membranes, 16, 23, 37-38
Nerve myelination, 17-18
Nervous system, patient assessment and,
176, 179
Neuroanatomy
dental neural plexus, 20-21
inadequate anesthesia and, 320
nerve axons, cell bodies, and
membranes, 16
nerve cell anatomy, 16
nerve fiber types, 19-20
nerve myelination, 17-18
overview, 16
peripheral, 19-20
saltatory conduction, 19
Neurolemmas, 16. See also Nerve
membranes
Neurons, 16
motor, 16
myelinated, 18
nonmyelinated, 18
sensory, 16
Neuropathic pain, 7-8
Neurophysiology, 21
Neutral base, 37
Neutral base molecules, 38-39
New York Heart Association, 92
NIOSH (National Institute for
Occupational Safety and Health),
409
Nitrous oxide, 391-392
adverse reactions, 397
calculating percentage of, 410
complications and revention of
adverse occurrences, 413-414
examples of industrial uses of, 398
examples of medical uses of, 398
excessive sedation signs, 413
in FDA Pregnancy Category C, 396
manufacturing process for, 399-409
occupational exposure risks, 414
optimal sedation signs, 412
sedation principles, 410
solubility in blood, 394
tanks, 400
usage employee safety and health
guidelines, 409
Nitrous oxide-oxygen sedation, 391,
419-424. See also Sedation
adverse reactions to, 397
anatomy and physiology involved in,
392-395
for anxiety control, 366
benefits, limitations, and precautions
of, 391
common indications for dental, 398
complications and revention of
adverse occurrences, 413-414
contraindications for, 398-399
currently used in dentistry, 392
delivery system components, 402, 423
effects on other body systems, 396,
396-397
effects on the cardiovascular system,
395
effects on the central nervous system,
395-396
employee safety and health guidelines,
409
enhancing, 410
equipment combustion risks, 399
ethical and legal issues relating,
414-415
safety mechanisms, 409
states and provincal statutes relating,
415
steps for administering, 410-416
Nociceptive pain, 6-7
Nociceptors, 6, 7
Nodes of Ranvier, 18, 1 9
Nonmyelinated nerves, 18, 19
Nonselective beta-blockers, 182
Norepinephrine, 79, 80, 85-86
Novalar Pharmaceuticals, 314
Novocaine, 33, 66
Novocol Company, 130
NP nerve blocks. See Nasopalatine (NP)
nerve blocks
N-Tralig, 146, 146
0
Obesity, pediatric drug doses and, 95, 371
Occult hematomas, 333
Occupational exposure, 414, 416
Occupational Safety and Health
Administration (OSHA), 138, 146,
200, 337
Ocular complications, 345
Office of Pharmaceutical Science, 46
Ointments, 1 05-106, 109
Oligodendrocytes, 17
Onpharma, 324, 325
Onset of action
of articaine, 58, 74
of benzocaine, 1 07-108, 121
of benzocaine, butamben, and
tetracaine combination, 1 1 3
o f bupivacaine, 6 6 , 77
of butamben, 125
of dyclonine, 1 10, 122
of lidocaine, 53, 73, 1 1 1 , 123
of lidocaine/prilocaine mixture, 1 15,
116
of mepivacaine, 6 1 , 75
of prilocaine, 63, 76
of procaine, 68
of tetracaine, 1 12, 124
Onset system, 313, 324, 325
Oral and maxillofacial surgery (OMFS) ,
382-384
Oraqix, 64, 106, 1 14-1 16
OraVerse, 338, 373-374
OraVerse®, 142
OSHA (Occupational Safety and Health
Administration) , 337
OSHA's Standard on Bending Needles,
337
Overdose, 332
initial signs and symptoms of, 346-347
later signs and symptoms of, 347
management of, 347-348
 INDEX 1-9

pathophysiology of, 346 NP nerve blocks, 248-252 GP nerve blocks, 261, 261
prevention of, 347 P-ASA nerve blocks, 252-254 lA nerve blocks, 270, 271, 272
recognition of, 347 techniques, 248 INBs, 287
Oxygen Palatal innervation of maxillary central for infiltrations inj ections, 20 1 , 219, 220
flow before sedation, 4 1 1 incisors, 327 intra osseous inj ections, 306, 307
tanks, 400 Para-aminobenzoic acid (PABA) , 349 intrapupal technique, 3 1 1
Parasympathetic system, 10 intraseptal technique, 3 1 0
p Paresthesia, 55, 57, 278, 338-342, 341, 342, 10 nerve blocks, 229, 229
Pain, 5 385, 386 LNBs, 280
acute, 6 articaine and, 57 mandibular infiltrations with articaine,
avoidance of, 5 incidence of, 339 276
chronic, 6 intraoral, 176 maxillary nerve block, 238, 238, 239
classification of, 6-8 management, 341-342 MNBs, 283-284
defined, 5, 360 prevention, 340-341 MSA nerve blocks, 226, 226
disorders, 8 response to, 341 mylohyoid nerve blocks, 278
duration, 6 strategies to reduce risks of, 340 NP nerve blocks, 249, 249
on inj ection, 335-336 Paroject, 146, 146 P-ASA nerve blocks, 253
neuropathic, 7-8 P-ASA nerve blocks. See Palatal anterior PDL inj ections, 302
nociception and, 6 superior alveolar (P-ASA) nerve PSA nerve blocks, 233 , 233
nociceptive, 6-7 blocks VA nerve blocks, 292
somatic, 6 Patches, 1 05 Peridental technique, 300
sympathetic nervous system and, 8 Patient assessment Perilemma, 19
threshold vs. tolerance, 5-6 contraindications to local anesthesia, Perineurium, 19
visceral, 6-7 178-183 Periodontal ligament (PDL) injection,
Pain control and informed consent, 410--4 1 1 300-305
devices for, 130 introduction, 170-171 Periodontal ligament inj ection manual
local anesthesia, 34 for nitrous oxide-oxygen sedation, devices, 146
origins of, 33 397-399 Periodontal ligament (PDL) inj ections,
pharmacology and technology systems review, 173-178 300-305. See also Inj ections
advances, 32--42 tools for, 171-173 Periodontics, 385
Pain disorders, 8 Patient assessment tools hemostasis in, 385
Pain management clinical examination, 172-173 mandibular techniques in, 385
classification by etiology, 6-8 comprehensive patient assessment, 171 maxillary techniques in, 385
for fearful patients, 360 medical and dental history, 171-172 Peripheral nerve anatomy, 19-20
implications for dentistry, 8-9 medical consultation, 173 Personal protective equipment (PPE),
nociception and, 6 Patient drug record, 172 200
pain duration, 6 Patient relaxation skill determination, pH
pain threshold vs. pain tolerance, 5-6 362 of articaine, 57, 58, 74
patient management perspectives, 9-1 1 Patterns of innervation, 226 of bupivacaine, 65, 66, 77
patient perspectives, 5 PDL inj ections, 300-305. See also of lidocaine, 48, 52
protective response, 5 Inj ections of mepivacaine, 60, 61, 75
sympathetic nervous system and, 8 Pediatric doses, 95-96 of prilocaine, 63, 76
Pain threshold, 5 Pedodontics of procaine, 67-68
Pain tolerance, 5 behavioral management techniques, relevance of, 39
Palatal anterior superior alveolar 375-376 Pharmacodynamics, 36
(P-ASA) nerve blocks, 252-254 drug dosages, 371 Pharmacokinetics, 36-37
anatomical factors, 253 inj ection management techniques, 375, Pharmacological compromise, 182
complications, 254 375 Pharmacological intervention, 1 1
confirming anesthesia, 254 inj ection technique variations for, Pharmacology
field of anesthesia, 252, 252-254 376-378 basics, 32--42
inj ection failure, common causes of, introduction, 370 developments in, 33
254 postoperative trauma, 372 dose calculations, 88-97
technique factors, 253 using appropriate terminology, introduction, 33-34
technique modifications and 370-371 local anesthesia, 34
alternatives, 254 using topical anesthetics, 374 of local anesthetic agents, 35-36
technique steps, 253 Penetrating end, of needle shaft, 136, 136 pharmacodynamics, 36--42
troubleshooting, 254 Penetration site pharmacokinetics, 36--42
Palatal inj ections. See also Inj ections AMSA nerve blocks, 256, 256 topical anesthetics, 103-1 19
AMSA nerve blocks, 254-260 ASA nerve blocks, 223 , 224 Pharynx, 392
case management on, 262 BNBs, 282 Phenothiazines, local anesthesia and, 193
GP nerve blocks, 260-262 explained, 198, 219, 248 Phenylephrine, 86
introduction, 248 GGs (or GGMNBs), 289 Phobia, defined, 360
1-1 0 INDEX

Physical barriers, to local anesthesia, of prilocaine, 63, 64, 76 Psychological barriers, to local
322-324 of procaine, 68 anesthesia, 322, 323
Physical Status Classification System of tetracaine, 1 12, 124 Psychological compromise, 183
(ASA), 170-171 Pregnancy ratings, 54 Pterygomandibular raphe, 269-270, 274
Physiological indicators of fear, 361 Pre-inj ection patient assessment, 199
Pin index safety system, 402-408, 405 Pre-inj ection preparation, 200, 202 Q
p450 isoenzyme system, 41 Premature contact, 275 QuickSleeper, 146, 147
Piston, 132, 133 Preoperative dietary restrictions, 4 1 1
pKa PREP (Prepare, Rehearse, Empower, and
of articaine, 57, 58 Praise) strategy, 9, 200 R
of bupivacaine, 65, 66, 77 Pressure anesthesia, 250 Rapid depolarization, 23-27
clinical application of, 39 Pressure variances, 399 Rapid drug tolerance. See Tachyphylaxis
of inj ectable local anesthetic drugs, 39 Prilocaine, 61-64 Rate of deposition, 205-206
of lidocaine, 48, 52, 73 AAPD maximum recommended Reaction, defined, 360
of mepivacaine, 60, 75 doses, 96 Re-aspiration, 205
of prilocaine, 63, 76 background, 61 Recapping, of needles, 145, 158-160
of procaine, 67 dentistry, formulations for use in, 61 Recreational drugs, 194
relevance of, 39 duration of action, 48, 61 Refractory state of membrane, 24
Plasma cholinesterase, 41, 66-67. See also excretion, 63 absolute, 24
Cholinesterase FDA-approved maximum relative, 25
atypical, 178 doses of, 89 Refrigerants, as topical anesthetics, 1 1 9
Pneumothorax, 414 FDA pregnancy category, 64 Regional nerve blocks, 170
Polarization, 26 half-life, 42, 54, 63-64 Regulators, 403 , 405
Polymodal receptors, 6 lactation, safety during, 64 Rehearsals, 363-364
Positive aspiration, 204-205, 206 metabolism, 63 Relative contraindications, 178, 398-399
Positive coping statements, 362 MRD, 62 Relative potency
Positive feedback, 375-376 onset of action, 63 of articaine, 56, 57
Postanesthetic mucosal lesions, 343-344 pH value, 53, 63 of bupivacaine, 65, 77
Postanesthetic trauma, 372 pKa of, 39, 53, 63 of butamben, 125
Posterior superior alveolar (PSA) nerve relative potency, 62 of dyclonine, 122
blocks, 232-236, 326 relative toxicity, 62-63 of lidocaine, 48-50, 73, 123
anatomical factors, 232-233 topical preparations, 64 of mepivacaine, 60, 75
complications, 235-236 vasoactivity, 63 of prilocaine, 62, 63, 76
confirming anesthesia, 234-235 Procaine, 33-34, 66-68 of procaine, 67
field of anesthesia, 232, 232 background, 66 of tetracaine, 124
inj ection failure, common causes of, biotransformation of, 41-42 Relative refractory state, 25
235 dentistry, formulations for use in, 66 Relaxation, 362-363
technique factors, 233 duration of action, 48, 66-67 Renal dysfunction, local anesthesia and,
technique modifications and excretion, 67 191
alternatives, 235 half-life, 54, 68 Repolarization, 26
technique steps, 233-234 lactation, safety during, 68 Reservoir bags, 403 , 405 , 406
Terminology for Needle Pathway for, metabolism, 67 Respiratory process, 393-394
235 MRD, 67 Respiratory system
troubleshooting, 235 onset of action, 68 lower and nitrous oxide-oxygen
Post-op anesthetic recovery, 366 pH value, 53, 67-68 sedation, 393
Postoperative trauma, 372 pKa, 39, 53, 67 upper and nitrous oxide-oxygen
Pre-anesthesia, 249, 250, 301 pregnancy category, 68 sedation, 392-393
Pregnancy, local anesthesia and, 181 relative potency, 67 Respiratory system, patient assessment
Pregnancy category relative toxicity, 67 and, 176
of articaine, 57, 58, 74 topical applications, 68 Response, defined, 360
of benzocaine, 108, 121 vasoactivity, 67 Resting state, 21, 22
of benzocaine, butamben, and Pro-Dex, 146 electrical potential, 21
tetracaine combination, 1 1 3 Progressive muscle relaxation (PMR) , return to, 26
o f bupivacaine, 6 5 , 6 6 , 77 363 Retrospective control, 362
of butamben, 125 Propagation, 21
of dyclonine, 1 10, 122 Propranolol, 174, 182 s
FDA guidelines for, 68 Protective response, 5 Safety syringes, 150
of lidocaine, 48, 53-54, 73 PSA nerve blocks. See Palatal anterior Safety Wand® handpiece, 150, 151
of lidocaine/prilocaine mixture, 1 16, superior alveolar (P-ASA) nerve Saltatory conduction, 19
1 17 blocks Sample device evaluation form, 154-155
of lidocaine topical, 1 1 1 , 123 Pseudocholinesterase, 68 Scavenging systems, 407-408, 408,
of mepivacaine, 60, 6 1 , 75 Psychogenic factors, 8 411, 423
 I N DEX 1-1 1

Schwann cells, 17-18 Strategy, defined, 360 Terminal arborizations, 16

nodes of Ranvier and, 18 Street drugs, 182-183 Tetracaine, 1 1 1
vs. perilemma, 20 cocaine, 182-183 biotransformation of, 41-42
Schwann cell sheath, 18 methamphetamine, 183 duration of action, 1 1 2
Scoop technique, 138 Stress reduction protocol (SRP) , 171 , 189 i n endodontics, 386
Second division nerve block, 236. See also Success, defined, 321 excretion, 1 1 2
Maxillary nerve block Sucrets, 1 1 0 metabolism, 1 1 2
Sedation. See also Nitrous oxide-oxygen Supplemental injections. See also M R D for, 1 1 2
sedation Inj ections onset o f action, 1 1 2
central supply delivery systems, 401-402 intra osseous, 305-309 in oral and maxillofacial surgery, 382
common symptoms of, 412 intrapulpal technique, 31 1-312 pregnancy category, 1 1 2
deep, 391 intraseptal technique, 309-3 1 1 toxicity, 1 1 2
defined, 391 introduction, 300 Thumb disk, 133
delivery systems, 400 PDL, 300-305 Thumb ring, 132, 133
minimal, 391-392 techniques, 300 Thyroid storm, 177
moderate, 391 Supportive communication, 200-20 1 Thyrotoxic crisis, 177
monitoring, 41 1-413 Supraperiosteal inj ections, 197. See also Thyrotoxicosis, 177
pin index safety system, 402-408 Inj ections Tidal volume, 394
portable delivery systems, 402 Sympathetic nervous system, 8 Time structuring, 364
Self-aspirating syringes, 130 Sympathomimetic amines, 79 Time-weighted dosimetry, 409
design and technique modifications Synapses, 16 Timolol, 182, 193
for, 133 Syncope, 345-346 Tofranil, 383
Self-injury, 337-338 Synthetic catecholamine, 79 Topical anesthetics
management of, 338 Syrij et, 118, 150 application methods, 105-106
prevention of, 338 Syrij et Mark II Needleless Injector, 1 1 9 benzocaine, 106-109
Self-report, 360 Syringe adaptor, 136 for children, 107, 374
Sensory modality, 6 Syringe barrel, 1 3 1 , 132 considerations in administration of,
Sensory nerves, 21 Syringes 1 17-1 18
Septodont Company, 35, 146, 151 anatomy of, 1 3 1-134, 132 dyclonine hydrochloride, 1 1 0
Septodont USA, 133, 146 breech-loading, 134 i n endodontics, 386
Shaft, 136 CCLAD vs. manual, 162-163 eutectic mixtures, 1 1 3-117
Shank, 136 Comfort Control Syringe (CCS), 147-148 future of, 1 19
Short-needle ia technique, 279 common PDL, 146 general considerations, 105
Sickle cell anemia, 175-176 defined, 130 introduction, 104
Single tooth anesthesia system (STA), harpoon-type aspirating, 130 jet inj ection devices, 1 18-1 19
130, 147-150, 166-167 history of, 130 lidocaine, 1 1 0-1 1 1
Skill, defined, 360 hypodermic, 130 local adverse reactions, 1 17
Slow depolarization, 23 introduction, 130-13 1 special considerations when using, 109
Sodium bicarbonate buffering, 324 j e t inj ectors, 150 systemic reactions, 1 17-1 18
Sodium channels, 23 safety syringes, 150-151 tetracaine, 1 1 1-112
Sodium ion pumps, 25 self-aspirating, 130, 133 topical drug combinations, 1 12-1 13
Soft-tissue anesthesia, 163, 166 stability of, 203 Topical applications
Somatic pain, 6 steps for disassembling, 144-145 of bupivacaine, 66
Specific protein receptor sites, 22, 37 steps for loading, 143-144, 156-157 of procaine, 68
Specific protein receptor theory, 37 technique specific, 146 Toxicity
Sphenopalatine nerve blocks, 248. See Systematic desensitization, 363 of articaine, 56-57
also Nasopalatine (NP) nerve blocks Systemic allergic reactions, 350 of benzocaine, 108
Spongy bone, 305 Systemic complications from local of benzocaine, butamben, and
Sprays, 106 anesthesia tetracaine combination, 1 1 3
STA (single tooth anesthesia system), allergies, 348-349 o f bupivacaine, 65
130, 147-150, 166-167 atypical plasma cholinesterase, 350 of dyclonine, 1 1 0
Stabident, 386 idiosyncratic events, 350 of lidocaine, 5 0
Stabident system, 146 methemoglobinemia, 350-351 o f lidocaine/prilocaine mixture, 1 15-117
Standard on Bending Needles, OSHA, overdose, 346-348 of lidocaine topical, 1 1 1
337 systemic allergic reactions, 350 o f mepivacaine, 60
Startle reaction, 363 Systemic reactions, to topical anesthetics, of prilocaine, 62-63
STA Single Tooth Anesthesia System® 1 17-1 18 of procaine, 67
Instrument, 148, 301 signs and symptoms of CNS overdose,
Stealth technique, 148 T 40
Stopper, of drug cartridge, 140 Taber's Cyclopedic Medical Dictionary, 5 of tetracaine, 1 1 2
Stopper displacement, 142 Tachyphylaxis, 324, 326 of vasoconstrictors, 84-85
Stopper leakage, 142 Takamine, Jokichi, 33 Trace gases, 409
1-1 2 INDEX

Trachea, 393 of prilocaine, 63 Vazirani-Akinosi (VA) nerve blocks,

Transient ischemic attacks (TIA), local of procaine, 67 292-294, 343
anesthesia and, 180 Vasoconstrictor dilutions, 93 Visceral pain, 6-7
Triazolam, 383 Vasoconstrictor drugs Visual scales (VAS) , 321
Tricyclic antidepressants (TCAs), 86, 192, calculating doses of, 93 V2 nerve block, 236. See also Maxillary
383 definition of maximum recommended nerve block
Trigger words, 370 doses for, 92-93 Vocal distraction, 375, 376
Trismus, 278 volume of drug per cartridge, 93 Voice box, 392
defined, 335 Vasoconstrictors, 34, 48
management of, 335 adrenergic actions of, 79-80
w
prevention of, 335 adverse events associated with, 81
The Wand, 130, 147-150, 162, 165-166
Troubleshooting strategies, 3 articaine and, 58
Wand STA (Wand STA Single Tooth
Tuberosity nerve block, 232, 240. See also biotransformation of, 84-85
Anesthesia System Instrument) , 130,
Posterior superior alveolar (PSA) of bupivacaine, 66
147-150, 166-167
nerve blocks calculating doses for, 92-95
Wand STA Single Tooth Anesthesia
Type 3 - high-density tissues, 162 cardiac considerations for, 94
System Instrument (Wand STA),
Type 1 - low-density tissues, 162 cardiac doses by drug ratio, 95
130, 147-150, 166-167
Type 2 - moderate-density tissues, 162 cartridge volume, 90
Wide open mouth technique, 291
considerations prior to using, 83
Window, of cartridges, 132
defined, 34
u Wong-Baker FACES Pain Rating Scale,
dosage, 84
Undiagnosed medical conditions, 173. 6, 8
epinephrine, 81-83
See also Medical conditions Work Practice Controls (WPC), 138
felypressin, 86
Undisclosed medical conditions, 173 . World Meteorological Organization, 400
introduction, 79
See also Medical conditions
levonordefrin, 83-84
Urticaria, 349
lidocaine and, 53 X
U.S. Bureau of Labor Statistics, 207
mepivacaine and, 61 Xenon anesthesia, 416
U.S. D epartment of Labor, 207
MRD related to, 94 X-Tip, 146, 147, 386
U.S. Department of Transportation
norepinephrine, 85-86 Xylocaine, 332
(D OT) , 400
overdose, 348 Xylocaine hydrochloride, 167
overdose of, 84-85
v in pediatric dentistry, 371
y
VA nerve blocks, 292-294, 343 phenylephrine, 86
Young's Rule, 95
Vasoactivity prilocaine of, 63
of articaine, 58 of procaine, 68
of bupivacaine, 66 toxicity and, 84-85, 383 z
of lidocaine, 51 use or avoidance of, 80-81 Zygomatic blocks, 232. See also Posterior
of local anesthesia, 39 Vasodilation, 39 superior alveolar (PSA) nerve
of mepivacaine, 60 Vasopressors, 79 blocks