Morgan and Mikhail's Clinical Anesthesiology, 5th Edition 5th Edition PDF

a LANGE medical book
Clinical
Anesthesiology
Morgan & Mikhails
F I F T H
E D I T I O N
John F. Butterworth IV, MD

Professor and Chairman
Department of Anesthesiology
Virginia Commonwealth University School of Medicine
VCU Health System
Richmond, Virginia
David C. Mackey, MD
Professor
Department of Anesthesiology and Perioperative Medicine
University of Texas M.D. Anderson Cancer Center
Houston, Texas
John D. Wasnick, MD, MPH

Steven L. Berk Endowed Chair for Excellence in Medicine
Professor and Chair
Department of Anesthesia
Texas Tech University Health Sciences Center
School of Medicine
Lubbock, Texas
New York Chicago San Francisco Lisbon London Madrid Mexico City
Milan New Delhi San Juan Seoul Singapore Sydney Toronto
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Morgan & Mikhails Clinical Anesthesiology, Fifth Edition

Copyright 2013, 2006, 2002 by The McGraw-Hill Companies, Inc. All rights reserved. Printed in the
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ISSN 1058-4277
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Contents
Chapter Authors v | Contributors vii
Research and Review ix | Foreword xi | Preface xiii
1 The Practice of Anesthesiology 1

SECTION
15 Hypotensive Agents 255

16 Local Anesthetics 263
Anesthetic Equipment
& Monitors
2 The Operating Room Environment 9

Charles E. Cowles, MD
3 Breathing Systems 29
17 Adjuncts to Anesthesia 277

SECTION
III
Anesthetic Management
4 The Anesthesia Machine 43
18 Preoperative Assessment, Premedication,

& Perioperative Documentation 295
5 Cardiovascular Monitoring 87
19 Airway Management 309
6 Noncardiovascular Monitoring 123
20 Cardiovascular Physiology
& Anesthesia 343
SECTION
II
Clinical Pharmacology
7 Pharmacological Principles 143

8 Inhalation Anesthetics 153
9 Intravenous Anesthetics 175
21 Anesthesia for Patients with

Cardiovascular Disease 375
22 Anesthesia for Cardiovascular
Surgery 435
23 Respiratory Physiology
& Anesthesia 487
10 Analgesic Agents 189
24 Anesthesia for Patients

with Respiratory Disease 527
11 Neuromuscular Blocking Agents 199
25 Anesthesia for Thoracic Surgery 545
12 Cholinesterase Inhibitors & Other

Pharmacologic Antagonists to
Neuromuscular Blocking Agents 223
26 Neurophysiology & Anesthesia 575
13 Anticholinergic Drugs 233

Neurologic & Psychiatric Diseases 613
14 Adrenergic Agonists & Antagonists 239
27 Anesthesia for Neurosurgery 593
iii
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iv
CONTENTS
29 Renal Physiology & Anesthesia 631

30 Anesthesia for Patients
with Kidney Disease 653
31 Anesthesia for Genitourinary
Surgery 671
32 Hepatic Physiology & Anesthesia 691
Michael Ramsay, MD, FRCA

Liver Disease 707

Endocrine Disease 727
Neuromuscular Disease 747
36 Anesthesia for Ophthalmic
Surgery 759
SECTION
IV
Regional Anesthesia &

Pain Management
45 Spinal, Epidural, & Caudal Blocks 937

46 Peripheral Nerve Blocks 975
Sarah J. Madison, MD and Brian M. Ilfeld, MD, MS
47 Chronic Pain Management 1023

Richard W. Rosenquist, MD
and Bruce M. Vrooman, MD
48 Perioperative Pain Management &

Enhanced Outcomes 1087
Francesco Carli, MD, MPhil and
Gabriele Baldini, MD, MSc
SECTION
Perioperative &
Critical Care Medicine
37 Anesthesia for Otorhinolaryngologic

Surgery 773
49 Management of Patients with

Fluid & Electrolyte Disturbances 1107
38 Anesthesia for Orthopedic Surgery 789
50 AcidBase Management 1141
Edward R. Mariano, MD, MAS
39 Anesthesia for Trauma &

Emergency Surgery 805
Brian P. McGlinch, MD
40 Maternal & Fetal Physiology

& Anesthesia 825
Michael A. Frlich, MD, MS
41 Obstetric Anesthesia 843

42 Pediatric Anesthesia 877

43 Geriatric Anesthesia 907
44 Ambulatory, Nonoperating
Room, & Oce-Based
Anesthesia 919
51 Fluid Management &

Blood Component Therapy 1161
52 Thermoregulation, Hypothermia,
& Malignant Hyperthermia 1183
53 Nutrition in Perioperative
& Critical Care 1193
54 Anesthetic Complications 1199
55 Cardiopulmonary Resuscitation 1231
Martin Giesecke, MD and Srikanth Hosur, MBBS, MD
56 Postanesthesia Care 1257

57 Critical Care 1277
58 Safety, Quality, & Performance
Improvement 1325
Index 1331
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Chapter Authors
Gabriele Baldini, MD, MSc
Assistant Professor
McGill University
Montreal, Quebec
Professor and Chairman
Virginia Commonwealth University School of Medicine
VCU Health System
Richmond, Virginia
Francesco Carli, MD, MPhil
Professor
McGill University
Montreal, Quebec
Charles E. Cowles, Jr, MD
Assistant Professor
and Perioperative Medicine
Chief Safety Officer
Perioperative Enterprise
University of Texas MD Anderson Cancer Center
Houston, Texas
Associate Professor
University of Alabama at Birmingham
Birmingham, Alabama
Martin Giesecke, MD
M.T. Pepper Jenkins Professor in Anesthesiology
Vice Chair, University Hospitals
Department of Anesthesiology and Pain Management
University of Texas Southwestern Medical Center
Dallas, Texas
Srikanth Hosur, MBBS, MD

Consultant in Intensive Care
QuestCare Intensivists
Dallas, Texas
Brian M. Ilfeld, MD, MS
Professor, In Residence
University of California, San Diego
San Diego, California
David C. Mackey, MD
Professor
Department of Anesthesiology and
Perioperative Medicine
University of Texas M.D. Anderson Cancer Center
Houston, Texas
Sarah J. Madison, MD
Assistant Clinical Professor of Anesthesiology
University of California, San Diego
San Diego, California
Edward R. Mariano, MD, MAS (Clinical Research)
Associate Professor of Anesthesia
Stanford University School of Medicine
Chief, Anesthesiology and Perioperative Care Service
VA Palo Alto Health Care System
Palo Alto, California
Brian P. McGlinch, MD
Associate Professor
Mayo Clinic
Rochester, Minnesota
Colonel, United States Army Reserve, Medical Corps
452 Combat Support Hospital
Fort Snelling, Minnesota
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vi
CHAPTER AUTHORS

Chairman Department of Anesthesiology
and Pain Management
Baylor University Medical Center
President Baylor Research Institute
Clinical Professor
University of Texas Southwestern Medical School
Dallas, Texas
Richard W. Rosenquist, MD
Chair, Pain Management Department
Anesthesiology Institute
Cleveland Clinic
Cleveland, Ohio
Morg_FM_i-xiv.indd vi
Bruce M. Vrooman, MD
Department of Pain Management
Anesthesiology Institute
Cleveland Clinic
Cleveland, Ohio
Steven L. Berk Endowed Chair for
Excellence in Medicine
Professor and Chair
School of Medicine
Lubbock, Texas
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Contributors
Kallol Chaudhuri, MD, PhD
Professor
Lubbock, Texas
Robert Johnston, MD
Associate Professor
Lubbock, Texas
Swapna Chaudhuri, MD, PhD

Professor
Lubbock, Texas
Sanford Littwin, MD
Assistant Professor
St. Lukes Roosevelt Hospital Center and Columbia
University College of Physicians and Surgeons
New York, New York
John Emhardt, MD
Indiana University School of Medicine
Indianapolis, Indiana
Suzanne N. Escudier, MD
Associate Professor
Lubbock, Texas
Aschraf N. Farag, MD
Assistant Professor
Lubbock, Texas
Herbert Gonzalez, MD
Assistant Professor
Lubbock, Texas
Kyle Gunnerson, MD
VCU School of Medicine
Richmond, Virginia
Alina Nicoara, MD
Assistant Professor
Duke University Medical Center
Durham, North Carolina
Bettina Schmitz, MD, PhD
Associate Professor
Lubbock, Texas
Steven L. Shafer, MD
Stanford University School of Medicine
Palo Alto, California
Christiane Vogt-Harenkamp, MD, PhD
Assistant Professor
Lubbock, Texas
Gary Zaloga, MD
Global Medical Affairs
Baxter Healthcare
Deerfield, Illinois
vii
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Research and Review

Jacqueline E. Geier, MD
Resident, Department of Anesthesiology
St. Lukes Roosevelt Hospital Center
New York, New York
Cecilia N. Pena, MD
Texas Tech University Medical Center Hospital
Lubbock, Texas
Brian Hirsch, MD
Texas Tech University Medical Center
Lubbock, Texas
Charlotte M. Walter, MD
Lubbock, Texas
Shane Huffman, MD
Lubbock, Texas
Karvier Yates, MD
Lubbock, Texas
Rahul K. Mishra, MD
Lubbock, Texas
ix
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Foreword
A little more than 25 years ago, Alexander Kugushev,
then the editor for Lange Medical Publications,
approached us to consider writing an introductory textbook in the specialty of anesthesiology that
would be part of the popular Lange series of medical books. Mr. Kugushev proved to be a convincing
salesman, in part by offering his experience with
scores of authors, all of whom opined that their most
satisfying career achievement was the fathering of
their texts. We could not agree more.
Now in its fifth edition, the overall stylistic goal
of Clinical Anesthesiology remains unchanged: to be
written simply enough so that a third year medical
student can understand all essential basic concepts,
yet comprehensively enough to provide a strong
foundation for a resident in anesthesiology. To quote
C. Philip Larson, Jr, MD from the Foreword of the
first edition: The text is complete; nothing of consequence is omitted. The writing style is precise, concise and highly readable.
The fifth edition features three new chapters:

Ambulatory, Nonoperating Room, and Officebased Anesthesia; Perioperative Pain Management
and Enhanced Outcomes; and Safety, Quality, and
Performance Improvement. There are approximately 70 new figures and 20 new tables. The adoption of full color dramatically improves the aesthetic
appeal of every page.
However, the biggest and most important
change in the fifth edition is the passing of the
baton to a distinguished and accomplished team of
authors and editors. We were thrilled to learn that
Drs. Butterworth, Mackey, and Wasnick would be
succeeding us. The result of their hard work proves
our enthusiasm was justified as they have taken
Clinical Anesthesiology to a new level. We hope you,
the readers, agree!
G. Edward Morgan, Jr, MD
Maged S. Mikhail, MD
xi
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Preface
Authors should be proud whenever a book is sufficiently successful to require a new edition. This is
especially true when a books consistent popularity over time leads to the succession of the original
authors by a new set of authors. This latter circumstance is the case for the fifth edition of what most
of us call Morgan and Mikhail. We hope that you
the reader will find this new edition as readable and
useful as you have found the preceding four editions
of the work.
This fifth edition, while retaining essential elements of its predecessors, represents a significant
revision of the text. Only those who have written a
book of this size and complexity will understand just
how much effort was involved. Entirely new subjects
(eg, Perioperative Pain Management and Enhanced
Outcomes) have been added, and many other topics
that previously lived in multiple chapters have been
moved and consolidated. We have tried to eliminate redundancies and contradictions. The number
of illustrations devoted to regional anesthesia and
analgesia has been greatly increased to adequately
address the rapidly growing importance of this
perioperative management topic. The clarity of the
illustrations is also enhanced by the widespread use
of color throughout the book. We hope the product
of this endeavor provides readers with as useful an
exercise as was experienced by the authors in composing it.
Key Concepts are listed at the beginning of
each chapter and a corresponding numbered
icon identifies the section(s) within the
chapter in which each concept is discussed.
These should help the reader focus on
important concepts that underlie the core of
anesthesiology.
Case Discussions deal with clinical problems

of current interest and are intended to
stimulate discussion and critical thinking.
The suggested reading has been revised and
updated to include pertinent Web addresses
and references to clinical practice guidelines
and practice parameters. We have not tried
to provide a comprehensive list of references:
we expect that most readers of this text would
normally perform their own literature searches
on medical topics using Google, PubMed,
and other electronic resources. Indeed, we
expect that an ever-increasing segment of our
readers will access this text in one of its several
electronic forms.
Multiple new illustrations and images have
been added to this edition.
Nonetheless, our goal remains the same as that of
the first edition: to provide a concise, consistent
presentation of the basic principles essential to the
modern practice of anesthesia.
We would like to thank Brian Belval, Harriet
Lebowitz, and Marsha Loeb for their invaluable
assistance.
Despite our best intentions, various errors
may have made their way into the fifth edition. We
will be grateful to readers who report these to us
at mm5edition@gmail.com so that we can correct
them in reprints and future editions.
David C. Mackey, MD
xiii
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SECTION II
C
Pharmacological Principles
KEY CONCEPTS
1
Drug molecules obey the law of mass action.

When the plasma concentration exceeds
the tissue concentration, the drug moves
from the plasma into tissue. When the
plasma concentration is less than the tissue
concentration, the drug moves from the
tissue back to plasma.
Most drugs that readily cross the bloodbrain

barrier (eg, lipophilic drugs like hypnotics
and opioids) are avidly taken up in body fat.
Biotransformation is the chemical process

by which the drug molecule is altered in
the body. The liver is the primary organ of
metabolism for drugs.
Small unbound molecules freely pass from

plasma into the glomerular ltrate. The
nonionized (uncharged) fraction of drug is
The clinical practice of anesthesiology is connected

more directly than any other specialty to the science of clinical pharmacology. One would think,
therefore, that the study of pharmacokinetics
and pharmacodynamics would receive attention
comparable to that given to airway assessment,
choice of inhalation anesthetic for ambulatory
surgery, or neuromuscular blockade in anesthesiology curricula and examinations. The frequent
reabsorbed in the renal tubules, whereas

the ionized (charged) portion is excreted
in urine.
5
Elimination half-life is the time required

for the drug concentration to fall by 50%.
For drugs described by multicompartment
pharmacokinetics (eg, all drugs used in
anesthesia), there are multiple elimination
half-lives.
The oset of a drugs eect cannot be

predicted from half-lives. The contextsensitive half-time is a clinically useful
concept to describe the rate of decrease
in drug concentration and should be
used instead of half-lives to compare the
pharmacokinetic properties of intravenous
drugs used in anesthesia.
misidentification or misuse of pharmacokinetic

principles and measurements suggests that this is
not the case.
PHARMACOKINETICS
Pharmacokinetics defines the relationships among
drug dosing, drug concentration in body fluids
and tissues, and time. It consists of four linked
143
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144
SECTION II
processes: absorption, distribution, biotransformation, and excretion.
Absorption
Absorption defines the processes by which a drug
moves from the site of administration to the bloodstream. There are many possible routes of drug
administration: oral, sublingual, rectal, inhalational,
transdermal, transmucosal, subcutaneous, intramuscular, and intravenous. Absorption is influenced
by the physical characteristics of the drug (solubility,
pKa, diluents, binders, and formulation), dose, and
the site of absorption (eg, gut, lung, skin, muscle).
Bioavailability is the fraction of the administered
dose reaching the systemic circulation. For example,
nitroglycerin is well absorbed by the gastrointestinal
tract but has low bioavailability when administered
orally. The reason is that nitroglycerin undergoes
extensive first-pass hepatic metabolism as it transits
the liver before reaching the systemic circulation.
Oral drug administration is convenient, inexpensive, and relatively tolerant of dosing errors.
However, it requires cooperation of the patient,
exposes the drug to first-pass hepatic metabolism,
and permits gastric pH, enzymes, motility, food, and
other drugs to potentially reduce the predictability
of systemic drug delivery.
Nonionized (uncharged) drugs are more readily
absorbed than ionized (charged) forms. Therefore,
an acidic environment (stomach) favors the absorption of acidic drugs (A + H+ AH), whereas a more
alkaline environment (intestine) favors basic drugs
(BH+ H+ + B). Most drugs are largely absorbed
from the intestine rather than the stomach because
of the greater surface area of the small intestine and
longer transit duration.
All venous drainage from the stomach and small
intestine flows to the liver. As a result, the bioavailability of highly metabolized drugs may be significantly
reduced by first-pass hepatic metabolism. Because
the venous drainage from the mouth and esophagus
flows into the superior vena cava rather than into the
portal system, sublingual or buccal drug absorption
bypasses the liver and first-pass metabolism. Rectal
administration partly bypasses the portal system,
and represents an alternative route in small children
or patients who are unable to tolerate oral ingestion.
Morg_Ch07_0143-0152.indd 144
However, rectal absorption can be erratic, and many

drugs irritate the rectal mucosa.
Transdermal drug administration can provide
prolonged continuous administration for some
drugs. However, the stratum corneum is an effective barrier to all but small, lipid-soluble drugs (eg,
clonidine, nitroglycerin, scopolamine, fentanyl, and
free-base local anesthetics [EMLA]).
Parenteral routes of drug administration
include subcutaneous, intramuscular, and intravenous injection. Subcutaneous and intramuscular
absorption depend on drug diffusion from the site
of injection to the bloodstream. The rate at which a
drug enters the bloodstream depends on both blood
flow to the injected tissue and the injectate formulation. Drugs dissolved in solution are absorbed
faster than those present in suspensions. Irritating
preparations can cause pain and tissue necrosis (eg,
intramuscular diazepam). Intravenous injections
completely bypass the process of absorption.
Distribution
Once absorbed, a drug is distributed by the bloodstream throughout the body. Highly perfused organs
(the so-called vessel-rich group) receive a disproportionate fraction of the cardiac output (Table71).
Therefore, these tissues receive a disproportionate
amount of drug in the first minutes following drug
administration. These tissues approach equilibration
with the plasma concentration more quickly than
less well perfused tissues due to the differences in
TABLE 71 Tissue group composition,

relative body mass, and percentage of
cardiac output.
Tissue
Group
Composition
Body
Mass (%)
Cardiac
Output (%)
Vessel-rich
Brain, heart,
liver, kidney,
endocrine
glands
10
75
Muscle
Muscle, skin
50
19
Fat
Fat
20
Vessel-poor
Bone, ligament,
cartilage
20
11/02/13 9:59 AM
CHAPTER 7 Pharmacological Principles
blood flow. However, less well perfused tissues such

as fat and skin may have enormous capacity to
absorb lipophilic drugs, resulting in a large reservoir
of drug following long infusions.
1 Drug molecules obey the law of mass action.
When the plasma concentration exceeds the
concentration in tissue, the drug moves from the
plasma into tissue. When the plasma concentration is less than the concentration in tissue, the drug
moves from the tissue back to plasma.
Distribution is a major determinant of endorgan drug concentration. The rate of rise in drug
concentration in an organ is determined by that
organs perfusion and the relative drug solubility
in the organ compared with blood. The equilibrium concentration in an organ relative to blood
depends only on the relative solubility of the drug
in the organ relative to blood, unless the organ is
capable of metabolizing the drug.
Molecules in blood are either free or bound to
plasma proteins and lipids. The free concentration
equilibrates between organs and tissues. However,
the equilibration between bound and unbound molecules is instantaneous. As unbound molecules of
drug diffuse into tissue, they are instantly replaced by
previously bound molecules. Plasma protein binding does not affect the rate of transfer directly, but
it does affect relative solubility of the drug in blood
and tissue. If the drug is highly bound in tissues,
and unbound in plasma, then the relative solubility
favors drug transfer into tissue. Put another way, a
drug that is highly bound in tissue, but not in blood,
will have a very large free drug concentration gradient driving drug into the tissue. Conversely, if the
drug is highly bound in plasma and has few binding
sites in the tissue, then transfer of a small amount of
drug may be enough to bring the free drug concentration into equilibrium between blood and tissue.
Thus, high levels of binding in blood relative to tissues increase the rate of onset of drug effect, because
fewer molecules need to transfer into the tissue to
produce an effective free drug concentration.
Albumin binds many acidic drugs (eg, barbiturates), whereas 1-acid glycoprotein (AAG) binds
basic drugs (local anesthetics). If the concentrations
of these proteins are diminished or (typically less
important) if the protein-binding sites are occupied
Morg_Ch07_0143-0152.indd 145
145
by other drugs, then the relative solubility of the

drugs in blood is decreased, increasing tissue uptake.
Kidney disease, liver disease, chronic congestive heart
failure, and malignancies decrease albumin production. Trauma (including surgery), infection, myocardial infarction, and chronic pain increase AAG levels.
Pregnancy is associated with reduced AAG concentrations. Note that these changes will have very little
effect on propofol, which is administered with its
own binding molecules (the lipid in the emulsion).
Lipophilic molecules can readily transfer
between the blood and organs. Charged molecules
are able to pass in small quantities into most organs.
However, the bloodbrain barrier is a special case.
Permeation of the central nervous system by ionized
drugs is limited by pericapillary glial cells and endo2 thelial cell tight junctions. Most drugs that
readily cross the bloodbrain barrier (eg, lipophilic drugs like hypnotics and opioids) are avidly
taken up in body fat.
The time course of distribution of drugs into
peripheral tissues is complex and can only be
assessed with computer models. Following intravenous bolus administration, rapid distribution
of drug from the plasma into peripheral tissues
accounts for the profound decrease in plasma concentration observed in the first few minutes. For
each tissue, there is a point in time at which the
apparent concentration in the tissue is the same as
the concentration in the plasma. The redistribution phase (for each tissue) follows this moment of
equilibration. During redistribution, drug returns
from peripheral tissues back into the plasma. This
return of drug back to the plasma slows the rate of
decline in plasma drug concentration.
Distribution generally contributes to rapid
emergence by removing drug from the plasma for
many minutes following administration of a bolus
infusion. Following prolonged infusions, redistribution generally delays emergence as drug returns
from tissue reservoirs to the plasma for many hours.
The complex process of drug distribution
into and out of tissues is one reason that half-lives
are clinically useless. The offset of a drugs clinical
actions are best predicted by computer models using
the context-sensitive half-time or decrement times.
The context-sensitive half-time is the time required
11/02/13 9:59 AM
146
SECTION II
for a 50% decrease in plasma drug concentration to

occur following a pseudo steady-state infusion (in
other words, an infusion that has continued long
enough to yield nearly steady-state concentrations).
Here the context is the duration of the infusion.
The context-sensitive decrement time is a more generalized concept referring to any clinically relevant
decreased concentration in any tissue, particularly
the brain or effect site.
The volume of distribution, Vd, is the apparent volume into which a drug has distributed (ie,
mixed). This volume is calculated by dividing a
bolus dose of drug by the plasma concentration at
time 0. In practice, the concentration used to define
the Vd is often obtained by extrapolating subsequent
concentrations back to 0 time when the drug was
injected, as follows:
Vd =
Bolus dose
Concentration time0
The concept of a single Vd does not apply to

any intravenous drugs used in anesthesia. All intravenous anesthetic drugs are better modeled with
at least two compartments: a central compartment
and a peripheral compartment. The behavior of
many of these drugs is best described using three
compartments: a central compartment, a rapidly
equilibrating peripheral compartment, and a slowly
equilibrating peripheral compartment. The central
compartment may be thought of as including the
blood and any ultra-rapidly equilibrating tissues
such as the lungs. The peripheral compartment is
composed of the other body tissues. For drugs with
two peripheral compartments, the rapidly equilibrating compartment comprises the organs and muscles,
while the slowly equilibrating compartment roughly
represents distribution of the drug into fat and skin.
These compartments are designated V1 (central),
V2 (rapid distribution), and V3 (slow distribution).
The volume of distribution at steady state, Vdss is the
algebraic sum of these compartment volumes. V1 is
calculated by the above equation showing the relationship between volume, dose, and concentration.
The other volumes are calculated through pharmacokinetic modeling.
A small Vdss implies that the drug has high
aqueous solubility and will remain largely within
the intravascular space. For example, the Vdss of
Morg_Ch07_0143-0152.indd 146
pancuronium is about 15 L in a 70-kg person, indicating that pancuronium is mostly present in body
water, with little distribution into fat. However, the
typical anesthetic drug is lipophilic, resulting in a
Vdss that exceeds total body water (approximately
40 L). For example, the Vdss for fentanyl is about 350
L in adults, and the Vdss for propofol may exceed
5000 L. Vdss does not represent a real volume but
rather reflects the volume into which the drug would
need to distribute to account for the observed plasma
concentration given the dose that was administered.
Biotransformation
3 Biotransformation is
the chemical process

by which the drug molecule is altered in the
body. The liver is the primary organ of metabolism
for drugs. The exception is esters, which undergo
hydrolysis in the plasma or tissues. The end products
of biotransformation are often (but not necessarily)
inactive and water soluble. Water solubility allows
excretion by the kidneys.
Metabolic biotransformation is frequently
divided into phase I and phase II reactions. Phase
I reactions convert a parent compound into more
polar metabolites through oxidation, reduction, or
hydrolysis. Phase II reactions couple (conjugate) a
parent drug or a phase I metabolite with an endogenous substrate (eg, glucuronic acid) to form watersoluble metabolites that can be eliminated in the
urine or stool. Although this is usually a sequential
process, phase I metabolites may be excreted without undergoing phase II biotransformation, and
a phase II reaction can precede or occur without a
phase I reaction.
Hepatic clearance is the volume of blood or
plasma (whichever was measured in the assay)
cleared of drug per unit of time. The units of clearance
are units of flow: volume per unit time. Clearance
may be expressed in milliliters per minute, liters per
hour, or any other convenient unit of flow.
If every molecule of drug that enters the liver
is metabolized, then hepatic clearance will equal
liver blood flow. This is true for very few drugs,
although it is very nearly the case for propofol. For
most drugs, only a fraction of the drug that enters
the liver is removed. The fraction removed is called
the extraction ratio. The hepatic clearance can therefore be expressed as the liver blood flow times the
11/02/13 9:59 AM
extraction ratio. If the extraction ratio is 50%, then

hepatic clearance is 50% of liver blood flow. The
clearance of drugs efficiently removed by the liver
(ie, having a high hepatic extraction ratio) is proportional to hepatic blood flow. For example, because
the liver removes almost all of the propofol that
goes through it, if the hepatic blood flow doubles,
then the clearance of propofol doubles. Induction
of liver enzymes has no effect on propofol clearance, because the liver so efficiently removes all of
the propofol that goes through it. Even severe loss
of liver tissue, as occurs in cirrhosis, has little effect
on propofol clearance. Drugs such as propofol have
flow-dependent clearance.
Many drugs have low hepatic extraction ratios
and are slowly cleared by the liver. For these drugs,
the rate-limiting step is not the flow of blood to the
liver, but rather the metabolic capacity of the liver
itself. Changes in liver blood flow have little effect
on the clearance of such drugs. However, if liver
enzymes are induced, then clearance will increase
because the liver has more capacity to metabolize
the drug. Conversely, if the liver is damaged, then
less capacity is available for metabolism and clearance is reduced. Drugs with low hepatic extraction
ratios thus have capacity-dependent clearance. The
extraction ratios of methadone and alfentanil are
10% and 15% respectively, making these capacitydependent drugs.
Excretion
Some drugs and many drug metabolites are excreted
by the kidneys. Renal clearance is the rate of elimination of a drug from the body by kidney excretion.
This concept is analogous to hepatic clearance, and
similarly, renal clearance can be expressed as the
renal blood flow times the renal extraction ratio.
4 Small unbound drugs freely pass from plasma
into the glomerular filtrate. The nonionized
(uncharged) fraction of drug is reabsorbed in the
renal tubules, whereas the ionized (charged) portion
is excreted in urine. The fraction of drug ionized
depends on the pH; thus renal elimination of drugs
that exist in ionized and nonionized forms depends
in part on urinary pH. The kidney actively secretes
some drugs into the renal tubules.
Many drugs and drug metabolites pass from the
liver into the intestine via the biliary system. Some
Morg_Ch07_0143-0152.indd 147
147
drugs excreted into the bile are then reabsorbed in

the intestine, a process called enterohepatic recirculation. Occasionally metabolites excreted in bile are
subsequently converted back to the parent drug. For
example, lorazepam is converted by the liver to lorazepam glucuronide. In the intestine, -glucuronidase
breaks the ester linkage, converting lorazepam glucuronide back to lorazepam.
Compartment Models
Multicompartment models provide a mathematical framework that can be used to relate drug
dose to changes in drug concentrations over time.
Conceptually, the compartments in these models are
tissues with a similar distribution time course. For
example, the plasma and lungs are components of
the central compartment. The organs and muscles,
sometimes called the vessel-rich group, could be
the second, or rapidly equilibrating, compartment.
Fat and skin have the capacity to bind large quantities of lipophilic drug but are poorly perfused.
These could represent the third, or slowly equilibrating, compartment. This is an intuitive definition
of compartments, and it is important to recognize
that the compartments of a pharmacokinetic model
are mathematical abstractions that relate dose to
observed concentration. A one-to-one relationship
does not exist between any compartment and any
organ or tissue in the body.
Many drugs used in anesthesia are well
described by a two-compartment model. This is
generally the case if the studies used to characterize
the pharmacokinetics do not include rapid arterial
sampling over the first few minutes (Figure 71).
Without rapid arterial sampling the ultra-rapid initial drop in plasma concentration immediately after
a bolus injection is missed, and the central compartment volume is blended into the rapidly equilibrating compartment. When rapid arterial sampling is
used in pharmacokinetic experiments, the results
are generally a three-compartment model. In these
cases the number of identifiable compartments is a
function of the experimental design and not a characteristic of the drug.
In compartmental models the instantaneous
concentration at the time of a bolus injection is
assumed to be the amount of the bolus divided
by the central compartment volume. This is not
11/02/13 9:59 AM
Plasma concentration
148
SECTION II
Distribution
phase
Elimination
phase
Time after dose

IV
bolus
FIGURE 71 Two-compartment model demonstrates

the distribution phase ( phase) and the elimination
phase ( phase). During the distribution phase, the drug
moves from the central compartment to the peripheral
compartment. The elimination phase consists of
metabolism and excretion.
equilibrating compartment is no longer removing

drug from the plasma. Instead, drug returns to the
plasma from the rapidly equilibrating compartment.
The reversed role of the rapidly equilibrating tissues
from extracting drug to returning drug accounts for
the slower rate of decline in plasma concentration in
this intermediate phase. Eventually there is an even
slower rate of decrease in plasma concentration,
which is log-linear until the drug is completely eliminated from the body. This terminal log-linear phase
occurs after the slowly equilibrating compartment
shifts from net removal of drug from the plasma to
net return of drug to the plasma. During this terminal phase the organ of elimination (typically the
liver) is exposed to the bodys entire body drug load,
which accounts for the very slow rate of decrease in
plasma drug concentration during this final phase.
The mathematical models used to describe
a drug with two or three compartments are,
respectively:
Cp(t) = Ae t + Bet
and
correct. If the bolus is given over a few seconds, the

instantaneous concentration is 0, because the drug
is all in the vein, still flowing to the heart. It takes
only a minute or two for the drug to mix in the central compartment volume. This misspecification is
common to conventional pharmacokinetic models. More physiologically based models, sometimes
called front-end kinetic models, can characterize
the initial delay in concentration. These models are
useful only if the concentrations over the first few
minutes are clinically important. After the first few
minutes, front-end models resemble conventional
compartmental models.
In the first few minutes following initial bolus
administration of a drug, the concentration drops
very rapidly as the drug quickly diffuses into peripheral compartments. The decline is typically an order
of magnitude over 10 minutes. For drugs with very
rapid hepatic clearance (eg, propofol) or those that
are metabolized in the blood (eg, remifentanil),
metabolism contributes significantly to the rapid initial drop in concentration. Following this very rapid
drop there is a period of slower decrease in plasma
concentration. During this period, the rapidly
Morg_Ch07_0143-0152.indd 148
Cp(t) = Ae t + Be t + Ce t
where Cp(t) equals plasma concentration at time t,
and , , and are the exponents that characterize the very rapid (ie, very steep), intermediate, and
slow (ie, log-linear) portions of the plasma concentration over time, respectively. Drugs described by
two-compartment and three-compartment models
will have two or three half-lives. Each half-life is calculated as the natural log of 2 (0.693), divided by the
exponent. The coefficients A, B, and C represent the
contribution of each of the exponents to the overall
decrease in concentration over time.
The two-compartment model is described by a
curve with two exponents and two coefficients,
whereas the three-compartment model is described
by a curve with three exponents and three coefficients. The mathematical relationships among compartments, clearances, coefficients, and exponents
are complex. Every coefficient and every exponent is
a function of every volume and every clearance.
5 Elimination half-life is the time required for the
drug concentration to fall by 50%. For drugs
described by multicompartment pharmacokinetics
11/02/13 9:59 AM
scale (Figure 72B), while the response is typically plotted either as the actual measured response
(Figure 72A) or as a fraction of the baseline or maximum physiological measurement (Figure 72B).
For our purposes here, basic pharmacodynamic
properties are described in terms of concentration,
but any metric of drug exposure (dose, area under
the curve, etc) could be used.
The shape of the relationship is typically sigmoidal, as shown in Figure 72. The sigmoidal
A
20
Drop in MAP (mm Hg)
(eg, all drugs used in anesthesia), there are multiple

elimination half-lives, in other words the elimination
6 half-time is context dependent. The offset of a
drugs effect cannot be predicted from halflives. Moreover, one cannot easily determine how
rapidly a drug effect will disappear simply by looking
at coefficients, exponents, and half-lives. For example,
the terminal half-life of sufentanil is about 10 h,
whereas that of alfentanil is 2 h. This does not mean
that recovery from alfentanil will be faster, because
clinical recovery from clinical dosing will be influenced by all half-lives, not just the terminal one.
Computer models readily demonstrate that recovery
from an infusion lasting several hours will be faster
when the drug administered is sufentanil than it will
be when the infused drug is alfentanil. The time
required for a 50% decrease in concentration depends
on the duration or context of the infusion. The context-sensitive half-time, discussed earlier, captures
this concept and should be used instead of half-lives
to compare the pharmacokinetic properties of intravenous drugs used in anesthesia.
149
15
10
PHARMACODYNAMICS
ExposureResponse Relationships
As the body is exposed to an increasing amount of
a drug, the response to the drug similarly increases,
typically up to a maximal value. This fundamental
concept in the exposure versus response relationship
is captured graphically by plotting exposure (usually
dose or concentration) on the x axis as the independent variable, and the bodys response on the y axis
as the dependent variable. Depending on the circumstances, the dose or concentration may be plotted on a linear scale (Figure 72A) or a logarithmic
Morg_Ch07_0143-0152.indd 149
10
20
30
Dose (mg)
40
B
100
% of maximal response
Pharmacodynamics, the study of how drugs affect

the body, involves the concepts of potency, efficacy,
and therapeutic window. Pharmacokinetic models can range from entirely empirical dose versus
response relationships to mechanistic models of
ligandreceptor binding. The fundamental pharmacodynamic concepts are captured in the relationship between exposure to a drug and physiological
response to the drug, often called the doseresponse
or concentrationresponse relationship.
75
50
25
10
Dose (mg)
100
1000
FIGURE 72 The shape of the doseresponse curve

depends on whether the dose or steady-state plasma
concentration (Ccpss) is plotted on a linear A: or logarithmic
B: scale. MAP, mean arterial pressure.
11/02/13 9:59 AM
150
SECTION II
shape reflects the observation that often a certain

amount of drug must be present before there is any
measurable physiological response. Thus, the left
side of the curve is flat until the drug concentration
reaches a minimum threshold. The right side is also
flat, reflecting the maximum physiological response
of the body, beyond which the body simply cannot
respond to additional drug (with the possible exception of eating and weight). Thus, the curve is flat on
both the left and right sides. A sigmoidal curve is
required to connect the baseline to the asymptote,
which is why sigmoidal curves are ubiquitous when
modeling pharmacodynamics
The sigmoidal relationship between exposure
and response is defined by one of two interchangeable relationships:
Effect = E0 + E max
C
C50 + C
or
Effect = E0 + (E max E 0 )
C
C + C
50
In both cases, E0 is the baseline effect in the

absence of drug, C is drug concentration, C50 is the
concentration associated with half-maximal effect,
and describes the steepness of the concentration versus response relationship. For the first equation, Emax
is the maximum change from baseline. In the second
equation, Emax is the maximum physiological measurement, not the maximum change from baseline.
Once defined in this fashion, each parameter
of the pharmacodynamic model speaks to the specific concepts mentioned earlier. Emax is related to
the intrinsic efficacy of a drug. Highly efficacious
drugs have a large maximum physiological effect,
characterized by a large Emax. For drugs that lack
efficacy, Emax will equal E0. C50 is a measure of drug
potency. Highly potent drugs have a low C50; thus
small amounts produce the drug effect. Drugs lacking potency have a high C50, indicating that a large
amount of drug is required to achieve the drug
effect. The parameter indicates steepness of the
relationship between concentration and effect. A
value less than 1 indicates a very gradual increase
in drug effect with increasing concentration. A
Morg_Ch07_0143-0152.indd 150
value greater than 4 suggests that once drug effect

is observed, small increases in drug concentration
produce large increases in drug effect until the maximum effect is reached.
The curve described above represents the relationship of drug concentration to a continuous
physiological response. The same relationship can
be used to characterize the probability of a binary
(yes/no) response to a drug dose:
Probability = P0 + (P max P 0 )
C
C + C
50
In this case, the probability (P) ranges from 0 (no

chance) to 1 (certainty). P0 is the probability of a yes
response in the absence of drug. Pmax is the maximum
probability, necessarily less than or equal to 1. As
before, C is the concentration, C50 is the concentration
associated with half-maximal effect, and describes
the steepness of the concentration versus response
relationship. Half-maximal effect is the same as 50%
probability of a response when P0 is 0 and Pmax is 1.
The therapeutic window for a drug is the range
between the concentration associated with a desired
therapeutic effect and the concentration associated
with a toxic drug response. This range can be measured either between two different points on the
same concentration versus response curve, or the
distance between two distinct curves. For a drug
such as sodium nitroprusside, a single concentration versus response curve defines the relationship
between concentration and decrease in blood pressure. The therapeutic window might be the difference in the concentration producing a desired 20%
decrease in blood pressure and a toxic concentration
that produces a 60% decrease in blood pressure.
However, for a drug such as lidocaine, the therapeutic window might be the difference between the
C50 for local anesthesia and the C50 for lidocaineinduced seizures, the latter being a separate concentration versus response relationship. The therapeutic
index is the C50 for toxicity divided by the C50 for
the desired therapeutic effect. Because of the risk of
ventilatory and cardiovascular depression (even at
concentrations only slightly greater than those producing anesthesia), most inhaled and intravenous
hypnotics are considered to have very low therapeutic indices relative to other drugs.
11/02/13 9:59 AM
then we can solve for receptor occupancy as:
Drug Receptors
Drug receptors are macromolecules, typically proteins, that bind a drug (agonist) and mediate the drug
response. Pharmacological antagonists reverse the
effects of the agonist but do not otherwise exert an
effect of their own. Competitive antagonism occurs
when the antagonist competes with the agonist for
the binding site, each potentially displacing the other.
Noncompetitive antagonism occurs when the antagonist, through covalent binding or another process,
permanently impairs the drugs access to the receptor.
The drug effect is governed by the fraction of
receptors that are occupied by an agonist. That fraction is based on the concentration of the drug, the
concentration of the receptor, and the strength of
binding between the drug and the receptor. This
binding is described by the law of mass action,
which states that the reaction rate is proportional to
the concentrations of the reactants:
[D][RU]
k on
[DR]
koff
where [D] is the concentration of the drug, [RU] is
the concentration of unbound receptor, and [DR] is
the concentration of bound receptor. The rate constant kon defines the rate of ligand binding to the
receptor. The rate constant koff defines the rate of
ligand unbinding from the receptor. According to
the law of mass action, the rate of receptor binding,
d[DR]/dt is:
d[DR]
= [D][RU] k on [DR]k off
dt
Steady state occurs almost instantly. Because the
rate of formation at steady state is 0, it follows that:
[D][RU] k on = [DR]k off
In this equation, kd is the dissociation rate constant, defined as kon /koff . If we define f, fractional
receptor occupancy, as:
[DR]
[DR] + [RU]
Morg_Ch07_0143-0152.indd 151
151
f=
[D]
kd + [D]
The receptors are half occupied when [D] = kd.

Thus, kd is the concentration of drug associated with
50% receptor occupancy.
Receptor occupancy is only the first step in
mediating drug effect. Binding of the drug to the
receptor can trigger a myriad of subsequent steps,
including opening or closing of an ion channel,
activation of a G protein, activation of an intracellular kinase, direct interaction with a cellular structure, or direct binding to DNA.
Like the concentration versus response curve,
the shape of the curve relating fractional receptor
occupancy to drug concentration is intrinsically
sigmoidal. However, the concentration associated
with 50% receptor occupancy and the concentration associated with 50% of maximal drug effect
are not necessarily the same. Maximal drug effect
could occur at very low receptor occupancy, or
(for partial agonists) at greater than 100% receptor
occupancy.
Prolonged binding and activation of a receptor
by an agonist may lead to hyporeactivity (desensitization) and tolerance. If the binding of an endogenous ligand is chronically blocked, then receptors
may proliferate resulting in hyperreactivity and
increased sensitivity.
SUGGESTED READING
Bauer LA (Ed): Applied Clinical Pharmacokinetics, 2nd
ed. McGraw-Hill, 2008: Chaps 1, 2.
Brunton LL, Chabner BA, Knollman BC (Eds): Goodman
& Gilmans The Pharmacological Basis of Therapeutics,
12th ed. McGraw-Hill, 2010: Chap 2.
Keifer J, Glass P: Context-sensitive half-time and anesthesia: How does theory match reality? Curr Opin
Anaesthesiol 1999;12:443.
Shargel L, Yu AB, Wu-Pong S (Eds): Applied
Biopharmaceutics & Pharmacokinetics, 6th ed.
McGraw-Hill, 2012.
11/02/13 9:59 AM
Morg_Ch07_0143-0152.indd 152
11/02/13 9:59 AM
Peripheral Nerve Blocks

Sarah J. Madison, MD and Brian M. Ilfeld, MD, MS
46
KEY CONCEPTS
1
In addition to potent analgesia, regional

anesthesia may lead to reductions in
the stress response, systemic analgesic
requirements, opioid-related side
eects, general anesthesia requirements,
and possibly the incidence of chronic pain.
The axillary, musculocutaneous, and medial

brachial cutaneous nerves branch from the
brachial plexus proximal to the location
in which local anesthetic is deposited
during an axillary nerve block, and thus
are usually spared.
Regional anesthetics should be

administered in an area where standard
hemodynamic monitors, supplemental
oxygen, and resuscitative medications and
equipment are readily available.
Local anesthetic may be deposited at any

point along the brachial plexus, depending
on the desired block eects: interscalene
for shoulder and proximal humerus
surgical procedures; and supraclavicular,
infraclavicular, and axillary for surgeries
distal to the mid-humerus.
Often it is necessary to anesthetize a single

terminal nerve, either for minor surgical
procedures with a limited eld or as a
supplement to an incomplete brachial plexus
block. Terminal nerves may be anesthetized
anywhere along their course, but the elbow
and the wrist are the two most favored sites.
Intravenous regional anesthesia, also called

a Bier block, can provide intense surgical
anesthesia for short surgical procedures
(4560 min) on an extremity.
A femoral nerve block alone will seldom

provide surgical anesthesia, but it is often
used to provide postoperative analgesia for
hip, thigh, knee, and ankle procedures.
A properly performed interscalene block

invariably blocks the ipsilateral phrenic
nerve, so careful consideration should be
given to patients with severe pulmonary
disease or preexisting contralateral phrenic
nerve palsy.
Brachial plexus block at the level of the
cords provides excellent anesthesia for
procedures at or distal to the elbow.
The upper arm and shoulder are not
anesthetized with this approach. As
with other brachial plexus blocks, the
intercostobrachial nerve (T2 dermatome)
is spared.
10 Posterior lumbar plexus blocks are useful
for surgical procedures involving areas

innervated by the femoral, lateral femoral
cutaneous, and obturator nerves. Complete
anesthesia of the knee can be attained
with a proximal sciatic nerve block.
11 Blockade of the sciatic nerve may occur
anywhere along its course and is indicated

for surgical procedures involving the hip,
thigh, knee, lower leg, and foot.
Continued next page
975
Morg_Ch46_0975-1022.indd 975
11/02/13 6:17 PM
976
SECTION IV
Regional Anesthesia & Pain Management
Continued
12 Popliteal nerve blocks provide excellent
coverage for foot and ankle surgery,

while sparing much of the hamstring
muscles, allowing lifting of the foot with
knee exion, thus easing ambulation. All
sciatic nerve blocks fail to provide complete
anesthesia for the cutaneous medial
leg and ankle joint capsule, but when a
saphenous (or femoral) block is added,
complete anesthesia below the knee is
provided.
13 A complete ankle block requires a series of
ve nerve blocks, but the process may be

streamlined to minimize needle insertions.
All ve injections are required to anesthetize
the entire foot; however, many surgical
procedures involve only a few terminal
nerves, and only aected nerves should
be blocked.
An understanding of regional anesthesia anatomy

and techniques is required of the well-rounded
anesthesiologist. Although anatomic relationships
have not changed over time, our ability to identify
them has evolved. From the paresthesia-seeking
techniques described by Winnie in the mid-twentieth century, to the popularization of the nerve
stimulator, to the introduction of ultrasound
guidance, anesthesiologists and their patients
have benefitted from technologys evolution. The
field of regional anesthesia has accordingly
expanded to one that addresses not only the intraoperative concerns of the anesthesiologist, but
also longer term perioperative pain management.
1 In addition to potent analgesia, regional
anesthesia may lead to reductions in the
stress response, systemic analgesic requirements,
opioid-related side effects, general anesthesia
requirements, and possibly the development of
chronic pain.
Morg_Ch46_0975-1022.indd 976
14 Intercostal blocks result in the highest
blood levels of local anesthetic per volume

injected of any block in the body, and care
must be taken to avoid toxic levels of local
anesthetic.
15 The thoracic paravertebral space is
dened posteriorly by the superior

costotransverse ligament, anterolaterally
by the parietal pleura, medially by the
vertebrae and the intervertebral foramina,
and inferiorly and superiorly by the heads
of the ribs.
16 The subcostal (T12), ilioinguinal (L1),
and iliohypogastric (L1) nerves are

targeted in the transversus abdominus
plane block, providing anesthesia to the
ipsilateral lower abdomen below the
umbilicus.
PATIENT SELECTION
The selection of a regional anesthetic technique is
a process that begins with a thorough history and
physical examination. Although many patients are
candidates for regional anesthesia/analgesia, as
with any medical procedure a riskbenefit analysis must be performed. The riskbenefit ratio often
favors regional anesthesia in patients with multiple
comorbidities for whom a general anesthetic carries a greater risk. In addition, patients intolerant to
systemic analgesics (eg, those with obstructive sleep
apnea or at high risk for nausea) may benefit from
the opioid-sparing effects of a regional analgesic.
Patients with chronic pain and opioid tolerance may
receive optimal analgesia with a continuous peripheral nerve block (so-called perineural local anesthetic infusion).
A comprehensive knowledge of anatomy and an
understanding of the planned surgical procedure are
11/02/13 6:17 PM
CHAPTER 46 Peripheral Nerve Blocks
important for selection of the appropriate regional

anesthetic technique. If possible, discussion with the
surgeon about various considerations (tourniquet
placement, bone grafting, projected surgical duration) is ideal. Also, knowing the anticipated course
of recovery and anticipated level of postoperative
pain will often influence specific decisions regarding
a regional anesthetic technique (eg, a single-injection versus continuous peripheral nerve block).
RISKS & CONTRAINDICATIONS

Patient cooperation and participation are key to
the success and safety of every regional anesthetic
procedure; patients who are unable to remain still
for a procedure may be exposed to increased risk.
Examples include younger pediatric patients and
some developmentally delayed individuals, as well
as patients with dementia or movement disorders.
Bleeding disorders and pharmacological anticoagulation heighten the risk of local hematoma or hemorrhage, and this risk must be balanced against the
possible benefits of regional block. Specific peripheral nerve block locations warranting the most concern are posterior lumbar plexus and paravertebral
blocks owing to their relative proximity to the retroperitoneal space and neuraxis, respectively.
Placement of a block needle through a site of
infection can theoretically track infectious material into the body, where it poses a risk to the target
nerve tissue and surrounding structures. Therefore,
the presence of a local infection is a relative contraindication to performing a peripheral nerve block.
Indwelling perineural catheters can serve as a nidus
of infection; however, the risk in patients with systemic infection remains unknown.
Although nerve injury is always a possibility with a regional anesthetic, some patients are at
increased risk. Individuals with a preexisting condition (eg, peripheral neuropathy or previous nerve
injury) may have a higher incidence of complications, including prolonged or permanent sensorimotor block. The precise mechanisms have yet to be
clearly defined but may involve local ischemia from
high injection pressure or vasoconstrictors, a neurotoxic effect of local anesthetics, or direct trauma to
nerve tissue.
Morg_Ch46_0975-1022.indd 977
977
Other risks associated with regional anesthesia

include local anesthetic toxicity from intravascular
injection or perivascular absorption. In the event of
a local anesthetic toxic reaction, seizure activity and
cardiovascular collapse may occur. Supportive measures should begin immediately, including solicitation of assistance with a code blue, the initiation
of cardiopulmonary resuscitation, lipid emulsion
administration to sequester local anesthetic, and
preparation for cardiopulmonary bypass.
Site-specific risks should also be considered for
each individual patient. In a patient with severe pulmonary compromise or hemidiaphragmatic paralysis, for example, a contralateral interscalene or deep
cervical plexus block with resultant phrenic nerve
block could be disastrous.
CHOICE OF LOCAL
ANESTHETIC
The decision about which local anesthetic to employ
for a particular nerve block depends on the desired
onset, duration, and relative blockade of sensory and
motor fibers. Potential for toxicity should be considered, as well as site-specific risks. A detailed discussion of local anesthetics is provided elsewhere (see
Chapter 16).
PREPARATION
2 Regional anesthetics should be administered
in an area where standard hemodynamic

monitors, supplemental oxygen, and resuscitative
medications and equipment are readily available.
Patients should be monitored with pulse oximetry,
noninvasive blood pressure, and electrocardiography; measurement of end-tidal CO2 and fraction
of inspired oxygen (Fio2) should also be available.
Positioning should be ergonomically favorable for
the practitioner and comfortable for the patient.
Intravenous premedication should be employed to
allay anxiety and minimize discomfort. A relatively
short-acting benzodiazepine and opioid are most
often used and should be titrated for comfort while
ensuring that patients respond to verbal cues. Sterile
technique should be strictly observed.
11/02/13 6:17 PM
978
SECTION IV
FIGURE 461 A eld block targets

terminal cutaneous nerves, such as
the intercostobrachial nerve.
BLOCK TECHNIQUES
Paresthesia Technique
Field Block Technique
Formerly the mainstay of regional anesthesia, this

technique is now rarely used for nerve localization. Using known anatomic relationships and surface landmarks as a guide, a block needle is placed
in proximity to the target nerve or plexus. When a
needle makes direct contact with a sensory nerve,
a paresthesia (abnormal sensation) is elicited in its
area of sensory distribution.
A field block is a local anesthetic injection that targets terminal cutaneous nerves (Figure 461). Field
blocks are used commonly by surgeons to minimize
incisional pain and may be used as a supplementary
technique or as a sole anesthetic for minor, superficial procedures. Anesthesiologists often use field
blocks to anesthetize the superficial cervical plexus
for procedures involving the neck or shoulder; the
intercostobrachial nerve for surgery involving the
medial upper extremity proximal to the elbow (in
combination with a brachial plexus nerve block);
and the saphenous nerve for surgery involving the
medial leg or ankle joint (in combination with a sciatic nerve block). Field blocks may be undesirable in
cases where they obscure the operative anatomy, or
where local tissue acidosis from infection prevents
effective local anesthetic functioning.
Morg_Ch46_0975-1022.indd 978
Nerve Stimulation Technique

For this technique, an insulated needle concentrates electrical current at the needle tip, while a
wire attached to the needle hub connects to a nerve
stimulatora battery-powered machine that emits a
small amount (05 mA) of electric current at a set
interval (usually 1 or 2 Hz). A grounding electrode
is attached to the patient to complete the circuit
(Figure 462). When the insulated needle is placed in
11/02/13 6:17 PM
979
technique, 3040 mL of anesthetic is usually injected

with gentle aspiration between divided doses.
Ultrasound Technique
FIGURE 462 A nerve stimulator delivers a small

amount of electric current to the block needle to facilitate
nerve localization.
proximity to a motor nerve, muscle contractions are
induced, and local anesthetic is injected. Although it
is common to redirect the block needle until muscle
contractions occur at a current less than 0.5 mA,
there is scant evidence to support this specific current in all cases. Similarly, although some have suggested that muscle contraction with current less
than 0.2 mA implies intraneural needle placement,
there is little evidence to support this specific cutoff.
Nonetheless, most practitioners inject local anesthetic when current between 0.2 and 0.5 mA results
in a muscle response. For most blocks using this
Linear
Ultrasound for peripheral nerve localization is

becoming increasingly popular; it may be used alone
or combined with other modalities such as nerve
stimulation. Ultrasound uses high-frequency (120
MHz) sound waves emitted from piezoelectric crystals that travel at different rates through tissues of different densities, returning a signal to the transducer.
Depending on the amplitude of signal received, the
crystals deform to create an electronic voltage that is
converted into a two-dimensional grayscale image.
The degree of efficiency with which sound passes
through a substance determines its echogenicity.
Structures and substances through which sound
passes easily are described as hypoechoic and appear
dark or black on the ultrasound screen. In contrast,
structures reflecting more sound waves appear
brighteror whiteon the ultrasound screen, and
are termed hyperechoic.
The optimal transducer varies depending upon
the depth of the target nerve and approach angle of
the needle relative to the transducer (Figure 463).
High-frequency transducers provide a high-resolution picture with a relatively clear image but
Curvilinear
No image
Poor
Good
FIGURE 463 A linear probe oers higher resolution with less penetration. A curvilinear probe provides better
penetration with lower resolution.
Morg_Ch46_0975-1022.indd 979
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980
SECTION IV
FIGURE 464 In-plane (A) and out-of-plane (B) ultrasound approaches.

offer poor tissue penetration and are therefore used
predominantly for more superficial nerves. Lowfrequency transducers provide an image of poorer
quality but have better tissue penetration and are
therefore used for deeper structures. Transducers
with a linear array offer an undistorted image and
are therefore often the first choice among practitioners. However, for deeper target nerves that require
a more acute angle between the needle and long-axis
of the transducer, a curved array (curvilinear) transducer will maximize returning ultrasound waves,
providing the optimal needle image (Figure 463).
Nerves are best imaged in cross-section, where
they have a characteristic honeycomb appearance
(short axis). Needle insertion can pass either parallel (in plane) or not parallel (out of plane) to
the plane of the ultrasound waves (Figure 464).
Unlike nerve stimulation alone, ultrasound guidance allows for a variable volume of local anesthetic
to be injected, with the final amount determined by
what is observed under direct vision. This technique
usually results in a far lower injected volume of local
anesthetic (1030 mL).
Continuous Peripheral Nerve Blocks

Also termed perineural local anesthetic infusion,
continuous peripheral nerve blocks involve the
Morg_Ch46_0975-1022.indd 980
placement of a percutaneous catheter adjacent

to a peripheral nerve, followed by local anesthetic administration to prolong a nerve block
(Figure 465). Potential advantages appear to
depend on successfully improving analgesia and
include reductions in resting and dynamic pain, supplemental analgesic requirements, opioid-related
side effects, and sleep disturbances. In some cases
patient satisfaction, ambulation, and functioning
may be improved; an accelerated resumption of
passive joint range-of-motion realized; and reduced
time until discharge-readiness as well as actual discharge from the hospital or rehabilitation center
achieved.
There are many types of catheters, including
nonstimulating and stimulating, flexible and more
rigid, through-the-needle and over-the-needle.
Currently, there is little evidence that a single
design results in superior effects. Local anesthetic
is the primary medication infused, as adjuvants
do not add benefits to perineural infusions (unlike
single-injection peripheral nerve blocks). Longacting local anesthetics (eg, ropivacaine) are more
commonly used as they provide a more favorable
sensory-to-motor block ratio (optimizing analgesia
while minimizing motor block). In an attempt to
further minimize any induced motor block, dilute
11/02/13 6:17 PM
981
FIGURE 465 Placement of a percutaneous catheter adjacent to a peripheral nerve.
local anesthetic (0.10.2%) is often infused; however, recent evidence suggests that it is the total dose,
and not concentration, that determines the majority of block effects. Unlike single-injection peripheral
nerve blocks, no adjuvant added to a perineural local
anesthetic infusion has been demonstrated to be of
benefit. The local anesthetic may be administered
exclusively as repeated bolus doses or a basal infusion, or as a combination of the two methods. Using
a small, portable infusion pump (Figure 466), continuous peripheral nerve blocks may be provided on
an ambulatory basis.
As with all medical procedures, there are
potential risks associated with continuous peripheral nerve blocks. Therefore, these infusions are
usually reserved for patients having procedures
expected to result in postoperative pain that is difficult to control with oral analgesics and will not
resolve in less time than the duration of a singleinjection peripheral nerve block. Serious complications, which are relatively rare, include systemic
local anesthetic toxicity, catheter retention, nerve
injury, infection, and retroperitoneal hematoma
Morg_Ch46_0975-1022.indd 981
formation. In addition, a perineural infusion affecting the femoral nerve increases the risk of falling, although to what degree and by what specific
mechanism (eg, sensory, motor, or proprioception
deficits) remain unknown.
UPPER EXTREMITY
PERIPHERAL NERVE BLOCKS
Brachial Plexus Anatomy
The brachial plexus is formed by the union of the
anterior primary divisions (ventral rami) of
the fifth through the eighth cervical nerves and
the first thoracic nerves. Contributions from C4
and T2 are often minor or absent. As the nerve
roots leave the intervertebral foramina, they converge, forming trunks, divisions, cords, branches,
and then finally terminal nerves. The three distinct
trunks formed between the anterior and middle
scalene muscles are termed superior, middle, and
inferior based on their vertical orientation. As the
trunks pass over the lateral border of the first rib
11/02/13 6:17 PM
982
SECTION IV
FIGURE 466 Elastomeric (A) and electronic (B) portable infusion pumps.
and under the clavicle, each trunk divides into

anterior and posterior divisions. As the brachial
plexus emerges below the clavicle, the fibers combine again to form three cords that are named
according to their relationship to the axillary
artery: lateral, medial, and posterior. At the lateral
border of the pectoralis minor muscle, each cord
gives off a large branch before ending as a major
terminal nerve. The lateral cord gives off the lateral
branch of the median nerve and terminates as the
musculocutaneous nerve; the medial cord gives off
the medial branch of the median nerve and terminates as the ulnar nerve; and the posterior cord
gives off the axillary nerve and terminates as the
3 radial nerve. Local anesthetic may be deposited at any point along the brachial plexus,
depending on the desired block effects
(Figure 467): interscalene for shoulder and proximal humerus surgical procedures; and supraclavicular, infraclavicular, and axillary for surgeries
distal to the mid-humerus.
Morg_Ch46_0975-1022.indd 982
Interscalene Block
An interscalene brachial plexus block is indicated
for procedures involving the shoulder and upper
arm (Figure 468). Roots C57 are most densely
blocked with this approach; and the ulnar nerve
originating from C8 and T1 may be spared. Therefore, interscalene blocks are not appropriate for surgery at or distal to the elbow. For complete surgical
anesthesia of the shoulder, the C3 and C4 cutaneous branches may need to be supplemented with a
superficial cervical plexus block or local infiltration.
Contraindications to an interscalene block
include local infection, severe coagulopathy, local
4 anesthetic allergy, and patient refusal. A
properly performed interscalene block invariably blocks the ipsilateral phrenic nerve (completely
for nerve stimulation techniques; unclear for ultrasound-guided techniques), so careful consideration
should be given to patients with severe pulmonary
disease or preexisting contralateral phrenic nerve
palsy. The hemidiaphragmatic paresis may result in
11/02/13 6:17 PM
983
Anterior (palmar) view
Supraclavicular
nerves
(from cervical
plexus)
Axillary nerve
Superior lateral
brachial cutaneous
nerve
Suprascapular
nerve
Radial nerve
Inferior lateral
brachial cutaneous
nerve
Intercostobrachial
and medial brachial
cutaneous nerve
Lateral
antebrachial
cutaneous nerve
(terminal part of
musculocutaneous
nerve)
Radial nerve
Superficial branch
Median nerve
Palmar and
palmar digital
branches
Posterior (dorsal) view
Medial
antebrachial
cutaneous nerve
Ulnar nerve
Palmar and
palmar digital
branches
Ulnar nerve
Dorsal branch,
dorsal digital
branches, and
proper palmar
digital branches
Axillary nerve
Superior lateral
brachial cutaneous
nerve
Radial nerve
Posterior brachial
cutaneous nerve,
inferior lateral
brachial cutaneous
nerve, and posterior
antebrachial
cutaneous nerve
Lateral
antebrachial
cutaneous nerve
(terminal part of
musculocutaneous
nerve)
Radial nerve
Superficial branch
and dorsal digital
branches
Median nerve
Proper palmar
digital branches
FIGURE 467 The location of local anesthetic deposition along the brachial plexus depends on the desired eects
of the block.
dyspnea, hypercapnia, and hypoxemia. A Horners

syndrome (myosis, ptosis, and anhidrosis) may
result from proximal tracking of local anesthetic
and blockade of sympathetic fibers to the cervicothoracic ganglion. Recurrent laryngeal nerve
involvement often induces hoarseness. In a patient
with contralateral vocal cord paralysis, respiratory
distress may ensue. Other site-specific risks include
vertebral artery injection (suspect if immediate seizure activity is observed), spinal or epidural injection, and pneumothorax. Even 1 mL of local
anesthetic delivered into the vertebral artery may
induce a seizure. Similarly, intrathecal, subdural,
and epidural local anesthetic spread is possible.
Morg_Ch46_0975-1022.indd 983
Lastly, pneumothorax is possible due to the close

proximity of the pleura.
The brachial plexus passes between the anterior
and middle scalene muscles at the level of the cricoid
cartilage, or C6 (Figure 469). Palpation of the interscalene groove is usually accomplished with the
patient supine and the head rotated 30 or less to the
contralateral side. The external jugular vein often
crosses the interscalene groove at the level of the
cricoid cartilage. The interscalene groove should not
be confused with the groove between the sternocleidomastoid and the anterior scalene muscle, which
lies further anterior. Having the patient lift and turn
the head against resistance often helps delineate the
11/02/13 6:17 PM
984
SECTION IV
Interscalene
Nerves or
plexus roots
C4
Trunks
C5
Divisions
C6
Cords
Upper
trunk
Main branches
ord
ral c
Late
ior
ster
cord
C7
run
et
ddl
Mi
C8
Po
Lower trunk
ord
T1
lc
edia
FIGURE 468 An interscalene block is appropriate for shoulder and proximal humerus procedures. The ventral rami of
C5C8 and T1 form the brachial plexus.
Morg_Ch46_0975-1022.indd 984
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985
Cricoid
cartilage
FIGURE 469 The brachial plexus passes between

the anterior and middle scalene muscles at the level of
the cricoid cartilage, or C6.
anatomy. If surgical anesthesia is desired for the

entire shoulder, the intercostobrachial nerve must
usually be targeted separately with a field block since
it originates from T2 and is not affected with an
interscalene block. Interscalene perineural infusions
provide potent analgesia following shoulder surgery.
A. Nerve Stimulation
A relatively short (5-cm) insulated needle is usually employed. The interscalene groove is palpated
using the nondominant hand, pressing firmly to
stabilize the skin against the underlying structures
(Figure 4610). After the skin is anesthetized, the
block needle is inserted at a slightly medial and caudad angle and advanced to optimally elicit a motor
response of the deltoid or biceps muscles (suggesting
stimulation of the superior trunk). A motor response
of the diaphragm indicates that the needle is placed
in too anterior a direction; a motor response of the
trapezius or serratus anterior muscles indicates that
the needle is placed in too posterior a direction. If
bone (transverse process) is contacted, the needle
should be redirected more anteriorly. Aspiration
of arterial blood should raise concern for vertebral
or carotid artery puncture; the needle should be
Morg_Ch46_0975-1022.indd 985
FIGURE 4610 Interscalene block using nerve

stimulation.
withdrawn, pressure held for 35 min, and landmarks reassessed.
B. Ultrasound
A needle in-plane or out-of-plane technique may
be used, and an insulated needle attached to a nerve
stimulator can be used to confirm the accuracy of
the targeted structure. For both techniques, after
identification of the sternocleidomastoid muscle
and interscalene groove at the approximate level
of C6, a high-frequency linear transducer is placed
perpendicular to the course of the interscalene muscles (short axis; Figure 4611). The brachial plexus
and anterior and middle scalene muscles should
be visualized in cross-section (Figure 4612). The
brachial plexus at this level appears as three to five
hypoechoic circles. The carotid artery and internal
jugular vein may be seen lying anterior to the anterior scalene muscle; the sternocleidomastoid is visible superficially as it tapers to form its lateral edge.
For an out-of-plane technique, the block needle is inserted just cephalad to the transducer and
advanced in a caudal direction toward the visualized plexus. After careful aspiration for nonappearance of blood, local anesthetic (hypoechoic) spread
11/02/13 6:17 PM
986
SECTION IV
middle scalene muscle until it has passed through

the fascia anteriorly into the interscalene groove.
The needle tip and shaft should be visualized during
the entire block performance. Depending on visualized spread relative to the target nerve(s), a lower
volume (10 mL) may be employed for postoperative
analgesia, whereas a larger volume (2030 mL) is
commonly used for surgical anesthesia.
Supraclavicular Block
Clavicle
FIGURE 4611 Ultrasound-guided interscalene block

(in-plane technique).
should occur adjacent to (sometimes surrounding)
the plexus.
For an in-plane technique, the needle is inserted
just posterior to the ultrasound transducer in a direction exactly parallel to the ultrasound beam. A longer block needle (8 cm) is usually necessary. It may
be helpful to have the patient turn slightly laterally
with the affected side up to facilitate manipulation
of the needle. The needle is advanced through the
Once described as the spinal of the arm, a supraclavicular block offers dense anesthesia of the
brachial plexus for surgical procedures at or distal to the elbow (Figure 4613). Historically, the
supraclavicular block fell out of favor due to the
high incidence of complications (namely, pneumothorax) that occurred with paresthesia and nerve
stimulator techniques. It has seen a resurgence in
recent years as the use of ultrasound guidance has
theoretically improved safety. The supraclavicular block does not reliably anesthetize the axillary
and suprascapular nerves, and thus is not ideal for
shoulder surgery. Sparing of distal branches, particularly the ulnar nerve, may occur. Supraclavicular perineural catheters provide inferior analgesia
compared with infraclavicular infusion and are
often displaced due to a lack of muscle mass to aid
catheter retention.
SCM
N
ASM
MSM
FIGURE 4612 Interscalene block.

Ultrasound image of the brachial plexus in
the interscalene groove. ASM, anterior scalene
muscle; MSM, middle scalene muscle; SCM,
sternocleidomastoid; N, brachial plexus nerve
roots in cross-section.
Morg_Ch46_0975-1022.indd 986
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987
Supraclavicular
Nerves or
plexus roots
C4
Trunks
C5
Divisions
C6
Cords
Upper
trunk
Main branches
ord
ral c
Late
ior
ster
cord
Po
C7
run
et
ddl
Mi
C8
Lower trunk
ord
T1
lc
edia
FIGURE 4613 A supraclavicular block can provide dense anesthesia for procedures at or distal to the elbow. Light
blue shading indicates regions of variable blockade; purple shading indicates regions of more reliable blockade.
Morg_Ch46_0975-1022.indd 987
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988
SECTION IV
Many of the same precautions that are taken

with patient selection for an interscalene block
should be exercised with a supraclavicular block.
Nearly half of patients undergoing supraclavicular block will experience ipsilateral phrenic nerve
palsy, although this incidence may be decreased by
using ultrasound guidance, allowing use of a minimal volume of local anesthetic. Horners syndrome
and recurrent laryngeal nerve palsy may also occur.
Pneumothorax and subclavian artery puncture,
although theoretically less likely under ultrasound
guidance, remain potential risks.
A. Ultrasound
The patient should be supine with the head turned
30o toward the contralateral side. A linear, highfrequency transducer is placed in the supraclavicular fossa superior to the clavicle and angled slightly
toward the thorax (Figure 4614). The subclavian
artery should be easily identified. The brachial plexus
appears as multiple hypoechoic disks just superficial
and lateral to the subclavian artery (Figure 4615).
The first rib should also be identified as a hyperechoic
line just deep to the artery. Pleura may be identified
adjacent to the rib, and can be distinguished from
bone by its movement with breathing.
For an out-of-plane technique, a short, 22-gauge
blunt-tipped needle is used. The skin is anesthetized, and the needle inserted just cephalad to the
ultrasound transducer in a posterior and caudad
FIGURE 4614 Ultrasound probe placement for

supraclavicular block (in-plane technique).
direction. After careful aspiration for the nonappearance of blood, 3040 mL of local anesthetic s
injected in 5-mL increments while visualizing local
anesthetic spread around the brachial plexus.
For an in-plane technique, a longer needle may
be necessary. The needle is inserted lateral to the
transducer in a direction parallel to the ultrasound
beam. The needle is advanced medially toward the
subclavian artery until the tip is visualized near the
brachial plexus just lateral and superficial to the
N
N
SA
N
R
FIGURE 4615 Supraclavicular block.

Ultrasound image of the brachial plexus in the
supraclavicular fossa. SA, subclavian artery;
R, rib; N, brachial plexus in cross-section.
Morg_Ch46_0975-1022.indd 988
11/02/13 6:17 PM
artery. Local anesthetic spread should be visualized

surrounding the plexus after careful aspiration and
incremental injection, which often requires injections in multiple locations and a highly variable volume (2030 mL).
Infraclavicular Block
5 Brachial plexus block at the level of the
cords provides excellent anesthesia for procedures at or distal to the elbow (Figure 4616).
The upper arm and shoulder are not anesthetized
with this approach. As with other brachial plexus
blocks, the intercostobrachial nerve (T2 dermatome) is spared. Site-specific risks of the infraclavicular approach include vascular puncture and
pneumothorax (although less common than with
supraclavicular block). It is often prudent to avoid
this approach in patients with vascular catheters in
the subclavian region, or patients with an ipsilateral pacemaker.
As the brachial plexus traverses beyond the first
rib and into the axilla, the cords are arranged around
the axillary artery according to their anatomic position: medial, lateral, and posterior.
The patient is positioned supine with the head turned
to the contralateral side, and the coracoid process is
identified (a bony prominence of the scapula that
can be palpated between the acromioclavicular
joint and the deltopectoral groove). The subclavian
artery and brachial plexus run deep to the coracoid process and can be found approximately 2 cm
medial and 2 cm caudad to it, about 45 cm deep
in the average patient (Figure 4617). A relatively
long (8cm) insulated needle is placed perpendicular to the skin and advanced directly posterior until
a motor response is elicited. An acceptable motor
response is finger flexion or extension at a current
less than 0.5mA, but not elbow flexion/extension.
B. Ultrasound
With the patient in the supine position, a small
curvilinear transducer is placed in the parasagittal plane over the point 2 cm medial and 2 cm
caudad to the coracoid process (Figure 4618A).
(Abducting the arm 90o improves axillary artery
imaging.) A high-frequency linear transducer will
Morg_Ch46_0975-1022.indd 989
989
often provide inadequate needle visualization due

to the relatively acute needle-to-transducer angle.
The axillary artery and vein are identified in crosssection (Figure 4618B). The medial, lateral, and
posterior cords appear as hyperechoic bundles positioned caudad, cephalad, and posterior to the artery,
respectively. A relatively long needle is inserted 23
cm cephalad to the transducer. Optimal needle
positioning is between the axillary artery and the
posterior cord. Three randomized, controlled trials
have demonstrated equivalent results with a single
30-mL injection adjacent to the posterior cord or
divided among each of the cords. Insertion of a
perineural catheter should always be in the same
location posterior to the axillary artery, and infraclavicular infusion has been shown to provide superior analgesia to both supraclavicular and axillary
catheters.
Axillary Block
At the lateral border of the pectoralis minor muscle,
the cords of the brachial plexus form large terminal
6 branches. The axillary, musculocutaneous,
and medial brachial cutaneous nerves branch
from the brachial plexus proximal to the location in
which local anesthetic is deposited during an axillary nerve block, and thus are usually spared
(Figure 4619). At this level, the major terminal
nerves often are separated by fascia; therefore multiple injections (10-mL each) may be required to
reliably produce anesthesia of the entire arm distal
to the elbow (Figure 4620).
There are few contraindications to axillary brachial plexus blocks. Local infection, neuropathy, and
bleeding risk must be considered. Because the axilla
is highly vascularized, there is a risk of local anesthetic uptake through small veins traumatized by
needle placement. The axilla is also a suboptimal site
for perineural catheter placement because of greatly
inferior analgesia versus an infraclavicular infusion,
as well as theoretically increased risks of infection
and catheter dislodgement.
All of the numerous axillary block techniques
require the patient to be positioned supine, with the
arm abducted 90o and the head turned toward the
contralateral side (Figure 4620). The axillary artery
pulse should be palpated and its location marked as
a reference point.
11/02/13 6:17 PM
990
SECTION IV
Infraclavicular
Nerves or
plexus roots
C4
Trunks
C5
Divisions
C6
Cords
Upper
trunk
Main branches
ord
ral c
Late
ior
ster
cord
Po
C7
run
et
ddl
Mi
C8
Lower trunk
ord
T1
lc
edia
FIGURE 4616 Infraclavicular block coverage and anatomy. Light blue shading indicates regions of variable blockade;
purple shading indicates regions of more reliable blockade.
Morg_Ch46_0975-1022.indd 990
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991
2 cm
2 cm
FIGURE 4617 Infraclavicular block using nerve stimulation: coracoid technique.
PMa
PMi
AV
N
N AA N
N
Morg_Ch46_0975-1022.indd 991
FIGURE 4618 Infraclavicular block. A: Use a small curvilinear

probe in a parasagittal plane to visualize the brachial plexus.
B: Ultrasound image of the brachial plexus surrounding the axillary
artery. AA, axillary artery; N, medial, lateral, and posterior cords of the
brachial plexus; AV, axillary vein; PMa, pectoralis major muscle; PMi,
pectoralis minor muscle. The red dot indicates the location of local
anesthetic deposition.
11/02/13 6:17 PM
992
SECTION IV
A. Transarterial Technique
This technique has fallen out of favor due to the
trauma of twice purposefully penetrating the axillary artery along with a theoretically increased risk
of inadvertent intravascular local anesthetic injection. The nondominant hand is used to palpate
and immobilize the axillary artery, and a 22-gauge
needle is inserted high in the axilla (Figure 4620)
until bright red blood is aspirated. The needle
is then slightly advanced until blood aspiration
ceases. Injection can be performed posteriorly,
anteriorly, or in both locations in relation to the
artery. A total of 3040 mL of local anesthetic is
typically used.
B. Nerve Stimulation
Again the nondominant hand is used to palpate
and immobilize the axillary artery. With the arm
abducted and externally rotated, the terminal nerves
usually lie in the following positions relative to
the artery (Figure 4621, although variations are

common): median nerve superior (wrist flexion,
thumb opposition, forearm pronation); ulnar nerve
inferior (wrist flexion, thumb adduction, fourth/
fifth digit flexion); and radial nerve inferiorposterior (digit/wrist/elbow extension, forearm supination). The musculocutaneous nerve (elbow flexion)
is separate and deep within the coracobrachialis
muscle, which is more superior (lateral) in this position and, as a consequence, is often not blocked with
this procedure (Figure 4621). A 2-in., 22-gauge
insulated needle is inserted proximal to the palpating fingers to elicit muscle twitches in the hand.
Once an acceptable muscle response is identified,
and after reducing the stimulation to less than 0.5
mA, careful aspiration is performed and local anesthetic is injected. Although a single injection of 40
mL may be used, greater success will be seen with
multiple nerve stimulations (ie, two or three nerves)
and divided doses of local anesthetic.
Musculocutaneous n.
Axillary n.
Medial brachial
cutaneous n.
FIGURE 4619 Axillary block. The axillary, musculocutaneous, and medial brachial cutaneous nerves are usually
spared with an axillary approach.
Morg_Ch46_0975-1022.indd 992
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993
FIGURE 4620 A: Patient positioning and needle angle for axillary brachial plexus block. B: A multiple injection
technique is more eective because of fascial separation between nerves.
Subcutaneous tissue
Skin
Intercostobrachial n.
Median n.
Brachial
plexus
Ulnar n.
Axillary a.
Radial n.
Biceps m.
Musculocutaneous n.
Axillary v.
Triceps m.
Coracobrachialis m.
FIGURE 4621 Positioning of terminal nerves about the axillary artery (variations are common).
Morg_Ch46_0975-1022.indd 993
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994
SECTION IV
U
AV
TM
M
AA
BM
MC
CB
Median n.
Brachial a.
FIGURE 4622 Ultrasound image of axillary brachial

plexus block. AA, Axillary artery; AV, axillary vein; U, ulnar
nerve; M, median nerve; MC, musculocutaneous nerve;
R, radial nerve; CB, coracobrachialis muscle; TM, triceps
muscle; BM, biceps muscle.
C. Ultrasound
Using a high-frequency linear array ultrasound
transducer, the axillary artery and vein are visualized in cross-section. The brachial plexus can be
identified surrounding the artery (Figure 4622).
The needle is inserted superior (lateral) to the transducer and advanced inferiorly (medially) toward the
plexus under direct visualization. Ten milliliters of
local anesthetic is then injected around each nerve
(including the musculocutaneous, if indicated).
Biceps tendon
Flexor carpi
radialis
Palmaris longus
Flexor digitorum
superficialis
Flexor digitorum
profundus
Palmar branch
Palmar
digital
nerves
Blocks of the Terminal Nerves

7 Often it is necessary to anesthetize a single ter-
minal nerve, either for minor surgical procedures with a limited field or as a supplement to an
incomplete brachial plexus block. Terminal nerves
may be anesthetized anywhere along their course, but
the elbow and the wrist are the two most favored sites.
FIGURE 4623 Median nerve course.
A. Median Nerve Block

The median nerve is derived from the lateral and
medial cords of the brachial plexus. It enters the
arm and runs just medial to the brachial artery
(Figure 4623). As it enters the antecubital space, it

lies medial to the brachial artery near the insertion
of the biceps tendon. Just distal to this point, it gives
off numerous motor branches to the wrist and finger
Morg_Ch46_0975-1022.indd 994
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995
flexors and follows the interosseous membrane to

the wrist. At the level of the proximal wrist flexion
crease, it lies directly behind the palmaris longus
tendon in the carpal tunnel.
To block the median nerve at the elbow, the
brachial artery is identified in the antecubital
crease just medial to the biceps insertion. A short
22-gauge insulated needle is inserted just medial
to the artery and directed toward the medial epicondyle until wrist flexion or thumb opposition is
elicited (Figure 4624); 35 mL of local anesthetic
is then injected. If ultrasound is used, the median
nerve may be identified in cross-section just medial
to the brachial artery and local anesthetic injected to
surround it (Figure 4625).
To block the median nerve at the wrist, the
palmaris longus tendon is first identified by asking the patient to flex the wrist against resistance.
A short 22-gauge needle is inserted just medial and
deep to the palmaris longus tendon, and 35 mL
Lateral
Medial
Brachial artery
Median nerve
Biceps
Medial epicondyle
Bicipital aponeurosis
Flexors
Dorsal
Palmar
FIGURE 4624 Median nerve block at the elbow.
Skin
Subcutaneous tissue
Biceps m.
Median n.
Brachial a.
Brachioradialis m.
Radial n.
Triceps m.
Brachialis m.
Humerus
FIGURE 4625 Cross-sectional anatomy of median nerve at the elbow.
Morg_Ch46_0975-1022.indd 995
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996
SECTION IV
Brachial a.
Ulnar n.
Medial
epicondyle
Biceps tendon
Arcuate
ligament
Ulnar a.
Radial a.
Flexor carpi
ulnaris
Flexor digitorum
profundus
Palmar
branch
Palmar
retinaculum
Median n.
Flexor carpi
radialis m.
Dorsal branch
Deep branch
Superficial branch
Palmaris
longus tendon
FIGURE 4626 Median nerve block at the wrist.

FIGURE 4627 Ulnar nerve course.
of local anesthetic is injected (Figure 4626). With
ultrasound, the median nerve may be identified at
the level of the mid-forearm between the muscle
bellies of the flexor digitorum profundus, flexor
digitorum superficialis, and flexor pollicis longus
(transducer faces perpendicular to the trajectory of
the nerves).
B. Ulnar Nerve Block

The ulnar nerve is the continuation of the medial
cord of the brachial plexus and maintains a position
medial to the axillary and brachial arteries in the
upper arm (Figure 4627). At the distal third of the
humerus, the nerve moves more medially and passes
under the arcuate ligament of the medial epicondyle.
The nerve is frequently palpable just proximal to the
medial epicondyle. In the mid-forearm, the nerve
Morg_Ch46_0975-1022.indd 996
lies between the flexor digitorum profundus and the

flexor carpi ulnaris. At the wrist, it is lateral to the
flexor carpi ulnaris tendon and medial to the ulnar
artery.
To block the ulnar nerve at the level of the
elbow, an insulated 22-gauge needle is inserted
approximately one fingerbreadth proximal to the
arcuate ligament (Figure 4628), and advanced
until fourth/fifth digit flexion or thumb adduction is
elicited; 35 mL of local anesthetic is then injected.
To block the ulnar nerve at the wrist, the ulnar artery
pulse is palpated just lateral to the flexor carpi ulnaris tendon. The needle is inserted just medial to the
artery (Figure 4629) and 35 mL of local anesthetic
is injected. If ultrasound is used, the ulnar nerve may
be identified just medial to the ulnar artery.
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997
Ulnar
nerve
Medial
epicondyle
Olecranon
process
Arcuate
ligament
Dorsal
Palmar
FIGURE 4628 Ulnar nerve block at the elbow with region of anesthesia illustrated on the hand.
Ulnar a.
Ulnar n.
Palmaris
longus tendon
Flexor carpi
ulnaris tendon
FIGURE 4629 Ulnar nerve block at the wrist.
Morg_Ch46_0975-1022.indd 997
C. Radial Nerve Block

The radial nervethe terminal branch of the posterior cord of the brachial plexuscourses posterior to the humerus, innervating the triceps muscle,
and enters the spiral groove of the humerus before
it moves laterally at the elbow (Figure 4630). Terminal sensory branches include the lateral cutaneous nerve of the arm and the posterior cutaneous
nerve of the forearm. After exiting the spiral groove
as it approaches the lateral epicondyle, the radial
nerve separates into superficial and deep branches.
The deep branch remains close to the periosteum
and innervates the postaxial extensor group of the
forearm. The superficial branch becomes superficial
and follows the radial artery to innervate the radial
aspects of the dorsal wrist and the dorsal aspect of
the lateral three digits and half of the fourth.
To block the radial nerve at the elbow, the
biceps tendon is identified in the antecubital fossa.
A short 22-gauge insulated needle is inserted just
lateral to the tendon and directed toward the lateral
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998
SECTION IV
Radial n.
Radial a.
Brachioradialis m.
Lateral
epicondyle
Deep branch
Flexor carpi
radialis m.
Posterior
interosseous n.
Superficial branch
Dorsal digital
nerves
FIGURE 4630 Radial nerve course.
epicondyle (Figure 4631) until wrist or finger

extension is elicited; 5 mL of local anesthetic is then
injected. With ultrasound, the radial nerve can be
identified in cross-section just proximal to the antecubital fossa between the biceps and brachioradialis
muscles.
At the wrist, the superficial branch of the radial
nerve lies just lateral to the radial artery, which can
be easily palpated lateral to the flexor carpi radialis tendon (Figure 4632). Using a short 22-gauge
needle, 35 mL local anesthetic is injected lateral to
the artery. Ultrasound may be used at the level of the
wrist or mid-forearm to identify the radial nerve just
lateral to the radial artery.
D. Musculocutaneous Nerve Block

A musculocutaneous nerve block is essential to
complete the anesthesia for the forearm and wrist
and is commonly included when performing the
axillary block. The musculocutaneous nerve is the
terminal branch of the lateral cord and the most
proximal of the major nerves to emerge from the
brachial plexus (Figure 4633). This nerve innervates the biceps and brachialis muscles and distally
terminates as the lateral antebrachial cutaneous
nerve, supplying sensory input to the lateral aspect
of the forearm and wrist.
Lateral
Medial
Brachialis m.
Biceps
Lateral
epicondyle
Median n.
Brachial a.
Radial n.
Brachioradialis m.
FIGURE 4631 Radial nerve block
Dorsal
Palmar
at the elbow.
Morg_Ch46_0975-1022.indd 998
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999
the coracobrachialis muscle is pierced, and 510 mL

of local anesthetic is injected, with or without elicitation of elbow flexion. (Simple infiltration may be
used, although the success rate using this technique
is questionable.) Ultrasound may be used to confirm the location of the musculocutaneous nerve in
the coracobrachialis muscle or between this muscle
and the biceps (see Figure 4622). Alternatively, the
block can be performed at the elbow as the nerve
courses superficially at the interepicondylar line.
The insertion of the biceps tendon is identified, and
a short 22-guage needle is inserted 12 cm laterally; 510 mL of local anesthetic is then injected as
a field block.
Radius
Radial nerve
Flexor carpi
radialis tendon
Ulnar styloid
process
Palmar longus
tendon
Radial artery
FIGURE 4632 Radial nerve block at the wrist.
To target the musculocutaneous nerve following an axillary block, the needle is redirected superior and proximal to the artery (see Figure 4621),
E. Digital Nerve Blocks

Digital nerve blocks are used for minor operations
on the fingers and to supplement incomplete brachial
plexus and terminal nerve blocks. Sensory innervation of each finger is provided by four small digital
nerves that enter each digit at its base in each of the
four corners (Figure 4634). A small-gauge needle is
inserted at the medial and lateral aspects of the base
of the selected digit, and 23 mL of local anesthetic
Dorsal
Digital
Palmar nerve
Musculocutaneous
nerve
Biceps muscle
Lateral antebrachial
cutaneous nerve
Coracobrachialis
muscle
Brachialis muscle
Anterior branch
Posterior branch
FIGURE 4633 Musculocutaneous nerve course.
Morg_Ch46_0975-1022.indd 999
FIGURE 4634 Sensory innervation of the ngers

is provided by the digital nerves.
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1000
SECTION IV
Skin wheal
T2
FIGURE 4636 Intercostobrachial nerve block.
FIGURE 4635 Intercostobrachial nerve cutaneous

innervation.
is inserted without epinephrine. Addition of a vasoconstrictor (epinephrine) has been claimed to seriously compromise blood flow to the digit; however,
there are no case reports involving lidocaine or other
modern local anesthetics to confirm this claim.
F. Intercostobrachial Nerve Block

The intercostobrachial nerve originates in the upper
thorax (T2) and becomes superficial on the medial
upper arm. It supplies cutaneous innervation to the
medial aspect of the proximal arm and is not anesthetized with a brachial plexus block (Figure 4635).
The patient should be supine with the arm abducted
and externally rotated. Starting at the deltoid prominence and proceeding inferiorly, a field block is
performed in a linear fashion using 5 mL of local
anesthetic, extending to the most inferior aspect of
the medial arm (Figure 4636).
intravenous catheter is usually inserted on the

dorsum of the hand (or foot) and a double pneumatic tourniquet is placed on the arm or thigh. The
extremity is elevated and exsanguinated by tightly
wrapping an Esmarch elastic bandage from a distal
to proximal direction. The proximal tourniquet is
inflated, the Esmarch bandage removed, and 0.5%
lidocaine (25mL for a forearm, 50 mL for an arm,
and 100mL for a thigh tourniquet) injected over 2
3 min through the catheter, which is subsequently
removed (Figure 4637). Anesthesia is usually
established after 510 min. Tourniquet pain usually
develops after 2030 min, at which time the distal
tourniquet is inflated and the proximal tourniquet
subsequently deflated. Patients usually tolerate
the distal tourniquet for an additional 1520 min
because it is inflated over an anesthetized area. Even
Intravenous Regional Anesthesia

8 Intravenous regional anesthesia, also called
a Bier block, can provide surgical anesthesia for short surgical procedures (4560 min)
on an extremity (eg, carpal tunnel release). An
Morg_Ch46_0975-1022.indd 1000
FIGURE 4637 Intravenous regional anesthesia

provides surgical anesthesia for procedures of short
duration.
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for surgical procedures of a very short duration, the

tourniquet must be left inflated for a total of at least
1520 min to avoid a rapid intravenous systemic
bolus of local anesthetic resulting in toxicity. Slow
deflation is also recommended to provide an additional margin of safety.
LOWER EXTREMITY
PERIPHERAL NERVE BLOCKS
Lumbar & Sacral Plexus Anatomy
The lumbosacral plexus provides innervation to
the lower extremities (Figure 4638). The lumbar
plexus is formed by the ventral rami of L14, with
occasional contribution from T12. It lies within
the psoas muscle with branches descending into
the proximal thigh. Three major nerves from the
1001
lumbar plexus make contributions to the lower

limb: the femoral (L24), lateral femoral cutaneous
(L13), and obturator (L24). These provide motor
and sensory innervation to the anterior portion of
the thigh and sensory innervation to the medial leg.
The sacral plexus arises from L45 and S14. The
posterior thigh and most of the leg and foot are supplied by the tibial and peroneal portions of the sciatic nerve. The posterior femoral cutaneous nerve
(S13), and not the sciatic nerve, provides sensory
innervation to the posterior thigh; it travels with
the sciatic nerve as it emerges around the piriformis muscle.
Femoral Nerve Block

The femoral nerve innervates the main hip flexors,
knee extensors, and provides much of the sensory
L1
L2
Inguinal nerve
L3
Genitofemoral nerve
L4
Lumbar plexus
L5
Lateral femoral
cutaneous nerve
S1
Femoral nerve
S3
S4
Sacral plexus
S2
Inguinal ligament
Sciatic nerve
Obturator nerve
FIGURE 4638 The ventral rami of L15 and S14 form the lumbosacral plexus, which provides innervation to the
lower extremities.
Morg_Ch46_0975-1022.indd 1001
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1002
SECTION IV
Lateral femoral
cutaneous nerve
Femoral nerve
Femoral nerve
Articular branch
Anterior femoral
cutaneous nerve
Quadriceps femoris
muscle
Obturator nerve
Rectus femoris muscle

(cut and reflected)
Vastus intermedius muscle
Vastus medialis muscle
Vastus lateralis muscle
Saphenous
nerve
FIGURE 4639 The femoral nerve provides sensory innervation to the hip and thigh, and to the medial leg via its
terminal branch, the saphenous nerve.
innervation of the hip and thigh (Figure 4639). Its

most medial branch is the saphenous nerve, which
innervates much of the skin of the medial leg and
ankle joint. The term 3-in-1 block refers to anesthetizing the femoral, lateral femoral cutaneous, and
obturator nerves with a single injection below the
inguinal ligament; this term has largely been abandoned as evidence accumulated demonstrating the
failure of most single injections to consistently affect
Morg_Ch46_0975-1022.indd 1002
9 all three nerves. A femoral nerve block alone
will seldom provide surgical anesthesia, but it

is often used to provide postoperative analgesia for
hip, thigh, knee, and ankle (for the saphenous nerve)
procedures. Femoral nerve blocks have a relatively
low rate of complications and few contraindications.
Local infection, previous vascular grafting, and local
adenopathy should be carefully considered in patient
selection.
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Anterior superior
iliac spine
1003
Femoral vein
Femoral artery
Lateral femoral
cutaneous nerve
Femoral nerve
Genitofemoral nerve
Inguinal
ligament
Pubic
symphysis
FIGURE 4640 Femoral block

using nerve stimulation.
With the patient positioned supine, the femoral artery
pulse is palpated at the level of the inguinal ligament. A
short (5-cm) insulated needle is inserted at a 45 angle
to the skin in a cephalad direction (Figure 4640)
until a clear quadriceps twitch is elicited at a current
below 0.5 mA (look for patella motion).
B. Ultrasound
A high-frequency linear ultrasound transducer is
placed over the area of the inguinal crease parallel to the crease itself, or slightly more transverse
(Figure 4641). The femoral artery and femoral
vein are visualized in cross-section, with the overlying fascia iliaca. Just lateral to the artery and deep to
the fascia iliaca, the femoral nerve appears in crosssection as a spindle-shaped structure with a honeycomb texture (Figure 4642).
For an out-of-plane technique, the block needle
is inserted just lateral to where the femoral nerve
is seen, and directed cephalad at an angle approximately 45 to the skin. The needle is advanced until
Morg_Ch46_0975-1022.indd 1003
it is seen penetrating the fascia iliaca, or (if using

concurrent electrical stimulation) until a motor
response is elicited. Following careful aspiration
for the nonappearance ofblood, 3040 mL of local
anesthetic is injected.
For an in-plane technique, a longer needle may
be used. The needle is inserted parallel to the ultrasound transducer just lateral to the outer edge. The
needle is advanced through the sartorius muscle,
deep to the fascia iliaca, until it is visualized just lateral to the femoral nerve. Local anesthetic is injected,
visualizing its hypoechoic spread deep to the fascia
iliaca and around the nerve.
C. Fascia Iliaca Technique

The goal of a fascia iliaca block is similar to that of
a femoral nerve block, but the approach is slightly
different. Without use of a nerve stimulator or
ultrasound machine, a relatively reliable level of
anesthesia may be attained simply with anatomic
landmarks and tactile sensation. Once the inguinal
ligament and femoral artery pulse are identified,
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1004
SECTION IV
SM
FV
FA
FN
IM
FIGURE 4642 Femoral nerve block. Ultrasound

image of the femoral nerve. FA, femoral artery; FV,
femoral vein; FN, femoral nerve; SM, Sartorius muscle;
IM, iliacus muscle.
local anesthetic is deposited under the fascia iliaca
between the two nerves which run in the same plane
between the fascia and underlying muscle.
Lateral Femoral
Cutaneous Nerve Block
FIGURE 4641 Ultrasound-guided femoral nerve

block (in-plane technique).
the length of the inguinal ligament is divided into
thirds (Figure 4643). Two centimeters distal to
the junction of the middle and outer thirds, a short,
blunt-tipped needle is inserted in a slightly cephalad
direction. As the needle passes through the two layers
of fascia in this region (fascia lata and fascia iliaca),
two pops will be felt. Once the needle has passed
through the fascia iliaca, careful aspiration is performed and 3040 mL of local anesthetic is injected.
This block usually anesthetizes both the femoral
nerve and lateral femoral cutaneous nerves, since the
Morg_Ch46_0975-1022.indd 1004
The lateral femoral cutaneous nerve provides sensory

innervation to the lateral thigh (see Figure 4639). It
may be anesthetized as a supplement to a femoral
nerve block or as an isolated block for limited anesthesia of the lateral thigh. As there are few vital structures in proximity to the lateral femoral cutaneous
nerve, complications with this block are exceedingly
rare. The lateral femoral cutaneous nerve (L23)
departs from the lumbar plexus, traverses laterally
from the psoas muscle, and courses anterolaterally along the iliacus muscle (see Figure 4638). It
emerges inferior and medial to the anterior superior
iliac spine to supply the cutaneous sensory innervation of the lateral thigh.
The patient is positioned supine or lateral, and
the point 2 cm medial and 2 cm distal to the anterior
superior iliac spine is identified. A short 22-gauge
block needle is inserted and directed laterally,
observing for a pop as it passes through the fascia
lata. A field block is performed with 1015 mL of
local anesthetic, which is deposited above and below
the fascia (Figure 4644).
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1005
Needle insertion point
FIGURE 4643 Fascia iliaca block.
2 cm
Femoral nerve
Anterior superior
iliac spine
Femoral vein
Femoral artery
Lateral femoral
cutaneous nerve
Genitofemoral nerve
Inguinal
ligament
FIGURE 4644 Lateral femoral

cutaneous nerve block.
Morg_Ch46_0975-1022.indd 1005
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1006
SECTION IV
L2
L3
L4
Obturator externus muscle
Adductor brevis muscle

Adductor longus muscle
Adductor magnus muscle

Gracilis muscle
FIGURE 4645 Obturator nerve innervation.
Obturator Nerve Block

A block of the obturator nerve is usually required
for complete anesthesia of the knee and is most
often performed in combination with femoral and
sciatic nerve blocks for this purpose. The obturator
nerve contributes sensory branches to the hip and
knee joints, a variable degree of sensation to the
medial thigh, and innervates the adductors of the
hip (Figure 4645). This nerve exits the pelvis and
enters the medial thigh through the obturator foramen, which lies beneath the superior pubic ramus.
After identification of the pubic tubercle, a long
(10-cm) block needle is inserted 1.5 cm inferior and
1.5cm lateral to the tubercle. The needle is advanced
Morg_Ch46_0975-1022.indd 1006
posteriorly until bone is contacted (Figure 4646).

Redirecting laterally and caudally, the needle is
advanced an additional 24 cm until a motor
response (thigh adduction) is elicited and maintained below 0.5 mA. Following careful aspiration
for the nonappearance of blood, 1520 mL of local
anesthetic is injected.
Posterior Lumbar Plexus

(Psoas Compartment) Block
10 Posterior lumbar plexus blocks are useful for
surgical procedures involving areas innervated by the femoral, lateral femoral cutaneous, and
obturator nerves (Figure 4647). These include
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1007
Obturator
nerve
Pubic ramus
Obturator
foramen
External
obturator
muscle
2
1
Obturator
nerve,
anterior
branch
Obturator
nerve,
posterior
branch
FIGURE 4646 Obturator nerve block.

Contact pubic tubercle (1), then redirect
laterally and caudally (2) until a motor
response is elicited.
Femoral nerve, lateral cutaneous

nerve of thigh, obturator nerve
Sciatic nerve, posterior femoral
cutaneous nerve
Needle insertion
point
Lateral femoral
cutaneous n.
Femoral n.
Obturator n.
FIGURE 4647 Lumbar plexus blocks provide anesthesia to the femoral, lateral femoral cutaneous, and
obturator nerves.
Morg_Ch46_0975-1022.indd 1007
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1008
SECTION IV
Inferior
vena cava
Ureter
Testicular/ovarian
vein and artery
Psoas muscle
FIGURE 4648 The lumbar plexus lies

in close proximity to several important
structures.
procedures on the hip, knee, and anterior thigh.

Complete anesthesia of the knee can be attained
with a proximal sciatic nerve block. The lumbar
plexus is relatively close to multiple sensitive structures (Figure 4648) and reaching it requires a very
long needle. Hence, the posterior lumbar plexus
block has one of the highest complication rates of
any peripheral nerve block; these include retroperitoneal hematoma, intravascular local anesthetic
injection with toxicity, intrathecal and epidural
injections, and renal capsular puncture with subsequent hematoma.
Lumbar nerve roots emerge into the body of
the psoas muscle and travel within the muscle compartment before exiting as terminal nerves (see
Figure 4638). Modern posterior lumbar plexus
blocks deposit local anesthetic within the body of
the psoas muscle. The patient is positioned in lateral
Morg_Ch46_0975-1022.indd 1008
Lumbar plexus
Spinal cord
decubitus with the side to be blocked in the nondependent position (Figure 4649). The midline is
palpated, identifying the spinous processes if possible. A line is first drawn through the lumbar spinous
processes, and both iliac crests are identified and
connected with a line to approximate the level of L4.
The posterior superior iliac spine is then palpated
and a line is drawn cephalad, parallel to the first line.
If available, ultrasound imaging of the transverse
process may be helpful to estimate lumbar plexus
depth. A long (10- to 15-cm) insulated needle is
inserted at the point of intersection between the
transverse (intercristal) line and the intersection of
the lateral and middle thirds of the two sagittal lines.
The needle is advanced in an anterior direction
until a femoral motor response is elicited (quadriceps contraction). If the transverse process is contacted, the needle should be withdrawn slightly
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1009
Curvilinear array
ultrasound transducer
Iliac crest
Posterior
superior
iliac spine
Needle entry
point
1/3
2/3
L4 L5
FIGURE 4649 Patient positioning and surface landmarks for posterior lumbar plexus block.
and walked off the transverse process in a caudal

direction, maintaining the needle in the parasagittal plane. The needle should never be inserted more
than 3 cm past the depth at which the transverse
process was contacted. Local anesthetic volumes
greater than 20 mL will increase the risk of bilateral
spread and contralateral limb involvement.
Morg_Ch46_0975-1022.indd 1009
Saphenous Nerve Block

The saphenous nerve is the most medial branch of
the femoral nerve and innervates the skin over the
medial leg and the ankle joint (see Figure 4639).
Therefore, this block is used mainly in conjunction with a sciatic nerve block to provide complete
anesthesia/analgesia below the knee.
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1010
SECTION IV
11 (see Figure 4638). Blockade of the sciatic
Tibial tuberosity
Line of injection
Lateral
Medial
FIGURE 4650 Proximal saphenous nerve block.
A. Trans-Sartorial Technique
The saphenous nerve may be accessed proximal
to the knee, just deep to the sartorius muscle. A
high-frequency linear probe is used to identify the
junction between the sartorius, vastus medialis,
and adductor muscles in cross-section just distal to
the adductor canal. A long needle is inserted from
medial to lateral (in-plane) or angled cephalad (outof-plane) and 510 mL of local anesthetic deposited
within this fascial plane.
nerve may occur anywhere along its course

and is indicated for surgical procedures involving
the hip, thigh, knee, lower leg, and foot. The posterior femoral cutaneous nerve is variably anesthetized as well, depending on the approach. If sacral
plexus or posterior femoral cutaneous nerve anesthesia is required, the parasacral approach is used
(a technique that is beyond the scope of this chapter).
A. Posterior (Classic or Labat) Approach

The patient is positioned laterally with the side
to be blocked in the nondependent position. The
patient is asked to bend the knee of the affected leg
and tilt the pelvis slightly forward (Sims position;
Figure 4651). The greater trochanter, posterior
superior iliac spine (PSIS), and sacral hiatus are then
identified. A line is drawn from the greater trochanter to the PSIS, its midpoint identified, and a perpendicular line extended in a caudal direction. Next,
a line is drawn from the greater trochanter to the
B. Proximal Saphenous Technique

A short block needle is inserted 2 cm distal to the
tibial tuberosity and directed medially, infiltrating
510 mL of local anesthetic as the needle passes
toward the posterior aspect of the leg (Figure 4650).
Ultrasound may be used to identify the saphenous
vein near the tibial tuberosity, facilitating a perivascular technique with infiltration about the vein.
C. Distal Saphenous Technique
The medial malleolus is identified, infiltrating 5mL
of local anesthetic in a line running anteriorly
around the ankle (see Ankle Block below).
Sciatic Nerve Block

The sciatic nerve originates from the lumbosacral
trunk and is composed of nerve roots L45 and S13
Morg_Ch46_0975-1022.indd 1010
Posterior
superior
iliac spine
5 cm
Sacral
hiatus
Greater
trochanter
FIGURE 4651 Patient positioning, surface landmarks,

and needle positioning for proximal sciatic nerve block
(classic approach).
11/02/13 6:17 PM
sacral hiatus and the intersection point is marked;

this is the initial needle insertion point. A long
(10-cm) insulated needle is inserted at an angle perpendicular to all planes to the skin (Figure 4651).
The needle is advanced through the gluteal muscles
(a motor response of these muscles may be encountered) until plantar- or dorsiflexion is elicited (plantarflexion or foot inversion is preferred for surgical
anesthesia). A local anesthetic volume of 25 mL provides surgical anesthesia.
B. Anterior Approach
After leaving the sciatic notch, the sciatic nerve
descends behind the lesser trochanter to a position
posterior to the femur. It can be accessed from the
anterior thigh just medial to the lesser trochanter.
Lateral or prone positioning may present a challenge
for some patients requiring a sciatic nerve block (ie,
elderly patients, pediatric patients under general
anesthesia). An anterior approach can be technically
challenging but offers an alternative path to the sciatic nerve. Before proceeding with this block, which
carries a risk of vascular puncture (femoral artery
and vein), patient-specific risks should be considered (eg, coagulopathy and vascular grafting). In
1011
addition, if combining this block with the femoral

nerve block in an unanesthetized patient, performing the sciatic block first is recommended to avoid
passing the block needle through a previously anesthetized femoral nerve. A local anesthetic volume of
25 mL provides surgical anesthesia.
1. Nerve stimulationWith the patient positioned
supine, a line is drawn along the inguinal ligament,
from the anterior superior iliac spine to the pubic
tubercle (Figure 4652). A second line is drawn parallel to the first that traverses the greater trochanter
(intertrochanteric line). Next, these two lines are
connected with a third line drawn from the point
between the medial one third and lateral two thirds
of the first line, at a 90 angle, and extended caudally
to intersect with the intertrochanteric line. A long
(10- to 15-cm) needle is inserted through this intersection and directly posterior until foot inversion
or plantarflexion is elicited (dorsiflexion is acceptable for postoperative analgesia). Often with this
approach, the femur is contacted before the needle
reaches the sciatic nerve. When this occurs, the needle should be withdrawn 23 cm, the patient should
be asked to internally rotate the leg, and then the
needle should be advanced. If the femur is contacted
Femoral artery
and vein
Anterior
superior
iliac spine
Pubic
tubercle
Greater
trochanter
Lesser
trochanter
Needle
insertion
point
FIGURE 4652 Anatomy and surface landmarks for anterior sciatic nerve block.
Morg_Ch46_0975-1022.indd 1011
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1012
SECTION IV
Greater trochanter
4 cm
Ischial tuberosity
FIGURE 4653 Patient positioning and surface landmarks for subgluteal sciatic block.
again, the landmarks may require reassessment. A

local anesthetic volume of 25 mL provides surgical
anesthesia.
2. UltrasoundWith the patient positioned supine
and the leg externally rotated, a low-frequency curvilinear transducer is placed transversely over the
medial thigh, approximately at the level of the lesser
trochanter. The femur, femoral vessels, adductor
muscles, and gluteus maximus are identified in crosssection. The elliptical, hyperechoic sciatic nerve is
found in the fascial plane between adductors and
gluteus muscles, posterior to the femur. Using a long
(10-cm) needle, the nerve is approached in-plane
(anterior to posterior) or out-of-plane (cephalad to
caudad), taking care to avoid femoral vessels, until
the needle tip lies in this muscle plane and a local
anesthetic injection can be observed as hypoechoic
spread surrounding the sciatic nerve.
C. Subgluteal Approach
A subgluteal approach to the sciatic nerve is a useful
alternative to the traditional posterior approach. In
many patients the landmarks are more easily identified, and less tissue is traversed. With the sciatic
nerve at a more superficial location, the exclusive
use of ultrasound becomes far more practical, as
well. If sciatic nerve block is being combined with
a femoral block and ambulation is desired within
the local anesthetic duration, consider a popliteal
approach (below) that will not affect the hamstring
muscles to the same degree, allowing knee flexion to
lift the foot with the use of crutches.
1. Nerve stimulationWith the patient in
Sims position, the greater trochanter and ischial
Morg_Ch46_0975-1022.indd 1012
tuberosity are identified and a line drawn between

them (Figure 4653). From the midpoint of this
line, a second line is drawn perpendicularly and
extended caudally 4 cm. Through this point a long
(10-cm) insulated needle is inserted directly slightly
cephalad until foot plantarflexion or inversion is
elicited (dorsiflexion is acceptable for analgesia). A
local anesthetic volume of 25 mL provides surgical
anesthesia.
2. UltrasoundUsing the same positioning and
landmarks (Figure 4653), a linear or low-frequency
curvilinear (best) ultrasound transducer is placed
over the midpoint between the ischial tuberosity
and the greater trochanter in a transverse orientation. Both bony structures should be visible in the
ultrasound field simultaneously. Gluteal muscles
are identified superficially, along with the fascial
layer defining their deep border. The triangular
sciatic nerve should be visible in cross-section just
deep to this layer in a location approximately midway between the ischial tuberosity and the greater
trochanter, superficial to the quadratus femoris
muscle.
For an out-of-plane ultrasound-guided sciatic
block, the block needle is inserted just caudad to
the ultrasound transducer and advanced in an anterior and cephalad direction. Once the needle passes
through the gluteus muscles with the tip next to
sciatic nerve, careful aspiration for the nonappearance of blood is performed and local anesthetic is
injected, visualizing spread around the nerve.
For an in-plane technique, the block needle is
inserted just lateral to the ultrasound transducer
near the greater trochanter. It is advanced through
11/02/13 6:17 PM
Semitendinosus m.
1013
Sciatic n.
Semimembranosus m.
Common peroneal n.
Tibial n.
Sural n.
Common
peroneal
nerve
Saphenous
nerve
Medial calcaneal
branches of
tibial nerve
Superficial
peroneal
nerve
Sural nerve
Deep peroneal
nerve
FIGURE 4654 The sciatic nerve divides into tibial and peroneal branches just proximal to the popliteal fossa and
provides sensory innervation to much of the lower leg.
the field of the ultrasound beam until the tip is visible deep to the gluteus maximus, next to the sciatic nerve. Again, local anesthetic spread around the
nerve should be visualized.
D. Popliteal Approach
12 Popliteal nerve blocks provide excellent coverage for foot and ankle surgery, while sparing
much of the hamstring muscles, allowing lifting of
the foot with knee flexion, thus easing ambulation.
All sciatic nerve blocks fail to provide complete
anesthesia for the cutaneous medial leg and ankle
joint capsule, but when a saphenous (or femoral)
Morg_Ch46_0975-1022.indd 1013
block is added, complete anesthesia below the knee

is provided. The major site-specific risk of a popliteal
block is vascular puncture, owing to the sciatic nerves
proximity to the popliteal vessels at this location.
The sciatic nerve divides into the tibial and
common peroneal nerves within or just proximal to
the popliteal fossa (Figure 4654). The upper popliteal fossa is bounded laterally by the biceps femoris tendon and medially by the semitendinosus and
semimembranosus tendons. Cephalad to the flexion
crease of the knee, the popliteal artery is immediately lateral to the semitendinosus tendon. The popliteal vein is lateral to the artery, and the tibial and
11/02/13 6:17 PM
1014
SECTION IV
common peroneal nerves are just lateral to the vein

and medial to the biceps tendon, 26 cm deep to
the skin. The tibial nerve continues deep behind the
gastrocnemius muscle, and the common peroneal
nerve leaves the popliteal fossa by passing between
the head and neck of the fibula to supply the lower
leg. The sciatic nerve is approached by either a posterior or a lateral approach. For posterior approaches,
the patient is usually positioned prone with the knee
slightly flexed by propping the ankle on pillows or
towels. For lateral approaches, the patient may be in
the lateral or supine position.
1. Nerve stimulation (posterior approach)With
the patient in the prone position, the apex of the
popliteal fossa is identified. The hamstring muscles
are palpated to locate the point where the biceps
femoris (lateral) and the semimembranosus/semitendinosus complex (medial) join (Figure 4655).
Having the patient flex the knee against resistance
facilitates recognition of these structures. The needle entry point is 1 cm caudad from the apex. An
insulated needle (510 cm) is advanced until foot
plantarflexion or inversion is elicited (dorsiflexion is
acceptable for analgesia). A volume of 3040 mL of
local anesthetic is often required for single-injection
poplitealsciatic nerve block.
2. Nerve stimulation (lateral approach)With
the patient in the supine position and the knee fully
extended, the intertendinous groove is palpated
between the vastus lateralis and biceps femoris
muscles approximately 10 cm proximal to the superior notch of the patella. A long (10-cm) insulated
needle is inserted at this point and advanced at a
30 angle posteriorly until an appropriate motor
response is elicited. If bone (femur) is contacted,
the needle is withdrawn and redirected slightly
posteriorly until an acceptable motor response is
encountered.
3. UltrasoundWith the patient positioned
prone, the apex of the popliteal fossa is identified,
as described above. Using a high-frequency linear
ultrasound transducer placed in a transverse orientation, the femur, biceps femoris muscle, popliteal
vessels, and sciatic nerve or branches are identified in cross-section (Figure 4655). The nerve is
usually posterior and lateral (or immediately posterior) to the vessels and is often located in close
Morg_Ch46_0975-1022.indd 1014
Proximal
Medial
Lateral
Distal
BFM
N
PV
PA
FIGURE 4655 Anatomy and sonoanatomy of the

sciatic nerve in the popliteal fossa. PA, popliteal artery;
PV, popliteal vein; N, sciatic nerve; BFM, biceps femoris
muscle; F, femur.
relationship to the bicepsfemoris muscle, just deep

to its medial edge.
For an out-of-plane technique, the needle is
inserted just caudad to the ultrasound transducer and
directed anteriorly and slightly cephalad. When the
needle is positioned in proximity to the sciatic nerve,
and following careful aspiration, local anesthetic
injected, observing for spread around the nerve.
11/02/13 6:17 PM
1015
For an in-plane technique, the block needle

is inserted lateral to the ultrasound transducer,
traversingor just anterior tothe biceps femoris
muscle (Figure 4656). The needle is advanced in
the ultrasound plane, while visualizing its approach
either deep or superficial to the nerve.
If surgical anesthesia is desired, local anesthetic
should be seen surrounding all sides of the nerve,
which usually requires multiple needle tip placements with incremental injection. For analgesia
alone, a single injection of local anesthetic is acceptable. Ultrasound-guided popliteal sciatic blocks
may be performed with the patient in the lateral or
supine positions (the latter with leg up-raised on
several pillows). These maneuvers are often more
technically challenging.
Ankle Block
For surgical procedures of the foot, an ankle block
is a fast, low-technology, low-risk means of providing anesthesia. Excessive injectate volume and use
of vasoconstrictors such as epinephrine must be
avoided to minimize the risk of ischemic complications. Since this block includes five separate injections, it is often uncomfortable for patients and
adequate premedication is required.
Five nerves supply sensation to the foot
(Figure 4657). The saphenous nerve is a terminal
branch of the femoral nerve and the only innervation
FIGURE 4656 Patient positioning, probe, and needle

orientation for popliteal block.
Common
peroneal
nerve
Saphenous
nerve
Superficial
peroneal
nerve
Medial calcaneal
branches of
tibial nerve
Sural nerve
Saphenous nerve
Sural nerve
Deep peroneal
nerve
Lateral plantar
nerve
Medial plantar
nerve
Medial calcaneal
branches
From
tibial
nerve
FIGURE 4657 Cutaneous innervation of the foot.
Morg_Ch46_0975-1022.indd 1015
11/02/13 6:17 PM
1016
SECTION IV
Tibial n.
Common
peroneal n.
Gastrocnemius m.
Peroneus longus
muscle (cut)
Extensor
digitorum
longus m.
Popliteus m.
Soleus m.
Superficial
peroneal n.
Deep
peroneal n.
Peroneus longus
and brevis m.
Tibialis posterior m.
Extensor hallucis
longus m.
Tibialis anterior m.
Flexor hallucis
longus m.
Tibial n.
FIGURE 4658 Tibial and common peroneal nerve courses.
of the foot not a part of the sciatic system. It supplies

superficial sensation to the anteromedial foot and is
most constantly located just anterior to the medial
malleolus. The deep peroneal nerve runs in the
anterior leg after branching off the common peroneal nerve, entering the ankle between the extensor
hallucis longus and the extensor digitorum longus
tendons (Figure 4658), just lateral to the dorsalis pedis artery. It provides innervation to the toe
extensors and sensation to the first dorsal webspace.
The superficial peroneal nerve, also a branch of the
common peroneal nerve, descends toward the ankle
in the lateral compartment, giving motor branches
Morg_Ch46_0975-1022.indd 1016
to the muscles of eversion. It enters the ankle just

lateral to the extensor digitorum longus and provides cutaneous sensation to the dorsum of the
foot and toes. The posterior tibial nerve is a direct
continuation of the tibial nerve and enters the foot
posterior to the medial malleolus, branching into
calcaneal, lateral plantar, and medial plantar nerves.
It is located behind the posterior tibial artery at the
level of the medial malleolus and provides sensory
innervation to the heel, the medial sole, and part of
the lateral sole of the foot, as well as the tips of the
toes. The sural nerve is a branch of the tibial nerve
and enters the foot between the Achilles tendon
11/02/13 6:17 PM
Tibialis anterior tendon

Deep peroneal nerve
Saphenous nerve
1017
Extensor hallucis
longus tendon
Superficial
peroneal nerve
Tibia
Fibula
Posterior tibial nerve

Achilles tendon
Sural nerve
FIGURE 4659 Needle placement for ankle block.
and the lateral malleolus to provide sensation to the

lateral foot.
13 A complete ankle block requires a series of five
nerve blocks, but the process may be streamlined to minimize needle insertions (Figure 4659).
All five injections are required to anesthetize the
entire foot; however, many surgical procedures
involve only a few terminal nerves, and only affected
nerves should be blocked. In addition, unlike a sciatic nerve block, an ankle block provides no analgesia for (below-the-knee) tourniquet pain, nor does it
allow for perineural catheter insertion. To block the
deep peroneal nerve, the groove between the extensor hallucis longus and extensor digitorum longus
tendons is identified. The dorsalis pedis pulse is
often palpable here. A short, small-gauge block needle is inserted perpendicular to the skin just lateral
to the pulse, bone is contacted, and 5 mL of local
anesthetic is infiltrated as the needle is withdrawn.
Continuing from this insertion site, a subcutaneous
wheal of 5 mL of local anesthetic is extended toward
the lateral malleolus to target the superficial peroneal nerve. The needle is withdrawn and redirected
from the same location in a medial direction, infiltrating 5 mL of local anesthetic toward the medial
malleolus to target the saphenous nerve. The posterior tibial nerve may be located by identifying the
Morg_Ch46_0975-1022.indd 1017
posterior tibial artery pulse behind the medial malleolus. A short, small-gauge block needle is inserted
just posterior to the artery and 5 mL of local anesthetic is distributed in the pocket deep to the flexor
retinaculum. To target the sural nerve, 5 mL of local
anesthetic is injected subcutaneously posterior to
the lateral malleolus.
PERIPHERAL NERVE
BLOCKS OF THE TRUNK
Supercial Cervical Plexus Block
The superficial cervical plexus block provides cutaneous analgesia for surgical procedures on the neck,
anterior shoulder, and clavicle. It is helpful to identify and avoid the external jugular vein. The cervical plexus is formed from the anterior rami of C14,
which emerge from the platysma muscle posterior to
the sternocleidomastoid (Figure 4660). It supplies
sensation to the jaw, neck, occiput, and areas of the
chest and shoulder.
The patient is positioned supine with the head
turned away from the side to be blocked. The sternocleidomastoid muscle is identified and its lateral
edge marked. At the junction of the upper and middle thirds, a short (5-cm) block needle is inserted,
11/02/13 6:18 PM
1018
SECTION IV
C2
C3
C4
FIGURE 4660 Distribution of the supercial cervical plexus.
directed cephalad toward the mastoid process,

and 5 mL of local anesthetic is injected in a subcutaneous plane. The needle is turned to advance
it in a caudad direction, maintaining a path along
the posterior border of sternocleidomastoid. An
additional 5 mL of local anesthetic is infiltrated
subcutaneously.
Intercostal Block
Intercostal blocks provide analgesia following thoracic and upper abdominal surgery, and relief of
pain associated with rib fractures, herpes zoster, and
cancer. These blocks require individual injections
delivered at the various vertebral levels that correspond to the area of body wall to be anesthetized.
14 Intercostal blocks result in the highest blood
levels of local anesthetic per volume injected
of any block in the body, and care must be taken to
avoid toxic levels of local anesthetic. The intercostal
block has one of the highest complication rates of
any peripheral nerve block due to the close proximity of the intercostal artery and vein (intravascular
local anesthetic injection), as well as underlying
pleura (pneumothorax). In addition, duration is
impressively short due to the high vascular flow, and
Morg_Ch46_0975-1022.indd 1018
placement of a perineural catheter is tenuous, at

best. With the advent of ultrasound guidance, the
paravertebral approach is rapidly replacing the
intercostal approach.
The intercostal nerves arise from the dorsal and
ventral rami of the thoracic spinal nerves. They exit
from the spine at the intervertebral foramen and
enter a groove on the underside of the corresponding rib, running with the intercostal artery and vein;
the nerve is generally the most inferior structure in
the neurovascular bundle (Figure 4661). Branches
are given off for sensation in a single dermatome
from the midline dorsally all the way to across the
midline ventrally.
With the patient in the lateral decubitus or
supine position, the level of each rib in the mid
and posterior axillary line is palpated and marked.
A small-gauge needle is inserted at the inferior
edge of each of the selected ribs, bone is contacted, and the needle is then walked off inferiorly (Figure 4661). The needle is redirected in a
slightly cephalad direction and advanced approximately 0.25cm. Following aspiration, observing for
blood or air, 35 mL of local anesthetic is injected
at each desired level.
11/02/13 6:18 PM
1019
Needle insertion
point
Intercostal nerve,
artery, and vein
FIGURE 4661 Anatomy and needle positioning for intercostal nerve block.
Paravertebral Block
Paravertebral blocks provide surgical anesthesia or
postoperative analgesia for procedures involving
the thoracic or abdominal wall, mastectomy, inguinal or abdominal hernia repair, and more invasive
unilateral procedures such as open nephrectomy.
Paravertebral blocks usually require individual
injections delivered at the various vertebral levels
that correspond to the area of body wall to be anesthetized. For example, a simple mastectomy would
require blocks at levels T36; for axillary node dissection, additional injections should be made from
C7 through T2. For inguinal hernia repair, blocks
should be performed at T10 through L2. Ventral
hernias require bilateral injections corresponding
to the level of the surgical site. The major complication of thoracic injections is pneumothorax,
whereas retroperitoneal structures may be at risk
with lumbar-level injections. Hypotension secondary to sympathectomy can be observed with
multilevel thoracic blocks. Unlike the intercostal
approach, long-acting local anesthetic will have a
nearly 24-hour duration, and perineural catheter
Morg_Ch46_0975-1022.indd 1019
insertion is a viable option (although local anesthetic spread from a single catheter to multiple levels is variable).
Each spinal nerve emerges from the intervertebral foramina and divides into two rami: a larger
anterior ramus, which innervates the muscles and
skin over the anterolateral body wall and limbs, and
a smaller posterior ramus, which reflects posteriorly
and innervates the skin and muscles of the back
15 and neck (Figure 4662). The thoracic paravertebral space is defined posteriorly by the
superior costotransverse ligament, anterolaterally by
the parietal pleura, medially by the vertebrae and the
intervertebral foramina, and inferiorly and superiorly by the heads of the ribs.
With the patient seated and vertebral column
flexed, each spinous process is palpated, counting
from the prominent C7 for thoracic blocks, and the
iliac crests as a reference for lumbar levels. From
the midpoint of the superior aspect of each spinous
process, a point 2.5 cm laterally is measured and
marked. In the thorax, the target nerve is located lateral to the spinous process above it, due to the steep
11/02/13 6:18 PM
1020
SECTION IV
2 1
Intervertebral
foramen
2.5 cm
Spinous
process
Transverse
process
Spinal nerve
Spinal cord
Pleura
Lung
FIGURE 4662 Paravertebral anatomy and traditional

approach. Contact transverse process (1), then redirect the
needle caudally (2) and advance 1 cm.
angulation of thoracic spinous processes (eg, the T4

nerve root is located lateral to the spinous process
of T3).
A. Traditional Technique
A pediatric Tuohy needle (20 gauge) is inserted at
each point and advanced perpendicular to the skin
(Figure 4662). Upon contact with the transverse
process, the needle is withdrawn slightly and redirected caudally an additional 1 cm (0.5 cm for lumbar placement). A pop or loss of resistance may be
felt as the needle passes through the costotransverse
ligament. Some practitioners use a loss-of-resistance
syringe to guide placement; others prefer use of a
nerve stimulator with chest wall motion for the end
point. Inject 5 mL of local anesthetic at each level.
The difficulty with this technique is that the depth
of the transverse process is simply estimated; thus
Morg_Ch46_0975-1022.indd 1020
the risk of pneumothorax is relatively high. Using

ultrasound to gauge transverse process depth prior
to needle insertion theoretically decreases the risk of
pneumothorax.
B. Ultrasound
An ultrasound transducer with a curvilinear array
is used, with the beam oriented in a parasagittal or
transverse plane. The transverse process, head of the
rib, costotransverse ligament, and pleura are identified. The paravertebral space may be approached
from a caudal-to-cephalad direction (parasagittal)
or a lateral-to-medial direction (transverse). It is
helpful to visualize the needle in-plane as it passes
through the costotransverse ligament and observe a
downward displacement of the pleura as local anesthetic is injected. At each level 5 mL of local anesthetic is injected.
11/02/13 6:18 PM
1021
External oblique muscle (cut)

Transversus abdominis muscle
Internal oblique muscle
Anterior and lateral cutaneous
branches of subcostal nerve (T12)
Anterior branch of
iliohypogastric nerve (L1)
Ilioinguinal nerve (L1)
Anterior cutaneous branch
of iliohypogastric nerve (L1)
Ilioinguinal nerve (L1)
FIGURE 4663 Transversus

abdominis plane (TAP)
anatomy.
Transversus Abdominis Plane Block

The transversus abdominis plane (TAP) block is
most often used to provide surgical anesthesia for
minor, superficial procedures on the lower abdominal wall, or postoperative analgesia for procedures
below the umbilicus. For hernia surgeries, intravenous or local supplementation may be necessary
to provide anesthesia during peritoneal traction.
Potential complications include violation of the
peritoneum with or without bowel perforation,
and the use of ultrasound is highly recommended
to minimize this risk.
16 The subcostal (T12), ilioinguinal (L1), and
iliohypogastric (L1) nerves are targeted in the
TAP block, providing anesthesia to the ipsilateral
Morg_Ch46_0975-1022.indd 1021
lower abdomen below the umbilicus (Figure 4663).

For part of their course, these three nerves travel in
the muscle plane between the internal oblique and
transversus abdominis muscles. Needle placement
should be between the two fascial layers of these
muscles, with local anesthetic filling the transversus
abdominis plane. The patient is ideally positioned in
lateral decubitus, but if mobility is limited the block
may be performed in the supine position.
A. Ultrasound
With a linear or curvilinear array transducer oriented parallel to the inguinal ligament, the layers of
the external oblique, internal oblique, and transversus abdominis muscles are identified just superior
11/02/13 6:18 PM
1022
SECTION IV
SQ
EO
IO
TAP
TA
FIGURE 4664 Ultrasound image of TAP block.

SQ, subcutaneous tissue; EO, external oblique; IO, internal
oblique; TA, transversus abdominis; TAP, transversus
abdominis plane.
to the anterior superior iliac spine (Figure 4664).

Muscles appear as striated hypoechoic structures
with hyperechoic layers of fascia at their borders.
A long (10-cm) needle is inserted in-plane just lateral (posterior) to the transducer and advanced,
noting tactile feedback from fascial planes, to the
hyperechoic effacement of the deep border of internal oblique and the superficial border of transversus abdominis. Following careful aspiration for the
nonappearance of blood, 20mL of local anesthetic
is injected, observing for an elliptical separation
between the two fascial layers (Figure 4664).
SUGGESTED READING
Capdevila X, Coimbra C, Choquet O: Approaches to
the lumbar plexus: Success, risks, and outcome. Reg
Anesth Pain Med 2005;30:150.
Morg_Ch46_0975-1022.indd 1022
Hadzic A (editor): Peripheral Nerve Blocks and Anatomy

for Ultrasound-guided Regional Anesthesia, 2nd ed.
McGraw-Hill Medical, 2012.
Hebl JR, Lennon RL (editors): Mayo Clinic Atlas of
Regional Anesthesia and Ultrasound-Guided Nerve
Blockade. Oxford University Press, 2010.
Heil JW, Ilfeld BM, Loland VJ, et al: Ultrasound-guided
transversus abdominis plane catheters and ambulatory
perineural infusions for outpatient inguinal hernia
repair. Reg Anesth Pain Med 2010;35:556.
Horn JL, Pitsch T, Salinas F, Benninger B: Anatomic basis
to the ultrasound-guided approach for saphenous
nerve blockade. Reg Anesth Pain Med 2009;34:486.
Ilfeld BM: Continuous peripheral nerve blocks:
A review of the published evidence. Anesth Analg
2011;113:904.
Ilfeld BM, Fredrickson MJ, Mariano ER: Ultrasoundguided perineural catheter insertion: Three
approaches, but little illuminating data. Reg Anesth
Pain Med 2010;35:123.
Mariano ER, Loland VJ, Sandhu NS, et al: Ultrasound
guidance versus electrical stimulation for femoral
perineural catheter insertion. J Ultrasound Med
2009;28:1453.
Perlas A, Brull R, Chan VW, et al: Ultrasound
guidance improves the success of sciatic nerve
block at the popliteal fossa. Reg Anesth Pain Med.
2008;33:259.
Perlas A, Chan VW, Simons M: Brachial plexus
examination and localization using ultrasound
and electrical stimulation: A volunteer study.
Anesthesiology 2003;99:429.
Sites BD, Brull R, Chan VW, et al: Artifacts and pitfall
errors associated with ultrasound-guided regional
anesthesia. Part I: Understanding the basic principles
of ultrasound physics and machine operations. Reg
Anesth Pain Med 2007;32: 412.
Sites BD, Brull R, Chan VW, et al: Artifacts and
pitfall errors associated with ultrasound-guided
regional anesthesia. Part II: A pictorial approach to
understanding and avoidance. Reg Anesth Pain Med.
2007;32:419.
11/02/13 6:18 PM
Anesthetic Complications
54
KEY CONCEPTS
1
The rate of anesthetic complications will

never be zero. All anesthesia practitioners,
irrespective of their experience, abilities,
diligence, and best intentions, will
participate in anesthetics that are
associated with patient injury.
Malpractice occurs when four
requirements have been met: (1) the
practitioner must have a duty to the
patient; (2) there must have been a breach
of duty (deviation from the standard of
care); (3) the patient (plainti ) must have
suered an injury; and (4) the proximate
cause of the injury must have been the
practitioners deviation from the standard
of care.
Anesthetic mishaps can be categorized

as preventable or unpreventable. Of
the preventable incidents, most involve
human error, as opposed to equipment
malfunctions.
The relative decrease in death attributed

to respiratory rather than cardiovascular
damaging events has been attributed to
the increased use of pulse oximetry and
capnometry.
Many anesthetic fatalities occur only after

a series of coincidental circumstances,
misjudgments, and technical errors coincide
(mishap chain).
Despite diering mechanisms, anaphylactic

and anaphylactoid reactions are typically
clinically indistinguishable and equally
life-threatening.
True anaphylaxis due to anesthetic agents

is rare; anaphylactoid reactions are much
more common. Muscle relaxants are the
most common cause of anaphylaxis during
anesthesia.
Patients with spina bida, spinal cord

injury, and congenital abnormalities of the
genitourinary tract have a very increased
incidence of latex allergy. The incidence of
latex anaphylaxis in children is estimated
to be 1 in 10,000.
Although there is no clear evidence that

exposure to trace amounts of anesthetic
agents presents a health hazard to
operating room personnel, the United
States Occupational Health and Safety
Administration continues to set maximum
acceptable trace concentrations of less
than 25 ppm for nitrous oxide and 0.5 ppm
for halogenated anesthetics (2 ppm if the
halogenated agent is used alone).
10 Hollow (hypodermic) needles pose a greater
risk than do solid (surgical) needles because

of the potentially larger inoculum. The use
of gloves, needleless systems, or protected
needle devices may decrease the incidence
of some (but not all) types of injury.
Continued next page
1199
Morg_Ch54_1199-1230.indd 1199
11/02/13 10:40 AM
1200
SECTION V
Perioperative & Critical Care Medicine
Continued
11 Anesthesiology is a high-risk medical
specialty for substance abuse.

12 The three most important methods of
minimizing radiation doses are limiting total
1 The rate of anesthetic complications will never
be zero. All anesthesia practitioners, irrespective of their experience, abilities, diligence, and best
intentions, will participate in anesthetics that are associated with patient injury. Moreover, unexpected
adverse perioperative outcomes can lead to litigation,
even if those outcomes did not directly arise from anesthetic mismanagement. This chapter reviews management approaches to complications secondary to
anesthesia and discusses medical malpractice and
legal issues from an American (USA) perspective.
Readers based in other countries may not find this
section to be as relevant to their practices.
LITIGATION AND ANESTHETIC

COMPLICATIONS
All anesthesia practitioners will have patients with
adverse outcomes, and in the USA most anesthesiologists will at some point in their career be involved
to one degree or another in malpractice litigation.
Consequently, all anesthesia staff should expect
litigation to be a part of their professional lives and
acquire suitably solvent medical malpractice insurance with coverage appropriate for the community
in which they practice.
When unexpected events occur, anesthesia staff
must generate an appropriate differential diagnosis,
seek necessary consultation, and execute a treatment plan to mitigate (to the greatest degree possible) any patient injury. Appropriate documentation
in the patient record is helpful, as many adverse
outcomes will be reviewed by facility-based and
practice-based quality assurance and performance
improvement authorities. Deviations from acceptable practice will likely be noted in the practitioners
Morg_Ch54_1199-1230.indd 1200
exposure time during procedures,

using proper barriers, and maximizing
ones distance from the source of
radiation.
quality assurance file. Should an adverse outcome

lead to litigation, the medical record documents
the practitioners actions at the time of the incident.
Often years pass before litigation proceeds to the
point where the anesthesia provider is asked about
the case in question. Although memories fade, a
clear and complete anesthesiology record can provide convincing evidence that a complication was
recognized and appropriately treated.
A lawsuit may be filed, despite a physicians best
efforts to communicate with the patient and family
about the intraoperative events, management decisions, and the circumstances surrounding an adverse
event. It is often not possible to predict which cases
will be pursued by plaintiffs! Litigation may be pursued when it is clear (at least to the defense team)
that the anesthesia care conformed to standards,
and, conversely, that suits may not be filed when
there is obvious anesthesia culpability. That said,
anesthetics that are followed by unexpected death,
paralysis, or brain injury of young, economically
productive individuals are particularly attractive to
plaintiff s lawyers. When a patient has an unexpectedly poor outcome, one should expect litigation
irrespective of ones positive relationship with the
patient or the injured patients family or guardians.
2 Malpractice occurs when four requirements
are met: (1) the practitioner must have a duty
to the patient; (2) there must have been a breach of
duty (deviation from the standard of care); (3) the
patient (plaintiff ) must have suffered an injury; and
(4) the proximate cause of the injury must have been
the practitioners deviation from the standard of care.
A duty is established when the practitioner has an
obligation to provide care (doctorpatient relationship). The practitioners failure to execute that duty
11/02/13 10:40 AM
CHAPTER 54 Anesthetic Complications
constitutes a breach of duty. Injuries can be physical, emotional, or financial. Causation is established;
if but for the breach of duty, the patient would not
have experienced the injury. When a claim is meritorious, the tort system attempts to compensate the
injured patient and/or family members by awarding
them monetary damages.
Being sued is stressful, regardless of the perceived merits of the claim. Preparation for defense
begins before an injury has occurred. Anesthesiology staff should carefully explain the risks and benefits of the anesthesia options available to the patient.
The patient grants informed consent following a
discussion of the risks and benefits. Informed consent does not consist of handing the patient a form
to sign. Informed consent requires that the patient
understand the choices being presented. As previously noted, appropriate documentation of patient
care activities, differential diagnoses, and therapeutic interventions helps to provide a defensible
record of the care that was provided, resistant to
the passage of time and the stress of the litigation
experience.
When an adverse outcome occurs, the hospital
and/or practice risk management group should be
immediately notified. Likewise, ones liability insurance carrier should be notified of the possibility of a
claim for damages. Some policies have a clause that
disallows the practitioner from admitting errors to
patients and families. Consequently, it is important
to know and obey the institutions and insurers
approach to adverse outcomes. Nevertheless, most
risk managers advocate a frank and honest disclosure of adverse events to patients or approved family
members. It is possible to express sorrow about an
adverse outcome without admitting guilt. Ideally,
such discussions should take place in the presence of
risk management personnel and/or a departmental
leader.
It must never be forgotten that the tort system
is designed to be adversarial. Unfortunately, this
makes every patient a potential courtroom adversary. Malpractice insurers will hire a defense firm
to represent the anesthesia staff involved. Typically,
multiple practitioners and the hospitals in which
they work will be named to involve the maximal
number of insurance policies that might pay in the
Morg_Ch54_1199-1230.indd 1201
1201
event of a plaintiff s victory, and to ensure that the

defendants cannot choose to attribute blame for
the adverse event to whichever person or entity
was not named in the suit. In some systems (usually when everyone in a health system is insured
by the same carrier), all of the named entities are
represented by one defense team. More commonly,
various insurers and attorneys represent specific
practitioners and institutional providers. In this
instance, those involved may deflect and diffuse
blame from themselves and focus blame on others
also named in the action. One should not discuss
elements of any case with anyone other than a risk
manager, insurer, or attorney, as other conversations
are not protected from discovery. Discovery is the
process by which the plaintiff s attorneys access the
medical records and depose witnesses under oath
to establish the elements of the case: duty, breach,
injury, and causation. False testimony can lead to
criminal charges of perjury.
Oftentimes, expediency and financial risk exposure will argue for settlement of the case. The practitioner may or may not be able to participate in
this decision depending upon the insurance policy.
Settled cases are reported to the National Practitioner Data Bank and become a part of the physicians
record. Moreover, malpractice suits, settlements, and
judgments must be reported to hospital authorities
as part of the credentialing process. When applying for licensure or hospital appointment, all such
actions must be reported. Failure to do so can lead
to adverse consequences.
The litigation process begins with the delivery
of a summons indicating that an action is pending.
Once delivered, the anesthesia defendant must contact his or her malpractice insurer/risk management
department, who will appoint legal counsel. Counsel
for both the plaintiff and defense will identify independent experts to review the cases. These experts
are paid for their time and expenses and can arrive at
dramatically different assessments of the case materials. Following review by expert consultants, the
plaintiff s counsel may depose the principal actors
involved in the case. Providing testimony can be
stressful. Generally, one should follow the advice of
ones defense attorney. Oftentimes, plaintiff s attorneys will attempt to anger or confuse the deponent,
11/02/13 10:40 AM
1202
SECTION V
hoping to provoke a response favorable to the claim.

Most defense attorneys will advise their clients to
answer questions as literally and simply as possible,
without offering extraneous commentary. Should
the plaintiff s attorney become abusive, the defense
attorney will object for the record. However, depositions, also known as examinations before trial, are
not held in front of a judge (only the attorneys, the
deponent, the court reporter[s], and [sometimes]
the videographer are present). Obligatory small
talk often occurs among the attorneys and the court
reporters. This is natural and should not be a source
of anxiety for the defendant, because in most localities, the same plaintiff s and defense attorneys see
each other regularly.
Following discovery, the insurers, plaintiffs, and
defense attorneys will value the case and attempt to
monetize the damages. Items, such as pain and suffering, loss of consortium with spouses, lost wages,
and many other factors, are included in determining
what the injury is worth. Also during this period,
the defense attorney may petition the court to grant
defendants a summary judgment, dismissing the
defendant from the case if there is no evidence of
malpractice elicited during the discovery process. At
times, the plaintiff s attorneys will dismiss the suit
against certain named individuals after they have
testified, particularly when their testimony implicates other named defendants.
Settlement negotiations will occur in nearly
every action. Juries are unpredictable, and both
parties are often hesitant to take a case to trial.
There are expenses associated with litigation, and,
consequently, both plaintiff and defense attorneys
will try to avoid uncertainties. Many anesthesia
providers will not want to settle a case because
the settlement must be reported. Nonetheless, an
award in excess of the insurance policy maximum
may (depending on the jurisdiction) place the
personal assets of the defendant providers at risk.
This underscores the importance of our advice
to all practitioners (not only those involved in a
lawsuit) to assemble their personal assets (house,
retirement fund, etc.) in a fashion that makes personal asset confiscation difficult in the event of a
negative judgment. One should remember that an
adverse judgment may arise from a case in which
Morg_Ch54_1199-1230.indd 1202
most anesthesiologists would find the care to meet

acceptable standards!
When a case proceeds to trial, the first step is
jury selection in the process of voir direfrom the
Frenchto see, to say. In this process, attorneys
for the plaintiff and defendant will use various profiling techniques to attempt to identify (and remove)
jurors who are less likely to be sympathetic to their
case, while keeping the jurors deemed most likely
to favor their side. Each attorney is able to strike a
certain number of jurors from the pool because they
perceive an inherent bias. The jurors will be questioned about such matters as their educational level,
history of litigation themselves, professions, and so
forth.
Following empanelment, the case is presented
to the jury. Each attorney attempts to educate the
jurorswho usually have limited knowledge of
healthcare (physicians and nurses will usually be
struck from the jury)as to the standard of care for
this or that procedure and how the defendants did
or did not breach their duty to the patient to uphold
those standards. Expert witnesses will attempt to
define what the standard of care is for the community, and the plaintiff and defendant will present
experts with views that are favorable to their respective cause. The attorneys will attempt to discredit
the opponents experts and challenge their opinions.
Exhibits are often used to explain to the jury what
should or should not have happened and why the
injuries for which damages are being sought were
caused by the practitioners negligence.
After the attorneys conclude their closing
remarks, the judge will charge the jurors with their
duty and will delineate what they can consider in
making their judgment. Once a case is in the hands
of a jury, anything can happen. Many cases will settle during the course of the trial, as neither party
wishes to be subject to the arbitrary decisions of an
unpredictable jury. Should the case not settle, the
jurors will reach a verdict. When a jury determines
that the defendants were negligent and negligence
was the cause of the plaintiff s injuries, the jury
will determine an appropriate award. If the award
is so egregiously large that it is inconsistent with
awards for similar injuries, the judge may reduce its
amount. Of course, following any verdict, there are
11/02/13 10:40 AM
numerous appeals that may be filed. It is important

to note that appeals typically do not relate to the
medical aspects of the case, but are filed because the
trial process itself was somehow flawed.
Unfortunately, a malpractice action can take
years to reach a conclusion. Consultation with a
mental health professional may be appropriate for
the defendant when the litigation process results in
unmanageable stress, depression, increased alcohol
consumption, or substance abuse.
Determining what constitutes the standard
of care is increasingly complicated. In the United
Sates, the definition of standard of care is made
separately by each state. The standard of care is NOT
necessarily best practices or even the care that
another physician would prefer. Generally, the standard of care is met when a patient receives carethat
other reasonable physicians in similar circumstances
would regard as adequate. The American Society of
Anesthesiologists (ASA) has published standards,
and these provide a basic framework for routine
anesthetic practice (eg, monitoring). Increasingly, a
number of guidelines have been developed by the
multiple specialty societies to identify best practices
in accordance with assessments of the evidence in the
literature. The increasing number of guidelines proffered by the numerous anesthesia and other societies and their frequent updating can make it difficult
for clinicians to stay abreast of the changing nature
of practice. This is a particular problem when two
societies produce conflicting guidelines on the same
topic using the same data. Likewise, the information
upon which guidelines are based can range from
randomized clinical trials to the opinion of experts
in the field. Consequently, guidelines do not hold the
same weight as standards. Guidelines produced by
reputable societies will generally include an appropriate disclaimer based on the level of evidence used
to generate the guideline. Nonetheless, plaintiff s
attorneys will attempt to use guidelines to establish
a standard of care, when, in fact, clinical guidelines are prepared to assist in guiding the delivery
of therapy. However, if deviation from guidelines is
required for good patient care, the rationale for such
actions should be documented on the anesthesia
record, as plaintiff s attorneys will attempt to use the
guideline as a de facto standard of care.
Morg_Ch54_1199-1230.indd 1203
1203
ADVERSE ANESTHETIC
OUTCOMES
Incidence
There are several reasons why it is difficult to
accurately measure the incidence of adverse
anesthesia-related outcomes. First, it is often difficult
to determine whether the cause of a poor outcome is
the patients underlying disease, the surgical procedure, or the anesthetic management. In some cases,
all three factors contribute to a poor outcome. Clinically important measurable outcomes are relatively
rare after elective anesthetics. For example, death is
a clear endpoint, and perioperative deaths do occur
with some regularity. But, because deaths attributable to anesthesia are much rarer, a very large series
of patients must be studied to assemble conclusions
that have statistical significance. Nonetheless, many
studies have attempted to determine the incidence
of complications due to anesthesia. Unfortunately,
studies vary in criteria for defining an anesthesiarelated adverse outcome and are limited by retrospective analysis.
Perioperative mortality is usually defined as
death within 48 hr of surgery. It is clear that most
perioperative fatalities are due to the patients preoperative disease or the surgical procedure. In a study
conducted between 1948 and 1952, anesthesia mortality in the United States was approximately 5100
deaths per year or 3.3 deaths per 100,000 population. A review of cause of death files in the United
States showed that the rate of anesthesia-related
deaths was 1.1/1,000,000 population or 1 anesthetic
death per 100,000 procedures between 1999 and
2005 (Figure 541). These results suggest a 97%
decrease in anesthesia mortality since the 1940s.
However, a 2002 study reported an estimated rate
of 1 death per 13,000 anesthetics. Due to differences
in methodology, there are discrepancies in the literature as to how well anesthesiology is doing in
achieving safe practice. In a 2008 study of 815,077
patients (ASA class 1, 2, or 3) who underwent elective surgery at US Department of Veterans Affairs
hospitals, the mortality rate was 0.08% on the day
of surgery. The strongest association with perioperative death was the type of surgery (Figure 542).
Other factors associated with increased risk of death
11/02/13 10:40 AM
1204
SECTION V
Deaths/million surgical discharges
25
20
15
10
04
514
1524 2534 3544 4554 5564 6574 7584
85
Age (years)
FIGURE 541 Annual in-hospital anesthesia-related

deaths rates per million hospital surgical discharges and
95% condence intervals by age, United States, 1999-2005.
(Reproduced, with permission, from Li G, Warner M, Lang B, et al:

Epidemiology of anesthesia-related mortality in the United States
1999-2005. Anesthesiology 2009;110:759.)
included dyspnea, reduced albumin concentrations,

increased bilirubin, and increased creatinine concentrations. A subsequent review of the 88 deaths
that occurred on the surgical day noted that 13 of
the patients might have benefitted from better anesthesia care, and estimates suggest that death might
have been prevented by better anesthesia practice in
1 of 13,900 cases. Additionally, this study reported
Spine
Intracranial
Urologic
Abdominal
Head/Neck
Other Vasc.
Aortic
Thoracic
Bone
0
20
40
60
80
100
120
140
160
Number of deaths
FIGURE 542 Total number of deaths by type of surgery in Veterans Aairs hospitals. (Reproduced, with permission, from
Bishop M, Souders J, Peterson C, et al: Factors associated with unanticipated day of surgery deaths in Department of Veterans Aairs hospitals.
Anesth Analg 2008;107:1924.)
Morg_Ch54_1199-1230.indd 1204
11/02/13 10:40 AM
that the immediate postsurgical period tended to

be the time of unexpected mortality. Indeed, often
missed opportunities for improved anesthetic care
occur following complications when failure to rescue contributes to patient demise.
American Society of
Anesthesiologists Closed
Claims Project
The goal of the ASA Closed Claims Project is to
identify common events leading to claims in anesthesia, patterns of injury, and strategies for injury
prevention. It is a collection of closed malpractice
claims that provides a snapshot of anesthesia liability rather than a study of the incidence of anesthetic
complications, as only events that lead to the filing
of a malpractice claim are considered. The Closed
Claims Project consists of trained physicians who
review claims against anesthesiologists represented
by some US malpractice insurers. The number of
claims in the database continues to rise each year as
new claims are closed and reported. The claims are
grouped according to specific damaging events and
complication type. Closed Claims Project analyses
have been reported for airway injury, nerve injury,
awareness, and so forth. These analyses provide
insights into the circumstances that result in claims;
however, the incidence of a complication cannot
be determined from closed claim data, because we
know neither the actual incidence of the complication (some with the complication may not file suit),
nor how many anesthetics were performed for which
the particular complication might possibly develop.
Other similar analyses have been performed in the
United Kingdom, where National Health Service
(NHS) Litigation Authority claims are reviewed.
Causes
1205
TABLE 541 Human errors that may lead

to preventable anesthetic accidents.
Unrecognized breathing circuit disconnection
Mistaken drug administration
Airway mismanagement
Anesthesia machine misuse
Fluid mismanagement
Intravenous line disconnection
malfunctions (Table 542). Unfortunately, some

rate of human error is inevitable, and a preventable accident is not necessarily evidence of incompetence. During the 1990s, the top three causes for
claims in the ASA Closed Claims Project were death
(22%), nerve injury (18%), and brain damage (9%).
In a 2009 report based on an analysis of NHS litigation records, anesthesia-related claims accounted
for 2.5% of total claims filed and 2.4% of the value
of all NHS claims. Moreover, regional and obstetrical anesthesia were responsible for 44% and 29%,
respectively, of anesthesia-related claims filed. The
authors of the latter study noted that there are two
ways to examine data related to patient harm: critical
incident and closed claim analyses. Clinical (or critical) incident data consider events that either cause
harm or result in a near-miss. Comparison between
clinical incident datasets and closed claims analyses
demonstrates that not all critical events generate
claims and that claims may be filed in the absence of
negligent care. Consequently, closed claims reports
must always be considered in this context.
MORTALITY AND
BRAIN INJURY
Trends in anesthesia-related death and brain damage have been tracked for many years. In a Closed
Claims Project report examining claims in the
3 Anesthetic mishaps can be categorized as
preventable or unpreventable. Examples of

the latter include sudden death syndrome, fatal
idiosyncratic drug reactions, or any poor outcome
that occurs despite proper management. However, studies of anesthetic-related deaths or near
misses suggest that many accidents are preventable. Of these preventable incidents, most involve
human error (Table 541), as opposed to equipment
Morg_Ch54_1199-1230.indd 1205
TABLE 542 Equipment malfunctions that

may lead to preventable anesthetic accidents.
Breathing circuit
Monitoring device
Ventilator
Anesthesia machine
Laryngoscope
11/02/13 10:40 AM
1206
SECTION V
# of claims per year
A
400
300
200
100
0
1975
1980
1985
1975
1980
1985
1990
1995
2000
% per year
B
60
40
20
0
1990
1995
2000
p<0.01 over years (logistic regression)
FIGURE 543 A: The total number of claims by the

year of injury. Retrospective data collection began in
1985. Data in this analysis includes data collected through
December 2003. B: Claims for death or permanent brain
damage as percentage of total claims per year by year of

injury. (Reproduced, with permission, from Cheney FW, Domino KB,
period between 1975 and 2000, there were 6750

claims (Figure 543A and B), 2613 of which were
for brain injury or death. The proportion of claims
for brain injury or death was 56% in 1975, but had
decreased to 27% by 2000. The primary pathological
mechanisms by which these outcomes occurred
were related to cardiovascular or respiratory problems. Early in the study period, respiratory-related
damaging events were responsible for more than
50% of brain injury/death claims, whereas cardiovascular-related damaging events were responsible
for 27% of such claims; however, by the late 1980s,
the percentage of damaging events related to respiratory issues had decreased, with both respiratory
and cardiovascular events being equally likely to
contribute to severe brain injury or death. Respiratory damaging events included difficult airway,
esophageal intubation, and unexpected extubation.
Cardiovascular damaging events were usually multifactorial. Closed claims reviewers found that anesthesia care was substandard in 64% of claims in
which respiratory complications contributed to
brain injury or death, but in only 28% of cases in
which the primary mechanism of patient injury was

cardiovascular in nature. Esophageal intubation,
premature extubation, and inadequate ventilation
were the primary mechanisms by which less than
optimal anesthetic care was thought to have contributed to patient injury related to respiratory events.
4 The relative decrease in causes of death being
attributed to respiratory rather cardiovascular
damaging events during the review period was
attributed to the increased use of pulse oximetry and
capnometry. Consequently, if expired gas analysis
was judged to be adequate, and a patient suffered
brain injury or death, a cardiovascular event was
more likely to be considered causative.
A 2010 study examining the NHS Litigation Authority dataset noted that airway-related
claims led to higher awards and poorer outcomes
than did nonairway-related claims. Indeed, airway
manipulation and central venous catheterization
claims in this database were most associated with
patient death. Trauma to the airway also generates
significant claims if esophageal or tracheal rupture
occur. Postintubation mediastinitis should always
Morg_Ch54_1199-1230.indd 1206
Caplan RA, Posner KL: Nerve injury associated with anesthesia: a closed
claims analysis. Anesthesiology 1999;90:1062.)
11/02/13 10:40 AM
1207
Swelling/
inflammation/
infection
17%
Nerve damage
17%
Skin slough
or necrosis
28%
Burns from
treatment of
IV infiltration
3%
Frivolous
6%
Fasciotomy scar
16%
Miscellaneous
6%
Air embolism
8%
be considered whenever there are repeated unsuccessful airway manipulations, as early intervention
presents the best opportunity to mitigate any injuries incurred.
VASCULAR CANNULATION
Claims related to central venous access in the ASA
database were associated with patient death 47% of
the time and represented 1.7% of the 6449 claims
reviewed. Complications secondary to guidewire or
catheter embolism, tamponade, bloodstream infections, carotid artery puncture, hemothorax, and pneumothorax all contributed to patient injury. Although
guidewire and catheter embolisms were associated
with generally lower level patient injuries, these complications were generally attributed to substandard
care. Tamponade claims following line placement
were often for patient death. The authors of a 2004
closed claims analysis recommended reviewing the
chest radiograph following line placement and repositioning lines found in the heart or at an acute angle
to reduce the likelihood of tamponade. Brain damage
and stroke are associated with claims secondary to
carotid cannulation. Multiple confirmatory methods
should be used to ensure that the internal jugular and
not the carotid artery is cannulated.
Claims related to peripheral vascular cannulation in the ASA database accounted for 2% of
6849 claims, 91% of which were for complications
secondary to the extravasation of fluids or drugs
Morg_Ch54_1199-1230.indd 1207
FIGURE 544 Injuries related to

IV catheters (n = 127). (Reproduced, with
permission, from Bhananker S, Liau D, Kooner P,
et al: Liability related to peripheral venous and
arterial catheterization: a closed claims analysis.
Anesth Analg 2009;109:124.)
from peripheral intravenous catheters that resulted

in extremity injury (Figure 544). Air embolisms,
infections, and vascular insufficiency secondary to
arterial spasm or thrombosis also resulted in claims.
Of interest, intravenous catheter claims in patients
who had undergone cardiac surgery formed the
largest cohort of claims related to peripheral intravenous catheters, most likely due to the usual practice
of tucking the arms alongside the patient during the
procedure, placing them out of view of the anesthesia providers. Radial artery catheters seem to generate few closed claims; however, femoral artery
catheters can lead to greater complications and
potentially increased liability exposure.
OBSTETRIC ANESTHESIA
Both critical incident and closed claims analyses
have been reported regarding complications and
mortality related to obstetrical anesthesia.
In a study reviewing anesthesia-related
maternal mortality in the United States using the
Pregnancy Mortality Surveillance System, which
collects data on all reported deaths causally related
to pregnancy, 86 of the 5946 pregnancy-related
deaths reported to the Centers for Disease Control
were thought to be anesthesia related or approximately 1.6% of total pregnancy related-deaths in
the period 19912002. The anesthesia mortality
rate in this period was 1.2 per million live births,
compared with 2.9 per million live births in the
11/02/13 10:40 AM
1208
SECTION V
period 19791990. The decline in anesthesiarelated maternal mortality may be secondary to the
decreased use of general anesthesia in parturients,
reduced concentrations of bupivacaine in epidurals, improved airway management protocols and
devices, and greater use of incremental (rather than
bolus) dosing of epidural catheters.
In a 2009 study examining the epidemiology of
anesthesia-related complications in labor and delivery in New York state in the period 20022005, an
anesthesia-related complication was reported in
4438 of 957,471 deliveries (0.46%). The incidence
of complications was increased in patients undergoing cesarean section, those living in rural areas,
and those with other medical conditions. Complications of neuraxial anesthesia (eg, postdural puncture
headache) were most common, followed by systemic complications, including aspiration or cardiac
events. Other reported problems related to anesthetic dose administration and unintended overdosages. African American women and those aged
4055 years were more likely to experience systemic
complications, whereas Caucasian women and those
aged 3039 were more likely to experience complications related to neuraxial anesthesia.
ASA Closed Claims Project analyses were
reported in 2009 for the period 19902003. Four
hundred twenty-six claims from this period were
compared with 190 claims in the database prior to
1990. After 1990, the proportion of claims for maternal or fetal demise was lower than that recorded
prior to 1990. After 1990, the number of claims for
maternal nerve injury increased. In the review of
claims in which anesthesia was thought to have contributed to the adverse outcome, anesthesia delay,
poor communication, and substandard care were
thought to have resulted in poor newborn outcomes.
Prolonged attempts to secure neuraxial blockade in
the setting of emergent cesarean section can contribute to adverse fetal outcome. Additionally, the closed
claims review indicated that poor communication
between the obstetrician and the anesthesiologist
regarding the urgency of newborn delivery was
likewise thought to have contributed to newborn
demise and neonatal brain injury.
Maternal death claims were secondary to airway
difficulty, maternal hemorrhage, and high neuraxial
Morg_Ch54_1199-1230.indd 1208
blockade. The most common claim associated with

obstetrical anesthesia was related to nerve injury
following regional anesthesia. Nerve injury can be
secondary to neuraxial anesthesia and analgesia,
but also due to obstetrical causes. Early neurological
consultation to identify the source of nerve injury is
suggested to discern if injury could be secondary to
obstetrical rather than anesthesia interventions.
REGIONAL ANESTHESIA
In a closed claims analysis, peripheral nerve blocks
were involved in 159 of the 6894 claims analyzed.
Peripheral nerve block claims were for death (8%),
permanent injuries (36%), and temporary injuries (56%). The brachial plexus was the most common location for nerve injury. In addition to ocular
injury, cardiac arrest following retrobulbar block
contributed to anesthesiology claims. Cardiac arrest
and epidural hematomas are two of the more common damaging events leading to severe injuries
related to regional anesthesia. Neuraxial hematomas
in both obstetrical and nonobstetrical patients were
associated with coagulopathy (either intrinsic to the
patient or secondary to medical interventions). In
one study, cardiac arrest related to neuraxial anesthesia contributed to roughly one-third of the death
or brain damage claims in both obstetrical and nonobstetrical patients. Accidental intravenous injection and local anesthesia toxicity also contributed to
claims for brain injury or death.
Nerve injuries constitute the third most common source of anesthesia litigation. A retrospective review of patient records and a claims database
showed that 112 of 380,680 patients (0.03%) experienced perioperative nerve injury. Patients with
hypertension and diabetes and those who were
smokers were at increased risk of developing perioperative nerve injury. Perioperative nerve injuries
may result from compression, stretch, ischemia,
other traumatic events, and unknown causes.
Improper positioning can lead to nerve compression, ischemia, and injury, however not every nerve
injury is the result of improper positioning. The care
received by patients with ulnar nerve injury was
rarely judged to be inadequate in the ASA Closed
Claims database. Even awake patients undergoing
11/02/13 10:40 AM
spinal anesthesia have been reported to experience

upper extremity injury. Moreover, many peripheral
nerve injuries do not become manifest until more
than 48 hr after anesthesia and surgery, suggesting that some nerve damage that occurs in surgical
patients may arise from events taking place after the
patient leaves the operating room setting.
PEDIATRIC ANESTHESIA
In a 2007 study reviewing 532 claims in pediatric
patients aged <16 years in the ASA Closed Claims
database from 19732000 (Figure 545), a decrease
in the proportion of claims for death and brain damage was noted over the three decades. Likewise, the
percentage of claims related to respiratory events
also was reduced. Compared with before 1990, the
percentage of claims secondary to respiratory events
decreased during the years 19902000, accounting for only 23 % of claims in the latter study years
compared with 51% of claims in the 1970s. Moreover, the percentage of claims that could be avoided
by better monitoring decreased from 63% in the
1970s to 16% in the 1990s. Death and brain damage constitute the major complications for which
claims are filed. In the 1990s, cardiovascular events
joined respiratory complications in sharing the primary causes of pediatric anesthesia litigation. In
1209
the study mentioned above, better monitoring and

newer airway management techniques may have
reduced the incidence of respiratory events leading
to litigation-generating complications in the latter
years of the review period. Additionally, the possibility of a claim being filed secondary to death or
brain injury is greater in children who are in ASA
classes 3, 4, or 5.
In a review of the Pediatric Perioperative
Cardiac Arrest Registry, which collects information from about 80 North American institutions
that provide pediatric anesthesia, 193 arrests were
reported in children between 1998 and 2004. During the study period, 18% of the arrests were drug
related, compared with 37% of all arrests during the
years 19941997. Cardiovascular arrests occurred
most often (41%), with hypovolemia and hyperkalemia being the most common causes. Respiratory
arrests (27%) were most commonly associated with
laryngospasm. Central venous catheter placement
with resultant vascular injury also contributed to
some perioperative arrests. Arrests from cardiovascular causes occurred most frequently during
surgery, whereas arrests from respiratory causes
tended to occur after surgery. The reduced use of
halothane seems to have decreased the incidence
of arrests secondary to medication administration.
However, hyperkalemia and electrolyte disturbances
90%
% of alms in time period
80%
Death or permanent brain damage
70%
60%
Preventable by monitoring
50%
40%
Respiratory events
30%
20%
10%
Cardiovascular events
19
7
3
19 19
77 76
19 19
79 78
19 19
81 80
19 19
83 82
19 19
85 84
19 19
87 86
19 19
89 88
19 19
91 90
19 19
93 92
19 19
95 94
19 19
97 96
2
00
0
0%
Morg_Ch54_1199-1230.indd 1209
FIGURE 545 Trends over time.

Outcome, type of event, and prevention by
better monitoring. Years are grouped for
illustration. (Reproduced, with permission, from
Jimenez N, Posner K, Cheney F, et al: An update on
pediatric anesthesia liability: a closed claims analysis.
Anesth Analg 2007;104:147.)
11/02/13 10:40 AM
1210
SECTION V
associated with transfusion and hypovolemia also

contribute to sources of cardiovascular arrest in children perioperatively.
A review of data from the Pediatric Perioperative Cardiac Arrest Registry with a focus on children with congenital heart disease found that such
children were more likely to arrest perioperatively
secondary to a cardiovascular cause. In particular,
children with a single ventricle were at increased risk
of perioperative arrest. Children with aortic stenosis
and cardiomyopathy were similarly found to be at
increased risk of cardiac arrest perioperatively.
OUT OF THE OPERATING ROOM

ANESTHESIA AND MONITORED
ANESTHESIA CARE
Review of the ASA Closed Claims Project database
indicates that anesthesia at remote (out of the operating room) locations poses a risk to patients secondary to hypoventilation and excessive sedation.
Remote location anesthesia care was more likely than
operating room anesthesia care to involve a claim for
death (54% vs 29%, respectively). The endoscopy
suite and cardiac catheterization laboratory were
the most frequent locations from which claims were
generated. Monitored Anesthesia Care (MAC) was
the most common technique employed in these
claims. Overwhelmingly, adverse respiratory events
were most frequently responsible for the injury.
An analysis of the ASA Closed Claims Project
database focusing on MAC likewise revealed that
oversedation and respiratory collapse most frequently lead to claims. Claims for burn injuries suffered in operating room fires were also found in the
database. Supplemental oxygen, draping, pooling of
flammable antiseptic preparatory solutions, and surgical cautery combine to produce the potential for
operating room fires.
EQUIPMENT PROBLEMS
Equipment problems is probably a misnomer;
the ASA Closed Claims Project review of 72 claims
involving gas delivery systems found that equipment
misuse was three times more common than equipment malfunction. The majority (76%) of adverse
Morg_Ch54_1199-1230.indd 1210
TABLE 543 Factors associated with human

errors and equipment misuse.
Factor
Example
Inadequate
preparation
No machine checkout or preoperative

evaluation; haste and carelessness;
production pressure
Inadequate
experience and
training
Unfamilarity with anesthetic

technique or equipment
Environmental
limitations
Inability to visualize surgical field:

poor communication with surgeons
Physical and
emotional factors
Fatigue; distraction caused by

personal problems
outcomes associated with gas delivery problems were

either death or permanent neurological damage.
Errors in drug administration also typically
involve human error. It has been suggested that as
many as 20% of the drug doses given to hospitalized
patients are incorrect. Errors in drug administration
account for 4% of cases in the ASA Closed Claims
Project, which found that errors resulting in claims
were most frequently due to either incorrect dosage
or unintentional administration of the wrong drug
(syringe swap). In the latter category, accidental
administration of epinephrine proved particularly
dangerous.
Another type of human error occurs when the
most critical problem is ignored because attention is
inappropriately focused on a less important problem
or an incorrect solution (fixation error). Serious
anesthetic mishaps are often associated with distractions and other factors (Table 543). The impact of
most equipment failures is decreased or avoided
when the problem is identified during a routine
preoperative checkout performed by adequately
5 trained personnel. Many anesthetic fatalities
occur only after a series of coincidental circumstances, misjudgments, and technical errors
coincide (mishap chain).
Prevention
Strategies to reduce the incidence of serious anesthetic complications include better monitoring and
anesthetic techniques, improved education, more
11/02/13 10:40 AM
comprehensive protocols and standards of practice, and active risk management programs. Better
monitoring and anesthetic techniques imply more
comprehensive monitoring and ongoing patient
assessments and better designed anesthesia equipment and workspaces. The fact that most accidents
occur during the maintenance phase of anesthesia
rather than during induction or emergenceimplies
a failure of vigilance.
Inspection, palpation, percussion, and auscultation of the patient provide important information.
Instruments should supplement (but never replace)
the anesthesiologists own senses. To minimize
errors in drug administration, drug syringes and
ampoules in the workspace should be restricted to
those needed for the current specific case. Drugs
should be consistently diluted to the same concentration in the same way for each use, and they should
be clearly labeled. Computer systems for scanning
bar-coded drug labels are available that may help to
reduce medication errors. The conduct of all anesthetics should follow a predictable pattern by which
the anesthetist actively surveys the monitors, the
surgical field, and the patient on a recurrent basis. In
particular, patient positioning should be frequently
reassessed to avoid the possibility of compression
or stretch injuries. When surgical necessity requires
patients to be placed in positions where harm may
occur or when hemodynamic manipulations (eg,
deliberate hypotension) are requested or required,
the anesthesiologist should note on the record the
surgical request and remind the surgeon of any
potential risks to the patient.
QUALITY MANAGEMENT
Risk management and continuous quality improvement programs at the departmental level may
reduce anesthetic morbidity and mortality rates
by addressing monitoring standards, equipment,
practice guidelines, continuing education, quality
of care, and staffing issues. Specific responsibilities
of peer review committees include identifying (and,
ideally, preventing) potential problems, formulating and periodically revising departmental policies,
ensuring the availability of properly functioning
anesthetic equipment, enforcing standards required
Morg_Ch54_1199-1230.indd 1211
1211
for clinical privileges, and evaluating the appropriateness and quality of patient care. A quality
improvement system impartially and continuously
reviews complications, compliance with standards,
and quality indicators.
AIRWAY INJURY
The daily insertion of endotracheal tubes, laryngeal mask airways, oral/nasal airways, gastric tubes,
transesophageal echocardiogram (TEE) probes,
esophageal (bougie) dilators, and emergency airways all involve the risk of airway structure damage.
Common morbid complaints, such as sore throat
and dysphagia, are usually self-limiting, but may
also be nonspecific symptoms of more ominous
complications.
The most common persisting airway injury is
dental trauma. In a retrospective study of 600,000
surgical cases, the incidence of injury requiring dental intervention and repair was approximately 1 in
4500. In most cases, laryngoscopy and endotracheal
intubation were involved, and the upper incisors
were the most frequently injured. Major risk factors for dental trauma included tracheal intubation,
preexisting poor dentition, and patient characteristics associated with difficult airway management
(including limited neck motion, previous head and
neck surgery, craniofacial abnormalities, and a history of difficult intubation).
Other types of airway trauma are rare. Although
there are scattered case reports in the literature, the
most comprehensive analysis was performed by the
ASA Closed Claims Project. This report describes
266 claims, of which the least serious were temporomandibular joint (TMJ) injuries that were all associated with otherwise uncomplicated intubations
and occurred mostly in females younger than age
60 years. Approximately 25% of these patients had
previous TMJ disease. Laryngeal injuries included
vocal cord paralysis, granuloma, and arytenoid dislocation. Most tracheal injuries were associated with
emergency surgical tracheotomy, but a few were
related to endotracheal intubation. Some injuries
occurred during seemingly easy, routine intubations. Proposed mechanisms include excessive tube
movement in the trachea, excessive cuff inflation
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1212
SECTION V
leading to pressure necrosis, and inadequate relaxation. Esophageal perforations contributed to death
in 5 of 13 patients. Esophageal perforation often
presents with delayed-onset subcutaneous emphysema or pneumothorax, unexpected febrile state,
and sepsis. Pharyngoesophageal perforation is associated with difficult intubation, age over 60 years,
and female gender. As in tracheal perforation, signs
and symptoms are often delayed in onset. Initial sore
throat, cervical pain, and cough often progressed
to fever, dysphagia, and dyspnea, as mediastinitis,
abscess, or pneumonia develop. Mortality rates of
up to 50% have been reported after esophageal perforation, with better outcomes attributable to rapid
detection and treatment.
Minimizing the risk of airway injury begins
with the preoperative assessment. A thorough airway examination will help to determine the risk
for difficulty Documentation of current dentition
(including dental work) should be included. Many
practitioners believe preoperative consent should
include a discussion of the risk of dental, oral, vocal
cord, and esophageal trauma in every patient who
could potentially need any airway manipulation. If
a difficult airway is suspected, a more detailed discussion of risks (eg, emergency tracheotomy) is
appropriate. In such cases, emergency airway supplies and experienced help should be available. The
ASA algorithm for difficult airway management is a
useful guide. After a difficult intubation, one should
seek latent signs of esophageal perforation and have
an increased level of suspicion for airway trauma.
When intubation cannot be accomplished by routine
means, the patient or guardian should be informed
to alert future anesthesia providers of potential airway difficulty.
Emergent nonoperating room intubations present unique challenges. In a review of 3423 out of the
operating room intubations, 10% were considered to
be difficult, and 4% of these intubations were associated with some form of complication, including
aspiration, esophageal intubation, or dental injury.
In this report, intubation bougies were employed in
56% of difficult intubations. The increased availability of video laryngoscopes and bougies have made
emergent intubations less stressful and less likely to
be unsuccessful.
Morg_Ch54_1199-1230.indd 1212
PERIPHERAL NERVE INJURY

Nerve injury is a complication of being hospitalized, with or without surgery, regional, or general
anesthesia. Peripheral nerve injury is a frequent
and vexing problem. In most cases, these injuries
resolve within 612 weeks, but some are permanent.
Because peripheral neuropathies are commonly
associated (often incorrectly!) with failures of patient
positioning, a review of mechanisms and prevention
is necessary.
The most commonly injured peripheral nerve
is the ulnar nerve (Figure 546). In a retrospective
study of over 1 million patients, ulnar neuropathy
(persisting for more than 3 months) occurred in
approximately 1 in 2700 patients. Of interest, initial symptoms were most frequently noted more
than 24 hr after a surgical procedure. Risk factors
included male gender, hospital stay greater than
14 days, and very thin or obese body habitus. More
than 50% of these patients regained full sensory and
motor function within 1 yr. Anesthetic technique
was not implicated as a risk factor; 25% of patients
with ulnar neuropathy underwent monitored care
or lower extremity regional technique. The ASA
Closed Claims Project findings support most of
these results, including the delayed onset of symptoms and the lack of relationship between anesthesia technique and injury. This study also noted that
many neuropathies occurred despite notation of
extra padding over the elbow area, further negating compression as a possible mechanism of injury.
Finally, the ASA Closed Claims Project investigators
found no deviation from the standard of care in the
majority of patients who manifested nerve damage
perioperatively.
The Role of Positioning

Other peripheral nerve injuries seem to be more
closely related to positioning or surgical procedure.
They may involve the peroneal nerve, the brachial
plexus, or the femoral and sciatic nerves. External
pressure on a nerve could compromise its perfusion,
disrupt its cellular integrity, and eventually result in
edema, ischemia, and necrosis. Pressure injuries are
particularly likely when nerves pass through closed
compartments or take a superficial course (eg, the
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1213
Humerus
Ulnar nerve
Medial epicondyle
Arcuate ligament
Olecranon process
Pronation
Supination
FIGURE 546 A: Pronation of the forearm can cause

external compression of the ulnar nerve in the cubital
tunnel. B: Forearm supination avoids this problem.
(Modied and reproduced, with permission, from Wadsworth TG: The

cubital tunnel and the external compression syndrome. Anesth Analg
1974;53:303.)
peroneal nerve around the fibula). Lower extremity

neuropathies, particularly those involving the peroneal nerve, have been associated with such factors as
extreme degrees (high) and prolonged (greater than
2 h) durations of the lithotomy position. But, these
nerve injuries also sometimes occur when such conditions are not present. Other risk factors for lower
extremity neuropathy include hypotension, thin
body habitus, older age, vascular disease, diabetes,
and cigarette smoking. An axillary (chest) roll is
commonly used to reduce pressure on the inferior
shoulder of patients in the lateral decubitus position.
This roll should be located caudad to the axilla to
prevent direct pressure on the brachial plexus and
large enough to relieve any pressure from the mattress on the lower shoulder.
The data are convincing that some peripheral nerve injuries are not preventable. The risk
of peripheral neuropathy should be included in
discussions leading to informed consent. When

reasonable, patients with contractures (or other
causes of limited flexibility) can be positioned before
induction of anesthesia to check for feasibility and
discomfort. Final positioning should be evaluated
prior to draping. In most circumstances, the head
and neck should be kept in a neutral position. Shoulder braces to support patients maintained in a Trendelenberg position should be avoided if possible,
and shoulder abduction and lateral rotation should
be minimized. The upper extremities should not be
extended greater than 90 at any joint. (There should
be no continuous external compression on the knee,
ankle, or heel.) Although injuries may still occur,
additional padding may be helpful in vulnerable
areas. Documentation should include information
on positioning, including the presence of padding.
Finally, patients who complain of sensory or motor
dysfunction in the postoperative period should be
Morg_Ch54_1199-1230.indd 1213
11/02/13 10:40 AM
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SECTION V
reassured that this is usually a temporary condition.

Motor and sensory function should be documented.
When symptoms persist for more than 24 hr, the
patient should be referred to a neurologist (or a
physiatrist or hand surgeon) who is knowledgeable
about perioperative nerve damage for evaluation.
Physiological testing, such as nerve conduction and
electromyographic studies, can be useful to document whether nerve damage is a new or chronic
condition. In the latter case, fibrillations will be
observed in chronically denervated muscles.
Complications Related to Positioning

Changes of body position have physiological consequences that can be exaggerated in disease states.
General and regional anesthesia may limit the cardiovascular response to such a change. Even positions that are safe for short periods may eventually
lead to complications in persons who are not able
to move in response to pain. For example, the alcoholic patient who passes out on a hard floor or a park
bench may awaken with a brachial plexus injury.
Similarly, regional and general anesthesia abolish
protective reflexes and predispose patients to injury.
Complications of postural hypotension, the

most common physiological consequence of positioning, can be minimized by avoiding abrupt or
extreme position changes (eg, sitting up quickly),
reversing the position if vital signs deteriorate, keeping the patient well hydrated, and having vasoactive drugs available to treat hypotension. Whereas
maintaining a reduced level of general anesthesia
will decrease the likelihood of hypotension, light
general anesthesia will increase the likelihood that
movement of the endotracheal tube during positioning will cause the patient to cough and become
hypertensive.
Many complications, including air embolism,
blindness from sustained pressure on the globe, and
finger amputation following a crush injury, can be
caused by improper patient positioning (Table 544).
These complications are best prevented by evaluating the patients postural limitations during the preanesthetic visit; padding pressure points, susceptible
nerves, and any area of the body that will possibly
be in contact with the operating table or its attachments; avoiding flexion or extension of a joint to its
limit; having an awake patient assume the position
TABLE 544 Complications associated with patient positioning.

Complication
Position
Prevention
Venous air embolism
Sitting, prone, reverse

Trendelenburg
Maintain adequate venous pressure; ligate open veins
Alopecia
Supine, lithotomy,
Trendelenburg
Avoid prolonged hypotension, padding, and occasional head turning.
Backache
Any
Lumbar support, padding, and slight hip flexion.
Extremity compartment
syndromes
Especially lithotomy
Maintain perfusion pressure and avoid external compression.
Corneal abrasion
Any, but especially prone
Taping and/or lubricating eye.
Digit amputation
Any
Check for protruding digits before changing table configuration.
Any
Lithotomy, lateral
decubitus
Any
Any
Prone, sitting
Any
Avoid stretching or direct compression at neck, shoulder, or axilla.

Avoid sustained pressure on lateral aspect of upper fibula.
Nerve palsies
Brachial plexus
Common peroneal
Radial
Ulnar
Retinal ischemia
Skin necrosis
Morg_Ch54_1199-1230.indd 1214
Avoid compression of lateral humerus.

Avoid sustained pressure on ulnar groove.
Avoid pressure on globe.
Avoid sustained pressure over bony prominences.
11/02/13 10:40 AM
to ensure comfort; and understanding the potential complications of each position. Monitors must
often be disconnected during patient repositioning,
making this a time of greater risk for unrecognized
hemodynamic derangement.
Compartment syndromes can result from
hemorrhage into a closed space following a vascular puncture or prolonged venous outflow obstruction, particularly when associated with hypotension.
In severe cases, this may lead to muscle necrosis,
myoglobinuria, and renal damage, unless the pressure within the extremity compartment is relieved
by surgical decompression (fasciotomy) or in the
abdominal compartment by laparotomy.
AWARENESS
A continuing series of media reports have imprinted
the fear of awareness under general anesthesia into
the psyche of the general population. Accounts of
recall and helplessness while paralyzed have made
unconsciousness a primary concern of patients
undergoing general anesthesia. When unintended
intraoperative awareness does occur, patients may
exhibit symptoms ranging from mild anxiety to
posttraumatic stress disorder (eg, sleep disturbances,
nightmares, and social difficulties).
Although the incidence is difficult to measure,
approximately 2% of the closed claims in the ASA
Closed Claims Project database relate to awareness
under anesthesia. Analysis of the NHS Litigation
Authority database from 19952007 revealed that
19 of 93 relevant claims were for awake paralysis.
Clearly, awareness is of great concern to patients and
may lead to litigation. Certain types of surgeries are
most frequently associated with awareness, including those for major trauma, obstetrics, and major
cardiac procedures. In some instances, awareness
may result from the reduced depth of anesthesia that
can be tolerated by the patient. In early studies, recall
rates for intraoperative events during major trauma
surgery have been reported to be as frequent as 43%;
the incidence of awareness during cardiac surgery
and cesarean sections is 1.5% and 0.4%, respectively.
As of 1999, the ASA Closed Claims Project reported
79 awareness claims; approximately 20% of the
claims were for awake paralysis, and the remainder
Morg_Ch54_1199-1230.indd 1215
1215
of the claims were for recall under general anesthesia. Most claims for awake paralysis were thought
to be due to errors in drug labeling and administration, such as administering paralytics before inducing narcosis. Since the 1999 review, another 71 cases
have appeared in the database. Claims for recall were
more likely in women undergoing general anesthesia
without a volatile agent. Patients with long term substance abuse may have increased anesthesia requirements which if not met can lead to awareness.
Other specific causes of awareness include inadequate inhalational anesthetic delivery (eg, from
vaporizer malfunction) and medication errors. Some
patients may complain of awareness, when, in fact,
they received regional anesthesia or monitored anesthesia care; thus, anesthetists should make sure that
patients have reasonable expectations when regional
or local techniques are employed. Likewise, patients
requesting regional or local anesthesia because they
want to see it all and/ or stay in control often can
become irate when sedation dulls their memory of
the perioperative experience. In all cases, frank discussion between anesthesia staff and the patient is
necessary to avoid unrealistic expectations.
Some clinicians routinely discuss the possibility of intraoperative recall and the steps that will be
taken to minimize it as part of the informed consent
for general anesthesia. This makes particular sense
for those procedures in which recall is more likely. It
is advisable to also remind patients who are undergoing monitored anesthesia care with sedation that
awareness is expected. Volatile anesthetics should
be administered at a level consistent with amnesia. If this is not possible, benzodiazepines (and/or
scopolamine) can be used. Movement of a patient
may indicate inadequate anesthetic depth. Documentation should include end-tidal concentrations
of anesthetic gases (when available) and dosages of
amnesic drugs. Use of a bispectral index scale (BIS)
monitor or similar monitors may be helpful although
randomized clinical trials have failed to demonstrate
a reduced incidence of awareness with use of BIS
when compared with a group receiving appropriate
concentrations of volatile agents. Finally, if there is
evidence of intraoperative awareness during postoperative rounds, the practitioner should obtain a
detailed account of the experience, answer patient
11/02/13 10:40 AM
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SECTION V
questions, be very empathetic, and refer the patient

for psychological counseling if appropriate.
EYE INJURY
A wide range of conditions from simple corneal
abrasion to blindness have been reported. Corneal
abrasion is by far the most common and transient
eye injury. The ASA Closed Claims Project identified
a small number of claims for abrasion, in which the
cause was rarely identified (20%) and the incidence
of permanent injury was low (16%). It also identified
a subset of claims for blindness that resulted from
patient movement during ophthalmological surgery.
These cases occurred in patients receiving either
general anesthesia or monitored anesthesia care.
Although the cause of corneal abrasion may not
be obvious, securely closing the eye lids with tape
after loss of consciousness (but prior to intubation)
and avoiding direct contact between eyes and oxygen masks, drapes, lines, and pillows (particularly
during monitored anesthesia care, in transport,
and in nonsupine positions) can help to minimize
the possibility of injury. Adequate anesthetic depth
(and, in most cases, paralysis) should be maintained
to prevent movement during ophthalmological surgery under general anesthesia. In patients scheduled
for MAC, the patient must understand that movement under monitored care is hazardous and, thus,
that only minimal sedation may be administered to
ensure that he or she can cooperate.
Ischemic optic neuropathy (ION) is a devastating perioperative complication. ION is now the
most common cause of postoperative vision loss.
Postoperative vision loss is most commonly reported
after cardiopulmonary bypass, radical neck dissection, and spinal surgeries in the prone position.
Both preoperative and intraoperative factors may
be contributory. Many of the case reports implicate
preexisting hypertension, diabetes, coronary artery
disease, and smoking, suggesting that preoperative
vascular abnormalities may play a role. Intraoperative deliberate hypotension and anemia have also
been implicated (in spine surgery), perhaps because
of their potential to reduce oxygen delivery. Finally,
prolonged surgical time in positions that compromise venous outflow (prone, head down, compressed
Morg_Ch54_1199-1230.indd 1216
abdomen) have also been found to be factors in spine

surgery. Symptoms are usually present immediately
upon awakening from anesthesia, but have been
reported up to 12 days postoperatively. Such symptoms range from decreased visual acuity to complete
blindness. Analysis of case records submitted to the
ASA Postoperative Vision Loss Registry revealed
that vision loss was secondary to ION in 83 of
93 cases. Instrumentation of the spine was associated with ION when surgery lasted more than 6 hr
and blood loss was more than 1 L. ION can occur in
patients whose eyes are free of pressure secondary to
the use of pin fixation, indicating that direct pressure
on the eye is not required to produce ION.
Increased venous pressure in patients in the
Trendelenberg position may reduce blood flow to
the optic nerve.
It is difficult to formulate recommendations
to prevent this complication because risk factors
for ION are often unavoidable. Steps that might be
taken include: (1) limiting the degree and duration
of hypotension during controlled (deliberate) hypotension, (2) administering a transfusion to severely
anemic patients who seem to be at risk of ION, and
(3) discussing with the surgeon the possibility of
staged operations in high-risk patients to limit prolonged procedures.
Of note, postoperative vision loss can be caused
by other mechanisms as well, including angle closure
glaucoma or embolic phenomenon to the cortex or
retina. Immediate evaluation is advised.
CARDIOPULMONARY ARREST
DURING SPINAL ANESTHESIA
Sudden cardiac arrest during an otherwise routine
administration of spinal anesthetics is an uncommon complication. The initial published report was
a closed claims analysis of 14 patients who experienced cardiac arrest during spinal anesthesia.
The cases primarily involved young (average age
36 years), relatively healthy (ASA physical status
III) patients who were given appropriate doses of
local anesthetic that produced a high dermatomal
level of block prior to arrest (T4 level). Respiratory
insufficiency with hypercarbia due to sedatives was
thought to be a potential contributing factor. The
11/02/13 10:40 AM
average time from induction of spinal anesthesia to

arrest was 36 min, and, in all cases, arrest was preceded by a gradual decline in heart rate and blood
pressure. Just prior to arrest, the most common signs
were bradycardia, hypotension, and cyanosis. Treatment consisted of ventilatory support, ephedrine,
atropine, cardiopulmonary resuscitation (average
duration 10.9 min), and epinephrine. Despite these
interventions, 10 patients remained comatose and
4 patients regained consciousness with significant
neurological deficits. A subsequent study concluded
that such arrests had little relationship to sedation,
but were related more to extensive degrees of sympathetic blockade, leading to unopposed vagal tone
and profound bradycardia. Rapid appropriate treatment of bradycardia and hypotension is essential to
minimize the risk of arrest. Early treatment of bradycardia with atropine may prevent a downward
spiral. Stepwise doses of ephedrine, epinephrine,
and other vasoactive drugs should be given to treat
hypotension. If cardiopulmonary arrest occurs, ventilatory support, cardiopulmonary resuscitation,
and full resuscitation doses of atropine and epinephrine should be administered without delay.
HEARING LOSS
Perioperative hearing loss is usually transient and
often goes unrecognized. The incidence of lowfrequency hearing loss following dural puncture may
be as high as 50%. It seems to be due to cerebrospinal
fluid leak, and, if persistent, can be relieved with an
epidural blood patch. Hearing loss following general
anesthesia can be due to a variety of causes and is
much less predictable. Mechanisms include middle
ear barotrauma, vascular injury, and ototoxicity of
drugs (aminoglycosides, loop diuretics, nonsteroidal
antiinflammatory drugs, and antineoplastic agents).
Hearing loss following cardiopulmonary bypass is
usually unilateral and is thought to be due to embolism and ischemic injury to the organ of Corti.
ALLERGIC REACTIONS
Hypersensitivity (or allergic) reactions are exaggerated immunological responses to antigenic stimulation in previously sensitized persons. The antigen, or
Morg_Ch54_1199-1230.indd 1217
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TABLE 545 Hypersensitivity reactions.

Type I (immediate)
Atopy
Urticariaangioedema
Anaphylaxis
Type II (cytotoxic)
Hemolytic transfusion reactions
Autoimmune hemolytic anemia
Heparin-induced thrombocytopenia
Type III (immune complex)
Arthus reaction
Serum sickness
Acute hypersensitivity pneumonitis
Type IV (delayed, cell-mediated)
Contact dermatitis
Tuberculin-type hypersensitivity
Chronic hypersensitivity pneumonitis
allergen, may be a protein, polypeptide, or smaller

molecule. Moreover, the allergen may be the substance itself, a metabolite, or a breakdown product.
Patients may be exposed to antigens through the
respiratory tract, gastrointestinal tract, eyes, skin
and from previous intravenous, intramuscular, or
peritoneal exposure.
Anaphylaxis occurs when inflammatory agents
are released from basophils and mast cells as a result
of an antigen interacting with the immunoglobulin
(Ig) E. Anaphylactoid reactions manifest themselves
in the same manner as anaphylactic reactions, but
are not the result of an interaction with IgE. Direct
activation of complement and IgG-mediated complement activation can result in similar inflammatory mediator release and activity.
Depending on the antigen and the immune system components involved, hypersensitivity reactions
are classically divided into four types (Table545).
In many cases, an allergen (eg, latex) may cause
more than one type of hypersensitivity reaction.
Type I reactions involve antigens that cross-link
IgE antibodies, triggering the release of inflammatory mediators from mast cells. In type II reactions,
complement-fixing (C1-binding) IgG antibodies
bind to antigens on cell surfaces, activating the classic
complement pathway and lysing the cells. Examples
of type II reactions include hemolytic transfusion
reactions and heparin-induced thrombocytopenia.
Type III reactions occur when antigenantibody
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SECTION V
(IgG or IgM) immune complexes are deposited in

tissues, activating complement and generating chemotactic factors that attract neutrophils to the area.
The activated neutrophils cause tissue injury by
releasing lysosomal enzymes and toxic products.
Type III reactions include serum sickness reactions
and acute hypersensitivity pneumonitis. Type IV
reactions, often referred to as delayed hypersensitivity reactions, are mediated by CD4+ T lymphocytes
that have been sensitized to a specific antigen by
prior exposure. Prior TH1 response causes expression of a T-cell receptor protein that is specific for
the antigen. Reexposure to the antigen causes these
lymphocytes to produce lymphokinesinterleukins
(IL), interferon (IFN), and tumor necrosis factor-
(TNF-)that attract and activate inflammatory
mononuclear cells over 4872 hr. Production of IL-1
and IL-6 by antigen-processing cells amplifies clonal
expression of the specific sensitized T cells and
attracts other types of T cells. IL-2 secretion transforms CD8+ cytotoxic T cells into killer cells; IL-4
and IFN- cause macrophages to undergo epithelioid transformation, often producing granuloma.
Examples of type IV reactions are those associated
with tuberculosis, histoplasmosis, schistosomiasis,
and hypersensitivity pneumonitis and some autoimmune disorders, such as rheumatoid arthritis and
Wegeners granulomatosis.
1. Immediate Hypersensitivity
Reactions
Initial exposure of a susceptible person to an antigen
induces CD4+ T cells to lymphokines that activate
and transform specific B lymphocytes into plasma
cells, producing allergen-specific IgE antibodies
(Figure 547). The Fc portion of these antibodies
then associates with high affinity receptors on the
cell surface of tissue mast cells and circulating basophils. During subsequent reexposure to the antigen,
it binds the Fab portion of adjacent IgE antibodies
on the mast cell surface, inducing degranulation and
release of inflammatory lipid mediators and additional cytokines from the mast cell. The end result
is the release of histamine, tryptase, proteoglycans
(heparin and chondroitin sulfate), and carboxypeptidases. Prostaglandin (mainly prostaglandin
Morg_Ch54_1199-1230.indd 1218
D2) and leukotriene (B4, C4, D4, E4, and plateletactivating factor) synthesis is also increased. The
combined effects of these mediators can produce
arteriolar vasodilatation, increased vascular permeability, increased mucus secretion, smooth muscle
contraction, and other clinical manifestations of
type I reactions.
Type I hypersensitivity reactions are classified
as atopic or nonatopic. Atopic disorders typically
affect the skin or respiratory tract and include allergic rhinitis, atopic dermatitis, and allergic asthma.
Nonatopic hypersensitivity disorders include urticaria, angioedema, and anaphylaxis; when these
reactions are mild, they are confined to the skin
(urticaria) or subcutaneous tissue (angioedema),
but when they are severe, they become generalized
and a life-threatening medical emergency (anaphylaxis). Urticarial lesions are characteristically
well-circumscribed skin wheals with raised erythematous borders and blanched centers; they are
intensely pruritic. Angioedema presents as deep,
nonpitting cutaneous edema from marked vasodilatation and increased permeability of subcutaneous
blood vessels. When angioedema is extensive, it can
be associated with large fluid shifts; when it involves
the pharyngeal or laryngeal mucosa, it can rapidly
compromise the airway.
2. Anaphylactic Reactions
Anaphylaxis is an exaggerated response to an
allergen (eg, antibiotic) that is mediated by a type
I hypersensitivity reaction. The syndrome appears
within minutes of exposure to a specific antigen in
a sensitized person and characteristically presents as
acute respiratory distress, circulatory shock, or both.
Death may occur from asphyxiation or irreversible
circulatory shock. The incidence of anaphylactic
reactions during anesthesia has been estimated at a
rate of 1:3500 to 1:20000 anesthetics. Mortality from
anaphylaxis can be as frequent as 4% of cases with
brain injury, occurring in another 2% of surviving
patients. A French study evaluating 789 anaphylactic
and anaphylactoid reactions reported that the most
common sources of perioperative anaphylaxis were
neuromuscular blockers (58%), latex (17%), and
antibiotics (15%).
11/02/13 10:40 AM
1219
Free drug
Fixation of IgE
antibodies to
mast cells and
blood basophils
Carrier
(eg, albumin)
Drugcarrier
complex
Prednisone
blocks
Mitosis
Macrophage
IgE antibody
producing cells
Reaginic (IgE)
antibody-forming
precursor cell
IgE reaginic
antibodies
Binding of allergen to specific IgE antibody

on surface of mast cell induces mediator release
Antihistamines
partially block
Histamine, kinins,
leukotrienes (SRS),
prostaglandins, serotonin,
platelet-activating factor
Degranulation and
mediator release
Smooth muscle
and other
end organs
Isoproterenol, theophylline,
epinephrine, and cromolyn
partially block
FIGURE 547 A: Induction of IgE-mediated allergic

sensitivity to drugs and other allergens. B: Response of
IgE-sensitized cells to subsequent exposure to allergens.
Ig, immunoglobulin. (Reproduced, with permission, from

Katzung BG [editor]: Basic & Clinical Pharmacology, 8th ed.
McGraw-Hill, 2001.)
The most important mediators of anaphylaxis

are histamine, leukotrienes, basophil kallikrein
(BK-A,) and platelet-activating factor. They increase
vascular permeability and contract smooth muscle.
H1-receptor activation contracts bronchial smooth
muscle, whereas H2-receptor activation causes
vasodilatation, enhanced mucus secretion, tachycardia, and increased myocardial contractility. BK-A
cleaves bradykinin from kininogen; bradykinin
increases vascular permeability and vasodilatation
and contracts smooth muscle. Activation of Hageman factor can initiate intravascular coagulation.
Morg_Ch54_1199-1230.indd 1219
11/02/13 10:40 AM
1220
SECTION V
TABLE 546 Clinical manifestations

of anaphylaxis.
Organ System
Signs and Symptoms
Cardiovascular
Hypotension,1 tachycardia, arrhythmias
Pulmonary
Bronchospasm,1 cough, dyspnea,

pulmonary edema, laryngeal edema,
hypoxia
Dermatological
Urticaria,1 facial edema, pruritus
Key signs during general anesthesia.
Eosinophil chemotactic factor of anaphylaxis, neutrophil chemotactic factor, and leukotriene B4 attract
inflammatory cells that mediate additional tissue
injury. Angioedema of the pharynx, larynx, and
trachea produce upper airway obstruction, whereas
bronchospasm and mucosal edema result in lower
airway obstruction. Histamine may preferentially
constrict large airways, whereas leukotrienes primarily affect smaller peripheral airways. Transudation of fluid into the skin (angioedema) and viscera
produces hypovolemia and shock, whereas arteriolar vasodilatation decreases systemic vascular
resistance. Coronary hypoperfusion and arterial

hypoxemia promote arrhythmias and myocardial
ischemia. Leukotriene and prostaglandin mediators may also cause coronary vasospasm. Prolonged
circulatory shock leads to progressive lactic acidosis and ischemic damage to vital organs. Table 546
summarizes important manifestations of anaphylactic reactions.
Anaphylactoid reactions resemble anaphylaxis
but do not depend on IgE antibody interaction with
antigen. A drug can directly release histamine from
mast cells (eg, urticaria following high-dose mor6 phine sulfate) or activate complement. Despite
differing mechanisms, anaphylactic and anaphylactoid reactions typically are clinically indistinguishable and equally life-threatening. Table 547
lists common causes of anaphylactic and anaphylactoid reactions.
Factors that may predispose patients to these
reactions include pregnancy, known atopy, and previous drug exposure. Such reactions are more common in younger than older patients. Laboratory
identification of patients who have experienced an
adverse allergic reaction or who may be particularly
TABLE 547 Causes of anaphylactic and anaphylactoid reactions.

Anaphylactic reactions against
polypeptides
Venoms (Hymenoptera, fire ant, snake, jellyfish)

Airborne allergens (pollen, molds, danders)
Foods (peanuts, milk, egg, seafood, grain)
Enzymes (trypsin, streptokinase, chymopapain, asparaginase)
Heterologous serum (tetanus antitoxin, antilymphocyte globulin, antivenin)
Human proteins (insulin, corticotropin, vasopressin, serum and seminal proteins)
Latex
Anaphylactic reactions against

hapten carrier
Antibiotics (penicillin, cephalosporins, sulfonamides)

Disinfectants (ethylene oxide, chlorhexidine)
Local anesthetics (procaine)
Anaphylactoid reactions
Polyionic solutions (radiocontrast medium, polymyxin B)

Opioids (morphine, meperidine)
Hypnotics (propofol, thiopental)
Muscle relaxants (rocuronium, succinylcholine, cisatracurium)
Synthetic membranes (dialysis)
Nonsteroidal antiinflammatory drugs
Preservatives (sulfites, benzoates)
Protamine
Dextran
Steroids
Exercise
Idiopathic
Adapted and reproduced, with permission, from Bochner BS, Lichtenstein LM: N Engl J Med 1991;324:1786.
Morg_Ch54_1199-1230.indd 1220
11/02/13 10:40 AM
TABLE 548 Treatment of anaphylactic

and anaphylactoid reactions.
Discontinue drug administration
Administer 100% oxygen
Epinephrine (0.010.5 mg IV or IM)1
Consider intubation
Intravenous fluid bolus
Diphenhydramine (5075 mg IV)
Ranitidine (150 mg IV)
Hydrocortisone (up to 200 mg IV) or methylprednisolone
(12 mg/kg)
1
The dose and route of epinephrine depend on the severity of the
reaction. An infusion of 15 mcg/min may be necessary in adults.
susceptible is often aided by intradermal skin testing,

leukocyte or basophil degranulation testing (histamine release test), or radio-allergosorbent testing
(RAST). The latter is capable of measuring the level
of drug-specific IgE antibody in the serum. Serum
tryptase measurement is helpful in confirming the
diagnosis of an anaphylactic reaction. Prophylactic
pretreatment with histamine receptor antagonists
and corticosteroids decreases the severity of the
reaction. Treatment must be immediate and tailored
to the severity of the reaction (Table 548).
3. Allergic Reactions
to Anesthetic Agents
7 True anaphylaxis due to anesthetic agents is
rare; anaphylactoid reactions are much more

common. Risk factors associated with hypersensitivity to anesthetics include female gender, atopic history, preexisting allergies, and previous anesthetic
exposures. Muscle relaxants are the most common
cause of anaphylaxis during anesthesia, with an estimated incidence of 1 in 6500 patients. They account
for almost 60% of perioperative anaphylactic reactions. In many instances, there was no previous
exposure to muscle relaxants. Investigators suggest
that over-the-counter drugs, cosmetics, and food
products, many of which contain tertiary or quaternary ammonium ions, can sensitize susceptible individuals. A French study found that, in decreasing
order of frequency, rocuronium, succinylcholine,
and atracurium were most often responsible; this
likely reflects the propensity to cause anaphylaxis,
together with frequency of use.
Morg_Ch54_1199-1230.indd 1221
1221
Although rarer, hypnotic agents can also be

responsible for some allergic reactions. The incidence of anaphylaxis for thiopental and propofol
is 1 in 30,000 and 1 in 60,000, respectively. Allergic
reactions to etomidate, ketamine, and benzodiazepines are exceedingly rare. True anaphylactic
reactions due to opioids are far less common than
nonimmune histamine release. Similarly, anaphylactic reactions to local anesthetics are much
less common than vasovagal reactions, toxic reactions to accidental intravenous injections, and side
effects from absorbed or intravenously injected epinephrine. IgE-mediated reactions to ester-type local
anesthetics, however, are well described secondary
to reaction to the metabolite, para-aminobenzoic
acid, In contrast, true anaphylaxis due to amidetype local anesthetics is very rare; in some instances,
the preservative (paraben or methylparaben) was
believed to be responsible for an apparent anaphylactoid reaction to a local anesthetic. Moreover, the
cross-reactivity between amide-type local anesthetics seems to be low. There are no reports of anaphylaxis to volatile anesthetics.
4. Latex Allergy
The severity of allergic reactions to latex-containing
products ranges from mild contact dermatitis to lifethreatening anaphylaxis. Latex allergy is the second
most common cause of anaphylaxis during anesthesia. Most serious reactions seem to involve a direct
IgE-mediated immune response to polypeptides in
natural latex, although some cases of contact dermatitis may be due to a type IV sensitivity reaction to
chemicals introduced in the manufacturing process.
Nonetheless, a relationship between the occurrence
of contact dermatitis and the probability of future
anaphylaxis has been suggested. Chronic exposure to
latex and a history of atopy increases the risk of sensitization. Healthcare workers and patients undergoing frequent procedures with latex items (eg,
repeated urinary bladder catheterization, barium
enema examinations) should therefore be consid8 ered at increased risk. Patients with spina
bifida, spinal cord injury, and congenital
abnormalities of the genitourinary tract have an
increased incidence of latex allergy. The incidence of
11/02/13 10:40 AM
1222
SECTION V
latex anaphylaxis in children is estimated to be 1 in

10,000. A history of allergic symptoms to latex
should be sought in all patients during the preanesthetic interview. Foods that cross-react with latex
include mango, kiwi, chestnut, avacado, passion
fruit, and banana.
IL-18 and IL-13 single nucleotide polymorphisms may affect the sensitivity of individuals to
latex and promote allergic responses.
Anaphylactic reactions to latex may be confused with reactions to other substances (eg, drugs,
blood products) because the onset of symptoms can
be delayed for more than 1 hr after initial exposure.
Treatment is the same as for other forms of anaphylactic reactions. Skin-prick tests, intradermal tests,
basophil histamine-release tests, and RAST have
been used to evaluate high-risk patients. Preventing a reaction in sensitized patients includes pharmacological prophylaxis and absolute avoidance
of latex. Preoperative administration of H1 and H2
histamine antagonists and steroids may provide
some protection, although their use is controversial. Although most pieces of anesthetic equipment
are now latex-free, some may still contain latex
(eg, gloves, tourniquets, some ventilator bellows,
intravenous injection ports, and older reusable face
masks). An allergic reaction has even been documented from inhalation of latex antigen contained
within aerosolized glove powder. Manufacturers
of latex-containing medical products must label
their products accordingly. Only devices specifically known not to contain latex (eg, polyvinyl or
neoprene gloves, silicone endotracheal tubes or
laryngeal masks, plastic face masks) can be used
in latex-allergic patients. Rubber stoppers should
be removed from drug vials prior to use, and injections should be made through plastic stopcocks, if
latex has not been eliminated from containers and
injection ports.
5. Allergies to Antibiotics
Many true drug allergies in surgical patients are due
to antibiotics, mainly -lactam antibiotics, such as
penicillins and cephalosporins. Although 1% to 4%
of -lactam administrations result in allergic reactions, only 0.004% to 0.015% of these reactions
Morg_Ch54_1199-1230.indd 1222
result in anaphylaxis. Up to 2% of the general

population is allergic to penicillin, but only 0.01%
of penicillin administrations result in anaphylaxis.
Cephalosporin cross-sensitivity in patients with
penicillin allergy is estimated to be 2% to 7%, but
a history of an anaphylactic reaction to penicillin increases the cross-reactivity rate up to 50%.
Patients with a prior history of an anaphylactic
reaction to penicillin should therefore not receive a
cephalosporin. Although imipenem exhibits similar
cross-sensitivity, aztreonam seems to be antigenically distinct and reportedly does not cross-react
with other -lactams. Sulfonamide allergy is also
relatively common in surgical patients. Sulfa drugs
include sulfonamide antibiotics, furosemide, hydrochlorothiazide, and captopril. Fortunately, the frequency of cross-reactivity among these agents is low.
Like cephalosporins, vancomycin is commonly
used for antibiotic prophylaxis in surgical patients.
Unfortunately, it is associated with adverse reactions. An anaphylactoid-type reaction, red man
syndrome, consists of intense pruritus, flushing,
and erythema of the head and upper torso, often
with arterial hypotension; this syndrome seems to
be related to a rapid rate of administration more
than to dose or allergy. Isolated systemic hypotension is a much more frequent side effect and seems
to be primarily mediated by histamine release,
because pretreatment with H1 and H2 antihistamines
can prevent hypotension, even with rapid rates of
administration.
Immunologic mechanisms are associated with
other perioperative pathologies. Transfusion-related
lung injury may be secondary to the activity of antibodies in the donor plasma, producing a hypersensitivity reaction that results in lung infiltrates
and respiratory failure. IgG antibody formation
directed at heparinPF4 complexes results in platelet activation, thrombosis, and heparin-induced
thrombocytopenia.
OCCUPATIONAL HAZARDS
IN ANESTHESIOLOGY
Anesthesiologists spend much of their workday
exposed to anesthetic gases, low-dose ionizing
radiation, electromagnetic fields, blood products,
11/02/13 10:40 AM
1223
TABLE 549 Relative rate ratios for drug and suicide deaths comparing
anesthesiologists with internists before and after January 1, 1987.
Anesthesiologists
(N)
Internists
(N)
RR1
95% CI
All drug-related deaths
<1987
1987
36
55
14
19
2.65
2.87
1.424.91
1.714.84
Drug-related suicides
<1987
1987
16
32
11
11
1.48
2.88
0.693.20
1.455.71
Suicides
<1987
1987
41
62
33
38
1.25
1.60
0.791.97
1.072.39
Cl, condence interval.

1
Ratio (RR) of anesthesiologists compared with internists for that time period, RR is adjusted for age, gender, and race.
Reproduced, with permission, from Alexander B, Checkoway H, Nagahama S, Domino K: Cause-specic mortality risks
of anesthesiologists. Anesthesiology 2000;93:922.
and workplace stress. Each of these can contribute

to negative health effects in anesthesia practitioners. A 2000 paper compared the mortality risks of
anesthesiologists and internists. Death from heart
disease or cancer did not differ between the groups;
however, anesthesiologists had an increased rate
of suicides and drug-related deaths (Table 549).
Anesthesiologists also had a greater chance of death
from external causes, such as boating, bicycling, and
aeronautical accidents compared with internists.
Nevertheless, both anesthesiologists and internists
had lower mortality than the general population,
likely due to their higher socioeconomic status.
Anesthesiologists access to intravenous opioids
likely contributes to a 2.21 relative risk for drugrelated deaths compared with that of internists.
low levels depends on efficient scavenging equipment, adequate operating room ventilation, and
conscientious anesthetic technique. Most people
cannot detect the odor of volatile agents at a concentration of less than 30 ppm. If there is no functioning
scavenging system, anesthetic gas concentrations
reach 3000 ppm for nitrous oxide and 50 ppm for
volatile agents.
Early studies indicated that female operating
room staff might be at increased risk of spontaneous
abortion compared with other women. It is unclear
if other factors related to operating room activity could also contribute to the possibly increased
potential for pregnancy loss.
1. Chronic Exposure
to Anesthetic Gases
Hospital workers are exposed to many infectious

diseases prevalent in the community (eg, respiratory
viral infections, rubella, and tuberculosis).
Herpetic whitlow is an infection of the finger
with herpes simplex virus type 1 or 2 and usually
involves direct contact of previously traumatized
skin with contaminated oral secretions. Painful vesicles appear at the site of infection. The diagnosis is
confirmed by the appearance of giant epithelial cells
or nuclear inclusion bodies in a smear taken from
the base of a vesicle, the presence of a rise in herpes
simplex virus titer, or identification of the virus with
antiserum. Treatment is conservative and includes
9 There is no clear evidence that exposure to
trace amounts of anesthetic agents presents a

health hazard to operating room personnel. However, because previous studies examining this issue
have yielded flawed but conflicting results, the US
Occupational Health and Safety Administration
continues to set maximum acceptable trace concentrations of less than 25 ppm for nitrous oxide and
0.5 ppm for halogenated anesthetics (2 ppm if the
halogenated agent is used alone). Achieving these
Morg_Ch54_1199-1230.indd 1223
2. Infectious Diseases
11/02/13 10:40 AM
1224
SECTION V
topical application of 5% acyclovir ointment. Prevention involves wearing gloves when contacting
oral secretions. Patients at risk of harboring the
virus include those suffering from other infections,
immunosuppression, cancer, and malnutrition. The
risk of this condition has virtually disappeared now
that anesthesia personnel routinely wear gloves during manipulation of the airway, which was not the
case in the 1980s and earlier.
Viral DNA has been identified in the smoke
plume generated during laser treatment of condylomata. The theoretical possibility of viral transmission from this source can be minimized by using
smoke evacuators, gloves, and appropriate OSHA
approved masks.
More disturbing is the potential of acquiring
serious blood-borne infections, such as hepatitis B,
hepatitis C, or human immunodeficiency virus
(HIV). Although parenteral transmission of these
diseases can occur following mucous membrane,
cutaneous, or percutaneous exposure to infected
body fluids, accidental injury with a needle contaminated with infected blood represents the most common occupational mechanism. The risk of
transmission can be estimated if three factors are
known: the prevalence of the infection within the
patient population, the incidence of exposure (eg,
frequency of needlestick), and the rate of seroconversion after a single exposure. The seroconversion
rate after a specific exposure depends on several factors, including the infectivity of the organism, the
stage of the patients disease (extent of viremia),
the size of the inoculum, and the immune status of
the healthcare provider. Rates of seroconversion following a single needlestick are estimated to range
10 between 0.3% and 30%. Hollow (hypodermic)
needles pose a greater risk than do solid (surgical) needles because of the potentially larger inoculum. The use of gloves, needleless systems, or
protected needle devices may decrease the incidence
of some (but not all) types of injury.
The initial management of needlesticks
involves cleaning the wound and notifying the
appropriate authority within the health care facility. After an exposure, anesthesia workers should
report to their institutions emergency or employee
health department for appropriate counseling on
Morg_Ch54_1199-1230.indd 1224
postexposure prophylaxis options. All OR staff

should be made aware of the institutions employee
health notification pathway for needle stick and
other injuries
Fulminant hepatitis B (1% of acute infections)
carries a 60% mortality rate. Chronic active hepatitis (<5% of all cases) is associated with an increased
incidence of cirrhosis of the liver and hepatocellular carcinoma. Transmission of the virus is primarily through contact with blood products or body
fluids. The diagnosis is confirmed by detection of
hepatitis B surface antigen (HBsAg). Uncomplicated recovery is signaled by the disappearance
of HBsAg and the appearance of antibody to the
surface antigen (anti-HBs). A hepatitis B vaccine is
available and is strongly recommended prophylactically for anesthesia personnel. The appearance of
anti-HBs after a three-dose regimen indicates successful immunization.
Hepatitis C is another important occupational
hazard in anesthesiology; 4% to 8% of hepatitis C
infections occur in healthcare workers. Most (50%
to 90%) of these infections lead to chronic hepatitis,
which, although often asymptomatic, can progress
to liver failure and death. In fact, hepatitis C is the
most common cause of nonalcoholic cirrhosis in the
United States. There is currently no vaccine to protect against hepatitis C infection.
Anesthesia personnel seem to be at a low, but
measureable, risk for the occupational contraction
of HIV. The risk of acquiring HIV infection following a single needlestick contaminated with blood
from an HIV-infected patient has been estimated at
0.4% to 0.5%. Because there are documented reports
of transmission of HIV from infected patients to
healthcare workers (including anesthesiologists),
the Centers for Disease Control and Prevention
proposed guidelines that apply to all categories of
patient contact. These universal precautions, which
are equally valid for protection against hepatitis B or
C infection, are as follows:
No recapping and the immediate disposal
ofcontaminated needles
Use of gloves and other barriers during contact
with open wounds and body fluids
Frequent hand washing
11/02/13 10:40 AM
Use of proper techniques for disinfection or the

disposal of contaminated materials
Particular caution by pregnant healthcare
workers, and no contact with patients by workers
who have exudative or weeping skin lesions
3. Substance Abuse
11 Anesthesiology is a high-risk medical spe-
cialty for substance abuse. Probable reasons

for this include the stress of anesthetic practice and
the easy availability of drugs with addiction potential (potentially attracting people at risk of addiction
to the field). The likelihood of developing substance
abuse is increased by coexisting personal problems
(eg, marital or financial difficulties) or a family history of alcoholism or drug addiction.
The voluntary use of nonprescribed moodaltering pharmaceuticals is a disease. If left untreated,
substance abuse often leads to death from drug
overdoseintentional or unintentional. One of the
greatest challenges in treating drug abuse is identifying the afflicted individual, as denial is a consistent
feature. Unfortunately, changes evident to an outside observer are often both vague and late: reduced
involvement in social activities, subtle changes in
appearance, extreme mood swings, and altered work
habits. Treatment begins with a careful, well-planned
intervention. Those inexperienced in this area would
be well advised to consult with their local medical
society or licensing authority about how to proceed.
The goal is to enroll the individual in a formal rehabilitation program. The possibility that one may
lose ones medical license and be unable to return to
practice provides powerful motivation. Some diversion programs report a success rate of approximately
70%; however, most rehabilitation programs report
a recurrence rate of at least 25%. Long-term compliance often involves continued participation in support groups (eg, Narcotics Anonymous), random
urine testing, and oral naltrexone therapy (a longacting opioid antagonist). Effective prevention strategies are difficult to formulate; better control of
drug availability is unlikely to deter a determined
individual. It is unlikely that education about the
severe consequences of substance abuse will bring
new information to the potential drug-abusing
Morg_Ch54_1199-1230.indd 1225
1225
physician. There remains controversy regarding the

rate at which anesthesia staff will experience recidivism. Many experts argue for a one strike and youre
out policy for anesthesiology residents who abuse
injectable drugs. The decision as to whether a fully
trained and certified physician who has been discovered to abuse injectable drugs should return to
anesthetic practice after completing a rehabilitation
program varies and depends on the rules and traditions of the practice group, the medical center,
the relevant medical licensing board, and the perceived likelihood of recidivism. Physicians returning to practice following successful completion of a
program must be carefully monitored over the long
term, as relapses can occur years after apparent successful rehabilitation. Alcohol abuse is a common
problem among physicians and nurses, and anesthesia personnel are no exception. Interventions for
alcohol abuse, as is true for injectable drug abuse,
must be carefully orchestrated. Guidance from the
local medical society or licensing authority is highly
recommended.
4. Ionizing Radiation Exposure

The use of imaging equipment (eg, fluoroscopy)
during surgery and interventional radiologic procedures exposes the anesthesiologist to the potential
12 risks of ionizing radiation. The three most
important methods of minimizing radiation
doses are limiting total exposure time during procedures, using proper barriers, and maximizing the
distance from the source of radiation. Anesthesiologists who routinely perform fluoroscopic image
guided invasive procedures should consider wearing
protective eyeware incorporating radiation shielding. Lead glass partitions or lead aprons with thyroid
shields are mandatory protection for all personnel
who are exposed to ionizing radiation. The inverse
square law states that the dosage of radiation varies
inversely with the square of the distance. Thus, the
exposure at 4 m will be one-sixteenth that at 1 m.
The maximum recommended occupational wholebody exposure to radiation is 5 rem/yr. This can be
monitored with an exposure badge. The health
impact on operating room personnel of exposure to
electromagnetic radiation remains unclear.
11/02/13 10:40 AM
1226
SECTION V
CASE DISCUSSION
Unexplained Intraoperative
Tachycardia & Hypertension
A 73-year-old man is scheduled for emergency
relief of an intestinal obstruction from a sigmoid
volvulus. The patient had a myocardial infarction 1 month earlier that was complicated by
congestive heart failure. His blood pressure is
160/90 mm Hg, pulse 110 beats/min, respiratory
rate 22 breaths/min, and temperature 38.8C.
Why is this case an emergency?
Strangulation of the bowel begins with venous
obstruction, but can quickly progress to arterial
occlusion, ischemia, infarction, and perforation.
Acute peritonitis could lead to severe dehydration,
sepsis, shock, and multiorgan failure.
What special monitoring is appropriate
for this patient?
Because of the history of recent myocardial
infarction and congestive heart failure, an arterial
line would be useful. Transesophageal echocardiography and pulse contour analysis monitors of
cardiac output could be used. Pulmonary arterial
otation catheters have often been used in the
past, but they are associated with signicant complications and current evidence does not indicate
that their use improves patient outcomes. Large
uid shifts should be anticipated. Furthermore,
information regarding myocardial supply (diastolic
blood pressure) and demand (systolic blood pressure, left ventricular wall stress, and heart rate)
should be continuously available. Central venous
pressure may not track left atrial pressure in a
patient with signicant left ventricular dysfunction.
What cardiovascular medications might
be useful during induction and maintenance
of general anesthesia?
Drugs causing severe tachycardia or extremes
in arterial blood pressure should be avoided.
During the laparotomy, gradual increases
in heart rate and blood pressure are noted.
ST-segment elevations appear on the electrocardiogram. A nitroglycerin infusion is started. The heart
Morg_Ch54_1199-1230.indd 1226
rate is now 130 beats/min, and the blood pressure

is 220/140 mm Hg. The concentration of volatile
anesthetic is increased, and metoprolol is administered intravenously in 1-mg increments. This results
in a decline in heart rate to 115 beats/min, with no
change in blood pressure. Suddenly, the rhythm
converts to ventricular tachycardia, with a profound
drop in blood pressure. As amiodarone is being
administered and the debrillation unit prepared,
the rhythm degenerates into ventricular brillation.
What can explain this series of events?
A dierential diagnosis of pronounced tachycardia and hypertension might include pheochromocytoma, malignant hyperthermia, or thyroid
storm. In this case, further inspection of the nitroglycerin infusion reveals a labeling error: although
the tubing was labeled nitroglycerin, the infusion
bag was labeled epinephrine.
How does this explain the paradoxic response
to metoprolol?
Metoprolol is a 1-adrenergic antagonist. It
inhibits epinephrines 1-stimulation of heart rate,
but does not antagonize -induced vasoconstriction. The net result is a decrease in heart rate, but a
sustained increase in blood pressure.
What is the cause of the ventricular
tachycardia?
An overdose of epinephrine can cause lifethreatening ventricular arrhythmias. In addition,
if the central venous catheter was malpositioned,
with its tip in the right ventricle, the catheter tip
could have stimulated ventricular arrhythmias.
What other factors may have contributed to this
anesthetic mishap?
Multiple factors will often combine to create an
anesthetic misadventure. Incorrect drug labels are
but one example of errors that can result in patient
injury. Inadequate preparation, technical failures,
knowledge decits, and practitioner fatigue or
distraction can all contribute to adverse outcomes.
Careful adherence to hospital policies, checklists,
patient identication procedures, and surgical and
regional block timeouts can all help to prevent iatrogenic complications.
11/02/13 10:40 AM
GUIDELINES
Practice advisory for the prevention of perioperative
peripheral neuropathies: a report by the American
Society of Anesthesiologists Task Force on prevention
of peripheral neuropathies. Anesthesiology
2000;92:1168.
SUGGESTED READING
Alexander B, Checkoway H, Nagahama S, Domino K:
Cause-specific mortality risks of anesthesiologists.
Berge E, Seppala M, Lanier W: The anesthesiology
communitys approach to opioid and anesthetic
abusing personnel: time to change course.
Bhananker S, Posner K, Cheney F, et al: Injury and
liability associated with monitored anesthesia care.
Bhananker S, Liau D, Kooner P, et al: Liability
related to peripheral venous and arterial
catheterization; a closed claims analysis. Anesth
Analg 2009;109:124.
Bishop M, Souders J, Peterson C, et al: Factors associated
with unanticipated day of surgery deaths in
Department of Veterans Affairs hospitals. Anesth
Analg 2008;107:1924.
Bowdle TA: Drug administration errors from
the ASA closed claims project. ASA Newslett
2003;67:11.
Brown RH, Schauble JF, Miller NR: Anemia and
hypotension as contributors to perioperative loss of
vision. Anesthesiology 1994;80:222.
Bryson E, Silverstein J: Addiction and substance abuse in
anesthesiology. Anesthesiology 2008;109:905.
Caplan RA, Ward RJ, Posner K, Cheney FW: Unexpected
cardiac arrest during spinal anesthesia: a closed claims
analysis of predisposing factors. Anesthesiology
1988;68:5.
Caplan RA, Vistica MF, Posner KL, Cheney FW: Adverse
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a LANGE medical book

John F. Butterworth IV, MD

John D. Wasnick, MD, MPH

Morgan & Mikhails Clinical Anesthesiology, Fifth Edition

This book was set in Minion Pro by Thomson Digital.

International Edition ISBN 978-0-07-181669-4 ; MHID 0-07-181669-0.

1 The Practice of Anesthesiology 1

15 Hypotensive Agents 255

2 The Operating Room Environment 9

17 Adjuncts to Anesthesia 277

4 The Anesthesia Machine 43

18 Preoperative Assessment, Premedication,

19 Airway Management 309

6 Noncardiovascular Monitoring 123

7 Pharmacological Principles 143

21 Anesthesia for Patients with

10 Analgesic Agents 189

24 Anesthesia for Patients

11 Neuromuscular Blocking Agents 199

25 Anesthesia for Thoracic Surgery 545

12 Cholinesterase Inhibitors & Other

26 Neurophysiology & Anesthesia 575

13 Anticholinergic Drugs 233

28 Anesthesia for Patients with

14 Adrenergic Agonists & Antagonists 239

27 Anesthesia for Neurosurgery 593

29 Renal Physiology & Anesthesia 631

33 Anesthesia for Patients with

34 Anesthesia for Patients with

Regional Anesthesia &

45 Spinal, Epidural, & Caudal Blocks 937

47 Chronic Pain Management 1023

48 Perioperative Pain Management &

37 Anesthesia for Otorhinolaryngologic

49 Management of Patients with

38 Anesthesia for Orthopedic Surgery 789

50 AcidBase Management 1141

Edward R. Mariano, MD, MAS

39 Anesthesia for Trauma &

40 Maternal & Fetal Physiology

41 Obstetric Anesthesia 843

42 Pediatric Anesthesia 877

51 Fluid Management &

56 Postanesthesia Care 1257

Srikanth Hosur, MBBS, MD

Michael Ramsay, MD, FRCA

Swapna Chaudhuri, MD, PhD

Research and Review

The fifth edition features three new chapters:

Case Discussions deal with clinical problems

Drug molecules obey the law of mass action.

Most drugs that readily cross the bloodbrain

Biotransformation is the chemical process

Small unbound molecules freely pass from

The clinical practice of anesthesiology is connected

reabsorbed in the renal tubules, whereas

Elimination half-life is the time required

The oset of a drugs eect cannot be

misidentification or misuse of pharmacokinetic

processes: absorption, distribution, biotransformation, and excretion.

However, rectal absorption can be erratic, and many

TABLE 71 Tissue group composition,

CHAPTER 7 Pharmacological Principles