a LANGE medical book
Clinical Anesthesiology Morgan & Mikh Mikhail’ ail’ss
F I F T H
E D I T I O N
John F. 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, MD, MPH Steven L. Berk Endowed Chair for Excellence in Medicine Professor and Chair Department of Anesthesia Texas Tex as Tech University Health Sciences Center School of Medicine Lubbock, Texas
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a LANGE medical book
Clinical Anesthesiology Morgan & Mikh Mikhail’ ail’ss
F I F T H
E D I T I O N
John F. 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, MD, MPH Steven L. Berk Endowed Chair for Excellence in Medicine Professor and Chair Department of Anesthesia Texas Tex as Tech University Health Sciences Center School of Medicine Lubbock, Texas
New York Chicago San Francisc Francisco o Lisbon London Madrid Mexico City Milan New Delhi San Juan Seoul Singapore Sydney Toronto
Morgan & Mikhail’s Clinical Anesthesiolog y, Fifth Edition Editi on
Copyright © 2013, 2006, 2002 by he McGraw-Hill Companies, Inc. All rights reserved. Printed in the United States. States. Except as permitted under the United States Copyright Act o 1976, no part o this publication may be reproduced or distributed in any orm or by any means, or stored in a data base or retrieval system, without the prior written permission o the publisher. Previous editions copyright © 1996, 1992 by Appleton Appleton & Lange. 1234567890
WC/WC
18 17 16 15 14 13
ISBN 978-0-07-1 978-0-07-162703-0 62703-0 MHID 0-07-16270 0-07-162703-0 3-0 ISSN 1058-4277
Notice Medicine is an ever-changing science. As n ew research and clinical experience broaden our knowledge, knowledge, changes in treatment and drug therapy are required. he authors and the publisher o this work have checked with sources believed to be reliable in their eorts to provide inormation that is complete and generally in accord with the standards accepted at the time o publication. However, in view o the possibility o human error or changes in medical sciences, neither the authors nor the publisher nor any other party who has been involved in the preparation or publication o this work warrants that the inormation contained herein is in every respect accurate or complete, and they disclaim all responsibility or any errors or omissions or or the results obtained rom use o the inormation contained in this work. Readers are encouraged to conirm the inormation contained herein with other sources. For example and in particular, readers are advised to check the product inormation sheet included in the package o each drug they plan to administer to be certain that the inormation contained in this work is accurate and that changes have not been made in the recommended dose or in the contraindications or administration. his recommendation is o particular importance in connection with new or inrequently used drugs.
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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
I
15 Hypotensive Agents 255 16 Local Anesthetics 263
Anesthetic Equipment & Monitors
2 The Operating Room Environment 9 Charles E. Cowles, MD
17 Adjuncts to Anesthesia 277 SECTION
III
Anesthetic Management
3 Breathing Systems 29 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
21 Anesthesia for Patients with
Cardiovascular Disease 375 22 Anesthesia for Cardiovascular
7 Pharmacological Principles 143 8 Inhalation Anesthetics 153 9 Intravenous Anesthetics 175 10 Analgesic Agents 189
Surgery 435 23 Respiratory Physiology
& Anesthesia 487 24 Anesthesia for Patients
with Respiratory Disease 527
11 Neuromuscular Blocking Agents 199
25 Anesthesia for Thoracic Surgery 545
12 Cholinesterase Inhibitors & Other
26 Neurophysiology & Anesthesia 575
Pharmacologic Antagonists to Neuromuscular Blocking Agents 223 13 Anticholinergic Drugs 233 14 Adrenergic Agonists & Antagonists 239
27 Anesthesia for Neurosurgery 593 28 Anesthesia for Patients with
Neurologic & Psychiatric Diseases 613
iii
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
33 Anesthesia for Patients with
Liver Disease 707 Michael Ramsay, MD, FRCA
34 Anesthesia for Patients with
Endocrine Disease 727
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
35 Anesthesia for Patients with
Neuromuscular Disease 747 36 Anesthesia for Ophthalmic
Surgery 759 37 Anesthesia for Otorhinolaryngologic
Surgery 773 38 Anesthesia for Orthopedic Surgery 789 Edward R. Mariano, MD, MAS
39 Anesthesia for Trauma &
Emergency Surgery 805 Brian P. McGlinch, MD
40 Maternal & Fetal Physiology
& Anesthesia 825 Michael A. Frölich, MD, MS
41 Obstetric Anesthesia 843 Michael A. Frölich, MD, MS
42 Pediatric Anesthesia 877 43 Geriatric Anesthesia 907 44 Ambulatory, Nonoperating
Room, & Offi ce-Based Anesthesia 919
SECTION
V
Perioperative & Critical Care Medicine
49 Management of Patients with
Fluid & Electrolyte Disturbances 1107 50 Acid–Base Management 1141 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
Chapter Authors Gabriele Baldini, MD, MSc Assistant Proessor Department o Anesthesia McGill University Montreal, Quebec John F. Butterworth IV, MD Proessor and Chairman Department o Anesthesiology Virginia Commonwealth University School o Medicine VCU Health System Richmond, Virginia Francesco Carli, MD, MPhil Proessor Department o Anesthesia McGill University Montreal, Quebec Charles E. Cowles, Jr, MD Assistant Proessor Department o Anesthesiology and Perioperative Medicine Chie Saety Offi cer Perioperative Enterprise University o exas MD Anderson Cancer Center Houston, exas Michael A. Frölich, MD, MS Associate Proessor Department o Anesthesiology University o Alabama at Birmingham Birmingham, Alabama Martin Giesecke, MD M.. “Pepper” Jenkins Proessor in Anesthesiology Vice Chair, University Hospitals Department o Anesthesiology and Pain Management University o exas Southwestern Medical Center Dallas, exas
Srikanth Hosur, MBBS, MD Consultant in Intensive Care QuestCare Intensivists Dallas, exas Brian M. Ilfeld, MD, MS Proessor, In Residence Department o Anesthesiology University o Caliornia, San Diego San Diego, Caliornia David C. Mackey, MD Proessor Department o Anesthesiology and Perioperative Medicine University o exas M.D. Anderson Cancer Center Houston, exas Sarah J. Madison, MD Assistant Clinical Proessor o Anesthesiology Department o Anesthesiology University o Caliornia, San Diego San Diego, Caliornia Edward R. Mariano, MD, MAS (Clinical Research) Associate Proessor o Anesthesia Stanord University School o Medicine Chie, Anesthesiology and Perioperative Care Service VA Palo Alto Health Care System Palo Alto, Caliornia Brian P. McGlinch, MD Associate Proessor Department o Anesthesiology Mayo Clinic Rochester, Minnesota Colonel, United States Army Reserve, Medical Corps 452 Combat Support Hospital Fort Snelling, Minnesota
v
vi
CHAPTER AUTHORS
Michael Ramsay, MD, FRCA Chairman Department o Anesthesiology and Pain Management Baylor University Medical Center President Baylor Research Institute Clinical Proessor University o exas Southwestern Medical School Dallas, exas Richard W. Rosenquist, MD Chair, Pain Management Department Anesthesiology Institute Cleveland Clinic Cleveland, Ohio
Bruce M. Vrooman, MD Department o Pain Management Anesthesiology Institute Cleveland Clinic Cleveland, Ohio John D. Wasnick, MD, MPH Steven L. Berk Endowed Chair or Excellence in Medicine Proessor and Chair Department o Anesthesia exas ech University Health Sciences Center School o Medicine Lubbock, exas
Contributors Kallol Chaudhuri, MD, PhD Proessor Department o Anesthesia exas ech University Health Sciences Center Lubbock, exas
Robert Johnston, MD Associate Proessor Department o Anesthesia exas ech University Health Sciences Center Lubbock, exas
Swapna Chaudhuri, MD, PhD Proessor Department o Anesthesia exas ech University Health Sciences Center Lubbock, exas
Sanford Littwin, MD Assistant Proessor Department o Anesthesiology St. Luke’s Roosevelt Hospital Center and Columbia University College o Physicians and Surgeons New York, New York
John Emhardt, MD Department o Anesthesia Indiana University School o Medicine Indianapolis, Indiana Suzanne N. Escudier, MD Associate Proessor Department o Anesthesia exas ech University Health Sciences Center Lubbock, exas Aschraf N. Farag, MD Assistant Proessor Department o Anesthesia exas ech University Health Sciences Center Lubbock, exas Herbert Gonzalez, MD Assistant Proessor Department o Anesthesia exas ech University Health Sciences Center Lubbock, exas Kyle Gunnerson, MD Department o Anesthesiology VCU School o Medicine Richmond, Virginia
Alina Nicoara, MD Assistant Proessor Department o Anesthesiology Duke University Medical Center Durham, North Carolina Bettina Schmitz, MD, PhD Associate Proessor Department o Anesthesia exas ech University Health Sciences Center Lubbock, exas Steven L. Shafer, MD Department o Anesthesia Stanord University School o Medicine Palo Alto, Caliornia Christiane Vogt-Harenkamp, MD, PhD Assistant Proessor Department o Anesthesia exas ech University Health Sciences Center Lubbock, exas Gary Zaloga, MD Global Medical Affairs Baxter Healthcare Deer�eld, Illinois
vii
Research and Review Jacqueline E. Geier, MD Resident, Department o Anesthesiology St. Luke’s Roosevelt Hospital Center New York, New York
Cecilia N. Pena, MD Resident, Department o Anesthesiology exas ech University Medical Center Hospital Lubbock, exas
Brian Hirsch, MD Resident, Department o Anesthesiology exas ech University Medical Center Lubbock, exas
Charlotte M. Walter, MD Resident, Department o Anesthesiology exas ech University Medical Center Lubbock, exas
Shane Huffman, MD Resident, Department o Anesthesiology exas ech University Medical Center Lubbock, exas
Karvier Yates, MD Resident, Department o Anesthesiology exas ech University Medical Center Lubbock, exas
Rahul K. Mishra, MD Resident, Department o Anesthesiology exas ech University Medical Center Lubbock, exas
ix
Foreword A little more than 25 years ago, Alexander Kugushev, then the editor or Lange Medical Publications, approached us to consider writing an introductory textbook in the specialty o anesthesiology that would be part o the popular Lange series o medical books. Mr. Kugushev proved to be a convincing salesman, in part by offering his experience with scores o authors, all o whom opined that their most satisying career achievement was the athering o their texts. We could not agree more. Now in its ith edition, the overall stylistic goal o 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 oundation or a resident in anesthesiology. o quote C. Philip Larson, Jr, MD rom the Foreword o the irst edition: “he text is complete; nothing o consequence is omitted. he writing style is precise, concise and highly readable.”
he ith edition eatures three new chapters: Ambulatory, Nonoperating Room, and Oicebased Anesthesia; Perioperative Pain Management and Enhanced Outcomes; and Saety, Quality, and Perormance Improvement. here are approximately 70 new igures and 20 new tables. he adoption o ull color dramatically improves the aesthetic appeal o every page. However, the biggest and most important change in the ith edition is the “passing o the baton” to a distinguished and accomplished team o authors and editors. We were thrilled to learn that Drs. Butterworth, Mackey, and Wasnick would be succeeding us. he result o their hard work proves our enthusiasm was justiied 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
Preface Authors should be proud whenever a book is su�ciently successul to require a new edition. Tis is especially true when a book’s consistent popularity over time leads to the succession o the original authors by a new set o authors. Tis latter circumstance is the case or the �fh edition o what most o us call “Morgan and Mikhail.” We hope that you the reader will �nd this new edition as readable and useul as you have ound the preceding our editions o the work. his ith edition, while retaining essential elements o its predecessors, represents a signiicant revision o the text. Only those who have written a book o this size and complexity will understand just how much eort 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. he number o illustrations devoted to regional anesthesia and analgesia has been greatly increased to adequately address the rapidly growing importance o this perioperative management topic. he clarity o the illustrations is also enhanced by the widespread use o color throughout the book. We hope the product o this endeavor provides readers with as useul an exercise as was experienced by the authors in composing it. • Key Concepts are listed at the beginning o each chapter and a corresponding numbered icon identi�es the section(s) within the chapter in which each concept is discussed. Tese should help the reader ocus on important concepts that underlie the core o anesthesiology.
• Case Discussions deal with clinical problems o current interest and are intended to stimulate discussion and critical thinking. • Te suggested reading has been revised and updated to include pertinent Web addresses and reerences to clinical practice guidelines and practice parameters. We have not tried to provide a comprehensive list o reerences: we expect that most readers o this text would normally perorm their own literature searches on medical topics using Google, PubMed, and other electronic resources. Indeed, we expect that an ever-increasing segment o our readers will access this text in one o its several electronic orms. • Multiple new illustrations and images have been added to this edition. Nonetheless, our goal remains the same as that o the �rst edition: “to provide a concise, consistent presentation o the basic principles essential to the modern practice o anesthesia.” We would like to thank Brian Belval, Harriet Lebowitz, and Marsha Loeb or their invaluable assistance. Despite our best intentions, various errors may have made their way into the ith edition. We will be grateul to readers who report these to us at
[email protected] so that we can correct them in reprints and uture editions. John F. Butterworth IV, MD David C. Mackey, MD John D. Wasnick, MD, MPH
xiii
SECTION II
Clinical Pharmacology C
Pharmacological Principles
H
A
P
T
E
R
7
KEY CO NCE PTS 1
2
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 blood–brain barrier (eg, lipophilic drugs like hypnotics and opioids) are avidly taken up in body fat.
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.
4
Small unbound molecules freely pass from plasma into the glomerular filtrate. The nonionized (uncharged) fraction of drug is
Te clinical practice o anesthesiology is connected more directly than any other specialty to the science o clinical pharmacology. One would think, thereore, that the study o pharmacokinetics and pharmacodynamics would receive attention comparable to that given to airway assessment, choice o inhalation anesthetic or ambulatory surgery, or neuromuscular blockade in anesthesiology curricula and examinations. Te requent
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.
6 The offset of a drug’s effect 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.
misidenti�cation or misuse o pharmacokinetic principles and measurements suggests that this is not the case.
PHARMACOKINETICS Pharmacokinetics de�nes the relationships among drug dosing, drug concentration in body �uids and tissues, and time. It consists o our linked 143
144
SECTION II
Clinical Pharmacology
processes: absorption, distribution, biotransormation, and excretion.
Absorption Absorption de�nes the processes by which a drug moves rom the site o administration to the bloodstream. Tere are many possible routes o drug administration: oral, sublingual, rectal, inhalational, transdermal, transmucosal, subcutaneous, intramuscular, and intravenous. Absorption is in�uenced by the physical characteristics o the drug (solubility, pK a, diluents, binders, and ormulation), dose, and the site o absorption (eg, gut, lung, skin, muscle). Bioavailability is the raction o the administered dose reaching the systemic circulation. For example, nitroglycerin is well absorbed by the gastrointestinal tract but has low bioavailability when administered orally. Te reason is that nitroglycerin undergoes extensive �rst-pass hepatic metabolism as it transits the liver beore reaching the systemic circulation. Oral drug administration is convenient, inexpensive, and relatively tolerant o dosing errors. However, it requires cooperation o the patient, exposes the drug to �rst-pass hepatic metabolism, and permits gastric pH, enzymes, motility, ood, and other drugs to potentially reduce the predictability o systemic drug delivery. Nonionized (uncharged) drugs are more readily absorbed than ionized (charged) orms. Tereore, an acidic environment (stomach) avors the absorption o acidic drugs (A– + H+ → AH), whereas a more alkaline environment (intestine) avors basic drugs (BH+ → H+ + B). Most drugs are largely absorbed rom the intestine rather than the stomach because o the greater surace area o the small intestine and longer transit duration. All venous drainage rom the stomach and small intestine �ows to the liver. As a result, the bioavailability o highly metabolized drugs may be signi�cantly reduced by �rst-pass hepatic metabolism. Because the venous drainage rom the mouth and esophagus �ows into the superior vena cava rather than into the portal system, sublingual or buccal drug absorption bypasses the liver and �rst-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.
However, rectal absorption can be erratic, and many drugs irritate the rectal mucosa. ransdermal drug administration can provide prolonged continuous administration or some drugs. However, the stratum corneum is an effective barrier to all but small, lipid-soluble drugs (eg, clonidine, nitroglycerin, scopolamine, entanyl, and ree-base local anesthetics [EMLA]). Parenteral routes o drug administration include subcutaneous, intramuscular, and intravenous injection. Subcutaneous and intramuscular absorption depend on drug diffusion rom the site o injection to the bloodstream. Te rate at which a drug enters the bloodstream depends on both blood �ow to the injected tissue and the injectate ormulation. Drugs dissolved in solution are absorbed aster than those present in suspensions. Irritating preparations can cause pain and tissue necrosis (eg, intramuscular diazepam). Intravenous injections completely bypass the process o absorption.
Distribution Once absorbed, a drug is distributed by the bloodstream throughout the body. Highly perused organs (the so-called vessel-rich group) receive a disproportionate raction o the cardiac output (Table 7–1). Tereore, these tissues receive a disproportionate amount o drug in the �rst minutes ollowing drug administration. Tese tissues approach equilibration with the plasma concentration more quickly than less well perused 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
6
Vessel-poor Bone, ligament, cartilage
20
0
CHAPTER 7
blood �ow. However, less well perused tissues such as at and skin may have enormous capacity to absorb lipophilic drugs, resulting in a l arge reservoir o drug ollowing long inusions. Drug molecules obey the law o mass action. 1 When the plasma concentration exceeds the concentration in tissue, the drug moves rom the plasma into tissue. When the plasma concentration is less than the concentration in tissue, the drug moves rom the tissue back to plasma. Distribution is a major determinant o endorgan drug concentration. Te rate o rise in drug concentration in an organ is determined by that organ’s perusion and the relative drug solubility in the organ compared with blood. Te equilibrium concentration in an organ relative to blood depends only on the relative solubility o the drug in the organ relative to blood, unless the organ is capable o metabolizing the drug. Molecules in blood are either ree or bound to plasma proteins and lipids. Te ree concentration equilibrates between organs and tissues. However, the equilibration between bound and unbound molecules is instantaneous. As unbound molecules o drug diffuse into tissue, they are instantly replaced by previously bound molecules. Plasma protein binding does not affect the rate o transer directly, but it does affect relative solubility o the drug in blood and tissue. I the drug is highly bound in tissues, and unbound in plasma, then the relative solubility avors drug transer into tissue. Put another way, a drug that is highly bound in tissue, but not in blood, will have a very large ree drug concentration gradient driving drug into the tissue. Conversely, i the drug is highly bound in plasma and has ew binding sites in the tissue, then transer o a small amount o drug may be enough to bring the ree drug concentration into equilibrium between blood and tissue. Tus, high levels o binding in blood relative to tissues increase the rate o onset o drug effect, because ewer molecules need to transer into the tissue to produce an effective ree drug concentration. Albumin binds many acidic drugs (eg, barbiturates), whereas α1-acid glycoprotein (AAG) binds basic drugs (local anesthetics). I the concentrations o these proteins are diminished or (typically less important) i the protein-binding sites are occupied
Pharmacological Principles
145
by other drugs, then the relative solubility o the drugs in blood is decreased, increasing tissue uptake. Kidney disease, liver disease, chronic congestive heart ailure, and malignancies decrease albumin production. rauma (including surgery), inection, myocardial inarction, and chronic pain increase AAG levels. Pregnancy is associated with reduced AAG concentrations. Note that these changes will have very little effect on propool, which is administered with its own binding molecules (the lipid in the emulsion). Lipophilic molecules can readily transer between the blood and organs. Charged molecules are able to pass in small quantities into most organs. However, the blood–brain barrier is a special case. Permeation o 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 blood–brain barrier (eg, lipophilic drugs like hypnotics and opioids) are avidly taken up in body at. Te time course o distribution o drugs into peripheral tissues is complex and can only be assessed with computer models. Following intra venous bolus administration, rapid distribution o drug rom the plasma into peripheral tissues accounts or the proound decrease in plasma concentration observed in the �rst ew 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. Te redistribution phase (or each tissue) ollows this moment o equilibration. During redistribution, drug returns rom peripheral tissues back into the plasma. Tis return o drug back to the plasma slows the rate o decline in plasma drug concentration. Distribution generally contributes to rapid emergence by removing drug rom the plasma or many minutes ollowing administration o a bolus inusion. Following prolonged inusions, redistribution generally delays emergence as drug returns rom tissue reservoirs to the plasma or many hours. Te complex process o drug distribution into and out o tissues is one reason that hal-lives are clinically useless. Te offset o a drug’s clinical actions are best predicted by computer models using the context-sensitive hal-time or decrement times. Te context-sensitive half-time is the time required
146
SECTION II
Clinical Pharmacology
or a 50% decrease in plasma drug concentration to occur ollowing a pseudo steady-state inusion (in other words, an inusion that has continued long enough to yield nearly steady-state concentrations). concentrations). Here the “context” is the duration o the inusion. Te context-sensitive decrement time is a more generalized concept reerring to any clinically relevant decreased concentration in any tissue, particularly the brain or effect site. Te volume o distribution, V d, is the apparent volume into which a drug has “distributed” (ie, mixed). Tis volume is calculated by dividing a bolus dose o drug by the plasma concentration at time 0. In practice, the t he concentration concentration used to de�ne the V d is ofen obtained by extrapolating subsequent concentrations back to “0 time” when the drug was injected, as ollows: V d =
Bolus dose Concentrationtime0
Te concept o a single V d does not apply to any intravenous drugs used in anesthesia. All intra venous anesthetic drugs are better modeled with at least two compartments: a central compartment and a peripheral compartment. Te behavior o many o these drugs is best described using three compartments: a central compartment, a rapidly equilibrating peripheral compartment, compartment, and a slowly equilibrating peripheral compartment. Te central compartment may be thought o as including the blood and any ultra-rapidly equilibrating tissues such as the lungs. Te peripheral compartment is composed o the other body tissues. For drugs with two peripheral compartments, the rapidly equilibrating compartment comprises comprises the organs and muscles, while the slowly equilibrating compartment compartment roughly represents represen ts distribution o the drug into at and skin. Tese compartments are designated V 1 (central), V 2 (rapid distribution), and V 3 (slow distribution). Te volume o distribution at steady state, V dss is the algebraic sum o these t hese compartment volumes. V 1 is calculated by the above equation showing the relationship between volume, dose, and concentration. Te other volumes are calculated through pharmacokinetic modeling. A small V dss implies that the drug has high aqueous solubility and will remain largely within the intravascular space. For example, the V dss o
pancuronium is about 15 L in a 70-kg person, indicating that pancuronium is mostly present in body water, with little distribution into at. However, the typical anesthetic drug is lipophilic, resulting in a V dss that exceeds total body water (approximately 40 L). For example, the V dss or entanyl is about 350 L in adults, and the V dss or propool may exceed 5000 L. V dss does not represent a real volume but rather re�ects the volume into which the drug would need to distribute to account or the observed plasma concentration concentra tion given the dose dos e that was administered.
Biotransformation 3 Biotransormation is the chemical process
by which the drug molecule is altered in the body. Te liver is the primary organ o metabolism or drugs. Te exception is esters, which undergo hydrolysis hydro lysis in the plasma or tissues. Te end products o biotransormation are ofen (but not necessarily) inactive and water soluble. Water solubility allows excretion by the kidneys. Metabolic biotransormation is requently 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 orm 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 biotransormation, and a phase II reaction can precede or occur without a phase I reaction. Hepatic clearance is the volume o blood or plasma (whichever was measured in the assay) cleared o drug per unit o time. Te units o clearance are units o �ow: volume per unit time. Clearance may be expressed in milliliters per minute minute,, liters per hour, or any other convenient unit o �ow. I every molecule o drug that enters the liver is metabolized, then hepatic clearance will equal liver blood �ow. Tis is true or very ew drugs, although it is very nearly the case or propool. For most drugs, only a raction o the drug that enters the liver is removed. Te raction removed is called the extraction ratio. ratio . Te hepatic clearance can theret hereore be expressed as the liver blood �ow times the
CHAPTER 7
extraction ratio. I the extraction ratio is 50%, then hepatic clearance is 50% o liver blood �ow. Te clearance o drugs efficiently removed rem oved by the liver (ie, having a high hepatic extraction ratio) is proportional to hepatic blood �ow. For example, because the liver removes almost all o the propool that goes through it, i the hepatic blood �ow doubles, then the clearance o propool doubles. Induction o liver enzymes has no effect on propool clearance, because bec ause the liver so efficiently removes re moves all o the propool that goes through it. Even severe loss o liver tissue, as occurs in cirrhosis, has little effect on propool clearance. Drugs such as propool have �ow-dependentt clearance. �ow-dependen Many drugs have low hepatic extraction ratios and are slowly cleared by the liver. For these drugs, the rate-limiting step is not the �ow o blood to the liver, but rather the metabolic capacity o the liver itsel. Changes in liver blood �ow have little effect on the clearance o such drugs. However, i liver enzymes are induced, then clearance will increase because the liver has more capacity to metabolize the drug. Conversely, i the liver is damaged, then less capacity is available or metabolism and clearance is reduced. Drugs with low hepatic extraction ratios thus have capacity-dependent clearance. Te extraction ratios o methadone and alentanil 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 o elimination o a drug rom the body by kidney excretion. Tis concept is analogous to hepatic clearance, and similarly, renal clearance can be expressed as the renal blood �ow times the renal extraction ratio. Small unbound drugs reely pass rom plasma 4 into the glomerular �ltrate. Te nonionized (uncharged) raction o drug is reabsorbed in the renal tubules, whereas the ionized (charged) portion is excreted in urine. Te raction o drug ionized depends on the pH; thus renal elimination o drugs that exist in ionized and nonionized orms depends in part on urinary pH. Te kidney actively secretes some drugs into the renal tubules. Many drugs and drug metabolites pass rom the liver into the intestine via the biliary system. Some
Pharmacological Principles
147
drugs excreted into the bile are then reabsorbed in the intestine, a process called enterohepatic recirculation.. Occasionally metabolites excreted in bile are lation subsequently converted converted back to the parent drug. For example,, lorazepam is converted by the liver to lorazexample epam glucuronide. In the intestine, β-glucuronidase breaks the ester linkage, converting lorazepam glucuronide back to lorazepam.
Compartment Models Multicompartment models provide a mathematical ramework that can be used to relate drug dose to changes in drug concentrations over time. Conceptually,, the compartmen Conceptually compartments ts in these models are tissues with a similar distribution time course. For example, the plasma and lungs are components o the central compartment. Te 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 o lipophilic drug but are poorly perused. Tese could represent the third, or slowly equilibrating, compartment. compartment. Tis is an intuitive de�nition o compartments, and it is important to recognize that the compartm compartments ents o a pharmacokin pharmacokinetic etic 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. Tis is generally the case i the studies used to characterize the pharmacokinetics do not include rapid arterial sampling over the �rst ew minutes (Figure 7–1). Without rapid arterial sampling the ultra-rapid initial drop in plasma concentration immediately afer 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 o identi�able compartments is a unction o the experimental design and not a characteristic o the drug. In compartmental models the instantaneous concentration at the time o a bolus injection is assumed to be the amount o the bolus divided by the central compartment volume. Tis is not
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Clinical Pharmacology
Distribution phase
Elimination phase
Time after dose IV bolus FIGURE 71 Two-compartment model demonstrates demonstrates the distribution phase ( α phase) and the elimination phase (β 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 rom the plasma. Instead, drug returns to the plasma rom the rapidly equilibrating compartment. compartment. Te reversed role o the rapidly equilibrating equilibrating tissues rom extracting drug to returning drug accounts or the slower rate o decline in plasma concentra concentration tion in this intermediate phase. Eventually there is an even slower rate o decrease in plasma concentration, which is log-linear until the drug is completely eliminated rom the body. Tis terminal log-linear phase occurs afer the slowly equilibrating compartment shifs rom net removal o drug rom the plasma to net return o drug to the plasma. During this terminal phase the organ o elimination (typically the liver) is exposed to the t he body’s body’s entire body drug load, which accounts or the very slow rate o decrease in plasma drug concentration during this �nal phase. Te mathematical models used to describe a drug with two or three compartments are, respectively: Cp(t) = Ae − αt + Be−βt and
correct. I the bolus is given over a ew seconds, the instantaneous concentration is 0, because the drug is all in the vein, still �owing to the heart. It takes only a minute or two or the drug to mix i n the central compartment volume. Tis misspeci�cation is common to conventional pharmacokinetic models. More physiologically based models, sometimes called front-end kinetic models models,, can characterize the initial delay in concentration. Tese models are useul only i the concentrations over the �rst ew minutes are clinically important. Afer the �rst ew minutes, ront-end models resemble conventional compartmental models. In the �rst ew minutes ollowing initial bolus administration o a drug, the concentration drops very rapidly rapidly as the drug quickly quickly diffuses into into peripheral compartments. Te decline is typically an order o magnitude over 10 minutes. For drugs with very rapid hepatic clearance (eg, propool) or those that are metabolized in the blood (eg, remientanil), metabolism contributes contributes signi�cantly to the rapid initial drop in concentra concentration. tion. Following this very rapid drop there is a period o slower decrease in plasma concentration. During this period, the rapidly
Cp(t) = Ae −αt + Be −βt + Ce −γ t
where Cp Cp((t ) equals plasma concentration at time t , and α, β, and γ are the exponents that characterize the very rapid (ie, very steep), intermediate, and slow (ie, log-linear) portions o the plasma concentration over time, respectively. Drugs described by two-compartment and three-compartment models will have two or three hal-lives. Each hal-lie i s calculated as the natural log o 2 (0.693), divided by the exponent. Te coeffi coe fficients cients A A,, B, and C represent represent the contribution o each o the exponents to the overall decrease in concentra concentration tion over time. Te two-compartment model is described by a curve with two exponents ex ponents and two coefficients, whereas the three-compartment model is described by a curve cur ve with three exponents e xponents and a nd three coefficients. Te mathematical relationships among compartments,, clearances, partments clear ances, coeffi c oefficients, and exponents expone nts are complex. Every coeffi c oefficient and every ever y exponent is a unction o every volume and every clearance. Elimination hal-lie is the time required or the 5 drug concentration to all by 50%. For drugs described by multicompartment pharmacokinetics
CHAPTER 7
(eg, all drugs used in anesthesia), there are multiple elimination hal-lives, in other words the elimination hal-time is context dependent. Te offset o a 6 drug’s effect cannot be predicted rom hallives. Moreover, one cannot easily determine how rapidly a drug effect will disappear simply by looking at coefficients, exponents, and hal-lives. For example, the terminal hal-lie o suentanil is about 10 h, whereas that o alentanil is 2 h. Tis does not mean that recovery rom alentanil will be aster, because clinical recovery rom clinical dosing will be in�uenced by all hal-lives, not just the terminal one. Computer models readily demonstrate that recovery rom an inusion lasting several hours will be aster when the drug administered is suentanil than it will be when the inused drug is alentanil. Te time required or a 50% decrease in concentration depends on the duration or “context” o the inusion. Te context-sensitive hal-time, discussed earlier, captures this concept and should be used instead o hal-lives to compare the pharmacokinetic properties o intra venous drugs used in anesthesia.
Pharmacological Principles
149
scale (Figure 7–2B), while the response is typically plotted either as the actual measured response (Figure 7–2A) or as a raction o the baseline or maximum physiological measurement (Figure 7–2B). For our purposes here, basic pharmacodynamic properties are described in terms o concentration, but any metric o drug exposure (dose, area under the curve, etc) could be used. Te shape o the relationship is typically sigmoidal, as shown in Figure 7–2. Te sigmoidal
A
20 ) g H 15 m m ( P A M10 n i p o r D
5
PHARMACODYNAMICS Pharmacodynamics, the study o how drugs affect the body, involves the concepts o potency, effi cacy, and therapeutic window. Pharmacokinetic models can range rom entirely empirical dose versus response relationships to mechanistic models o ligand–receptor binding. Te undamental pharmacodynamic concepts are captured in the relationship between exposure to a drug and physiological response to the drug, ofen called the dose–response or concentration–response relationship.
Exposure–Response Relationships As the body is exposed to an increasing amount o a drug, the response to the drug similarly increases, typically up to a maximal value. Tis undamental 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 body’s 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 7–2A) or a logarithmic
10
20 30 Dose (mg)
40
B
100 e s n o 75 p s e r l a m i x 50 a m f o %
25
1
10 Dose (mg)
100
1000
FIGURE 72 The shape of the dose–response curve
depends on whether the dose or steady-state plasma concentration (C cpss) is plotted on a linear A: or logarithmic B: scale. MAP, mean arterial pressure.
150
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shape re�ects the observation that ofen a certain amount o drug must be present beore there is any measurable physiological response. Tus, the lef side o the curve is �at until the drug concentration reaches a minimum threshold. Te right side is also �at, re�ecting the maximum physiological response o the body, beyond which the body simply cannot respond to additional drug (with the possible exception o eating and weight). Tus, the curve is �at on both the lef 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 Te sigmoidal relationship between exposure and response is de�ned by one o two interchangeable relationships: E�ect = E0 + E max
C γ C 50γ + C γ
or C γ E�ect = E0 + (E max − E 0 ) C 50γ + C γ
In both cases, E0 is the baseline effect in the absence o drug, C is drug concentration, C 50 is the concentration associated with hal-maximal effect, and γ describes the steepness o the concentration versus response relationship. For the �rst equation, Emax is the maximum change rom baseline. In the second equation, Emax is the maximum physiological measurement, not the maximum change rom baseline. Once de�ned in this ashion, each parameter o the pharmacodynamic model speaks to the speci�c concepts mentioned earlier. Emax is related to the intrinsic effi cacy o a drug. Highly efficacious drugs have a large maximum physiological effect, characterized by a large Emax. For drugs that lack effi cacy, Emax will equal E0. C 50 is a measure o drug potency. Highly potent drugs have a low C 50; thus small amounts produce the drug effect. Drugs lacking potency have a high C 50, indicating that a large amount o drug is required to achieve the drug effect. Te parameter γ indicates steepness o the relationship between concentration and effect. A γ value less than 1 indicates a very gradual increase in drug effect with increasing concentration. A
γ 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. Te curve described above represents the relationship o drug concentration to a continuous physiological response. Te same relationship can be used to characterize the probability o a binary (yes/no) response to a drug dose: Probability = P 0 + (P max − P 0 )
C γ C 50γ + C γ
In this case, the probability (P ) ranges rom 0 (no chance) to 1 (certainty). P 0 is the probability o a “yes” response in the absence o drug. P max is the maximum probability, necessarily less than or equal to 1. As beore, C is the concentration, C 50 is the concentration associated with hal-maximal effect, and γ describes the steepness o the concentration versus response relationship. Hal-maximal effect is the same as 50% probability o a response when P 0 is 0 and P max is 1. Te therapeutic window or a drug is the range between the concentration associated with a desired therapeutic effect and the concentration associated with a toxic drug response. Tis 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 de�nes the relationship between concentration and decrease in blood pressure. Te 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, or a drug such as lidocaine, the therapeutic window might be the difference between the C 50 or local anesthesia and the C 50 or lidocaineinduced seizures, the latter being a separate concentration versus response relationship. Te therapeutic index is the C 50 or toxicity divided by the C 50 or the desired therapeutic effect. Because o the risk o 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.
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Pharmacological Principles
151
then we can solve or 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 o the agonist but do not otherwise exert an effect o their own. Competitive antagonism occurs when the antagonist competes with the agonist or the binding site, each potentially displacing the other. Noncompetitive antagonism occurs when the antagonist, through covalent binding or another process, permanently impairs the drug’s access to the receptor. Te drug effect is governed by the raction o receptors that are occupied by an agonist. Tat raction is based on the concentration o the drug, the concentration o the receptor, and the strength o binding between the drug and the receptor. Tis binding is described by the law o mass action, which states that the reaction rate is proportional to the concentrations o the reactants: [D][RU ]
k on
[DR]
koff
where [D] is the concentration o the drug, [RU ] is the concentration o unbound receptor, and [DR] is the concentration o bound receptor. Te rate constant kon de�nes the rate o ligand binding to the receptor. Te rate constant koff de�nes the rate o ligand unbinding rom the receptor. According to the law o mass action, the rate o receptor binding, d [DR]/dt is: d [DR] = [D][RU ] k on − [DR]k off dt
Steady state occurs almost instantly. Because the rate o ormation at steady state is 0, it ollows that: [D][RU ] k on = [DR] k off
In this equation, kd is the dissociation rate constant, de�ned as kon /koff . I we de�ne f , ractional receptor occupancy, as: [DR] [DR] + [ RU ]
f =
[D]
kd
+
[D]
Te receptors are hal occupied when [D] = kd. Tus, kd is the concentration o drug associated with 50% receptor occupancy. Receptor occupancy is only the �rst step in mediating drug effect. Binding o the drug to the receptor can trigger a myriad o subsequent steps, including opening or closing o an ion channel, activation o a G protein, activation o an intracellular kinase, direct interaction with a cellular structure, or direct binding to DNA. Like the concentration versus response curve, the shape o the curve relating ractional receptor occupancy to drug concentration is intrinsically sigmoidal. However, the concentration associated with 50% receptor occupancy and the concentration associated with 50% o maximal drug effect are not necessarily the same. Maximal drug effect could occur at very low receptor occupancy, or (or partial agonists) at greater than 100% receptor occupancy. Prolonged binding and activation o a receptor by an agonist may lead to hyporeactivity (“desensitization”) and tolerance. I the binding o an endogenous ligand is chronically blocked, then receptors may prolierate 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 & Gilman’s Te Pharmacological Basis of Terapeutics, 12th ed. McGraw-Hill, 2010: Chap 2. Keier J, Glass P: Context-sensitive hal-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.
C
Peripheral Nerve Blocks Sarah J. Madison, MD and Brian M. Ilfeld, MD, MS
H
A
P
T
E
R
46
KEY CO NCE PTS 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 incidence of chronic pain.
6 The axillary, musculocutaneous, and medial
2
Regional anesthetics should be administered in an area where standard hemodynamic monitors, supplemental oxygen, and resuscitative medications and equipment are readily available.
7
3
Local anesthetic may be deposited at any point along the brachial plexus, depending on the desired block effects: 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 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.
8
Intravenous regional anesthesia, also called a Bier block, can provide intense surgical anesthesia for short surgical procedures (45–60 min) on an extremity.
9
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.
1
4
5
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.
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.
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
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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 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) block is added, complete anesthesia below the knee is provided. 13 A complete ankle block requires a series of
five nerve blocks, but the process may be streamlined to minimize needle insertions. 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.
An understanding o regional anesthesia anatomy and techniques is required o the well-rounded anesthesiologist. Although anatomic relationships have not changed over time, our ability to identiy them has evolved. From the paresthesia-seeking techniques described by Winnie in the mid-twentieth century, to the popularization o the nerve stimulator, to the introduction o ultrasound guidance, anesthesiologists and their patients have beneitted rom technology’s evolution. he ield o regional anesthesia has accordingly expanded to one that addresses not only the intraoperative concerns o the anesthesiologist, but also longer term perioperative pain management. In addition to potent analgesia, regional 1 anesthesia may lead to reductions in the stress response, systemic analgesic requirements, opioid-related side eects, general anesthesia requirements, and possibly the development o chronic pain.
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
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. 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 Te selection o a regional anesthetic technique is a process that begins with a thorough history and physical examination. Although many patients are candidates or regional anesthesia/analgesia, as with any medical procedure a risk–bene�t analysis must be perormed. Te risk–bene�t ratio ofen avors regional anesthesia in patients with multiple comorbidities or whom a general anesthetic carries a greater risk. In addition, patients intolerant to systemic analgesics (eg, those with obstructive sl eep apnea or at high risk or nausea) may bene�t rom the opioid-sparing effects o 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 inusion). A comprehensive knowledge o anatomy and an understanding o the planned surgical procedure are
CHAPTER 46 Peripheral Nerve Blocks
important or selection o the appropriate regional anesthetic technique. I possible, discussion with the surgeon about various considerations (tourniquet placement, bone grafing, projected surgical duration) is ideal. Also, knowing the anticipated course o recovery and anticipated level o postoperative pain will ofen in�uence speci�c 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 saety o every regional anesthetic procedure; patients who are unable to remain still or 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 o local hematoma or hemorrhage, and this risk must be balanced against the possible bene�ts o regional block. Speci�c 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 o a block needle through a site o inection can theoretically track inectious material into the body, where it poses a risk to the target nerve tissue and surrounding structures. Tereore, the presence o a local inection is a relative contraindication to perorming a peripheral nerve block. Indwelling perineural catheters can serve as a nidus o inection; however, the risk in patients with systemic inection 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 o complications, including prolonged or permanent sensorimotor block. Te precise mechanisms have yet to be clearly de�ned but may involve local ischemia rom high injection pressure or vasoconstrictors, a neurotoxic effect o local anesthetics, or direct trauma to nerve tissue.
977
Other risks associated with regional anesthesia include local anesthetic toxicity rom intravascular injection or perivascular absorption. In the event o a local anesthetic toxic reaction, seizure activity and cardiovascular collapse may occur. Supportive measures should begin immediately, including solicitation o assistance with a code blue, the initiation o cardiopulmonary resuscitation, lipid emulsion administration to sequester local anesthetic, and preparation or cardiopulmonary bypass. Site-speci�c risks should also be considered or each individual patient. In a patient with severe pulmonary compromise or hemidiaphragmatic paralysis, or example, a contralateral interscalene or deep cervical plexus block with resultant phrenic nerve block could be disastrous.
CHOICE OF LOCAL ANESTHETIC Te decision about which local anesthetic to employ or a particular nerve block depends on the desired onset, duration, and relative blockade o sensory and motor �bers. Potential or toxicity should be considered, as well as site-speci�c risks. A detailed discussion o local anesthetics is provided elsewhere (see Chapter 16).
PREPARATION 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 o end-tidal CO2 and raction o inspired oxygen (Fi�2) should also be available. Positioning should be ergonomically avorable or the practitioner and comortable or the patient. Intravenous premedication should be employed to allay anxiety and minimize discomort. A relatively short-acting benzodiazepine and opioid are most ofen used and should be titrated or comort while ensuring that patients respond to verbal cues. Sterile technique should be strictly observed.
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FIGURE 461 A field block targets terminal cutaneous nerves, such as the intercostobrachial nerve.
BLOCK TECHNIQUES Field Block Technique A �eld block is a local anesthetic injection that targets terminal cutaneous nerves (Figure 46–1). Field blocks are used commonly by surgeons to minimize incisional pain and may be used as a supplementary technique or as a sole anesthetic or minor, super�cial procedures. Anesthesiologists ofen use �eld blocks to anesthetize the super�cial cervical plexus or procedures involving the neck or shoulder; the intercostobrachial nerve or surgery involving the medial upper extremity proximal to the elbow (in combination with a brachial plexus nerve block); and the saphenous nerve or 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 rom inection prevents effective local anesthetic unctioning.
Paresthesia Technique Formerly the mainstay o regional anesthesia, this technique is now rarely used or nerve localization. Using known anatomic relationships and surace 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 o sensory distribution.
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 stimulator—a battery-powered machine that emits a small amount (0–5 mA) o electric current at a set interval (usually 1 or 2 Hz). A grounding electrode is attached to the patient to complete the circuit (Figure 46–2). When the insulated needle is placed in
CHAPTER 46 Peripheral Nerve Blocks
979
technique, 30–40 mL o 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 speci�c 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 speci�c 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 or peripheral nerve localization is becoming increasingly popular; it may be used alone or combined with other modalities such as nerve stimulation. Ultrasound uses high-requency (1–20 MHz) sound waves emitted rom piezoelectric crystals that travel at different rates through tissues o dierent densities, returning a signal to the transducer. Depending on the amplitude o signal received, the crystals deorm to create an electronic voltage that is converted into a two-dimensional grayscale image. Te degree o 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 re�ecting more sound waves appear brighter—or white—on the ultrasound screen, and are termed hyperechoic. Te optimal transducer varies depending upon the depth o the target nerve and approach angle o the needle relative to the transducer (Figure 46–3). High-requency transducers provide a high-resolution picture with a relatively clear image but
Curvilinear
No image Poor Good
FIGURE 463 A linear probe offers higher resolution with less penetration. A curvilinear probe provides better penetration with lower resolution.
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A
B
FIGURE 464 In-plane (A) and out-of-plane (B) ultrasound approaches.
offer poor tissue penetration and are thereore used predominantly or more super�cial nerves. Lowrequency transducers provide an image o poorer quality but have better tissue penetration and are thereore used or deeper structures. ransducers with a linear array offer an undistorted image and are thereore ofen the �rst choice among practitioners. However, or deeper target nerves that require a more acute angle between the needle and long-axis o the transducer, a curved array (curvilinear) transducer will maximize returning ultrasound waves, providing the optimal needle image (Figure 46–3). 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 o plane”) to the plane o the ultrasound waves (Figure 46–4). Unlike nerve stimulation alone, ultrasound guidance allows or a variable volume o local anesthetic to be injected, with the �nal amount determined by what is observed under direct vision. Tis technique usually results in a ar lower injected volume o local anesthetic (10–30 mL).
Continuous Peripheral Nerve Blocks Also termed perineural local anesthetic infusion, continuous peripheral nerve blocks involve the
placement o a percutaneous catheter adjacent to a peripheral nerve, ollowed by local anesthetic administration to prolong a nerve block (Figure 46–5). Potential advantages appear to depend on successully improving analgesia and include reductions in resting and dynamic pain, supplemental analgesic requirements, opioid-related side effects, and sleep disturbances. In some cases patient satisaction, ambulation, and unctioning may be improved; an accelerated resumption o passive joint range-o-motion realized; and reduced time until discharge-readiness as well as actual discharge rom the hospital or rehabilitation center achieved. Tere are many types o catheters, including nonstimulating and stimulating, �exible 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 inused, as adjuvants do not add bene�ts to perineural inusions (unlike single-injection peripheral nerve blocks). Longacting local anesthetics (eg, ropivacaine) are more commonly used as they provide a more avorable sensory-to-motor block ratio (optimizing analgesia while minimizing motor block). In an attempt to urther minimize any induced motor block, dilute
CHAPTER 46 Peripheral Nerve Blocks
981
FIGURE 465 Placement of a percutaneous catheter adjacent to a peripheral nerve.
local anesthetic (0.1–0.2%) is ofen inused; however, recent evidence suggests that it is the total dose, and not concentration, that determines the majority o block effects. Unlike single-injection peripheral nerve blocks, no adjuvant added to a perineural local anesthetic infusion has been demonstrated to be o bene�t. Te local anesthetic may be administered exclusively as repeated bolus doses or a basal inusion, or as a combination o the two methods. Using a small, portable inusion pump ( Figure 46–6), 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. Tereore, these inusions are usually reserved or patients having procedures expected to result in postoperative pain that is di�cult to control with oral analgesics and will not resolve in less time than the duration o a singleinjection peripheral nerve block. Serious complications, which are relatively rare, include systemic local anesthetic toxicity, catheter retention, nerve injury, inection, and retroperitoneal hematoma
ormation. In addition, a perineural inusion affecting the emoral nerve increases the risk o alling, although to what degree and by what speci�c mechanism (eg, sensory, motor, or proprioception de�cits) remain unknown.
UPPER EXTREMITY PERIPHERAL NERVE BLOCKS Brachial Plexus Anatomy Te brachial plexus is ormed by the union o the anterior primary divisions (ventral rami) o the �fh through the eighth cervical nerves and the �rst thoracic nerves. Contributions rom C4 and 2 are ofen minor or absent. As the nerve roots leave the intervertebral oramina, they con verge, orming trunks, divisions, cords, branches, and then �nally terminal nerves. Te three distinct trunks ormed between the anterior and middle scalene muscles are termed superior, middle, and inerior based on their vertical orientation. As the trunks pass over the lateral border o the �rst rib
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Regional Anesthesia & Pain Management
B
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 �bers combine again to orm three cords that are named according to their relationship to the axillary artery: lateral, medial, and posterior. At the lateral border o the pectoralis minor muscle, each cord gives off a large branch beore ending as a major terminal nerve. Te lateral cord gives off t he lateral branch o the median nerve and terminates as the musculocutaneous nerve; the medial cord gives off the medial branch o 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 46–7): interscalene or shoulder and proximal humerus surgical procedures; and supracla vicular, inraclavicular, and axillar y or surgeries distal to the mid-humerus.
Interscalene Block An interscalene brachial plexus block is indicated or procedures involving the shoulder and upper arm (Figure 46–8). Roots C5–7 are most densely blocked with this approach; and the ulnar nerve originating rom C8 and 1 may be spared. Tereore, interscalene blocks are not appropriate or surgery at or distal to the elbow. For complete surgical anesthesia o the shoulder, the C3 and C4 cutaneous branches may need to be supplemented with a super�cial cervical plexus block or local in�ltration. Contraindications to an interscalene block include local inection, severe coagulopathy, local 4 anesthetic allergy, and patient reusal. A properly perormed interscalene block invariably blocks the ipsilateral phrenic nerve (completely or nerve stimulation techniques; unclear or ultrasound-guided techniques), so careul consideration should be given to patients with severe pulmonary disease or preexisting contralateral phrenic nerve palsy. Te hemidiaphragmatic paresis may result in
CHAPTER 46 Peripheral Nerve Blocks
Anterior (palmar) view
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
Supraclavicular nerves (from cervical plexus)
Axillary nerve Superior lateral brachial cutaneous nerve
983
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 effects of the block.
dyspnea, hypercapnia, and hypoxemia. A Horner’s syndrome (myosis, ptosis, and anhidrosis) may result rom proximal tracking o local anesthetic and blockade o sympathetic �bers to the cervicothoracic ganglion. Recurrent laryngeal nerve involvement ofen induces hoarseness. In a patient with contralateral vocal cord paralysis, respiratory distress may ensue. Other site-speci�c risks include vertebral artery injection (suspect i immediate seizure activity is observed), spinal or epidural injection, and pneumothorax. Even 1 mL o local anesthetic delivered into the vertebral artery may induce a seizure. Similarly, intrathecal, subdural, and epidural local anesthetic spread is possible.
Lastly, pneumothorax is possible due to the close proximity o the pleura. Te brachial plexus passes between the anterior and middle scalene muscles at the level o the cricoid cartilage, or C6 (Figure 46–9). Palpation o the interscalene groove is usually accomplished with the patient supine and the head rotated 30° or less to the contralateral side. Te external jugular vein ofen crosses the interscalene groove at the level o the cricoid cartilage. Te interscalene groove should not be conused with the groove between the sternocleidomastoid and the anterior scalene muscle, which lies urther anterior. Having the patient lif and turn the head against resistance ofen helps delineate the
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Interscalene
Nerves or plexus roots C4 Trunks C5
Divisions
C6
Cords Upper trunk
Main branches r a l L a t e
c o r d
o r d io r c r e s t P o
o r d i a l c d e M
u n k e t r l d M i d
C7
C8 Lower trunk T1
FIGURE 468 An interscalene block is appropriate for shoulder and proximal humerus procedures. The ventral rami of C5–C8 and T1 form the brachial plexus.
CHAPTER 46 Peripheral Nerve Blocks
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. I surgical anesthesia is desired or the entire shoulder, the intercostobrachial nerve must usually be targeted separately with a �eld block since it originates rom 2 and is not affected with an interscalene block. Interscalene perineural inusions provide potent analgesia ollowing shoulder surgery.
A. Nerve Stimulation A relatively short (5-cm) insulated needle is usually employed. Te interscalene groove is palpated using the nondominant hand, pressing �rmly to stabilize the skin against the underlying structures (Figure 46–10). Afer the skin is anesthetized, the block needle is inserted at a slightly medial and caudad angle and advanced to optimally elicit a motor response o the deltoid or biceps muscles (suggesting stimulation o the superior trunk). A motor response o the diaphragm indicates that the needle is placed in too anterior a direction; a motor response o the trapezius or serratus anterior muscles indicates t hat the needle is placed in too posterior a direction. I bone (transverse process) is contacted, the needle should be redirected more anteriorly. Aspiration o arterial blood should raise concern or vertebral or carotid artery puncture; the needle should be
FIGURE 4610 Interscalene block using nerve stimulation.
withdrawn, pressure held or 3–5 min, and landmarks reassessed.
B. Ultrasound A needle in-plane or out-o-plane technique may be used, and an insulated needle attached to a nerve stimulator can be used to con�rm the accuracy o the targeted structure. For both techniques, afer identi�cation o the sternocleidomastoid muscle and interscalene groove at the approximate level o C6, a high-requency linear transducer is placed perpendicular to the course o the interscalene muscles (short axis; Figure 46–11). Te brachial plexus and anterior and middle scalene muscles should be visualized in cross-section (Figure 46–12). Te brachial plexus at this level appears as three to �ve hypoechoic circles. Te carotid artery and internal jugular vein may be seen lying anterior to the anterior scalene muscle; the sternocleidomastoid is visible super�cially as it tapers to orm its lateral edge. For an out-o-plane technique, the block needle is inserted just cephalad to the transducer and advanced in a caudal direction toward the visualized plexus. Afer careul aspiration or nonappearance o blood, local anesthetic (hypoechoic) spread
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middle scalene muscle until it has passed through the ascia anteriorly into the interscalene groove. Te needle tip and shaf should be visualized during the entire block perormance. Depending on visualized spread relative to the target nerve(s), a lower volume (10 mL) may be employed or postoperative analgesia, whereas a larger volume (20–30 mL) is commonly used or 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 helpul to have the patient turn slightly laterally with the affected side up to acilitate manipulation o the needle. Te needle is advanced through the
Once described as the “spinal o the arm,” a supraclavicular block offers dense anesthesia o the brachial plexus or surgical procedures at or distal to the elbow ( Figure 46–13). Historically, the supraclavicular block ell out o avor due to the high incidence o complications (namely, pneumothorax) that occurred with paresthesia and nerve stimulator techniques. It has seen a resurgence in recent years as the use o ultrasound guidance has theoretically improved saety. Te supraclavicular block does not reliably anesthetize the axillary and suprascapular nerves, and thus is not ideal or shoulder surgery. Sparing o distal branches, particularly the ulnar nerve, may occur. Supraclavicular perineural catheters provide inerior analgesia compared with inraclavicular inusion and are ofen displaced due to a lack o muscle mass to aid catheter retention.
SCM
N ASM
N N
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.
MSM
CHAPTER 46 Peripheral Nerve Blocks
987
Supraclavicular
Nerves or plexus roots C4 Trunks C5
Divisions
C6
Cords Upper trunk
Main branches r d l c o a r e L a t r d r c o o i r s t e P o
o r d i a l c d e M
u n k e t r l d M i d
C7
C8 Lower trunk T1
FIGURE 4613 A supraclavicular block can provide dense anesthesia for procedures at or distal to the elbow. Light blue shading indicates regions of variable block ade; purple shading indicates regions of more reliable blockade.
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Many o the same precautions that are taken with patient selection or an interscalene block should be exercised with a supraclavicular block. Nearly hal o patients undergoing supraclavicular block will experience ipsilateral phrenic nerve palsy, although this incidence may be decreased by using ultrasound guidance, allowing use o a minimal volume o local anesthetic. Horner’s 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 Te patient should be supine with the head turned 30o toward the contralateral side. A linear, highrequency transducer is placed in the supraclavicular ossa superior to the clavicle and angled slightly toward the thorax (Figure 46–14). Te subclavian artery should be easily identi�ed. Te brachial plexus appears as multiple hypoechoic disks just super�cial and lateral to the subclavian artery (Figure 46–15). Te �rst rib should also be identi�ed as a hyperechoic line just deep to the artery. Pleura may be identi�ed adjacent to the rib, and can be distinguished rom bone by its movement with breathing. For an out-o-plane technique, a short, 22-gauge blunt-tipped needle is used. Te 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. Afer careul aspiration or the nonappearance o blood, 30–40 mL o 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. Te needle is inserted lateral to the transducer in a direction parallel to the ultrasound beam. Te needle is advanced medially toward the subclavian artery until the tip is visualized near the brachial plexus just lateral and super�cial 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.
CHAPTER 46 Peripheral Nerve Blocks
artery. Local anesthetic spread should be visualized surrounding the plexus afer careul aspiration and incremental injection, which ofen requires injections in multiple locations and a highly variable volume (20–30 mL).
Infraclavicular Block Brachial plexus block at the level o the cords provides excellent anesthesia or procedures at or distal to the elbow ( Figure 46–16). Te upper arm and shoulder are not anesthetized with this approach. As with other brachial plexus blocks, the intercostobrachial nerve (2 dermatome) is spared. Site-speci�c risks o the inracla vicular approach include vascular puncture and pneumothorax (although less common than with supraclavicular block). It is ofen 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 �rst rib and into the axilla, the cords are arranged around the axillary artery according to their anatomic position: medial, lateral, and posterior.
5
A. Nerve Stimulation Te patient is positioned supine with the head turned to the contralateral side, and the coracoid process is identi�ed (a bony prominence o the scapula that can be palpated between the acromioclavicular joint and the deltopectoral groove). Te subclavian artery and brachial plexus run deep to the coracoid process and can be ound approximately 2 cm medial and 2 cm caudad to it, about 4–5 cm deep in the average patient (Figure 46–17). A relatively long (8 cm) insulated needle is placed perpendicular to the skin and advanced directly posterior until a motor response is elicited. An acceptable motor response is �nger �exion or extension at a current less than 0.5 mA, but not elbow �exion/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 46–18A). (Abducting the arm 90o improves axillary artery imaging.) A high-requency linear transducer will
989
ofen provide inadequate needle visualization due to the relatively acute needle-to-transducer angle. Te axillary artery and vein are identi�ed in crosssection (Figure 46–18B). Te medial, lateral, and posterior cords appear as hyperechoic bundles positioned caudad, cephalad, and posterior to the ar tery, respectively. A relatively long needle is inserted 2–3 cm cephalad to the transducer. Optimal needle positioning is between the axillary artery and the posterior cord. Tree randomized, controlled trials have demonstrated equivalent results with a single 30-mL injection adjacent to the posterior cord or divided among each o the cords. Insertion o a perineural catheter should always be in the same location posterior to the axillary artery, and inraclavicular inusion has been shown to provide superior analgesia to both supraclavicular and axillary catheters.
Axillary Block At the lateral border o the pectoralis minor muscle, the cords o the brachial plexus orm large terminal 6 branches. Te axillary, musculocutaneous, and medial brachial cutaneous nerves branch rom the brachial plexus proximal to the location in which local anesthetic is deposited during an axillary nerve block, and thus are usually spared (Figure 46–19). At this level, the major terminal nerves ofen are separated by ascia; thereore multiple injections (10-mL each) may be required to reliably produce anesthesia o the entire arm distal to the elbow ( Figure 46–20). Tere are ew contraindications to axillary brachial plexus blocks. Local inection, neuropathy, and bleeding risk must be considered. Because the axilla is highly vascularized, there is a risk o local anesthetic uptake through small veins traumatized by needle placement. Te axilla is also a suboptimal site or perineural catheter placement because o greatly inerior analgesia versus an inraclavicular inusion, as well as theoretically increased risks o inection and catheter dislodgement. All o 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 46–20). Te axillary artery pulse should be palpated and its location marked as a reerence point.
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Infraclavicular
Nerves or plexus roots C4 Trunks C5
Divisions
C6
Cords Upper trunk
Main branches r a l L a t e
c o r d
r d r c o o i r s t e P o
o r d i a l c d e M
u n k e t r l d M i d
C7
C8 Lower trunk T1
FIGURE 4616 Infraclavicular block coverage and anatomy. Light blue shading indicates regions of variable block ade; purple shading indicates regions of more reliable blockade.
CHAPTER 46 Peripheral Nerve Blocks
991
2 cm 2 cm
FIGURE 4617 Infraclavicular block using nerve stimulation: coracoid technique.
PMa PMi
AV
N AA
N
N
B
A
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.
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A. Transarterial Technique Tis technique has allen out o avor due to the trauma o twice purposeully penetrating the axillary artery along with a theoretically increased risk o inadvertent intravascular local anesthetic injection. Te nondominant hand is used to palpate and immobilize the axillary artery, and a 22-gauge needle is inserted high in the axilla (Figure 46–20) until bright red blood is aspirated. Te needle is then slightly advanced until blood aspiration ceases. Injection can be perormed posteriorly, anteriorly, or in both locations in relation to the artery. A total o 30–40 mL o 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 ollowing positions relative to
the artery (Figure 46–21, although variations are common): median nerve superior (wrist �exion, thumb opposition, orearm pronation); ulnar nerve inerior (wrist �exion, thumb adduction, ourth/ �fh digit �exion); and radial nerve inerior–posterior (digit/wrist/elbow extension, orearm supination). Te musculocutaneous nerve (elbow �exion) is separate and deep within the coracobrachialis muscle, which is more superior (lateral) in this p osition and, as a consequence, is ofen not blocked with this procedure (Figure 46–21). A 2-in., 22-gauge insulated needle is inserted proximal to the palpating �ngers to elicit muscle twitches in the hand. Once an acceptable muscle response is identi�ed, and afer reducing the stimulation to less than 0.5 mA, careul aspiration is perormed and local anesthetic is injected. Although a single injection o 40 mL may be used, greater success will be seen with multiple nerve stimulations (ie, two or three nerves) and divided doses o 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.
CHAPTER 46 Peripheral Nerve Blocks
A
B
FIGURE 4620 A: Patient positioning and needle angle for axillary brachial plexus block. B: A multiple injection technique is more effective 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).
993
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SECTION IV
Regional Anesthesia & Pain Management
U AV TM
R
AA
M BM
MC CB
Median n. Brachial a.
FIGURE 4622 Ultrasound image of axillary brachial plexus block. AA, Axillary ar tery; 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-requency linear array ultrasound transducer, the axillary artery and vein are visualized in cross-section. Te brachial plexus can be identi�ed surrounding the artery (Figure 46–22). Te needle is inserted superior (lateral) to the transducer and advanced ineriorly (medially) toward the plexus under direct visualization. en milliliters o local anesthetic is then injected around each nerve (including the musculocutaneous, i 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 Ofen it is necessary to anesthetize a single ter-
minal nerve, either or minor surgical procedures with a limited �eld or as a supplement to an incomplete brachial plexus block. erminal nerves may be anesthetized anywhere along their course, but the elbow and the wrist are the two most avored sites.
FIGURE 4623 Median nerve course.
A. Median Nerve Block Te median nerve is derived rom the lateral and medial cords o the brachial plexus. It enters the arm and runs just medial to the brachial artery
(Figure 46–23). As it enters the antecubital space, it lies medial to the brachial artery near the insertion o the biceps tendon. Just distal to this point, it gives off numerous motor branches to the wrist and �nger
CHAPTER 46 Peripheral Nerve Blocks
�exors and ollows the interosseous membrane to the wrist. At the level o the proximal wrist �exion crease, it lies directly behind the palmaris longus tendon in the carpal tunnel. o block the median nerve at the elbow, the brachial artery is identi�ed 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 �exion or thumb opposition is elicited (Figure 46–24); 3–5 mL o local anesthetic is then injected. I ultrasound is used, the median nerve may be identi�ed in cross-section just medial to the brachial artery and local anesthetic injected to surround it (Figure 46–25). o block the median nerve at the wrist, the palmaris longus tendon is �rst identi�ed by asking the patient to �ex the wrist against resistance. A short 22-gauge needle is inserted just medial and deep to the palmaris longus tendon, and 3–5 mL
Lateral
995
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.
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Brachial a. Ulnar n. Medial epicondyle
Biceps tendon
Arcuate ligament Ulnar a. Radial a.
Flexor carpi ulnaris
Flexor digitorum profundus Palmar
Dorsal branch
branch
Palmar retinaculum Median n. Flexor carpi radialis m.
Deep branch
Superficial branch
Palmaris longus tendon
FIGURE 4626 Median nerve block at the wrist. FIGURE 4627 Ulnar nerve course.
o local anesthetic is injected (Figure 46–26). With ultrasound, the median nerve may be identi�ed at the level o the mid-orearm between the muscle bellies o the �exor digitorum proundus, �exor digitorum super�cialis, and �exor pollicis longus (transducer aces perpendicular to the t rajectory o the nerves).
B. Ulnar Nerve Block Te ulnar nerve is the continuation o the medial cord o the brachial plexus and maintains a position medial to the axillary and brachial arteries in the upper arm (Figure 46–27). At the distal third o the humerus, the nerve moves more medially and passes under the arcuate ligament o the medial epicondyle. Te nerve is requently palpable just proximal to the medial epicondyle. In the mid-orearm, the nerve
lies between the �exor digitorum proundus and the �exor carpi ulnaris. At the wrist, it is lateral to the �exor carpi ulnaris tendon and medial to the ulnar artery. o block the ulnar nerve at the level o the elbow, an insulated 22-gauge needle is inserted approximately one �ngerbreadth proximal to the arcuate ligament (Figure 46–28), and advanced until ourth/�fh digit �exion or thumb adduction is elicited; 3–5 mL o local anesthetic is then injected. o block the ulnar nerve at the wrist, the ulnar artery pulse is palpated just lateral to the �exor carpi ulnaris tendon. Te needle is inserted just medial to the artery (Figure 46–29) and 3–5 mL o local anesthetic is injected. I ultrasound is used, the ulnar nerve may be identi�ed just medial to the ulnar artery.
CHAPTER 46 Peripheral Nerve Blocks
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.
C. Radial Nerve Block Te radial nerve—the terminal branch o the posterior cord o the brachial plexus—courses posterior to the humerus, innervating the triceps muscle, and enters the spiral groove o the humerus beore it moves laterally at the elbow (Figure 46–30). erminal sensory branches include the lateral cutaneous nerve o the arm and the posterior cutaneous nerve o the orearm. Afer exiting the spiral groove as it approaches the lateral epicondyle, the radial nerve separates into super�cial and deep branches. Te deep branch remains close to the periosteum and innervates the postaxial extensor group o the orearm. Te super�cial branch becomes super�cial and ollows the radial artery to innervate the radial aspects o the dorsal wrist and the dorsal aspect o the lateral three digits and hal o the ourth. o block the radial nerve at the elbow, the biceps tendon is identi�ed in the antecubital ossa. A short 22-gauge insulated needle is inserted just lateral to the tendon and directed toward the lateral
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Regional Anesthesia & Pain Management
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 46–31) until wrist or �nger extension is elicited; 5 mL o local anesthetic is then injected. With ultrasound, the radial nerve can be identi�ed in cross-section just proximal to the antecubital ossa between the biceps and brachioradialis muscles. At the wrist, the super�cial branch o the radial nerve lies just lateral to the radial artery, which can be easily palpated lateral to the �exor carpi radialis tendon (Figure 46–32). Using a short 22-gauge needle, 3–5 mL local anesthetic is injected lateral to the artery. Ultrasound may be used at the level o the wrist or mid-orearm to identiy the radial nerve just lateral to the radial artery.
D. Musculocutaneous Nerve Block A musculocutaneous nerve block is essential to complete the anesthesia or the orearm and wrist and is commonly included when perorming the axillary block. Te musculocutaneous nerve is the terminal branch o the lateral cord and the most proximal o the major nerves to emerge rom the brachial plexus ( Figure 46–33). Tis nerve inner vates the biceps and brachialis muscles and distally terminates as the lateral antebrachial cutaneous nerve, supplying sensory input to the lateral aspect o the orearm and wrist.
Lateral
Medial
Brachialis m.
Biceps
Lateral epicondyle
Median n. Brachial a.
Radial n. Brachioradialis m.
FIGURE 4631 Radial nerve block at the elbow.
Dorsal
Palmar
CHAPTER 46 Peripheral Nerve Blocks
999
the coracobrachialis muscle is pierced, and 5–1 0 mL o local anesthetic is injected, with or without elicitation o elbow �exion. (Simple in�ltration may be used, although the success rate using this technique is questionable.) Ultrasound may be used to con�rm the location o the musculocutaneous nerve in the coracobrachialis muscle or between this muscle and the biceps (see Figure 46–22). Alternatively, the block can be perormed at the elbow as the nerve courses super�cially at the interepicondylar line. Te insertion o the biceps tendon is identi�ed, and a short 22-guage needle is inserted 1–2 cm laterally; 5–10 mL o local anesthetic is then injected as a �eld block.
Radius Radial nerve Flexor carpi radialis tendon
Ulnar styloid process Palmar longus tendon
Radial artery
FIGURE 4632 Radial nerve block at the wrist.
o target the musculocutaneous nerve ollowing an axillary block, the needle is redirected superior and proximal to the artery (see Figure 46–21),
E. Digital Nerve Blocks Digital nerve blocks are used or minor operations on the �ngers and to supplement incomplete brachial plexus and terminal nerve blocks. Sensory innervation o each �nger is provided by our small digital nerves that enter each digit at its base in each o the our corners (Figure 46–34). A small-gauge needle is inserted at the medial and lateral aspects o the base o the selected digit, and 2–3 mL o 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.
FIGURE 4634 Sensory innervation of the fingers is provided by the digital ner ves.
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Regional Anesthesia & Pain Management
Skin wheal
T2
FIGURE 4636 Intercostobrachial nerve block.
FIGURE 4635 Intercostobrachial nerve cutaneous innervation.
is inserted without epinephrine. Addition o a vasoconstrictor (epinephrine) has been claimed to seriously compromise blood �ow to the digit; however, there are no case reports involving lidocaine or other modern local anesthetics to con�rm this claim.
F. Intercostobrachial Nerve Block Te intercostobrachial nerve originates in the upper thorax (2) and becomes super�cial on the medial upper arm. It supplies cutaneous innervation to the medial aspect o the proximal arm and is not anesthetized with a brachial plexus block ( Figure 46–35). Te patient should be supine with the arm abducted and externally rotated. Starting at the deltoid prominence and proceeding ineriorly, a �eld block is perormed in a linear ashion using 5 mL o local anesthetic, extending to the most inerior aspect o the medial arm (Figure 46–36).
intravenous catheter is usually inserted on the dorsum o the hand (or oot) and a double pneumatic tourniquet is placed on the arm or thigh. Te extremity is elevated and exsanguinated by tightly wrapping an Esmarch elastic bandage rom a distal to proximal direction. Te proximal tourniquet is in�ated, the Esmarch bandage removed, and 0.5% lidocaine (25 mL or a orearm, 50 mL or an arm, and 100 mL or a thigh tourniquet) injected over 2– 3 min through the catheter, which is subsequently removed (Figure 46–37). Anesthesia is usually established afer 5–10 min. ourniquet pain usually develops afer 20–30 min, at which time the distal tourniquet is in�ated and the proximal tourniquet subsequently de�ated. Patients usually tolerate the distal tourniquet or an additional 15–20 min because it is in�ated over an anesthetized area. Even
Intravenous Regional Anesthesia Intravenous regional anesthesia, also called a Bier block, can provide surgical anesthesia or short surgical procedures (45–60 min) on an extremity (eg, carpal tunnel release). An
8
FIGURE 4637 Intravenous regional anesthesia provides surgical anesthesia for procedures of short duration.
CHAPTER 46 Peripheral Nerve Blocks
or surgical procedures o a very short duration, the tourniquet must be lef in�ated or a total o at least 15–20 min to avoid a rapid intravenous systemic bolus o local anesthetic resulting in toxicity. Slow de�ation is also recommended to provide an additional margin o saety.
LOWER EXTREMITY PERIPHERAL NERVE BLOCKS Lumbar & Sacral Plexus Anatomy Te lumbosacral plexus provides innervation to the lower extremities (Figure 46–38). Te lumbar plexus is ormed by the ventral rami o L1–4, with occasional contribution rom 12. It lies within the psoas muscle with branches descending into the proximal thigh. Tree major nerves rom the
1001
lumbar plexus make contributions to the lower limb: the emoral (L2–4), lateral emoral cutaneous (L1–3), and obturator (L2–4). Tese provide motor and sensory innervation to the anterior portion o the thigh and sensory innervation to the medial leg. Te sacral plexus arises rom L4–5 and S1–4. Te posterior thigh and most o the leg and oot are supplied by the tibial and peroneal portions o the sciatic nerve. Te posterior emoral cutaneous nerve (S1–3), and not the sciatic nerve, provides sensory innervation to the posterior thigh; it travels with the sciatic nerve as it emerges around the piriormis muscle.
Femoral Nerve Block Te emoral nerve innervates the main hip �exors, knee extensors, and provides much o the sensory
L1 L2 Inguinal nerve
L3
Genitofemoral nerve
L4
Lumbar plexus
L5
Lateral femoral cutaneous nerve
S1
Femoral nerve
S3
Sacral plexus
S2 S4
Inguinal ligament
Sciatic nerve Obturator nerve
FIGURE 4638 The ventral rami of L1–5 and S1–4 form the lumbosacral plexus, which provides innervation to the lower extremities.
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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 o the hip and thigh ( Figure 46–39). Its most medial branch is the saphenous nerve, which innervates much o the skin o the medial leg and ankle joint. Te term 3-in-1 block reers to anesthetizing the emoral, lateral emoral cutaneous, and obturator nerves with a single injection below the inguinal ligament; this term has largely been abandoned as evidence accumulated demonstrating the ailure o most single injections to consistently affect
9 all three nerves. A emoral nerve block alone
will seldom provide surgical anesthesia, but it is ofen used to provide postoperative analgesia or hip, thigh, knee, and ankle (or the saphenous nerve) procedures. Femoral nerve blocks have a relatively low rate o complications and ew contraindications. Local inection, previous vascular grafing, and local adenopathy should be careully considered in patient selection.
CHAPTER 46 Peripheral Nerve Blocks
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.
A. Nerve Stimulation With the patient positioned supine, the emoral artery pulse is palpated at the level o the inguinal ligament. A short (5-cm) insulated needle is inserted at a 45° angle to the skin in a cephalad direction ( Figure 46–40) until a clear quadriceps twitch is elicited at a current below 0.5 mA (look or patella motion). B. Ultrasound A high-requency linear ultrasound transducer is placed over the area o the inguinal crease parallel to the crease itsel, or slightly more transverse (Figure 46–41). Te emoral artery and emoral vein are visualized in cross-section, with the overlying ascia iliaca. Just lateral to the artery and deep to the ascia iliaca, the emoral nerve appears in crosssection as a spindle-shaped structure with a “honeycomb” texture (Figure 46–42). For an out-o-plane technique, the block needle is inserted just lateral to where the emoral nerve is seen, and directed cephalad at an angle approximately 45° to the skin. Te needle is advanced until
it is seen penetrating the ascia iliaca, or (i using concurrent electrical stimulation) until a motor response is elicited. Following careul aspiration or the nonappearance o blood, 30–40 mL o local anesthetic is injected. For an in-plane technique, a longer needle may be used. Te needle is inserted parallel to the ultrasound transducer just lateral to the outer edge. Te needle is advanced through the sartorius muscle, deep to the ascia iliaca, until it is visualized just lateral to the emoral nerve. Local anesthetic is injected, visualizing its hypoechoic spread deep to the ascia iliaca and around the nerve.
C. Fascia Iliaca Technique Te goal o a ascia iliaca block is similar to that o a emoral nerve block, but the approach is slightly different. Without use o a nerve stimulator or ultrasound machine, a relatively reliable level o anesthesia may be attained simply with anatomic landmarks and tactile sensation. Once the inguinal ligament and emoral artery pulse are identi�ed,
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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 ascia iliaca between the two nerves which run in the same plane between the ascia and underlying muscle.
Lateral Femoral Cutaneous Nerve Block
FIGURE 4641 Ultrasound-guided femoral nerve block (in-plane technique).
the length o the inguinal ligament is divided into thirds (Figure 46–43). wo centimeters distal to the junction o 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 o ascia in this region (ascia lata and ascia iliaca), two “pops” will be elt. Once the needle has passed through the ascia iliaca, careul aspiration is perormed and 30–40 mL o local anesthetic is injected. Tis block usually anesthetizes both the emoral nerve and lateral emoral cutaneous nerves, since the
Te lateral emoral cutaneous nerve provides sensory innervation to the lateral thigh (see Figure 46–39). It may be anesthetized as a supplement to a emoral nerve block or as an isolated block or limited anesthesia o the lateral thigh. As there are ew vital structures in proximity to the lateral emoral cutaneous nerve, complications with this block are exceedingly rare. Te lateral emoral cutaneous nerve (L2–3) departs rom the lumbar plexus, traverses laterally rom the psoas muscle, and courses anterolaterally along the iliacus muscle (see Figure 46–38). It emerges inerior and medial to the anterior superior iliac spine to supply the cutaneous sensory innervation o the lateral thigh. Te patient is positioned supine or lateral, and the point 2 cm medial and 2 cm distal to the anterior superior iliac spine is identi�ed. A short 22-gauge block needle is inserted and directed laterally, observing or a “pop” as it passes through the ascia lata. A �eld block is perormed with 10–15 mL o local anesthetic, which is deposited above and below the ascia (Figure 46–44).
CHAPTER 46 Peripheral Nerve Blocks
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.
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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 o the obturator nerve is usually required or complete anesthesia o the knee and is most ofen perormed in combination with emoral and sciatic nerve blocks or this purpose. Te obturator nerve contributes sensory branches to the hip and knee joints, a variable degree o sensation to the medial thigh, and innervates the adductors o the hip (Figure 46–45). Tis nerve exits the pelvis and enters the medial thigh through the obturator oramen, which lies beneath the superior pubic ramus. Afer identi�cation o the pubic tubercle, a long (10-cm) block needle is inserted 1.5 cm inerior and 1.5 cm lateral to the tubercle. Te needle is advanced
posteriorly until bone is contacted (Figure 46–46). Redirecting laterally and caudally, the needle is advanced an additional 2–4 cm until a motor response (thigh adduction) is elicited and maintained below 0.5 mA. Following careul aspiration or the nonappearance o blood, 15–20 mL o local anesthetic is injected.
Posterior Lumbar Plexus (Psoas Compartment) Block 10 Posterior lumbar plexus blocks are useul or
surgical procedures involving areas inner vated by the emoral, lateral emoral cutaneous, and obturator nerves ( Figure 46–47). Tese include
CHAPTER 46 Peripheral Nerve Blocks
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 cu taneous, and obturator nerves.
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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 o the knee can be attained with a proximal sciatic nerve block. Te lumbar plexus is relatively close to multiple sensitive structures (Figure 46–48) and reaching it requires a very long needle. Hence, the posterior lumbar plexus block has one o the highest complication rates o 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 o the psoas muscle and travel within the muscle compartment beore exiting as terminal nerves (see Figure 46–38). Modern posterior lumbar plexus blocks deposit local anesthetic within the body o the psoas muscle. Te patient is positioned in lateral
Lumbar plexus Spinal cord
decubitus with the side to be blocked in the nondependent position (Figure 46–49). Te midline is palpated, identiying the spinous processes i possible. A line is �rst drawn through the lumbar spinous processes, and both iliac crests are identi�ed and connected with a line to approximate the level o L4. Te posterior superior iliac spine is then palpated and a line is drawn cephalad, parallel to the �rst line. I available, ultrasound imaging o the transverse process may be helpul to estimate lumbar plexus depth. A long (10- to 15-cm) insulated needle is inserted at the point o intersection between the transverse (intercristal) line and the intersection o the lateral and middle thirds o the two sagittal lines. Te needle is advanced in an anterior direction until a emoral motor response is elicited (quadriceps contraction). I the transverse process is contacted, the needle should be withdrawn slightly
CHAPTER 46 Peripheral Nerve Blocks
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. Te 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 o bilateral spread and contralateral limb involvement.
Saphenous Nerve Block Te saphenous nerve is the most medial branch o the emoral nerve and innervates the skin over the medial leg and the ankle joint (see Figure 46–39). Tereore, this block is used mainly in conjunction with a sciatic nerve block to provide complete anesthesia/analgesia below the knee.
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11 (see Figure 46–38). Blockade o the sciatic
Tibial tuberosity Line of injection Lateral
Medial
FIGURE 4650 Proximal saphenous nerve block.
A. Trans-Sartorial Technique Te saphenous nerve may be accessed proximal to the knee, just deep to the sartorius muscle. A high-requency linear probe is used to identiy the junction between the sartorius, vastus medialis, and adductor muscles in cross-section just distal to the adductor canal. A long needle is inserted rom medial to lateral (in-plane) or angled cephalad (outo-plane) and 5–10 mL o local anesthetic deposited within this ascial plane.
nerve may occur anywhere along its course and is indicated or surgical procedures involving the hip, thigh, knee, lower leg, and oot. Te posterior emoral cutaneous nerve is variably anesthetized as well, depending on the approach. I sacral plexus or posterior emoral cutaneous nerve anesthesia is required, the parasacral approach is used (a technique that is beyond the scope o this chapter).
A. Posterior (Classic or Labat) Approach Te patient is positioned laterally with the side to be blocked in the nondependent position. Te patient is asked to bend the knee o the affected leg and tilt the pelvis slightly orward (Sim’s position; Figure 46–51). Te greater trochanter, posterior superior iliac spine (PSIS), and sacral hiatus are then identi�ed. A line is drawn rom the greater trochanter to the PSIS, its midpoint identi�ed, and a perpendicular line extended in a caudal direction. Next, a line is drawn rom 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, in�ltrating 5–10 mL o local anesthetic as the needle passes toward the posterior aspect o the leg (Figure 46–50). Ultrasound may be used to identiy the saphenous vein near the tibial tuberosity, acilitating a perivascular technique with in�ltration about the vein. C. Distal Saphenous Technique Te medial malleolus is identi�ed, in�ltrating 5 mL o local anesthetic in a line running anteriorly around the ankle (see Ankle Block below).
Sciatic Nerve Block Te sciatic nerve originates rom the lumbosacral trunk and is composed o nerve roots L4–5 and S1–3
Posterior superior iliac spine 5 cm
Sacral hiatus
Greater trochanter
FIGURE 4651 Patient positioning, surface landmarks, and needle positioning for proximal sciatic ner ve block (classic approach).
CHAPTER 46 Peripheral Nerve Blocks
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 46–51). Te needle is advanced through the gluteal muscles (a motor response o these muscles may be encountered) until plantar- or dorsi�exion is elicited (plantar�exion or oot inversion is preerred or surgical anesthesia). A local anesthetic volume o 25 mL pro vides surgical anesthesia.
B. Anterior Approach Afer leaving the sciatic notch, the sciatic nerve descends behind the lesser trochanter to a position posterior to the emur. It can be accessed rom the anterior thigh just medial to the lesser trochanter. Lateral or prone positioning may present a challenge or 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. Beore proceeding with this block, which carries a risk o vascular puncture (emoral artery and vein), patient-speci�c risks should be considered (eg, coagulopathy and vascular grafing). In
addition, i combining this block with the emoral nerve block in an unanesthetized patient, perorming the sciatic block �rst is recommended to avoid passing the block needle through a previously anesthetized emoral nerve. A local anesthetic volume o 25 mL provides surgical anesthesia. 1. Nerve stimulation—With the patient positioned supine, a line is drawn along the inguinal ligament, rom the anterior superior iliac spine to the pubic tubercle (Figure 46–52). A second line is drawn parallel to the �rst that traverses the greater trochanter (intertrochanteric line). Next, these two lines are connected with a third line drawn rom the point between the medial one third and lateral two thirds o the �rst 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 oot inversion or plantar�exion is elicited (dorsi�exion is acceptable or postoperative analgesia). Ofen with this approach, the emur is contacted beore the needle reaches the sciatic nerve. When this occurs, the needle should be withdrawn 2–3 cm, the patient should be asked to internally rotate the leg, and then the needle should be advanced. I the emur is contacted
Femoral artery and vein Anterior superior iliac spine Pubic tubercle Greater trochanter
1011
Lesser trochanter
Needle insertion point
FIGURE 4652 Anatomy and surface landmarks for anterior sciatic nerve block.
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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 o 25 mL provides surgical anesthesia. 2. Ultrasound—With the patient positioned supine and the leg externally rotated, a low-requency cur vilinear transducer is placed transversely over the medial thigh, approximately at the level o the lesser trochanter. Te emur, emoral vessels, adductor muscles, and gluteus maximus are identi�ed in crosssection. Te elliptical, hyperechoic sciatic nerve is ound in the ascial plane between adductors and gluteus muscles, posterior to the emur. Using a long (10-cm) needle, the nerve is approached in-plane (anterior to posterior) or out-o-plane (cephalad to caudad), taking care to avoid emoral 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 useul alternative to the traditional posterior approach. In many patients the landmarks are more easily identi�ed, and less tissue is traversed. With the sciatic nerve at a more super�cial location, the exclusive use o ultrasound becomes ar more practical, as well. I sciatic nerve block is being combined with a emoral 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 �exion to lif the oot with the use o crutches. 1. Nerve stimulation—With the patient in Sim’s position, the greater trochanter and ischial
tuberosity are identi�ed and a line drawn between them (Figure 46–53). From the midpoint o this line, a second line is drawn perpendicularly and extended caudally 4 cm. Trough this point a long (10-cm) insulated needle is inserted directly slig htly cephalad until oot plantar�exion or inversion is elicited (dorsi�exion is acceptable or analgesia). A local anesthetic volume o 25 mL provides surgical anesthesia. 2. Ultrasound—Using the same positioning and landmarks (Figure 46–53), a linear or low-requency 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 �eld simultaneously. Gluteal muscles are identi�ed super�cially, along with the ascial layer de�ning their deep border. Te 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, super�cial to the quadratus emoris muscle. For an out-o-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, careul aspiration or the nonappearance o blood is perormed 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
CHAPTER 46 Peripheral Nerve Blocks
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 �eld o 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 Popliteal nerve blocks provide excellent cover12 age or oot and ankle surgery, while sparing much o the hamstring muscles, allowing lifing o the oot with knee �exion, thus easing ambulation. All sciatic nerve blocks ail to provide complete anesthesia or the cutaneous medial leg and ankle joint capsule, but when a saphenous (or emoral)
block is added, complete anesthesia below the knee is provided. Te major site-speci�c risk o a popliteal block is vascular puncture, owing to the sciatic nerve’s proximity to the popliteal vessels at this location. Te sciatic nerve divides into the tibial and common peroneal nerves within or just proximal to the popliteal ossa (Figure 46–54). Te upper popliteal ossa is bounded laterally by the biceps emoris tendon and medially by the semitendinosus and semimembranosus tendons. Cephalad to the �exion crease o the knee, the popliteal artery is immediately lateral to the semitendinosus tendon. Te popliteal vein is lateral to the artery, and the tibial and
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common peroneal nerves are just lateral to the vein and medial to the biceps tendon, 2–6 cm deep to the skin. Te tibial nerve continues deep behind the gastrocnemius muscle, and the common peroneal nerve leaves the popliteal ossa by passing between the head and neck o the �bula to supply the lower leg. Te 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 �exed 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 o the popliteal ossa is identi�ed. Te hamstring muscles are palpated to locate the point where the biceps emoris (lateral) and the semimembranosus/semitendinosus complex (medial) join (Figure 46–55). Having the patient �ex the knee against resistance acilitates recognition o these structures. Te needle entry point is 1 cm caudad rom the apex. An insulated needle (5–10 cm) is advanced until oot plantar�exion or inversion is elicited (dorsi�exion is acceptable or analgesia). A volume o 30–40 mL o local anesthetic is ofen required or single-injection popliteal–sciatic nerve block. 2. Nerve stimulation (lateral approach)—With the patient in the supine position and the knee ully extended, the intertendinous groove is palpated between the vastus lateralis and biceps emoris muscles approximately 10 cm proximal to the superior notch o 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. I bone (emur) is contacted, the needle is withdrawn and redirected slightly posteriorly until an acceptable motor response is encountered. 3. Ultrasound—With the patient positioned prone, the apex o the popliteal ossa is identi�ed, as described above. Using a high-requency linear ultrasound transducer placed in a transverse orientation, the emur, biceps emoris muscle, popliteal vessels, and sciatic nerve or branches are identi�ed in cross-section (Figure 46–55). Te nerve is usually posterior and lateral (or immediately posterior) to the vessels and is ofen located in close
Proximal
Medial
Lateral
Distal
BFM N
PV PA
F
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 biceps emoris muscle, just deep to its medial edge. For an out-o-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 ollowing careul aspiration, local anesthetic injected, observing or spread around the nerve.
CHAPTER 46 Peripheral Nerve Blocks
1015
For an in-plane technique, the block needle is inserted lateral to the ultrasound transducer, traversing—or just anterior to—the biceps emoris muscle (Figure 46–56). Te needle is advanced in the ultrasound plane, while visualizing its approach either deep or super�cial to the nerve. I surgical anesthesia is desired, local anesthetic should be seen surrounding all sides o the nerve, which usually requires multiple needle tip placements with incremental injection. For analgesia alone, a single injection o local anesthetic is acceptable. Ultrasound-guided popliteal sciatic blocks may be perormed with the patient in the lateral or supine positions (the latter with leg up-raised on several pillows). Tese maneuvers are ofen more technically challenging.
Ankle Block For surgical procedures o the oot, an ankle block is a ast, low-technology, low-risk means o providing anesthesia. Excessive injectate volume and use o vasoconstrictors such as epinephrine must be avoided to minimize the risk o ischemic complications. Since this block includes �ve separate injections, it is ofen uncomortable or patients and adequate premedication is required. Five nerves supply sensation to the oot (Figure 46–57). Te saphenous nerve is a terminal branch o the emoral 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
FIGURE 4657 Cutaneous innervation of the foot.
Saphenous nerve
Sural nerve
Deep peroneal nerve
Lateral plantar nerve Medial plantar nerve Medial calcaneal branches
From tibial nerve
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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.
o the oot not a part o the sciatic system. It supplies super�cial sensation to the anteromedial oot and is most constantly located just anterior to the medial malleolus. Te deep peroneal nerve runs in the anterior leg afer branching off the common peroneal nerve, entering the ankle between the extensor hallucis longus and the extensor digitorum longus tendons (Figure 46–58), just lateral to the dorsalis pedis artery. It provides innervation to the toe extensors and sensation to the �rst dorsal webspace. Te super�cial peroneal nerve, also a branch o the common peroneal nerve, descends toward the ankle in the lateral compartment, giving motor branches
to the muscles o eversion. It enters the ankle just lateral to the extensor digitorum longus and pro vides cutaneous sensation to the dorsum o the oot and toes. Te posterior tibial nerve is a direct continuation o the tibial nerve and enters the oot 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 o the medial malleolus and provides sensory innervation to the heel, the medial sole, and part o the lateral sole o the oot, as well as the tips o the toes. Te sural nerve is a branch o the tibial nerve and enters the oot between the Achilles tendon
CHAPTER 46 Peripheral Nerve Blocks
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
A
B
FIGURE 4659 Needle placement for ankle block.
and the lateral malleolus to provide sensation to the lateral oot. 13 A complete ankle block requires a series o �ve nerve blocks, but the process may be streamlined to minimize needle insertions (Figure 46–59). All �ve injections are required to anesthetize the entire oot; however, many surgical procedures involve only a ew terminal nerves, and only affected nerves should be blocked. In addition, unlike a sciatic nerve block, an ankle block provides no analgesia or (below-the-knee) tourniquet pain, nor does it allow or perineural catheter insertion. o block the deep peroneal nerve, the groove between the extensor hallucis longus and extensor digitorum longus tendons is identi�ed. Te dorsalis pedis pulse is ofen 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 o local anesthetic is in�ltrated as the needle is withdrawn. Continuing rom this insertion site, a subcutaneous wheal o 5 mL o local anesthetic is extended toward the lateral malleolus to target the super�cial peroneal nerve. Te needle is withdrawn and redirected rom the same location in a medial direction, in�ltrating 5 mL o local anesthetic toward the medial malleolus to target the saphenous nerve. Te posterior tibial nerve may be located by identiying the
posterior tibial artery pulse behind the medial malleolus. A short, small-gauge block needle is inserted just posterior to the artery and 5 mL o local anesthetic is distributed in the pocket deep to the �exor retinaculum. o target the sural nerve, 5 mL o local anesthetic is injected subcutaneously posterior to the lateral malleolus.
PERIPHERAL NERVE BLOCKS OF THE TRUNK Superficial Cervical Plexus Block Te super�cial cervical plexus block provides cutaneous analgesia or surgical procedures on the neck, anterior shoulder, and clavicle. It is helpul to identiy and avoid the external jugular vein. Te cervical plexus is ormed rom the anterior rami o C1–4, which emerge rom the platysma muscle posterior to the sternocleidomastoid (Figure 46–60). It supplies sensation to the jaw, neck, occiput, and areas o the chest and shoulder. Te patient is positioned supine with the head turned away rom the side to be blocked. Te sternocleidomastoid muscle is identi�ed and its lateral edge marked. At the junction o the upper and middle thirds, a short (5-cm) block needle is inserted,
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C2 C3 C4
FIGURE 4660 Distribution of the superficial cervical plexus.
directed cephalad toward the mastoid process, and 5 mL o local anesthetic is injected in a subcutaneous plane. Te needle is turned to advance it in a caudad direction, maintaining a path along the posterior border o sternocleidomastoid. An additional 5 mL o local anesthetic is in�ltrated subcutaneously.
Intercostal Block Intercostal blocks provide analgesia ollowing thoracic and upper abdominal surgery, and relie o pain associated with rib ractures, herpes zoster, and cancer. Tese blocks require individual injections delivered at the various vertebral levels that correspond to the area o body wall to be anesthetized. 14 Intercostal blocks result in the highest blood levels o local anesthetic per volume injected o any block in the body, and care must be taken to avoid toxic levels o local anesthetic. Te intercostal block has one o the highest complication rates o any peripheral nerve block due to the close proximity o 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 �ow, and
placement o a perineural catheter is tenuous, at best. With the advent o ultrasound guidance, the paravertebral approach is rapidly replacing the intercostal approach. Te intercostal nerves arise rom the dorsal and ventral rami o the thoracic spinal nerves. Tey exit rom the spine at the intervertebral oramen and enter a groove on the underside o the corresponding rib, running with the intercostal artery and vein; the nerve is generally the most inerior structure in the neurovascular bundle (Figure 46–61). Branches are given off or sensation in a single dermatome rom the midline dorsally all the way to across the midline ventrally. With the patient in the lateral decubitus or supine position, the level o each rib in the mid and posterior axillary line is palpated and marked. A small-gauge needle is inserted at the inerior edge o each o the selected ribs, bone is contacted, and the needle is then “walked off” ineriorly (Figure 46–61). Te needle is redirected in a slightly cephalad direction and advanced approximately 0.25 cm. Following aspiration, observing or blood or air, 3–5 mL o local anesthetic is injected at each desired level.
CHAPTER 46 Peripheral Nerve Blocks
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 or 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 o body wall to be anesthetized. For example, a simple mastectomy would require blocks at levels 3–6; or axillary node dissection, additional injections should be made rom C7 through 2. For inguinal hernia repair, blocks should be perormed at 10 through L2. Ventral hernias require bilateral injections corresponding to the level o the surgical site. Te major complication o 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
insertion is a viable option (although local anesthetic spread rom a single catheter to multiple levels is variable). Each spinal nerve emerges rom the intervertebral oramina 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 re�ects posteriorly and innervates the skin and muscles o the back 15 and neck (Figure 46–62). Te thoracic para vertebral space is de�ned posteriorly by the superior costotransverse ligament, anterolaterally by the parietal pleura, medially by the vertebrae and the intervertebral oramina, and ineriorly and superiorly by the heads o the ribs. With the patient seated and vertebral column �exed, each spinous process is palpated, counting rom the prominent C7 or thoracic blocks, and the iliac crests as a reerence or lumbar levels. From the midpoint o the superior aspect o 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
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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 o thoracic spinous processes (eg, the 4 nerve root is located lateral to the spinous process o 3).
A. Traditional Technique A pediatric uohy needle (20 gauge) is inserted at each point and advanced perpendicular to the skin (Figure 46–62). Upon contact with the transverse process, the needle is withdrawn slightly and redirected caudally an additional 1 cm (0.5 cm or lumbar placement). A “pop” or loss o resistance may be elt as the needle passes through the costotransverse ligament. Some practitioners use a loss-o-resistance syringe to guide placement; others preer use o a nerve stimulator with chest wall motion or the end point. Inject 5 mL o local anesthetic at each level. Te diffi culty with this technique is that the depth o the transverse process is simply estimated; thus
the risk o pneumothorax is relatively high. Using ultrasound to gauge transverse process depth prior to needle insertion theoretically decreases the risk o pneumothorax.
B. Ultrasound An ultrasound transducer with a curvilinear array is used, with the beam oriented in a parasagittal or transverse plane. Te transverse process, head o the rib, costotransverse ligament, and pleura are identi�ed. Te paravertebral space may be approached rom a caudal-to-cephalad direction (parasagittal) or a lateral-to-medial direction (transverse). It is helpul to visualize the needle in-plane as it passes through the costotransverse ligament and observe a downward displacement o the pleura as local anesthetic is injected. At each level 5 mL o local anesthetic is injected.
CHAPTER 46 Peripheral Nerve Blocks
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 Te transversus abdominis plane (AP) block is most ofen used to provide surgical anesthesia or minor, super�cial procedures on the lower abdominal wall, or postoperative analgesia or procedures below the umbilicus. For hernia surgeries, intravenous or local supplementation may be necessary to provide anesthesia during peritoneal traction. Potential complications include violation o the peritoneum with or without bowel peroration, and the use o ultrasound is highly recommended to minimize this risk. 16 Te subcostal (12), ilioinguinal (L1), and iliohypogastric (L1) nerves are targeted in the AP block, providing anesthesia to the ipsilateral
lower abdomen below the umbilicus ( Figure 46–63). For part o 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 ascial layers o these muscles, with local anesthetic �lling the transversus abdominis plane. Te patient is ideally positioned in lateral decubitus, but i mobility is limited the block may be perormed in the supine position.
A. Ultrasound With a linear or curvilinear array transducer oriented parallel to the inguinal ligament, the layers o the external oblique, internal oblique, and transversus abdominis muscles are identi�ed just superior
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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 46–64). Muscles appear as striated hypoechoic structures with hyperechoic layers o ascia at their borders. A long (10-cm) needle is inserted in-plane just lateral (posterior) to the transducer and advanced, noting tactile eedback rom ascial planes, to the hyperechoic effacement o the deep border o internal oblique and the super�cial border o transversus abdominis. Following careul aspiration or the nonappearance o blood, 20 mL o local anesthetic is injected, observing or an elliptical separation between the two ascial layers (Figure 46–64).
SUGGESTED READING Capdevila X, Coimbra C, Choquet O: Approaches to the lumbar plexus: Success, risks, and outcome. Reg Anesth Pain Med 2005;30:150.
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. Oxord University Press, 2010. Heil JW, Ileld BM, Loland VJ, et al: Ultrasound-guided transversus abdominis plane catheters and ambulatory perineural inusions or outpatient inguinal hernia repair. Reg Anesth Pain Med 2010;35:556. Horn JL, Pitsch , Salinas F, Benninger B: Anatomic basis to the ultrasound-guided approach or saphenous nerve blockade. Reg Anesth Pain Med 2009;34:486. Ileld BM: Continuous peripheral nerve blocks: A review o the published evidence. Anesth Analg 2011;113:904. Ileld BM, Fredrickson MJ, Mariano ER: Ultrasoundguided perineural catheter insertion: Tree 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 or emoral perineural catheter insertion. J Ultrasound Med 2009;28:1453. Perlas A, Brull R, Chan VW, et al: Ultrasound guidance improves the success o sciatic nerve block at the popliteal ossa. 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: Artiacts and pitall errors associated with ultrasound-guided regional anesthesia. Part I: Understanding the basic principles o ultrasound physics and machine operations. Reg Anesth Pain Med 2007;32: 412. Sites BD, Brull R, Chan VW, et al: Artiacts and pitall errors associated with ultrasound-guided regional anesthesia. Part II: A pictorial approach to understanding and avoidance. Reg Anesth Pain Med. 2007;32:419.
C
Anesthetic Complications
H
A
P
T
E
R
54
KEY CO NCE PTS 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. 2
3
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 (plaintiff) must have suffered an injury; and (4) the proximate cause of the injury must have been the practitioner’s 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.
4 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. 5
Many anesthetic fatalities occur only after a series of coincidental circumstances, misjudgments, and technical errors coincide (mishap chain).
6
Despite differing mechanisms, anaphylactic and anaphylactoid reactions are typically clinically indistinguishable and equally life-threatening.
7 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. 8
Patients with spina bifida, 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.
9
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
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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 Te rate o anesthetic complications will never
be zero. All anesthesia practitioners, irrespective o 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 i those outcomes did not directly arise rom anesthetic mismanagement. Tis chapter reviews management approaches to complications secondary to anesthesia and discusses medical malpractice and legal issues rom an American (USA) perspective. Readers based in other countries may not �nd 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 o their proessional lives and acquire suitably solvent medical malpractice insurance with coverage appropriate or 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 helpul, as many adverse outcomes will be reviewed by acility-based and practice-based quality assurance and perormance improvement authorities. Deviations rom acceptable practice will likely be noted in the practitioner’s
exposure time during procedures, using proper barriers, and maximizing one’s distance from the source of radiation.
quality assurance �le. Should an adverse outcome lead to litigation, the medical record documents the practitioner’s actions at the time o the incident. Ofen years pass beore litigation proceeds to the point where the anesthesia provider is asked about the case in question. Although memories ade, a clear and complete anesthesiology record can pro vide convincing evidence that a complication was recognized and appropriately treated. A lawsuit may be �led, despite a physician’s best efforts to communicate with the patient and amily about the intraoperative events, management decisions, and the circumstances surrounding an adverse event. It is ofen not possible to predict which cases will be pursued by plaintiffs! Litigation may be pursued when it is clear (at least to the deense team) that the anesthesia care conormed to standards, and, conversely, that suits may not be �led when there is obvious anesthesia culpability. Tat said, anesthetics that are ollowed by unexpected death, paralysis, or brain injury o young, economically productive individuals are particularly attractive to plaintiff’s lawyers. When a patient has an unexpectedly poor outcome, one should expect litigation irrespective o one’s “positive” relationship with the patient or the injured patient’s amily or guardians. Malpractice occurs when our requirements 2 are met: (1) the practitioner must have a duty to the patient; (2) there must have been a breach o duty (deviation rom the standard o care); (3) the patient (plaintiff) must have suffered an injury; and (4) the proximate cause o the injury must have been the practitioner’s deviation rom the standard o care. A duty is established when the practitioner has an obligation to provide care (doctor–patient relationship). Te practitioner’s ailure to execute that duty
CHAPTER 54 Anesthetic Complications
constitutes a breach o duty. Injuries can be physical, emotional, or �nancial. Causation is established; i but or the breach o 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 amily members by awarding them monetary damages. Being sued is stressul, regardless o the perceived “merits” o the claim. Preparation or deense begins beore an injury has occurred. Anesthesiology staff should careully explain the risks and b ene�ts o the anesthesia options available to the patient. Te patient grants inormed consent ollowing a discussion o the risks and bene�ts. Inormed consent does not consist o handing the patient a orm to sign. Inormed consent requires that the patient understand the choices being presented. As previously noted, appropriate documentation o patient care activities, differential diagnoses, and therapeutic interventions helps to provide a deensible record o the care that was provided, resistant to the passage o time and the stress o the litigation experience. When an adverse outcome occurs, the hospital and/or practice risk management group should be immediately noti�ed. Likewise, one’s liability insurance carrier should be noti�ed o the possibility o a claim or damages. Some policies have a clause that disallows the practitioner rom admitting errors to patients and amilies. Consequently, it is important to know and obey the institution’s and insurer’s approach to adverse outcomes. Nevertheless, most risk managers advocate a rank and honest disclosure o adverse events to patients or approved amily members. It is possible to express sorrow about an adverse outcome without admitting “guilt.” Ideally, such discussions should take place in t he presence o risk management personnel and/or a departmental leader. It must never be orgotten that the tort system is designed to be adversarial. Unortunately, this makes every patient a potential courtroom adversary. Malpractice insurers will hire a deense �rm to represent the anesthesia staff involved. ypically, multiple practitioners and the hospitals in which they work will be named to involve the maximal number o insurance policies that might pay in the
1201
event o a plaintiff ’s victory, and to ensure that the deendants cannot choose to attribute “blame” or 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 o the named entities are represented by one deense team. More commonly, various insurers and attorneys represent speci�c practitioners and institutional providers. In this instance, those involved may de�ect and diffuse blame rom themselves and ocus blame on others also named in the action. One should not discuss elements o any case with anyone other than a risk manager, insurer, or attorney, as other conversations are not protected rom discovery. Discovery is the process by which the plaintiff’s attorneys access the medical records and depose witnesses under oath to establish the elements o the case: duty, breach, injury, and causation. False testimony can lead to criminal charges o perjury. Ofentimes, expediency and �nancial risk exposure will argue or settlement o the case. Te 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 o the physician’s record. Moreover, malpractice suits, settlements, and judgments must be reported to hospital authorities as part o the credentialing process. When applying or licensure or hospital appointment, all such actions must be reported. Failure to do so can lead to adverse consequences. Te litigation process begins with the delivery o a summons indicating that an action is pending. Once delivered, the anesthesia deendant must contact his or her malpractice insurer/risk management department, who will appoint legal counsel. Counsel or both the plaintiff and deense will identiy “independent experts” to review the cases. Tese “experts” are paid or their time and expenses and can arrive at dramatically different assessments o 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 stressul. Generally, one should ollow the advice o one’s deense attorney. Ofentimes, plaintiff ’s attorneys will attempt to anger or conuse the deponent,
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hoping to provoke a response avorable to the claim. Most deense 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 deense attorney will object or the record. However, depositions, also known as “examinations beore trial,” are not held in ront o a judge (only the attorneys, the deponent, the court reporter[s], and [sometimes] the videographer are present). Obligatory small talk ofen occurs among the attorneys and the court reporters. Tis is natural and should not be a source o anxiety or the deendant, because in most localities, the same plaintiff’s and deense attorneys see each other regularly. Following discovery, the insurers, plaintiffs, and deense attorneys will “value” the case and attempt to monetize the damages. Items, such as pain and suering, loss o consortium with spouses, lost wages, and many other actors, are included in determining what the injury is worth. Also during this period, the deense attorney may petition the court to grant deendants a “summary judgment,” dismissing the deendant rom the case i there is no evidence o malpractice elicited during the discovery process. At times, the plaintiff ’s attorneys will dismiss the suit against certain named individuals afer they have testi�ed, particularly when their testimony implicates other named deendants. Settlement negotiations will occur in nearly every action. Juries are unpredictable, and both parties are ofen hesitant to take a case to trial. Tere are expenses associated with litigation, and, consequently, both plaintiff and deense 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 o the insurance policy maximum may (depending on the jurisdiction) place the personal assets o the deendant providers at risk. Tis underscores the importance o our advice to all practitioners (not only those involved in a lawsuit) to assemble their personal assets (house, retirement und, etc.) in a ashion that makes personal asset con�scation difficult in the event o a negative judgment. One should remember that an adverse judgment may arise rom a case in which
most anesthesiologists would �nd the care to meet acceptable standards! When a case proceeds to trial, the �rst step is jury selection in the process o voir dire—rom the French—“to see, to say.” In this process, attorneys or the plaintiff and deendant will use various pro�ling techniques to attempt to identiy (and remove) jurors who are less likely to be sympathetic to their case, while keeping the jurors deemed most likely to avor their side. Each attorney is able to strike a certain number o jurors rom the pool because they perceive an inherent bias. Te jurors will be questioned about such matters as their educational level, history o litigation themselves, proessions, and so orth. Following empanelment, the case is presented to the jury. Each attorney attempts to educate the jurors—who usually have limited knowledge o healthcare (physicians and nurses will usually be struck rom the jury)—as to the standard o care or this or that procedure and how the deendants did or did not breach their duty to the patient to uphold those standards. Expert witnesses will attempt to de�ne what the standard o care is or the community, and the plaintiff and deendant will present experts with views that are avorable to their respective cause. Te attorneys will attempt to discredit the opponent’s experts and challenge their opinions. Exhibits are ofen used to explain to the jury what should or should not have happened and why the injuries or which damages are being sought were caused by the practitioner’s negligence. Afer 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 o a jury, anything can happen. Many cases will settle during the course o the trial, as neither party wishes to be subject to the arbitrary decisions o an unpredictable jury. Should the case not settle, the jurors will reach a verdict. When a jury determines that the deendants were negligent and negligence was the cause o the plaintiff ’s injuries, the jury will determine an appropriate award. I the award is so egregiously large that it is inconsistent with awards or similar injuries, the judge may reduce its amount. O course, ollowing any verdict, there are
CHAPTER 54 Anesthetic Complications
numerous appeals that may be �led. It is important to note that appeals typically do not relate to the medical aspects o the case, but are �led because the trial process itsel was somehow �awed. Unortunately, a malpractice action can take years to reach a conclusion. Consultation with a mental health proessional may be appropriate or the deendant when the litigation process results in unmanageable stress, depression, increased alcohol consumption, or substance abuse. Determining what constitutes the “standard o care” is increasingly complicated. In the United Sates, the de�nition o “standard o care” is made separately by each state. Te standard o care is NO necessarily “best practices” or even the care that another physician would preer. Generally, the standard o care is met when a patient receives care that other reasonable physicians in similar circumstances would regard as adequate. Te American Society o Anesthesiologists (ASA) has published standards, and these provide a basic ramework or routine anesthetic practice (eg, monitoring). Increasingly, a number o “guidelines” have been developed by the multiple specialty societies to identiy best practices in accordance with assessments o the evidence in the literature. Te increasing number o guidelines proered by the numerous anesthesia and other societies and their requent updating can make it difficult or clinicians to stay abreast o the changing nature o practice. Tis is a particular problem when two societies produce con�icting guidelines on the same topic using the same data. Likewise, the inormation upon which guidelines are based can range rom randomized clinical trials to the opinion o “experts” in the �eld. 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 o evidence used to generate the guideline. Nonetheless, plaintiff’s attorneys will attempt to use guidelines to establish a “standard o care,” when, in act, clinical guidelines are prepared to assist in guiding the delivery o therapy. However, i deviation rom guidelines is required or good patient care, the rationale or such actions should be documented on the anesthesia record, as plaintiff’s attorneys will attempt to use the guideline as a de facto standard o care.
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ADVERSE ANESTHETIC OUTCOMES Incidence Tere are several reasons why it is difficult to accurately measure the incidence o adverse anesthesia-related outcomes. First, it is ofen diffi cult to determine whether the cause o a poor outcome is the patient’s underlying disease, the surgical procedure, or the anesthetic management. In some cases, all three actors contribute to a poor outcome. Clinically important measurable outcomes are relatively rare afer 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 o patients must be studied to assemble conclusions that have statistical signi�cance. Nonetheless, many studies have attempted to determine the incidence o complications due to anesthesia. Unortunately, studies vary in criteria or de�ning an anesthesiarelated adverse outcome and are limited by retrospective analysis. Perioperative mortality is usually de�ned as death within 48 hr o surgery. It is clear that most perioperative atalities are due to the patient’s 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 o cause o death �les in the United States showed that the rate o anesthesia-related deaths was 1.1/1,000,000 population or 1 anesthetic death per 100,000 procedures between 1999 and 2005 (Figure 54–1). Tese results suggest a 97% decrease in anesthesia mortality since the 1940s. However, a 2002 study reported an estimated rate o 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 sae practice. In a 2008 study o 815,077 patients (ASA class 1, 2, or 3) who underwent elective surgery at US Department o Veterans Affairs hospitals, the mortality rate was 0.08% on the day o surgery. Te strongest association with perioperative death was the type o surgery ( Figure 54–2). Other actors associated with increased risk o death
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25
s e 20 g r a h c s i d l a 15 c i g r u s n o i l l i 10 m / s h t a e D 5
0
0–4
5–14
15–24 25–34 35–44 45–54 55–64 65–74 75–84
≥85
Age (years)
FIGURE 541 Annual in-hospital anesthesia-related deaths rates per million hospital surgical discharges and 95% confidence intervals by age, United States, 1999-2005.
(Reproduced, with permission, from Li G, Warner M, Lang B, et al:
included dyspnea, reduced albumin concentrations, increased bilirubin, and increased creatinine concentrations. A subsequent review o the 88 deaths that occurred on the surgical day noted that 13 o
the patients might have bene�tted rom better anesthesia care, and estimates suggest that death might have been prevented by better anesthesia practice in 1 o 13,900 cases. Additionally, this study reported
Epidemiology of anesthesia-related mortality in the United States 1999-2005. Anesthesiology 2009;110:759.)
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 Affairs 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 Affairs hospitals. Anesth Analg 2008;107:1924.)
CHAPTER 54 Anesthetic Complications
that the immediate postsurgical period tended to be the time o unexpected mortality. Indeed, ofen missed opportunities or improved anesthetic care occur ollowing complications when “ailure to rescue” contributes to patient demise.
American Society of Anesthesiologists Closed Claims Project Te goal o the ASA Closed Claims Project is to identiy common events leading to claims in anesthesia, patterns o injury, and strategies or injury prevention. It is a collection o closed malpractice claims that provides a “snapshot” o anesthesia liability rather than a study o the incidence o anesthetic complications, as only events that lead to the �ling o a malpractice claim are considered. Te Closed Claims Project consists o trained physicians who review claims against anesthesiologists represented by some US malpractice insurers. Te number o claims in the database continues to rise each year as new claims are closed and reported. Te claims are grouped according to speci�c damaging events and complication type. Closed Claims Project analyses have been reported or airway injury, nerve injury, awareness, and so orth. Tese analyses provide insights into the circumstances that result in claims; however, the incidence o a complication cannot be determined rom closed claim data, because we know neither the actual incidence o the complication (some with the complication may not �le suit), nor how many anesthetics were perormed or which the particular complication might possibly develop. Other similar analyses have been perormed in the United Kingdom, where National Health Service (NHS) Litigation Authority claims are reviewed.
Causes Anesthetic mishaps can be categorized as preventable or unpreventable. Examples o the latter include sudden death syndrome, atal idiosyncratic drug reactions, or any poor outcome that occurs despite proper management. However, studies o anesthetic-related deaths or near misses suggest that many accidents are preventable. O these preventable incidents, most involve human error (Table 54–1), as opposed to equipment
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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
malunctions (Table 54–2). Unortunately, some rate o human error is inevitable, and a preventable accident is not necessarily evidence o incompetence. During the 1990s, the top three causes or 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 o NHS litigation records, anesthesia-related claims accounted or 2.5% o total claims �led and 2.4% o the value o all NHS claims. Moreover, regional and obstetrical anesthesia were responsible or 44% and 29%, respectively, o anesthesia-related claims �led. Te authors o 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 �led in the absence o negligent care. Consequently, closed claims reports must always be considered in this context.
MORTALITY AND BRAIN INJURY rends in anesthesia-related death and brain damage have been tracked or many years. In a Closed Claims Project report examining claims in the
3
TABLE 542 Equipment malfunctions that
may lead to preventable anesthetic accidents. Breathing circuit Monitoring device Ventilator Anesthesia machine Laryngoscope
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A
r 400 a e y r 300 e p s 200 m i a l c 100 f o # 0
1975
1980
1985
1990
1995
2000
1975
1980
1985
1990
1995
2000
B
r 60 a e 40 y r e p 20 %
0
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
period between 1975 and 2000, there were 6750 claims (Figure 54–3A and B), 2613 o which were or brain injury or death. Te proportion o claims or brain injury or death was 56% in 1975, but had decreased to 27% by 2000. Te 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 or more than 50% o brain injury/death claims, whereas cardio vascular-related damaging events were responsible or 27% o such claims; however, by the late 1980s, the percentage o 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 multiactorial. Closed claims reviewers ound that anesthesia care was substandard in 64% o claims in which respiratory complications contributed to brain injury or death, but in only 28% o cases in
damage as percentage of total claims per year by year of injury. (Reproduced, with permission, from Cheney FW, Domino KB, Caplan RA, Posner KL: Nerve injury associated with anesthesia: a closed claims analysis. Anesthesiology 1999;90:1062.)
which the primary mechanism o 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 Te relative decrease in causes o death being attributed to respiratory rather cardiovascular damaging events during the review period was attributed to the increased use o pulse oximetry and capnometry. Consequently, i 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. rauma to the airway also generates signi�cant claims i esophageal or tracheal rupture occur. Postintubation mediastinitis should always
CHAPTER 54 Anesthetic Complications
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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 unsuccessul 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% o the time and represented 1.7% o the 6449 claims reviewed. Complications secondary to guidewire or catheter embolism, tamponade, bloodstream inections, 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. amponade claims ollowing line placement were ofen or patient death. Te authors o a 2004 closed claims analysis recommended reviewing the chest radiograph ollowing line placement and repositioning lines ound in the heart or at an acute angle to reduce the likelihood o tamponade. Brain damage and stroke are associated with claims secondary to carotid cannulation. Multiple con�rmatory 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 or 2% o 6849 claims, 91% o which were or complications secondary to the extravasation o �uids or drugs
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.)
rom peripheral intravenous catheters that resulted in extremity injury (Figure 54–4). Air embolisms, inections, and vascular insuffi ciency secondary to arterial spasm or thrombosis also resulted in claims. O interest, intravenous catheter claims in patients who had undergone cardiac surgery ormed the largest cohort o claims related to peripheral intravenous catheters, most likely due to the usual practice o tucking the arms alongside the patient during the procedure, placing them out o view o the anesthesia providers. Radial artery catheters seem to generate ew closed claims; however, emoral 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 o the 5946 pregnancy-related deaths reported to the Centers or Disease Control were thought to be anesthesia related or approximately 1.6% o total pregnancy related-deaths in the period 1991–2002. Te anesthesia mortality rate in this period was 1.2 per million live births, compared with 2.9 per million live births in the
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period 1979–1990. Te decline in anesthesiarelated maternal mortality may be secondary to the decreased use o general anesthesia in parturients, reduced concentrations o bupivacaine in epidurals, improved airway management protocols and devices, and greater use o incremental (rather than bolus) dosing o epidural catheters. In a 2009 study examining the epidemiology o anesthesia-related complications in labor and delivery in New York state in the period 2002–2005, an anesthesia-related complication was reported in 4438 o 957,471 deliveries (0.46%). Te incidence o complications was increased in patients undergoing cesarean section, those living in rural areas, and those with other medical conditions. Complications o neuraxial anesthesia (eg, postdural puncture headache) were most common, ollowed by systemic complications, including aspiration or cardiac events. Other reported problems related to anesthetic dose administration and unintended overdosages. Arican American women and those aged 40–55 years were more likely to experience systemic complications, whereas Caucasian women and those aged 30–39 were more likely to experience complications related to neuraxial anesthesia. ASA Closed Claims Project analyses were reported in 2009 or the period 1990–2003. Four hundred twenty-six claims rom this period were compared with 190 claims in the database prior to 1990. Afer 1990, the proportion o claims or maternal or etal demise was lower than that recorded prior to 1990. Afer 1990, the number o claims or maternal nerve injury increased. In the review o 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 o emergent cesarean section can contribute to adverse etal outcome. Additionally, the closed claims review indicated that poor communication between the obstetrician and the anesthesiologist regarding the urgency o newborn delivery was likewise thought to have contributed to newborn demise and neonatal brain injury. Maternal death claims were secondary to air way difficulty, maternal hemorrhage, and high neuraxial
blockade. Te most common claim associated with obstetrical anesthesia was related to nerve injury ollowing regional anesthesia. Nerve injury can be secondary to neuraxial anesthesia and analgesia, but also due to obstetrical causes. Early neurological consultation to identiy the source o nerve injury is suggested to discern i injury could be secondary to obstetrical rather than anesthesia interventions.
REGIONAL ANESTHESIA In a closed claims analysis, peripheral nerve blocks were involved in 159 o the 6894 claims analyzed. Peripheral nerve block claims were or death (8%), permanent injuries (36%), and temporary injuries (56%). Te brachial plexus was the most common location or nerve injury. In addition to ocular injury, cardiac arrest ollowing retrobulbar block contributed to anesthesiology claims. Cardiac arrest and epidural hematomas are two o 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 o the death or brain damage claims in both obstetrical and nonobstetrical patients. Accidental intravenous injection and local anesthesia toxicity also contributed to claims or brain injury or death. Nerve injuries constitute the third most common source o anesthesia litigation. A retrospective review o patient records and a claims database showed that 112 o 380,680 patients (0.03%) experienced perioperative nerve injury. Patients with hypertension and diabetes and those who were smokers were at increased risk o developing perioperative nerve injury. Perioperative nerve injuries may result rom compression, stretch, ischemia, other traumatic events, and unknown causes. Improper positioning can lead to nerve compression, ischemia, and injury, however not every ner ve injury is the result o improper positioning. Te care received by patients with ulnar nerve injury was rarely judged to be inadequate in the ASA Closed Claims database. Even awake patients undergoing
CHAPTER 54 Anesthetic Complications
spinal anesthesia have been reported to experience upper extremity injury. Moreover, many peripheral nerve injuries do not become maniest until more than 48 hr afer anesthesia and surgery, suggesting that some nerve damage that occurs in surgical patients may arise rom events taking place afer 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 rom 1973–2000 (Figure 54–5), a decrease in the proportion o claims or death and brain damage was noted over the three decades. Likewise, the percentage o claims related to respiratory events also was reduced. Compared with beore 1990, the percentage o claims secondary to respiratory events decreased during the years 1990–2000, accounting or only 23 % o claims in the latter study years compared with 51% o claims in the 1970s. Moreover, the percentage o claims that could be avoided by better monitoring decreased rom 63% in the 1970s to 16% in the 1990s. Death and brain damage constitute the major complications or which claims are �led. In the 1990s, cardiovascular events joined respiratory complications in sharing the primary causes o pediatric anesthesia litigation. In
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the study mentioned above, better monitoring and newer airway management techniques may have reduced the incidence o respiratory events leading to litigation-generating complications in the latter years o the review period. Additionally, the possibility o a claim being �led secondary to death or brain injury is greater in children who are in ASA classes 3, 4, or 5. In a review o the Pediatric Perioperative Cardiac Arrest Registry, which collects inormation rom about 80 North American institutions that provide pediatric anesthesia, 193 arrests were reported in children between 1998 and 2004. During the study period, 18% o the arrests were “drug related,” compared with 37% o all arrests during the years 1994–1997. Cardiovascular arrests occurred most ofen (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 rom cardio vascular causes occurred most requently during surgery, whereas arrests rom respiratory causes tended to occur afer surgery. Te reduced use o halothane seems to have decreased the incidence o arrests secondary to medication administration. However, hyperkalemia and electrolyte disturbances
90% 80% d 70% o i r e 60% p e m i t 50% n i s 40% m l a f 30% o %20%
10% 0%
Death or permanent brain damage
Preventable by monitorin g Respiratory events
Cardiovascular events
6 7 8 8 0 8 2 8 4 8 6 8 8 9 0 9 2 9 4 9 6 0 0 7 9 9 1 9 1 9 1 9 1 9 1 9 1 9 1 9 1 9 1 9 2 0 1 1 3 – 7 7 – 7 9 – 8 1 – 8 3 – 8 5 – 8 7 – 8 9 – 9 1 – 9 3 – 9 5 – 9 7 – 7 9 9 1 9 1 9 1 9 1 9 1 9 1 9 1 9 1 9 1 9 1 9 1 1
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.)
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associated with transusion and hypovolemia also contribute to sources o cardiovascular arrest in children perioperatively. A review o data rom the Pediatric Perioperative Cardiac Arrest Registry with a ocus on children with congenital heart disease ound 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 o perioperative arrest. Children with aortic stenosis and cardiomyopathy were similarly ound to be at increased risk o cardiac arrest perioperatively.
OUT OF THE OPERATING ROOM ANESTHESIA AND MONITORED ANESTHESIA CARE Review o the ASA Closed Claims Project database indicates that anesthesia at remote (out o 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 or death (54% vs 29%, respectively). Te endoscopy suite and cardiac catheterization laboratory were the most requent locations rom which claims were generated. Monitored Anesthesia Care (MAC) was the most common technique employed in these claims. Overwhelmingly, adverse respiratory events were most requently responsible or the injury. An analysis o the ASA Closed Claims Project database ocusing on MAC likewise revealed that oversedation and respiratory collapse most requently lead to claims. Claims or burn injuries suered in operating room �res were also ound in t he database. Supplemental oxygen, draping, pooling o �ammable antiseptic preparatory solutions, and surgical cautery combine to produce the potential or operating room �res.
EQUIPMENT PROBLEMS “Equipment problems” is probably a misnomer; the ASA Closed Claims Project review o 72 claims involving gas delivery systems ound that equipment misuse was three times more common than equipment malfunction. Te majority (76%) o adverse
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% o the drug doses given to hospitalized patients are incorrect. Errors in drug administration account or 4% o cases in the ASA Closed Claims Project, which ound that errors resulting in claims were most requently due to either incorrect dosage or unintentional administration o the wrong drug (syringe swap). In the latter category, accidental administration o epinephrine proved particularly dangerous. Another type o human error occurs when the most critical problem is ignored because attention is inappropriately ocused on a less important problem or an incorrect solution (�xation error). Serious anesthetic mishaps are ofen associated with distractions and other actors (Table 54–3). Te impact o most equipment ailures is decreased or avoided when the problem is identi�ed during a routine preoperative checkout perormed by adequately 5 trained personnel. Many anesthetic atalities occur only afer a series o coincidental circumstances, misjudgments, and technical errors coincide (mishap chain).
Prevention Strategies to reduce the incidence o serious anesthetic complications include better monitoring and anesthetic techniques, improved education, more
CHAPTER 54 Anesthetic Complications
comprehensive protocols and standards o 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. Te act that most accidents occur during the maintenance phase o anesthesia— rather than during induction or emergence—implies a ailure o vigilance. Inspection, palpation, percussion, and auscultation o the patient provide important inormation. Instruments should supplement (but never replace) the anesthesiologist’s own senses. o minimize errors in drug administration, drug syringes and ampoules in the workspace should be restricted to those needed or the current speci�c case. Drugs should be consistently diluted to the same concentration in the same way or each use, and they should be clearly labeled. Computer systems or scanning bar-coded drug labels are available that may help to reduce medication errors. Te conduct o all anesthetics should ollow a predictable pattern by which the anesthetist actively surveys the monitors, the surgical �eld, and the patient on a recurrent basis. In particular, patient positioning should be requently reassessed to avoid the possibility o 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 o 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 o care, and staffing issues. Speci�c responsibilities o peer review committees include identiying (and, ideally, preventing) potential problems, ormulating and periodically revising departmental policies, ensuring the availability o properly unctioning anesthetic equipment, enorcing standards required
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or clinical privileges, and evaluating the appropriateness and quality o patient care. A quality improvement system impartially and continuously reviews complications, compliance with standards, and quality indicators.
AIRWAY INJURY Te daily insertion o endotracheal tubes, laryngeal mask airways, oral/nasal airways, gastric tubes, transesophageal echocardiogram (EE) probes, esophageal (bougie) dilators, and emergency airways all involve the risk o airway structure damage. Common morbid complaints, such as sore throat and dysphagia, are usually sel-limiting, but may also be nonspeci�c symptoms o more ominous complications. Te most common persisting airway injury is dental trauma. In a retrospective study o 600,000 surgical cases, the incidence o 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 requently injured. Major risk actors or dental trauma included tracheal intubation, preexisting poor dentition, and patient characteristics associated with diffi cult airway management (including limited neck motion, previous head and neck surgery, cranioacial abnormalities, and a history o difficult intubation). Other types o airway trauma are rare. Although there are scattered case reports in the literature, the most comprehensive analysis was perormed by the ASA Closed Claims Project. Tis report describes 266 claims, o which the least serious were temporomandibular joint (MJ) injuries that were all associated with otherwise uncomplicated intubations and occurred mostly in emales younger than age 60 years. Approximately 25% o these patients had previous MJ disease. Laryngeal injuries included vocal cord paralysis, granuloma, and arytenoid dislocation. Most tracheal injuries were associated with emergency surgical tracheotomy, but a ew were related to endotracheal intubation. Some injuries occurred during seemingly easy, routine intubations. Proposed mechanisms include excessive tube movement in the trachea, excessive cuff in�ation
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leading to pressure necrosis, and inadequate relaxation. Esophageal perorations contributed to death in 5 o 13 patients. Esophageal peroration ofen presents with delayed-onset subcutaneous emphysema or pneumothorax, unexpected ebrile state, and sepsis. Pharyngoesophageal peroration is associated with difficult intubation, age over 60 years, and emale gender. As in tracheal peroration, signs and symptoms are ofen delayed in onset. Initial sore throat, cervical pain, and cough ofen progressed to ever, dysphagia, and dyspnea, as mediastinitis, abscess, or pneumonia develop. Mortality rates o up to 50% have been reported afer esophageal peroration, with better outcomes attributable to rapid detection and treatment. Minimizing the risk o airway injury begins with the preoperative assessment. A thorough airway examination will help to determine the risk or difficulty Documentation o current dentition (including dental work) should be included. Many practitioners believe preoperative consent should include a discussion o the risk o dental, oral, vocal cord, and esophageal trauma in every patient who could potentially need any airway manipulation. I a diffi cult airway is suspected, a more detailed discussion o risks (eg, emergency tracheotomy) is appropriate. In such cases, emergency airway supplies and experienced help should be available. Te ASA algorithm or diffi cult airway management is a useul guide. Afer a difficult intubation, one should seek latent signs o esophageal peroration and have an increased level o suspicion or airway trauma. When intubation cannot be accomplished by routine means, the patient or guardian should be inormed to alert uture anesthesia providers o potential airway difficulty. Emergent nonoperating room intubations present unique challenges. In a review o 3423 out o the operating room intubations, 10% were considered to be “difficult,” and 4% o these intubations were associated with some orm o complication, including aspiration, esophageal intubation, or dental injury. In this report, intubation bougies were employed in 56% o difficult intubations. Te increased availability o video laryngoscopes and bougies have made emergent intubations less stressul and less likely to be unsuccessul.
PERIPHERAL NERVE INJURY Nerve injury is a complication o being hospitalized, with or without surgery, regional, or general anesthesia. Peripheral nerve injury is a requent and vexing problem. In most cases, these injuries resolve within 6–12 weeks, but some are permanent. Because peripheral neuropathies are commonly associated (ofen incorrectly!) with ailures o patient positioning, a review o mechanisms and prevention is necessary. Te most commonly injured peripheral nerve is the ulnar nerve (Figure 54–6). In a retrospective study o over 1 million patients, ulnar neuropathy (persisting or more than 3 months) occurred in approximately 1 in 2700 patients. O interest, initial symptoms were most requently noted more than 24 hr afer a surgical procedure. Risk actors included male gender, hospital stay greater than 14 days, and very thin or obese body habitus. More than 50% o these patients regained ull sensory and motor unction within 1 yr. Anesthetic technique was not implicated as a risk actor; 25% o patients with ulnar neuropathy underwent monitored care or lower extremity regional technique. Te ASA Closed Claims Project �ndings support most o these results, including the delayed onset o symptoms and the lack o relationship between anesthesia technique and injury. Tis study also noted that many neuropathies occurred despite notation o extra padding over the elbow area, urther negating compression as a possible mechanism o injury. Finally, the ASA Closed Claims Project investigators ound no deviation rom the standard o care in the majority o patients who maniested nerve damage perioperatively.
The Role of Positioning Other peripheral nerve injuries seem to be more closely related to positioning or surgical procedure. Tey may involve the peroneal nerve, the brachial plexus, or the emoral and sciatic nerves. External pressure on a nerve could compromise its perusion, 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 super�cial course (eg, the
CHAPTER 54 Anesthetic Complications
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Humerus
Ulnar nerve Medial epicondyle
Arcuate ligament Olecranon process
A
Pronation
B
Supination
FIGURE 546 A: Pronation of the forearm can c ause external compression of the ulnar nerve in the cubital tunnel. B: Forearm supination avoids this problem.
(Modified and reproduced, with permission, from Wadsworth TG: The cubital tunnel and the external compression syndrome. Anesth Analg
peroneal nerve around the �bula). Lower extremity neuropathies, particularly those involving the peroneal nerve, have been associated with such actors as extreme degrees (high) and prolonged (greater than 2 h) durations o the lithotomy position. But, these nerve injuries also sometimes occur when such conditions are not present. Other risk actors or 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 inerior shoulder o patients in the lateral decubitus position. Tis roll should be located caudad to the axilla to prevent direct pressure on the brachial plexus and large enough to relieve any pressure rom the mattress on the lower shoulder. Te data are convincing that some peripheral nerve injuries are not preventable. Te risk o peripheral neuropathy should be included in
discussions leading to inormed consent. When reasonable, patients with contractures (or other causes o limited �exibility) can be positioned beore induction o anesthesia to check or easibility and discomort. 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 rendelenberg position should be avoided i possible, and shoulder abduction and lateral rotation should be minimized. Te upper extremities should not be extended greater than 90° at any joint. (Tere should be no continuous external compression on the knee, ankle, or heel.) Although injuries may still occur, additional padding may be helpul in vulnerable areas. Documentation should include inormation on positioning, including the presence o padding. Finally, patients who complain o sensory or motor dysunction in the postoperative period should be
1974;53:303.)
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reassured that this is usually a temporary condition. Motor and sensory unction should be documented. When symptoms persist or more than 24 hr, the patient should be reerred to a neurologist (or a physiatrist or hand surgeon) who is knowledgeable about perioperative nerve damage or evaluation. Physiological testing, such as nerve conduction and electromyographic studies, can be useul to document whether nerve damage is a new or chronic condition. In the latter case, �brillations will be observed in chronicall chronicallyy denervated muscles.
Complications Related to Positioning Changes o 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 sae or 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 �oor or a park bench may awaken with a brachial plexus injury. Similarly, regional and general anesthesia abolish protective re�exes and predispose patients to injury.
Complications o postural hypotension, the most common physiological consequence o positioning, can be minimized by avoiding abrupt or extreme position changes (eg, sitting up quickly), reversing the position i vital signs deteriorate, keeping the patient well hydrated, and having vasoactive drugs available to treat hypotension. Whereas maintaining a reduced level o general anesthesia will decrease the likelihood o hypotension, light general anesthesia will increase the likelihood that movement o the endotracheal tube during positioning will cause the patient to cough and become hypertensive. Many complications, including air embolism, blindness rom sustained pressure pressure on the globe, g lobe, and �nger amputation ollowing a crush injury, can be 54– 4). caused by improper patient positioning (Table 54–4 Tese complications are best prevented by evaluating the patient’s postural limitations during the preanesthetic visit; padding pressure points, susceptible possibly ly nerves, and any area o the body that will possib be in contact with the operating table or its attachments; avoiding �exion or extension o a joint to its limit; having an awake patient assume the position
TABLE 544 Complications associated with patient positioning. Complication
Position
Prevention
Ven eno ous ai airr emb embol olis ism m
Sitt Si ttin ing g, pr pron one e, rev rever erse se Trendelenburg
Maintain adequate venous pressure; ligate “open” “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
Espe Es peci cial ally ly li lith thot otom omy y
Maint Ma intai ain n pe perfu rfusi sion on pr pres essu sure re an and d av avoi oid d ext exter erna nall co compr mpres essi sion on..
Corneal abrasion
Any, bu butt especially prone
Taping and/or lubricating eye.
Digit amputation
Any
Check for protruding digits before changing table configuration.
Any Lith Li thot otom omy y, la late tera rall decubitus Any Any Prone, sitting Any
Avoid stretching or direct compression at neck, shoulder, or axilla. Avoid sustained pressure on lateral aspect of up per fibula.
Nerve palsies Brachial plexus Com ommo mon n pe perron onea eall Radial Ulnar Retinal ischemia Skin necrosis
Avoid compression of lateral humerus. Avoid sustained pressure on ulnar groove. Avoid pressure on globe. Avoid sustained pressure over bony prominences.
CHAPTER 54 Anesthetic Complications
to ensure comort; and understanding the potential complications o each position. Monitors must ofen be disconnected during patient repositioning, making this a time o greater risk or unrecognized hemodynamic derangement. Compartment syndromes can result rom hemorrhage into a closed space ollowing a vascular puncture or prolonged venous out�ow 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 (asciotomy) or in the abdominal compartment by laparotomy.
AWARENESS A continuing series o media reports have imprinted the ear o awareness under general anesthesia into the psyche o the general population. Accounts o recall and helplessness while paralyzed have made unconsciousness a primary concern o patients undergoing general anesthesia. When unintended intraoperative awareness does occur, patients may exhibit symptoms ranging rom mild anxiety to posttraumatic posttrauma tic stress disorder (eg, sleep disturbances, nightmares,, and social diffi nightmares di fficulties culties). ). Although the t he incidence inciden ce is diffi cult to measure, meas ure, approximately 2% o the closed claims in the ASA Closed Claims Project database relate to awareness under anesthesia. Analysis o the NHS Litigation Authority database rom 1995–2007 revealed that 19 o 93 relevant claims were or “awake paralysis.” Clearly, awareness is o great concern to patients and may lead to litigation. Certain types o surgeries are most requently associated with awareness, including those or major trauma, obstetrics, and major cardiac procedures. In some instances, awareness may result rom the reduced depth o anesthesia that can be tolerated by the patient. In early studies, recall rates or intraoperative events during major trauma surgery have been reported to be as requent as 43%; the incidence o awareness during cardiac surgery and cesarean sections is 1.5% and 0.4%, respectively respectively.. As o 1999, the ASA Closed Claims Project reported 79 awareness claims; approximately 20% o the claims were or awake paralysis, and the remainder
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o the claims were or recall under general anesthesia. Most claims or awake paralysis were thought to be due to errors in drug labeling and administration, such as administering paralytics beore inducing narcosis. Since the 1999 review review,, another 71 cases have appeared in the database. Claims or 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 i not met can lead to awareness. Other speci�c causes o awareness include inadequate inhalational anesthetic delivery (eg, rom vaporizer malunction) and medication errors. Some patients may complain o awareness, when, in act, they received regional anesthesia or monitor monitored ed 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” ofen can become irate when sedation dulls their memory o the perioperative experience. In all cases, rank discussion between anesthesia staff and the patient is necessary to avoid unrealistic expectations. Some clinicians routinely discuss the possibility o intraoperative recall and the steps that will be taken to minimize it as part o the inormed consent or general anesthesia. Tis makes particular sense or 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. I this is not possible, benzodiazepines (and/or scopolamine) can be used. Movement o a patient may indicate inadequate anesthetic depth. Documentation should include end-tidal concentrations o anesthetic gases (when available) and dosages o amnesic drugs. Use o a bispectral index scale (BIS) monitor or similar monitors may be helpul although randomized clinical trials have ailed to demonstrate a reduced incidence o awareness with use o BIS when compared with a group receiving appropriate concentrations o volatile agents. Finally, i there is evidence o intraoperative awareness during postoperative rounds, the practitioner should obtain a detailed account o the experience, answer patient
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questions, be very empathetic, and reer the patient or psychological counseling i appr appropriate. opriate.
EYE INJURY A wide range o conditions rom simple corneal abrasion to blindness have been reported. Corneal abrasion is by ar the most common and transient eye injury. injury. Te ASA Closed Claims Project identi�ed a small number o claims or abrasion, in which the cause was rarely identi�ed (20%) and the incidence o permanent injury was low (16%). It also identi�ed a subset o claims or blindness that resulted rom patient movement during ophthalmological surgery. Tese cases occurred in patients receiving either general anesthesia or monito monitored red anesthesia care. Although the cause o corneal abrasion may not be obvious, securely closing the eye lids with tape afer loss o 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 o injury. Adequate anesthetic depth (and, in most cases, paralysis) should be maintained to prevent movement during ophthalmological surgery under general anesthesia. In patients scheduled or 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 o postoperative vision loss. Postoperative vision loss is most commonly reported afer cardiopulmonary bypass, radical neck dissection, and spinal surgeries in the prone position. Both preoperative and intraoperative actors may be contributory. Many o 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 o their potential to reduce oxygen delivery. Finally, prolonged surgical time in positions that compromise venous out�ow (prone, head down, compressed
abdomen) have also been ound to be actors in spine surgery. Symptoms are usually present immediately upon awakening rom anesthesia, but have been reported up to 12 days postoperatively. Such symptoms range rom decreased visual acuity to complete blindness. Analysis o case records submitted to the ASA Postoperative Vision Loss Registry revealed that vision loss was secondary to ION in 83 o 93 cases. Instrumentation o 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 ree o pressure secondary to the use o pin �xation, indicating that direct pressure on the eye is not required to produce ION. Increased venous pressure in patients in the rendelenberg position may reduce blood �ow to the optic nerve. It is difficult to ormulate or mulate recommendations to prevent this complication because risk actors or ION are ofen unavoidable. Steps that might be taken include: (1) limiting the degree and duration o hypotension during controlled (deliberate) hypotension, (2) administering a transusion to severely anemic patients who seem to be at risk o ION, and (3) discussing with the surgeon the possibility o staged operations in high-risk patients to limit prolonged procedures. O 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 o spinal anesthetics is an uncommon complication. Te initial published report was a closed claims analysis o 14 patients who experienced cardiac arrest during spinal anesthesia. Te cases primarily involved young (average age 36 years), relatively healthy (ASA physical status I–II) patients who were given appropriate doses o local anesthetic that produced a high dermatomal level o block prior to arrest (4 level). Respiratory insufficienc ciencyy with hypercarbia hypercar bia due to sedatives s edatives was w as thought to be a potential contributing actor. Te
CHAPTER 54 Anesthetic Complications
average time rom induction o 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. reatment consisted o 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 signi�cant neurological de�cits. A subsequent study concluded that such arrests had little relationship to sedation, but were related more to extensive degrees o sympathetic blockade, leading to unopposed vagal tone and proound bradycardia. Rapid appropriate treatment o bradycardia and hypotension is essential to minimize the risk o arrest. Early treatment o bradycardia with atropine may prevent a downward spiral. Stepwise doses o ephedrine, epinephrine, and other vasoactive drugs should be given to treat hypotension. I cardiopulmonary arrest occurs, ventilatory support, cardiopulmonary resuscitation, and ull resuscitation doses o atropine and epinephrine should be administered without delay.
HEARING LOSS Perioperative hearing loss is usually transient and ofen goes unrecognized. Te incidence o lowrequency hearing loss ollowing dural puncture may be as high as 50%. It seems to be due to cerebrospinal �uid leak, and, i persistent, can be relieved with an epidural blood patch. Hearing loss ollowing general anesthesia can be due to a variety o causes and is much less predictable. Mechanisms include middle ear barotrauma, vascular injury, and ototoxicity o drugs (aminoglycosides, loop diuretics, nonsteroidal antiin�ammatory drugs, and antineoplastic agents). Hearing loss ollowing cardiopulmonary bypass is usually unilateral and is thought to be due to embolism and ischemic injury to the organ o Corti.
ALLERGIC REACTIONS Hypersensitivity (or allergic) reactions are exaggerated immunological responses to antigenic stimulation in previously sensitized persons. Te antigen, or
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TABLE 545 Hypersensitivity reactions. Type I (immediate) Atopy Urticaria—angioedema 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 itsel, a metabolite, or a breakdown product. Patients may be exposed to antigens through the respiratory tract, gastrointestinal tract, eyes, skin and rom previous intravenous, intramuscular, or peritoneal exposure. Anaphylaxis occurs when in�ammatory agents are released rom basophils and mast cells as a result o an antigen interacting with the immunoglobulin (Ig) E. Anaphylactoid reactions maniest themselves in the same manner as anaphylactic reactions, but are not the result o an interaction with IgE. Direct activation o complement and IgG-mediated complement activation can result in similar in�ammatory mediator release and activity. Depending on the antigen and the immune system components involved, hypersensitivity reactions are classically divided into our types ( Table 54–5). In many cases, an allergen (eg, latex) may cause more than one type o hypersensitivity reaction. ype I reactions involve antigens that cross-link IgE antibodies, triggering the release o in�ammatory mediators rom mast cells. In type II reactions, complement-�xing (C1-binding) IgG antibodies bind to antigens on cell suraces, activating the classic complement pathway and lysing the cells. Examples o type II reactions include hemolytic transusion reactions and heparin-induced thrombocytopenia. ype III reactions occur when antigen–antibody
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(IgG or IgM) immune complexes are deposited in tissues, activating complement and generating chemotactic actors that attract neutrophils to the area. Te activated neutrophils cause tissue injury by releasing lysosomal enzymes and toxic products. ype III reactions include serum sickness reactions and acute hypersensitivity pneumonitis. ype IV reactions, ofen reerred to as delayed hypersensitivity reactions, are mediated by CD4+ lymphocytes that have been sensitized to a speci�c antigen by prior exposure. Prior H1 response causes expression o a -cell receptor protein that is speci�c or the antigen. Reexposure to the antigen causes these lymphocytes to produce lymphokines—interleukins (IL), intereron (IFN), and tumor necrosis actor-γ (NF-γ )—that attract and activate in�ammatory mononuclear cells over 48–72 hr. Production o IL-1 and IL-6 by antigen-processing cells ampli�es clonal expression o the speci�c sensitized cells and attracts other types o cells. IL-2 secretion transorms CD8+ cytotoxic cells into killer cells; IL-4 and IFN-γ cause macrophages to undergo epithelioid transormation, ofen producing granuloma. Examples o type IV reactions are those associated with tuberculosis, histoplasmosis, schistosomiasis, and hypersensitivity pneumonitis and some autoimmune disorders, such as rheumatoid arthritis and Wegener’s granulomatosis.
1. Immediate Hypersensitivity Reactions Initial exposure o a susceptible person to an antigen induces CD4+ cells to lymphokines that activate and transorm speci�c B lymphocytes into plasma cells, producing allergen-speci�c IgE antibodies (Figure 54–7). Te Fc portion o these antibodies then associates with high affi nity receptors on the cell surace o tissue mast cells and circulating basophils. During subsequent reexposure to the antigen, it binds the Fab portion o adjacent IgE antibodies on the mast cell surace, inducing degranulation and release o in�ammatory lipid mediators and additional cytokines rom the mast cell. Te end result is the release o histamine, tryptase, proteoglycans (heparin and chondroitin sulate), and carboxypeptidases. Prostaglandin (mainly prostaglandin
D2) and leukotriene (B 4, C4, D4, E4, and plateletactivating actor) synthesis is also increased. Te combined effects o these mediators can produce arteriolar vasodilatation, increased vascular permeability, increased mucus secretion, smooth muscle contraction, and other clinical maniestations o type I reactions. ype I hypersensitivity reactions are classi�ed 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 con�ned to the skin (urticaria) or subcutaneous tissue (angioedema), but when they are severe, they become generalized and a lie-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 rom marked vasodilatation and increased permeability o subcutaneous blood vessels. When angioedema is extensive, it can be associated with large �uid shifs; when it i nvolves 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. Te syndrome appears within minutes o exposure to a speci�c antigen in a sensitized person and characteristically presents as acute respiratory distress, circulatory shock, or both. Death may occur rom asphyxiation or irreversible circulatory shock. Te incidence o anaphylactic reactions during anesthesia has been estimated at a rate o 1:3500 to 1:20000 anesthetics. Mortality rom anaphylaxis can be as requent as 4% o cases with brain injury, occurring in another 2% o surviving patients. A French study evaluating 789 anaphylactic and anaphylactoid reactions reported that the most common sources o perioperative anaphylaxis were neuromuscular blockers (58%), latex (17%), and antibiotics (15%).
CHAPTER 54 Anesthetic Complications
A
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Free drug Fixation of IgE antibodies to mast cells and blood basophils
Carrier (eg, albumin)
Drugcarrier complex
Prednisone blocks
Mitosis Macrophage
B
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.
Te most important mediators o anaphylaxis are histamine, leukotrienes, basophil kallikrein (BK-A,) and platelet-activating actor. Tey increase vascular permeability and contract smooth muscle. H1-receptor activation contracts bronchial smooth muscle, whereas H2-receptor activation causes
Ig, immunoglobulin. (Reproduced, with permission, from Katzung BG [editor]: Basic & Clinical Pharmacology, 8th ed. McGraw-Hill, 2001.)
vasodilatation, enhanced mucus secretion, tachycardia, and increased myocardial contractility. BK-A cleaves bradykinin rom kininogen; bradykinin increases vascular permeability and vasodilatation and contracts smooth muscle. Activation o Hageman actor can initiate intravascular coagulation.
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TABLE 546 Clinical manifestations
of anaphylaxis.
1
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 actor o anaphylaxis, neutrophil chemotactic actor, and leukotriene B4 attract in�ammatory cells that mediate additional tissue injury. Angioedema o the pharynx, larynx, and trachea produce upper airway obstruction, whereas bronchospasm and mucosal edema result in lower airway obstruction. Histamine may preerentially constrict large airways, whereas leukotrienes primarily affect smaller peripheral airways. ransudation o �uid into the skin (angioedema) and viscera produces hypovolemia and shock, whereas arteriolar vasodilatation decreases systemic vascular
resistance. Coronary hypoperusion 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 54–6 summarizes important maniestations o anaphylactic reactions. Anaphylactoid reactions resemble anaphylaxis but do not depend on IgE antibody interaction with antigen. A drug can directly release histamine rom mast cells (eg, urticaria ollowing high-dose morphine sulate) or activate complement. Despite 6 differing mechanisms, anaphylactic and anaphylactoid reactions typically are clinically indistinguishable and equally lie-threatening. Table 54–7 lists common causes o anaphylactic and anaphylactoid reactions. Factors that may predispose patients to these reactions include pregnancy, known atopy, and pre vious drug exposure. Such reactions are more common in younger than older patients. Laboratory identi�cation o 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.
CHAPTER 54 Anesthetic Complications
TABLE 548 Treatment of anaphylactic
and anaphylactoid reactions. Discontinue drug administration Administer 100% oxygen Epinephrine (0.01–0.5 mg IV or IM)1 Consider intubation Intravenous fluid bolus Diphenhydramine (50–75 mg IV) Ranitidine (150 mg IV) Hydrocortisone (up to 200 mg IV) or methylprednisolone (1–2 mg/kg) 1
The dose and route of epinephrine depend on the severity of the reaction. An infusion of 1–5 mcg/min may be necessary in adults.
susceptible is ofen aided by intradermal skin testing, leukocyte or basophil degranulation testing (histamine release test), or radio-allergosorbent testing (RAS). Te latter is capable o measuring the level o drug-speci�c IgE antibody in the serum. Serum tryptase measurement is helpul in con�rming the diagnosis o an anaphylactic reaction. Prophylactic pretreatment with histamine receptor antagonists and corticosteroids decreases the severity o the reaction. reatment must be immediate and tailored to the severity o the reaction (Table 54–8).
3. Allergic Reactions to Anesthetic Agents 7 rue anaphylaxis due to anesthetic agents is
rare; anaphylactoid reactions are much more common. Risk actors associated with hypersensitivity to anesthetics include emale gender, atopic history, preexisting allergies, and previous anesthetic exposures. Muscle relaxants are the most common cause o anaphylaxis during anesthesia, with an estimated incidence o 1 in 6500 patients. Tey account or almost 60% o perioperative anaphylactic reactions. In many instances, there was no previous exposure to muscle relaxants. Investigators suggest that over-the-counter drugs, cosmetics, and ood products, many o which contain tertiary or quaternary ammonium ions, can sensitize susceptible indi viduals. A French study ound that, in decreasing order o requency, rocuronium, succinylcholine, and atracurium were most ofen responsible; this likely re�ects the propensity to cause anaphylaxis, together with requency o use.
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Although rarer, hypnotic agents can also be responsible or some allergic reactions. Te incidence o anaphylaxis or thiopental and propool is 1 in 30,000 and 1 in 60,000, respectively. Allergic reactions to etomidate, ketamine, and benzodiazepines are exceedingly rare. rue anaphylactic reactions due to opioids are ar 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 rom 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 or an apparent anaphylactoid reaction to a local anesthetic. Moreover, the cross-reactivity between amide-type local anesthetics seems to be low. Tere are no reports o anaphylaxis to volatile anesthetics.
4. Latex Allergy Te severity o allergic reactions to latex-containing products ranges rom mild contact dermatitis to liethreatening anaphylaxis. Latex allergy is the second most common cause o anaphylaxis during anesthesia. Most serious reactions seem to involve a direct IgE-mediated immune response to polypeptides in natural latex, although some cases o contact dermatitis may be due to a type IV sensitivity reaction to chemicals introduced in the manuacturing process. Nonetheless, a relationship between the occurrence o contact dermatitis and the probability o uture anaphylaxis has been suggested. Chronic exposure to latex and a history o atopy increases the risk o sensitization. Healthcare workers and patients undergoing requent procedures with latex items (eg, repeated urinary bladder catheterization, barium enema examinations) should thereore be considered at increased risk. Patients with spina 8 bi�da, spinal cord injury, and congenital abnormalities o the genitourinary tract have an increased incidence o latex allergy. Te incidence o
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latex anaphylaxis in children is estimated to be 1 in 10,000. A history o 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 ruit, and banana. IL-18 and IL-13 single nucleotide polymorphisms may affect the sensitivity o individuals to latex and promote allergic responses. Anaphylactic reactions to latex may be conused with reactions to other substances (eg, drugs, blood products) because the onset o symptoms can be delayed or more than 1 hr afer initial exposure. reatment is the same as or other orms o anaphylactic reactions. Skin-prick tests, intradermal tests, basophil histamine-release tests, and RAS have been used to evaluate high-risk patients. Preventing a reaction in sensitized patients includes pharmacological prophylaxis and absolute avoidance o latex. Preoperative administration o H1 and H2 histamine antagonists and steroids may provide some protection, although their use is controversial. Although most pieces o anesthetic equipment are now latex-ree, some may still contain latex (eg, gloves, tourniquets, some ventilator bellows, intravenous injection ports, and older reusable ace masks). An allergic reaction has even been documented rom inhalation o latex antigen contained within aerosolized glove powder. Manuacturers o latex-containing medical products must label their products accordingly. Only devices speci�cally 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 rom drug vials prior to use, and injections should be made through plastic stopcocks, i latex has not been eliminated rom containers and injection ports.
5. Allergies to Antibiotics Many true drug allergies in surgical patients are due to antibiotics, mainly β-lactam antibiotics, such as penicillins and cephalosporins. Although 1% to 4% o β-lactam administrations result in allergic reactions, only 0.004% to 0.015% o these reactions
result in anaphylaxis. Up to 2% o the general population is allergic to penicillin, but only 0.01% o penicillin administrations result in anaphylaxis. Cephalosporin cross-sensitivity in patients with penicillin allergy is estimated to be 2% to 7%, but a history o an anaphylactic reaction to penicillin increases the cross-reactivity rate up to 50%. Patients with a prior history o an anaphylactic reaction to penicillin should thereore not receive a cephalosporin. Although imipenem exhibits similar cross-sensitivity, aztreonam seems to be antigenically distinct and reportedly does not cross-react with other β-lactams. Sulonamide allergy is also relatively common in surgical patients. Sula drugs include sulonamide antibiotics, urosemide, hydrochlorothiazide, and captopril. Fortunately, the requency o cross-reactivity among these agents is low. Like cephalosporins, vancomycin is commonly used or antibiotic prophylaxis in surgical patients. Unortunately, it is associated with adverse reactions. An anaphylactoid-type reaction, “red man syndrome,” consists o intense pruritus, �ushing, and erythema o the head and upper torso, ofen with arterial hypotension; this syndrome seems to be related to a rapid rate o administration more than to dose or allergy. Isolated systemic hypotension is a much more requent 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 o administration. Immunologic mechanisms are associated with other perioperative pathologies. ransusion-related lung injury may be secondary to the activity o antibodies in the donor plasma, producing a hypersensitivity reaction that results in lung in�ltrates and respiratory ailure. IgG antibody ormation directed at heparin–PF4 complexes results in platelet activation, thrombosis, and heparin-induced thrombocytopenia.
OCCUPATIONAL HAZARDS IN ANESTHESIOLOGY Anesthesiologists spend much o their workday exposed to anesthetic gases, low-dose ionizing radiation, electromagnetic �elds, blood products,
CHAPTER 54 Anesthetic Complications
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
1.42–4.91 1.71–4.84
Drug-related suicides
<1987 ≥1987
16 32
11 11
1.48 2.88
0.69–3.20 1.45–5.71
Suicides
<1987 ≥1987
41 62
33 38
1.25 1.60
0.79–1.97 1.07–2.39
Cl, confidence 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-specific mortality risks of anesthesiologists. Anesthesiology 2000;93:922.
and workplace stress. Each o these can contribute to negative health effects in anesthesia practitioners. A 2000 paper compared the mortality risks o anesthesiologists and internists. Death rom heart disease or cancer did not differ between the groups; however, anesthesiologists had an increased rate o suicides and drug-related deaths (Table 54–9). Anesthesiologists also had a greater chance o death rom 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 or drugrelated deaths compared with that o internists.
1. Chronic Exposure to Anesthetic Gases 9 Tere is no clear evidence that exposure to
trace amounts o anesthetic agents presents a health hazard to operating room personnel. However, because previous studies examining this issue have yielded �awed but con�icting results, the US Occupational Health and Saety Administration continues to set maximum acceptable trace concentrations o less than 25 ppm or nitrous oxide and 0.5 ppm or halogenated anesthetics (2 ppm i the halogenated agent is used alone). Achieving these
low levels depends on efficient scavenging equipment, adequate operating room ventilation, and conscientious anesthetic technique. Most people cannot detect the odor o volatile agents at a concentration o less than 30 ppm. I there is no unctioning scavenging system, anesthetic gas concentrations reach 3000 ppm or nitrous oxide and 50 ppm or volatile agents. Early studies indicated that emale operating room staff might be at increased risk o spontaneous abortion compared with other women. It is unclear i other actors related to operating room activity could also contribute to the possibly increased potential or pregnancy loss.
2. Infectious Diseases Hospital workers are exposed to many inectious diseases prevalent in the community (eg, respiratory viral inections, rubella, and tuberculosis). Herpetic whitlow is an inection o the �nger with herpes simplex virus type 1 or 2 and usually involves direct contact o previously traumatized skin with contaminated oral secretions. Painul vesicles appear at the site o inection. Te diagnosis is con�rmed by the appearance o giant epithelial cells or nuclear inclusion bodies in a smear taken rom the base o a vesicle, the presence o a rise in herpes simplex virus titer, or identi�cation o the virus with antiserum. reatment is conservative and includes
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topical application o 5% acyclovir ointment. Pre vention involves wearing gloves when contacting oral secretions. Patients at risk o harboring the virus include those suffering rom other inections, immunosuppression, cancer, and malnutrition. Te risk o this condition has virtually disappeared now that anesthesia personnel routinely wear gloves during manipulation o the airway, which was not the case in the 1980s and earlier. Viral DNA has been identi�ed in the smoke plume generated during laser treatment o condylomata. Te theoretical possibility o viral transmission rom this source can be minimized by using smoke evacuators, gloves, and appropriate OSHA approved masks. More disturbing is the potential o acquiring serious blood-borne inections, such as hepatitis B, hepatitis C, or human immunode�ciency virus (HIV). Although parenteral transmission o these diseases can occur ollowing mucous membrane, cutaneous, or percutaneous exposure to inected body �uids, accidental injury with a needle contaminated with inected blood represents the most common occupational mechanism. Te risk o transmission can be estimated i three actors are known: the prevalence o the inection within the patient population, the incidence o exposure (eg, requency o needlestick), and the rate o serocon version afer a single exposure. Te seroconversion rate afer a speci�c exposure depends on several actors, including the inectivity o the organism, the stage o the patient’s disease (extent o viremia), the size o the inoculum, and the immune status o the healthcare provider. Rates o seroconversion ollowing a single needlestick are estimated to range between 0.3% and 30%. Hollow (hypodermic) 10 needles pose a greater risk than do solid (surgical) needles because o the potentially larger inoculum. Te use o gloves, needleless systems, or protected needle devices may decrease the incidence o some (but not all) types o injury. Te initial management o needlesticks involves cleaning the wound and notiying the appropriate authority within the health care acility. Afer an exposure, anesthesia workers should report to their institution’s emergency or employee health department or appropriate counseling on
postexposure prophylaxis options. All OR staff should be made aware o the institution’s employee health noti�cation pathway or needle stick and other injuries Fulminant hepatitis B (1% o acute inections) carries a 60% mortality rate. Chronic active hepatitis (<5% o all cases) is ass ociated with an increased incidence o cirrhosis o the liver and hepatocellular carcinoma. ransmission o the virus is primarily through contact with blood products or body �uids. Te diagnosis is con�rmed by detection o hepatitis B surace antigen (HBsAg). Uncomplicated recovery is signaled by the disappearance o HBsAg and the appearance o antibody to the surace antigen (anti-HBs). A hepatitis B vaccine is available and is strongly recommended prophylactically or anesthesia personnel. Te appearance o anti-HBs afer a three-dose regimen indicates successul immunization. Hepatitis C is another important occupational hazard in anesthesiology; 4% to 8% o hepatitis C inections occur in healthcare workers. Most (50% to 90%) o these inections lead to chronic hepatitis, which, although ofen asymptomatic, can progress to liver ailure and death. In act, hepatitis C is the most common cause o nonalcoholic cirrhosis in the United States. Tere is currently no vaccine to protect against hepatitis C inection. Anesthesia personnel seem to be at a low, but measureable, risk or the occupational contraction o HIV. Te risk o acquiring HIV inection ollowing a single needlestick contaminated with blood rom an HIV-inected patient has been estimated at 0.4% to 0.5%. Because there are documented reports o transmission o HIV rom inected patients to healthcare workers (including anesthesiologists), the Centers or Disease Control and Prevention proposed guidelines that apply to all categories o patient contact. Tese universal precautions, which are equally valid or protection against hepatitis B or C inection, are as ollows: • No recapping and the immediate disposal o contaminated needles • Use o gloves and other barriers during contact with open wounds and body �uids • Frequent hand washing
CHAPTER 54 Anesthetic Complications
• Use o proper techniques or disinection or the disposal o 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 Anesthesiology is a high-risk medical specialty or substance abuse. Probable reasons or this include the stress o anesthetic practice and the easy availability o drugs with addiction potential (potentially attracting people at risk o addiction to the �eld). Te likelihood o developing substance abuse is increased by coexisting personal problems (eg, marital or �nancial diffi culties) or a amily history o alcoholism or drug addiction. Te voluntary use o nonprescribed moodaltering pharmaceuticals is a disease. I lef untreated, substance abuse ofen leads to death rom drug overdose—intentional or unintentional. One o the greatest challenges in treating drug abuse is i dentiying the affl icted individual, as denial is a consistent eature. Unortunately, changes evident to an outside observer are ofen both vague and late: reduced involvement in social activities, subtle changes in appearance, extreme mood swings, and altered work habits. reatment begins with a careul, well-planned intervention. Tose inexperienced in this area would be well advised to consult with their local medical society or licensing authority about how to proceed. Te goal is to enroll the individual in a ormal rehabilitation program. Te possibility that one may lose one’s medical license and be unable to return to practice provides powerul motivation. Some diversion programs report a success rate o approximately 70%; however, most rehabilitation programs report a recurrence rate o at least 25%. Long-term compliance ofen involves continued participation in support groups (eg, Narcotics Anonymous), random urine testing, and oral naltrexone therapy (a longacting opioid antagonist). Effective prevention strategies are diffi cult to ormulate; “better” control o drug availability is unlikely to deter a determined individual. It is unlikely that education about the severe consequences o substance abuse will bring new inormation to the potential drug-abusing
11
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physician. Tere remains controversy regarding the rate at which anesthesia staff will experience recidi vism. Many experts argue or a “one strike and you’re out” policy or anesthesiology residents who abuse injectable drugs. Te decision as to whether a ully trained and certi�ed physician who has been discovered to abuse injectable drugs should return to anesthetic practice afer completing a rehabilitation program varies and depends on the rules and traditions o the practice group, the medical center, the relevant medical licensing board, and the perceived likelihood o recidivism. Physicians returning to practice ollowing successul completion o a program must be careully monitored over the long term, as relapses can occur years afer apparent successul rehabilitation. Alcohol abuse is a common problem among physicians and nurses, and anesthesia personnel are no exception. Interventions or alcohol abuse, as is true or injectable drug abuse, must be careully orchestrated. Guidance rom the local medical society or licensing authority is highly recommended.
4. Ionizing Radiation Exposure Te use o imaging equipment (eg, �uoroscopy) during surgery and interventional radiologic procedures exposes the anesthesiologist to the potential risks o ionizing radiation. Te three most 12 important methods o minimizing radiation doses are limiting total exposure time during procedures, using proper barriers, and maximizing the distance rom the source o radiation. Anesthesiologists who routinely perorm �uoroscopic image guided invasive procedures should consider wearing protective eyeware incorporating radiation shielding. Lead glass partitions or lead aprons with thyroid shields are mandatory protection or all personnel who are exposed to ionizing radiation. Te inverse square law states that the dosage o radiation varies inversely with the square o the distance. Tus, the exposure at 4 m will be one-sixteenth that at 1 m. Te maximum recommended occupational wholebody exposure to radiation is 5 rem/yr. Tis can be monitored with an exposure badge. Te health impact on operating room personnel o exposure to electromagnetic radiation remains unclear.
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Perioperative & Critical Care Medicine
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 38.8°C. 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 flotation catheters have often been used in the past, but they are associated with significant complications and current evidence does not indicate that their use improves patient outcomes. Large fluid 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 significant 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
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 defibrillation unit prepared, the rhythm degenerates into ventricular fibrillation. What can explain this series of events? A differential 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 β1-adrenergic antagonist. It inhibits epinephrine’s β1-stimulation of heart rate, but does not antagonize α-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 deficits, and practitioner fatigue or distraction can all contribute to adverse outcomes. Careful adherence to hospital policies, checklists, patient identification procedures, and surgical and regional block timeouts can all help to prevent iatrogenic complications.
CHAPTER 54 Anesthetic Complications
GUIDELINES Practice advisory or the prevention o perioperative peripheral neuropathies: a report by the American Society o Anesthesiologists ask Force on prevention o peripheral neuropathies. Anesthesiology 2000;92:1168.
SUGGESTED READING Alexander B, Checkoway H, Nagahama S, Domino K: Cause-speci�c mortality risks o anesthesiologists. Anesthesiology 2000;93:922. Berge E, Seppala M, Lanier W: Te anesthesiology community’s approach to opioid and anesthetic abusing personnel: time to change course. Anesthesiology 2008;109:762. Bhananker S, Posner K, Cheney F, et al: Injury and liability associated with monitored anesthesia care. Anesthesiology 2006;104:228. 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 o surgery deaths in Department o Veterans Affairs hospitals. Anesth Analg 2008;107:1924. Bowdle A: Drug administration errors rom the ASA closed claims project. ASA Newslett 2003;67:11. Brown RH, Schauble JF, Miller NR: Anemia and hypotension as contributors to perioperative loss o 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 o predisposing actors. Anesthesiology 1988;68:5. Caplan RA, Vistica MF, Posner KL, Cheney FW: Adverse anesthetic outcomes arising rom gas delivery equipment: a closed claims analysis. Anesthesiology 1997;87:741. Chadwick HS: An analysis o obstetric anesthesia cases rom the American Society o Anesthesiologists closed claims project database. Int J Obstet Anesth 1996;5:258. Cheesman K, Brady J, Flood P, Li G: Epidemiology o anesthesia-related complications in labor and delivery, New York state, 2002-2005. Anesth Analg 2009;109:1174.
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Cheney FW: Te American Society o Anesthesiologists closed claims project: what have we learned, how has it affected practice, and how will it affect practice in the uture? Anesthesiology 1999;91:552. Cheney FW, Posner KL, Caplan RA, Gild WM: Burns rom warming devices in anesthesia. Anesthesiology 1994;80:806. Cheney FW, Domino KB, Caplan RA, Posner KL: Nerve injury associated with anesthesia: a closed claims analysis. Anesthesiology 1999;90:1062. Cheney F, Posner K, Lee L, et al: rends in anesthesiarelated death and brain damage. Anesthesiology 2006;105:1071. Cook , Bland L, Mihai R, Scott S: Litigation related to anaesthesia: an analysis o claims against the NHS in England 1995-2007. Anaesthesia 2009;64:706. Cook , Scott S, Mihai R: Litigation related to airway and respiratory complications o anaesthesia: an analysis o claims against the NHS i n England 1995-2007. Anaesthesia 2010;65:556. Coppieters MW, Van De Velde M, Stappaerts KH: Positioning in anesthesiology. oward a better understanding o stretch-induced perioperative neuropathies. Anesthesiology 2002;97:75. Cranshaw J, Gupta K, Cook : Litigation related to drug errors in anaesthesia: an analysis o claims against the NHS in England 1995-2009. Anaesthesia 2009;64:1317. Crosby E: Medical malpractice and anesthesiology: literature review and role o the expert witness. Can J Anesth 2007;54:227. Davies J, Posner K, Lee L, et al: Liability associated with obstetric anesthesia. Anesthesiology 2009;110:131. Domino KB, Posner Kl, Caplan RA, Cheney FW: Awareness during anesthesia: a closed claims analysis. Anesthesiology 1999;90:1053. Domino KB, Posner KL, Caplan RA, Cheney FW: Airway injury during anesthesia: a closed claims analysis. Anesthesiology 1999;91:1703. Domino K, Bowdle , Posner K, et al: Injuries and liability related to central vascular catheters. Anesthesiology 2004;100:1411. Edbril SD, Lagasse RS: Relationship between malpractice litigation and human errors. Anesthesiology 1999;91:848. Fisher DM: New York State guidelines on the topical use o phenylephrine in operating rooms. Anesthesiology 2000;92:858. Fitzgibbon DR, Posner KL, Domino KB, et al: Chronic pain management: American Society o Anesthesiologists Closed Claims Project. Anesthesiology 2004;100:98.
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Gayer S: Prone to blindness: answers to postoperative visual loss. Anesth Analg 2011;112:11. Ghoneim MM: Awareness during anesthesia. Anesthesiology 2000;92:597. Gild WM, Posner KL, Caplan RA, Cheney FW: Eye injuries associated with anesthesia. Anesthesiology 1992;76:204. Hawkins J, Chang J, Palmer S, et al: Anesthesia-related maternal mortality in the United States: 1979-2002. Obstet Gynecol 2011;117:69. Hepner DL, Castells MC: Anaphylaxis during the perioperative period. Anesth Analg 2003;97:1381. Jimenez N, Posner K, Cheney F, et al: An update on pediatric anesthesia liability: a closed claims analysis. Anesth Analg 2007;104:147. Lagasse R: Anesthesia saety: model or myth? Anesthesiology 2002;97:1336. Lagasse R: o see or not to see. Anesthesiology 2006; 105:1971. Lagasse R: Innocent prattle. Anesthesiology 2009;110:698. Lee LA: Postoperative visual loss data gathered and analyzed. ASA Newslett 2000;64:25. Lee L, Posner K, DominoK, et al: Injuries associated with regional anesthesia in the 1980s and 1990s. Anesthesiology 2004;101:143. Lee L, Posner K, Cheney F, et al: Complications associated with eye blocks and peripheral nerve blocks: an American Society o Anesthesiologists Closed Claims analysis. Reg Anesth Pain Med 2008;33:416. Lee LA, Rothe S, Posner KL, et al: Te American Society o Anesthesiologists Postoperative Visual Loss Registry: analysis o 93 spine surgery cases with postoperative visual loss. Anesthesiology 2006;105:652. Lesser JB, Sanborn KV, Valskys R, Kuroda M: Severe bradycardia during spinal and epidural anesthesia recorded by an anesthesia inormation management system. Anesthesiology 2003;99:859. Levy J, Adkinson N: Anaphylaxis during cardiac surgery: implications or clinicians. Anesth Analg 2008;106:392. Li G, Warner M, Lang B, et al: Epidemiology o anesthesia related mortality in the United States 1999-2005. Anesthesiology 2009;110:759. Liang B: “Standards” o anesthesia: law and ASA guidelines. J Clin Anesth 2008;20:393. Lineberger C: Impairment in anesthesiology: awareness and education. Int Anesth Clin 2008;46:151. Marco A: Inormed consent or surgical anesthesia care: has the time come or separate consent? Anesth Analg 2009;110:280.
Martin L, Mhyre J, Shanks A, et al: 3,423 emergency tracheal intubations at a university hospital: airway outcomes and complications. Anesthesiology 2011;114:42. Martin J: Compartment syndromes: concepts and perspectives or the anesthesiologist. Anesth Analg 1992;75:275. Metzner J, Posner K, Domino K: Te risk and s aety o anesthesia at remote locations: the US closed claims analysis. Curr Opin Anaesthesiol 2009;22:502. Monitto C, Hamilton R, Levey E, et al: Genetic predisposition to natural rubber latex allergy differs between health care workers and high risk patients. Anesth Analg 2010;110:1310. Morray JP, Geiduschek JM, Caplan RA: A comparison o pediatric and adult anesthesia closed malpractice claims. Anesthesiology 1993;78:461. Newland MC, Ellis SJ, Lydiatt CA, et al: Anestheticrelated cardiac arrest and its mortality. Anesthesiology 2002;97:108. Pollard JB: Cardiac arrest during spinal anesthesia: common mechanisms and strategies or prevention. Anesth Analg 2001;92:252. Ramamoorthy C, Haberkern C, Bhananker S, et al: Anesthesia-related cardiac arrest in children with heart disease: data rom the pediatric perioperative cardiac arrest (POCA) registry. Anesth Analg 2010;110:1376. Ranta SOV, Lauila R, Saario J, et al: Awareness with recall during general anesthesia: incidence and risk actors. Anesth Analg 1998;86:1084. Roh J, Kim D, Lee S, et al: Intensity o extremely low requency electromagnetic �elds produced in operating rooms during surgery at the standing position o anesthesiologists. Anesthesiology 2009;111:275. Rose G, Brown R: Te impaired anesthesiologist: not just about drugs and alcohol anymore. J Clin Anesthesiol 2010;22:379. Sharma AD, Parmley CL, Sreeram G, Grocott HP: Peripheral nerve injuries during cardiac surgery: risk actors, diagnosis, prognosis, and prevention. Anesth Analg 2000;91:1358. Silverstein JH, Silva DA, Iberti J: Opioid addiction in anesthesiology. Anesthesiology 1993;79:354. Sprung J, Bourke DL, Contreras MG, et al: Perioperative hearing impairment. Anesthesiology 2003;98:241. ait AR: Occupational transmission o tuberculosis: implications or anesthesiologists. Anesth Analg 1997;85:444.
CHAPTER 54 Anesthetic Complications
Warner MA, Warner ME, Martin J: Ulnar neuropathy. Incidence, outcome, and risk actors in sedated or anesthetized patients. Anesthesiology 1994;81:1332. Warner MA, Warner DO, Harper CM: Lower extremity neuropathies associated with lithotomy positions. Anesthesiology 2000;93:938. Warner ME, Beneneld SM, Warner MA, et al: Perianesthetic dental injuries. Anesthesiology 1999;90:1302. Weinger MB, Englund CE: Ergonomic and human actors affecting anesthetic vigilance and monitoring
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perormance in the operating room environment. Anesthesiology 1990;73:995. Welch M, Brummett C, Welch , et al: Perioperative nerve injuries: a retrospective study o 380,680 cases during a 10-year period at a single institution. Anesthesiology 2009;111:490. Williams EL, Hart WM Jr, empelhoff R: Postoperative ischemic optic neuropathy. Anesth Analg 1995;80:1018. Yuill G, Saroya D, Yuill S: A national survey o the provision or patients with l atex allergy. Anaesthesiology 2003;58:775.
