Complications in Anesthesia, Second Edition

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Section Editors JOHN L. ATLEE, MD

TERRI G. MONK, MD

Professor of Anesthesiology Department of Anesthesiology Medical College of Wisconsin Milwaukee, Wisconsin

Professor Department of Anesthesiology Duke University Medical Center Durham, North Carolina

BRENDA A. BUCKLIN, MD

TIMOTHY E. MOREY, MD

Associate Professor of Anesthesiology Department of Anesthesiology University of Colorado Health Sciences Center Denver, Colorado

Associate Professor of Anesthesiology Department of Anesthesiology University of Florida College of Medicine Gainesville, Florida

MARK A. CHANEY, MD

MICHAEL J. MURRAY, MD, PHD

Associate Professor of Anesthesiology Department of Anesthesia and Critical Care University of Chicago Pritzker School of Medicine Chicago, Illinois

DONN M. DENNIS, MD, FAHA Joachim S. Gravenstein, MD, Professor of Anesthesiology Department of Anesthesiology University of Florida College of Medicine Gainesville, Florida Vice President-Pharmacology, ARYx Therapeutics, Inc. Santa Clara, California

JOHN ELLIS, MD Professor of Anesthesiology Department of Anesthesia and Critical Care University of Chicago Pritzker School of Medicine Chicago, Illinois

JOEL M. GUNTER, MD Professor of Clinical Anesthesia and Pediatrics Department of Anesthesia University of Cincinnati School of Medicine Attending Anesthesiologist Department of Anesthesia Children’s Hospital Medical Center Cincinnati, Ohio

ROSEMARY HICKEY, MD

Professor of Anesthesiology and Chair Department of Anesthesiology Mayo Clinic College of Medicine Jacksonville, Florida

NADER D. NADER, MD Associate Professor of Anesthesiology, Surgery and Pathology State University of New York at Buffalo School of Medicine Buffalo, New York

MICHAEL F. O’CONNOR, MD Associate Professor Department of Anesthesia and Critical Care University of Chicago Pritzker School of Medicine Chicago, Illinois

KERRI M. ROBERTSON, MD Associate Clinical Professor of Anesthesiology Chief, General, Vascular, High-Risk Transplant and Surgical Critical Care Medicine Division Chief, Transplant Services Duke University School of Medicine Department of Anesthesiology Durham, North Carolina

SCOTT R. SPRINGMAN, MD

Professor and Program Director Department of Anesthesiology University of Texas Health Science Center at San Antonio San Antonio, Texas

Professor Departments of Anesthesiology and Surgery University of Wisconsin Medical School Madison, Wisconsin

BRIAN M. ILFELD, MD

KEVIN K. TREMPER, MD

Associate Professor Department of Anesthesia University of California, San Diego San Diego, California

Professor and Chairman Department of Anesthesiology University of Michigan Medical Center Ann Arbor, Michigan

DONALD A. KROLL, MD, PHD

B. CRAIG WELDON, MD

Staff Anesthesiologist Department of Surgery Veterans Affairs Medical Center Biloxi, Mississippi

Associate Professor Department of Anesthesiology and Pediatrics Duke University School of Medicine Durham, North Carolina

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1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA 19103-2899

COMPLICATIONS IN ANESTHESIA, 2nd edition

ISBN-13: 978-1-4160-2215-2 ISBN-10: 1-4160-2215-5

Copyright © 2007, 1999 by Saunders, an imprint of Elsevier Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Permissions may be sought directly from Elsevier’s Health Sciences Rights Department in Philadelphia, PA, USA: phone: (+1) 215 239 3804, fax: (+1) 215 239 3805, e-mail: [email protected]. You may also complete your request on-line via the Elsevier homepage (http://www.elsevier.com), by selecting ‘Customer Support’ and then ‘Obtaining Permissions’.

Notice Knowledge and best practice in this field are constantly changing. As new research and experience broaden our knowledge, changes in practice, treatment, and drug therapy may become necessary or appropriate. Readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of the practitioner, relying on his or her own experience and knowledge of the patient, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the Editors assumes any liability for any injury and/or damage to persons or property arising out of or related to any use of the material contained in this book. The Publisher

Library of Congress Cataloging-in-Publication Data Complications in anesthesia / [edited by] John L. Atlee. -- 2nd ed. p. ; cm. Includes bibliographical references and index. ISBN 1-4160-2215-5 1. Anesthesia--Complications. I. Atlee, John L. [DNLM: 1. Anesthesia--adverse effects. 2. Anesthetics--adverse effects. WO 245 C7369 2007] RD82.5.C63 2007 617.9′6041--dc22 2006040549

Executive Publisher: Natasha Andjelkovic Developmental Editor: Jean Nevius Publishing Services Manager: Tina Rebane Project Manager: Amy Norwitz Marketing Manager: Dana Butler

Printed in the United States of America Last digit is the print number: 9 8 7 6 5 4 3 2 1

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To all who have contributed to this work, and to the patients we serve.

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Preface An ounce of prevention is worth a pound of cure. –ANONYMOUS The second edition of Complications in Anesthesia, like its first edition, is intended to provide all practitioners of anesthesia and critical care medicine with a comprehensive source of information for most complications that might be faced in clinical practice. Topics are addressed in ten sections: Pharmacology; General Anesthesia; Regional Anesthesia and Pain Management; Cardiothoracic and Vascular Surgery; Physiologic Imbalance and Coexisting Disease; Equipment and Monitoring; Pediatrics and Neonatology; Neurosurgery, Ophthalmology, and ENT; Other Surgical Subspecialties (subdivided into Obstetrics and Gynecology, General Surgery, Urologic Surgery, and Orthopedic Surgery); and Special Topics (subdivided into Postanesthesia Care Unit, Diagnostic or Therapeutic Intervention, and Medicolegal Aspects). Section Editors were selected based on their special expertise and knowledge of the topics addressed in each section. Each chapter is presented in a highly structured format (in accordance with problem-based learning) under the following headings and subheadings: Case Synopsis, Problem Analysis (divided into Definition, Recognition, Risk Assessment, Implications), Management, and Prevention; in chapters with more than one topic, each topic is addressed

using the same headings. Schematics, figures, and tables are used liberally to illustrate key points or to summarize important information. Key references are listed at the end of each chapter under “Further Reading,” avoiding in-text citations that might distract the reader. Some chapters contain footnotes that provide further explanations. In this way, the reader can gain useful insight into a topic of interest in the minimal amount of time and with maximal retention. Also, thumb indexing and liberal cross-referencing are intended to reduce the need for time-consuming index searches. Finally, under Further Reading, in text, or in footnotes, there are references to Web sites for more or updated information. In that way, the reader can keep abreast of new developments. I hope this unconventional treatment of complications in anesthesia and critical care will serve several purposes: first, to permit quick location and researching of topics of interest to busy practitioners in the least amount of time; second, to organize the thought processes involved in medical decisionmaking in an attractive format—i.e., akin to Sherlock Holmes’ “who done it?”; and third and most importantly, to reduce the risk to our patients for unexpected and untoward events. John L. Atlee, MD

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Contributors Mark Abel, MD

Lori A. Aronson, MD, FAAP

Clinical Assistant Professor, Department of Anesthesiology, Mount Sinai Medical Center, New York, New York Vaporizers

Assistant Professor of Clinical Anesthesia and Pediatrics, Department of Anesthesia, University of Cincinnati College of Medicine; Assistant Professor, Clinical Anesthesia and Pediatrics, Department of Anesthesia, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio Hypoxemia

Gaury S. Adhikary, MD, FRCA Assistant Professor, Department of Anesthesiology, University of Michigan Hospitals, Ann Arbor, Michigan Carbon Dioxide Absorbers

Maurice S. Albin, MD, MSc (Anes) Professor of Anesthesiology, Department of Anesthesiology, University of Alabama School of Medicine, Birmingham, Alabama Venous Air Embolism

Stacey L. Allen, MD Assistant Professor of Anesthesiology, Department of Anesthesiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas Corneal Injury; Open Globe Injury

Steven J. Allen, MD Professor of Anesthesiology, Ohio State University College of Medicine; Chief Executive Officer, Columbus Children’s Hospital, Columbus, Ohio Autonomic Hyperreflexia

Jonathan M. Anagnostou, MD Associate Professor of Clinical Anesthesia, Department of Anesthesia, Indiana University School of Medicine; Staff Anesthesiologist, Medical Director of Respiratory Care, Department of Anesthesia, Respiratory Care, Indiana University Hospital, Indianapolis, Indiana Blood and Blood Products: Hepatitis and HIV

Maged Argalious, MD

John L. Atlee, MD Professor of Anesthesiology, Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, Wisconsin Adenosine; Disorders of Potassium Balance; Nonbarbiturate Anesthetics; Chemotherapeutic Agents; Cardiac Risk Assessment; Postobstruction Pulmonary Edema; Perioperative Tachyarrhythmias; Tachyarrhythmias with Ventricular Preexcitation; Long QT Syndromes and Ventricular Arrhythmias; Patients with Cardiac Rhythm Management Devices; Disorders of Water Homeostasis: Hyponatremia and Hypernatremia

Michael S. Avidan, MD Associate Professor of Anesthesiology and Surgery; Division Chief, CT Anesthesiology and CT Intensive Care, Washington University School of Medicine, St. Louis, Missouri HIV Infection and AIDS

Isaac Azar, MD Professor of Anesthesiology, Albert Einstein College of Medicine; Consultant, Department of Anesthesiology, Beth Israel Medical Center, New York, New York Scavenging Systems

James E. Baker, MD, FRCPC Assistant Professor and Anesthesiologist, Department of Anesthesia and Perioperative Care, University of California, San Francisco, San Francisco, California Postoperative Pulmonary Hypertension

Staff Anesthesiologist, Departments of General Anesthesiology and Critical Care Medicine, Cleveland Clinic Foundation, Cleveland, Ohio Complications of Trauma Surgery

Narayan Baliga, MD

George A. Arndt, MD

Shahar Bar-Yosef, MD

Professor (CHS), Department of Anesthesiology, University of Wisconsin Medical School, Madison, Wisconsin Difficult Airway: Cannot Ventilate, Cannot Intubate

Assistant Professor, Department of Anesthesiology and Critical Care, Duke University School of Medicine, Durham, North Carolina Complications of Laparoscopic Surgery

Staff Anesthesiologist, Kenosha Hospital and Medical Center, Kenosha, Wisconsin Difficult Airway: Opiate-Induced Muscle Rigidity

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Contributors

Juliana Barr, MD

Lois L. Bready, MD

Associate Professor, Department of Anesthesiology, Stanford University School of Medicine, Stanford, California; Staff Intensivist and Anesthesiologist, Veterans Affairs Palo Alto Health Care System, Anesthesiology Service, Palo Alto, California Reversal Agents: Naloxone and Flumazenil

Professor and Vice Chair, Department of Anesthesiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas Corneal Injury

Curtis L. Baysinger, MD Associate Professor, Department of Anesthesiology, Vanderbilt University School of Medicine, Nashville, Tennessee Hypertensive Disorders of Pregnancy

Eric Bedell, MD Associate Professor, Department of Anesthesiology, University of Texas Medical Branch, Galveston, Texas Posterior Fossa Surgery

Joan Benca, MD Associate Professor, Department of Anesthesiology, University of Wisconsin Hospital and Clinics, Madison, Wisconsin Bronchospasm

Patrick E. Benedict, MD Assistant Professor of Anesthesiology, University of Michigan Medical School, Ann Arbor, Michigan Transesophageal Echocardiography

Thomas P. Broderick, MD Assistant Professor, Department of Anesthesiology, University of Wisconsin Hospital and Clinics, Madison, Wisconsin Preanesthetic Evaluation: Inadequate or Missing Test Result

David L. Brown, MD Edward Rotan Distinguished Professor and Chairman, Department of Anesthesiology and Pain Medicine, M.D. Anderson Cancer Center, Houston, Texas Celiac Plexus Block: Side Effects and Complications

Adrie Bruijinzeel, MD Assistant Professor, Department of Psychiatry, Evelyn and William McKnight Brain Institute, University of Florida College of Medicine, Gainesville, Florida Chemical Dependency: Opioids

Brenda A. Bucklin, MD Associate Professor of Anesthesiology, Department of Anesthesiology, University of Colorado Health Sciences Center, Denver, Colorado Fetal Distress

Matthew D. Caldwell, MD David G. Bjoraker, MD Associate Professor, Department of Anesthesiology, University of Florida College of Medicine, Gainesville, Florida Anaphylaxis and Anaphylactoid Reactions

Assistant Professor, Department of Anesthesiology, University of Michigan Medical School, Ann Arbor, Michigan Pulmonary Artery Pressure Monitoring

William R. Camann, MD Susan Black, MD Professor, Department of Anesthesiology, University of Alabama School of Medicine, Birmingham, Alabama Antidepressants

Associate Professor, Department of Anesthesia, Harvard Medical School; Director of Obstetric Anesthesia, Brigham and Women’s Hospital, Boston, Massachusetts Pulmonary Aspiration in the Parturient

Maria I. Castro, PhD William S. Blau, MD, PhD Associate Professor of Anesthesiology, University of North Carolina School of Medicine, Chapel Hill, North Carolina Opioid Tolerance

Assistant Professor, Department of Anesthesiology, University of Arkansas for Medical Sciences, Little Rock, Arkansas Class II Antiarrhythmic Drugs: β-Blockers—Heart Block or Bradycardia

Steffan Blumenthal, MD

Kevin P. Chan, MD

Assistant Professor, Department of Anesthesiology and Reanimation, Orthopedic University Clinic Balgrist/Zurich, Zurich, Switzerland Interscalene Nerve Block: Potential Severe Complications

Fellow in Cardiovascular Anesthesia, Stanford University School of Medicine, Stanford, California Nonbarbiturate Anesthetics

Mark A. Chaney, MD John C. Boncyk, MD Assistant Professor, Department of Anesthesiology, University of Wisconsin Hospital and Clinics, Madison, Wisconsin Perioperative Hypoxia

Associate Professor of Anesthesiology, Department of Anesthesia and Critical Care, University of Chicago Pritzker School of Medicine, Chicago, Illinois Perioperative Myocardial Ischemia and Infarction; Adverse Neurologic Sequelae: Central Neurologic Impairment; Hypercoagulable States: Thrombosis and Embolism

Alain Borgeat, MD Professor and Chief of Staff, Department of Anesthesiology and Reanimation, Orthopedic University Clinic Balgrist/Zurich, Zurich, Switzerland Interscalene Nerve Block: Potential Severe Complications

Amit V. Chawla, MD Consultant, Department of Anesthesia, Guy’s Hospital, London, United Kingdom Inspiratory and Expiratory Gas Monitoring

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David C. H. Cheng, MD, MSc, FRCPC

James C. Crews, MD

Professor and Chair, Department of Anesthesia and Perioperative Medicine, University of Western Ontario; Anesthesiologist in Chief, London Health Sciences Center and St. Joseph’s Health Care, London, Ontario, Canada Fast-Track Cardiac Surgery

Associate Professor of Anesthesiology, Section of Regional Anesthesia and Acute Pain Management, Department of Anesthesiology, Wake Forest University School of Medicine, Winston-Salem, North Carolina Infectious Complications of Central Neuraxial Block

Deborah A. Davis, MD S. Devi Chiravuri, MD Assistant Professor, Department of Anesthesiology, University of Michigan Medical School, Ann Arbor, Michigan Rapid Fluid and Blood Delivery Systems

Gordon Lee Collins, MD Clinical Fellow, Department of Anesthesiology, Washington University School of Medicine, St. Louis, Missouri Complications after Pneumonectomy

Lois A. Connolly, MD Associate Professor, Department of Anesthesiology, Medical College of Wisconsin, Froedtert Memorial Lutheran Hospital, Milwaukee, Wisconsin Unstable Cervical Spine, Atlantoaxial Subluxation

D. Ryan Cook, MD Professor of Anesthesiology, Department of Anesthesiology, Children’s Hospital of Pittsburgh, Pittsburgh, Pennsylvania Hypoglycemia and Hyperglycemia

Clinical Professor of Anesthesiology, Department of Anesthesiology, Thomas Jefferson University – Jefferson Medical College, Philadelphia, Pennsylvania; Pediatric Anesthesiologist/Intensivist, Nemours Cardiac Center, A.I. duPont Hospital for Children, Wilmington, Delaware Pulmonary Hypertension

Martin L. De Ruyter, MD Associate Professor of Anesthesiology, Department of Anesthesiology, Kansas University School of Medicine, Kansas City, Kansas Hyperglycemia and Diabetic Ketoacidosis; Sarcoidosis

Hernando De Soto, MD Associate Professor, Department of Pediatric Anesthesia, University of Florida Health Science Center; Staff Anesthesiologist/Medical Director of the OR, Department of Anesthesiology, SHANDS Jacksonville, Jacksonville, Florida Difficult Pediatric Airway

Donn M. Dennis, MD, FAHA

Assistant Professor of Anesthesia, Department of Anesthesiology and Critical Care Medicine, University of Pennsylvania School of Medicine; Associate Anesthesiologist, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania Ophthalmic Problems and Complications

Joachim S. Gravenstein, MD, Professor of Anesthesiology, Department of Anesthesiology, University of Florida College of Medicine, Gainesville, Florida; Vice PresidentPharmacology, ARYx Therapeutics, Inc., Santa Clara, California Class III Antiarrhythmic Drugs: Potassium Channel Blockers; Class IV Antiarrhythmic Drugs: Calcium Channel Blockers

Victoria Coon, CRNA, MS

Ronak Desai, DO

Scott D. Cook-Sather, MD

Perioperative Director and Anesthesiology Department Administrator, Kaiser Permanente, West Los Angeles, Los Angeles, California Quality Assurance; Cost Containment

Resident, CA-2, Department of Anesthesia and Critical Care, University of Chicago Pritzker School of Medicine, Chicago, Illinois Peripheral Vascular Surgery

John R. Cooper, Jr., MD

Cheryl DeSimone, MD

Clinical Associate Professor of Anesthesiology, University of Texas Health Science Center; Associate Chief, Cardiovascular Anesthesia; Co-Director, Cullen Cardiovascular Research Laboratories, Texas Heart Institute, Houston, Texas Troubleshooting Common Problems during Cardiopulmonary Bypass

Cyrus DeSouza, MB,BS, FANZCA

Associate Professor of Anesthesiology, Obstetrics and Gynecology, Department of Anesthesiology, Albany Medical College; Director of Obstetric Anesthesia, Albany Medical Center, Albany, New York Embolic Events of Pregnancy

Director of Clinical Research in Pediatric Anesthesia, Department of Anesthesiology, Massachusetts General Hospital, Boston, Massachusetts Sedation of Pediatric Patients

Acting Assistant Professor, Cardiothoracic Anesthesiologist, Department of Anesthesiology, University of Washington Medical Center, Seattle, Washington; Staff Specialist Anaesthetist, Department of Anaesthetics, St. Georges Hospital, Sydney, NSW, Australia Chronotropic Drugs

Douglas B. Coursin, MD

Clifford S. Deutschman, MD

Professor of Anesthesiology and Internal Medicine, Department of Anesthesiology, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin Adrenal Insufficiency

Professor, Department of Anesthesia and Surgery, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania Sepsis, Systemic Inflammatory Response Syndrome, and Multiple Organ Dysfunction Syndrome

Charles J. Coté, MD

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Pema Dorje, MD

Brenda G. Fahy, MD, FCCP, FCCM

Clinical Assistant Professor, Department of Anesthesiology, University of Michigan Medical School, Ann Arbor, Michigan Arterial Blood Pressure Monitoring

Professor, Department of Anesthesiology, University of Kentucky; Director of Critical Care, Department of Anesthesiology, AB Chandler Medical Center, Lexington, Kentucky Disorders of Water Homeostasis: Hyponatremia and Hypernatremia

Anthony R. Doyle, BSc, MB,BS, FRCA Formerly, Visiting Instructor in Anesthesiology, University of Michigan Medical School, Ann Arbor, Michigan; Consultant Anaesthetist, Dorset County Hospital, Dorchester, United Kingdom Fires in the Operating Room

Kenneth Drasner, MD Professor, Department of Anesthesiology and Perioperative Care, University of California, San Francisco, San Francisco, California Local Anesthetic Neurotoxicity: Cauda Equina Syndrome

Catherine Drexler, MD Vice Chair, Department of Anesthesiology, ColumbiaSt. Mary’s-Milwaukee Campus, Milwaukee, Wisconsin Angioedema and Urticaria

Zhuang T. Fang, MD, MSPH Assistant Clinical Professor, Department of Anesthesiology, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California Unanticipated Hospital Admission and Readmission

Doron Feldman, MD Associate Professor of Clinical Anesthesiology, State University of New York at Buffalo School of Medicine; Attending in Anesthesiology, Children’s Hospital of Buffalo, Buffalo, New York The Hostile-Combative Patient

Lynne R. Ferrari, MD

Ellen Duncan, MD

Associate Professor, Department of Anesthesia, Harvard Medical School; Medical Director, Perioperative Services, Children’s Hospital, Boston, Massachusetts Adenotonsillectomy

Tejas Anesthesia, San Antonio, Texas Open Globe Injury

Matthew P. Feuer, MD

Martin W. Dünser, MD Resident in Anesthesiology and Critical Care Medicine, Department of Anesthesiology and Critical Care Medicine, Medical University Innsbruck, Innsbruck, Austria Vasopressors: Vasoconstrictor Drugs

Jörg Dziersk, MD, FRCA Assistant Professor of Anesthesiology, Department of Anesthesiology, University of Washington School of Medicine, Seattle, Washington Vasodilator Drugs

Michael P. Eaton, MD Associate Professor, Department of Anesthesiology, University of Rochester School of Medicine and Dentistry, Rochester, New York Proportioning Systems; Patient Warming Systems

Charles E. Edmiston, Jr., MS, PhD Associate Professor, Department of Surgery; Director, Surgical Microbiology Research Laboratory, Medical College of Wisconsin, Milwaukee, Wisconsin Nosocomial Infections: Bacterial Pneumonia

Staff Anesthesiologist, Department of Anesthesiology, Virginia Mason Medical Center, Seattle, Washington Spinal Anesthesia: Post–Dural Puncture Headache

Stephanie S. F. Fischer, MD Visiting Associate in Cardiothoracic and Critical Care, Division of Pediatric Anesthesiology, Duke University School of Medicine, Durham, North Carolina Cardiomyopathies

M. Pamela Fish, MB,ChB Associate Professor, Department of Anesthesiology, Stanford University School of Medicine, Stanford, California; Staff Physician, Veterans Affairs Palo Alto Health Care System, Palo Alto, California Antiemetic Drugs

Randall Flick, MD, MPH Assistant Professor of Anesthesiology and Pediatrics, Department of Anesthesiology and Pediatrics, Mayo Clinic College of Medicine; Chair, Section of Pediatric Anesthesiology, Mayo Clinic, Rochester, Minnesota Anterior Mediastinal Mass

Michael P. Ford, MD

Professor of Anesthesiology, Mount Sinai School of Medicine, New York, New York Vaporizers

Assistant Professor of Anesthesiology, Department of Anesthesiology, University of Wisconsin Medical School, Madison, Wisconsin Preanesthetic Evaluation: False-Positive Tests; Difficult Airway: Cannot Ventilate, Cannot Intubate

John Ellis, MD

Jennifer T. Fortney, MD

Professor of Anesthesiology, Department of Anesthesia and Critical Care, University of Chicago Pritzker School of Medicine, Chicago, Illinois Carotid Endarterectomy; Thoracic Aortic Aneurysm

Assistant Clinical Professor, Department of Anesthesiology, Duke University School of Medicine, Durham, North Carolina Fat Embolism Syndrome

James B. Eisenkraft, MD

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James M. T. Foster, MD

Mark S. Gold, MD

Clinical Assistant Professor of Anesthesiology, Department of Anesthesiology, State University of New York at Buffalo School of Medicine; Director of Anesthesiology Services, Kaleida Health, Buffalo, New York The Hostile-Combative Patient

Distinguished Professor and Chief, Departments of Psychiatry, Neuroscience, Anesthesiology, Community Health and Family Medicine, Evelyn and William McKnight Brain Institute, University of Florida College of Medicine, Gainesville, Florida Chemical Dependency: Opioids; Chemical Dependency: Nonopioids

Melissa Franckowiak, MD Resident, Department of Anesthesiology, State University of New York at Buffalo School of Medicine, Buffalo, New York Cardioversion

Eugene B. Freid, MD Associate Professor, Departments of Anesthesiology and Pediatrics, University of North Carolina Hospitals, Chapel Hill, North Carolina Succinylcholine

Kimberly Frost-Pineda, MD Assistant in Psychiatry, Department of Psychiatry, Director of Public Health Research, University of Florida College of Medicine, Gainesville, Florida Chemical Dependency: Opioids; Chemical Dependency: Nonopioids

Jeffrey L. Galinkin, MD Associate Professor, Department of Anesthesia, Children’s Hospital, Denver, Colorado Fetal Intrauterine Surgery

Arjunan Ganesh, MD Assistant Professor of Anesthesia, Department of Anesthesia, University of Pennsylvania School of Medicine; Assistant Anesthesiologist, Department of Anesthesiology and Critical Care Medicine, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania Upper Respiratory Tract Infection

Hind M. Gautam, MD Clinical Assistant Professor, Department of Anesthesiology, Veterans Affairs Medical Center, Buffalo, New York Magnetic Resonance Imaging

Rodolfo Gebhardt, MD

Stuart Grant, MD Assistant Professor, Department of Anesthesiology, Duke University School of Medicine, Durham, North Carolina Continuous Nerve Blocks: Perineural Local Anesthetic Infusion

Glenn P. Gravlee, MD Professor, Department of Anesthesiology, Ohio State University Hospitals, Columbus, Ohio Hemodilution and Blood Conservation

Ivar Gunnarsson, MD Landspítali—háskólasjúkrahús, Reykjavik, Iceland Oxygen Flush Valve

Mary Ann Gurkowski, MD Professor of Anesthesiology, University of Texas Health Science Center at San Antonio; Clinical Staff/Director of Medical Students, Department of Anesthesiology/Crossappointed to Otorhinolaryngology, University Hospital; Attending Staff, Department of Anesthesiology, Audie Murphy Veterans Affairs Hospital, San Antonio, Texas Foreign Body Aspiration

Jacob Gutsche, MD Physician, Department of Anesthesia, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania Sepsis, Systemic Inflammatory Response Syndrome, and Multiple Organ Dysfunction Syndrome

Thomas S. Guyton, MD Staff Anesthesiologist, Methodist Healthcare of Memphis, Memphis, Tennessee Magnesium; Antibiotics

Assistant Professor of Clinical Anesthesiology, Department of Anesthesiology, Department of Clinical Anesthesiology, Veterans Affairs Medical Center, Buffalo New York Uncontrolled Pain

Ali Habibi, MD

Jeremy M. Geiduschek, MD

Saeed Habibi, MD

Clinical Professor, Department of Anesthesiology, University of Washington School of Medicine; Director, Clinical Anesthesia Services, Department of Anesthesiology, Children’s Hospital and Regional Medical Center, Seattle, Washington Intraoperative Cardiac Arrest

J. C. Gerancher, MD Associate Professor and Section Head, Regional Anesthesia and Acute Pain Management, Department of Anesthesiology, Wake Forest University School of Medicine, Winston-Salem, North Carolina Epidural Anesthesia: Unintended Intrathecal Injection; Epidural Anesthesia: Unintended Subdural Injection

Adjunct Clinical Faculty, Anesthesiology, Stanford University School of Medicine, Stanford, California Antihistamines: H1- and H2-Blockers Chair, Department of Anesthesiology, Columbia– St. Mary’s–Milwaukee Campus, Milwaukee, Wisconsin Angioedema and Urticaria

Charles B. Hantler, MD Professor, Department of Anesthesiology, Washington University School of Medicine, St. Louis, Missouri Bradyarrhythmias

H. David Hardman, MD, MBA Assistant Clinical Professor, Department of Anesthesiology, Duke University School of Medicine, Durham, North Carolina Extremity Tourniquets

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Contributors

Barry A. Harrison, MB,BS

Liana Hosu, MD

Assistant Professor of Anesthesiology, Department of Anesthesiology, Mayo Clinic College of Medicine, Jacksonville, Florida Hyperglycemia and Diabetic Ketoacidosis; Sarcoidosis

Assistant Professor of Anesthesia and Pediatrics, Department of Anesthesiology, University of Cincinnati College of Medicine; Staff Anesthesiologist, Department of Anesthesiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio Postoperative Apnea in Infants

Joy L. Hawkins, MD Professor of Anesthesiology and Director of Obstetric Anesthesia, University of Colorado School of Medicine, Denver, Colorado Nonobstetric Surgery during Pregnancy

Christopher M. B. Heard, MB,ChB, FRCA Research Assistant Professor, Department of Anesthesiology and Division of Pediatric Critical Care, State University of New York at Buffalo School of Medicine; Assistant Attending, Children’s Hospital of Buffalo, Buffalo, New York Magnetic Resonance Imaging; Alleged Malpractice; The HostileCombative Patient

Stephen O. Heard, MD Interim Chair, Professor of Anesthesiology and Surgery, University of Massachusetts Medical School, Worcester, Massachusetts Perioperative Care of Immunocompromised Patients

James R. Hebl, MD Assistant Professor, Department of Anesthesiology, Mayo Clinic College of Medicine, Rochester, Minnesota Anticoagulants and Peripheral Nerve Block

Robert F. Helfand, MD Associate Professor, Cleveland Clinic Lerner College of Medicine; Staff Anesthesiologist; Vice Chairman, Department of General Anesthesiology; Section Head of Orthopedic Anesthesia, Glickman Urological Center, Cleveland Clinic Foundation, Cleveland, Ohio Thromboembolic Complications

Rosemary Hickey, MD Professor and Program Director, Department of Anesthesiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas Intracranial Hypertension

Kate Huncke, MD Clinical Associate Professor, Department of Anesthesiology, New York University School of Medicine, New York, New York Radiation Oncology

Samuel A. Irefin, MD Associate Professor of Anesthesiology, Cleveland Clinic Lerner College of Medicine; Staff Anesthesiologist, Department of Anesthesiology and Critical Care Medicine, Cleveland Clinic Foundation, Cleveland, Ohio Complications of Thyroid Surgery

William Jacobs, MD Associate Professor, Departments of Psychiatry and Anesthesiology, University of Florida College of Medicine, Gainesville, Florida Chemical Dependency: Opioids; Chemical Dependency: Nonopioids

Eric Jacobsohn, MB,ChB, MHPE, FRCPC Associate Professor of Anesthesiology, Department of Anesthesiology, Washington University School of Medicine, St. Louis, Missouri Complications after Pneumonectomy

J. Michael Jaeger, MD, PhD Associate Professor of Anesthesiology and Neurological Surgery; Director, Thoracic Anesthesia, Department of Anesthesiology, University of Virginia Health Sciences Center, Charlottesville, Virginia Class IV Antiarrhythmic Drugs: Calcium Channel Blockers

George A. Higgins, BSN, MS, CRNA Adjunct Faculty, Department of Nursing, University of Southern California; Senior Nurse Anesthetist, Department of Anesthesiology, Department of Veterans Affairs Medical Center, Los Angeles, California Embolization Procedures

Scott Holliday, MD Resident, Department of Anesthesiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas Foreign Body Aspiration

William Hope, MD, PhD Assistant Professor, Department of Anesthesiology, Medical College of Wisconsin, Froedtert Memorial Lutheran Hospital East, Milwaukee, Wisconsin Laryngeal and Tracheal Injury

Michael F. M. James, MB,ChB, PhD, FRCA, FCA(SA) Professor and Head, Department of Anesthesia, University of Cape Town; Professor and Chief Anaesthetist, Department of Anaesthesia, Groote Schuur Hospital, Cape Town, Western Cape, South Africa Complications of Adrenal Surgery

Gregory M. Janelle, MD Assistant Professor, Chief of Cardiovascular Anesthesia, Department of Anesthesiology, University of Florida College of Medicine, Gainesville, Florida Phosphodiesterase Inhibitors

David R. Jobes, MD Terese T. Horlocker, MD Professor, Department of Anesthesiology, Mayo Clinic College of Medicine, Rochester, Minnesota Spinal Hematoma; Persistent Paresthesia

Professor of Anesthesia, Department of Anesthesia and Critical Care Medicine, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania Complications of Massive Transfusion

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Nicola Jones, MA, MB,BS, DTM&H, MRCP, MRCPath, PhD Consultant in Microbiology and Infectious Diseases, Departments of Microbiology and Infectious Diseases, Nuffield Department of Clinical Laboratory Sciences, John Radcliffe Hospital, University of Oxford, Oxford, United Kingdom HIV Infection and AIDS

Shailendra Joshi, MD Assistant Professor of Anesthesiology, Department of Anesthesiology, College of Physicians and Surgeons of Columbia University, New York, New York Arteriovenous Malformation: Normal Perfusion Pressure Breakthrough

Zeev N. Kain, MD Professor of Anesthesiology, Department of Anesthesiology, Yale University School of Medicine, New Haven, Connecticut Perioperative Psychological Trauma

Wendy B. Kang, MD Associate Professor and Chair, Residency Education Committee, Department of Anesthesiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas Retrobulbar Block

Shubjeet Kaur, MD Clinical Vice Chair, Department of Anesthesiology, University of Massachussets Memorial Medical Center, Worcester, Massachusetts Perioperative Care of Immunocompromised Patients

Robert D. Kaye, MD Assistant Professor of Clinical Anesthesiology and Pediatrics, State University of New York at Buffalo School of Medicine; Attending Anesthesiologist, Children’s Hospital of Buffalo, Buffalo, New York Alleged Malpractice

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Jonathan T. Ketzler, MD Associate Professor of Anesthesiology; Associate Director, Trauma and Life Support Center, Department of Anesthesiology, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin Adrenal Insufficiency

Evan D. Kharasch, MD, PhD Assistant Dean for Clinical Research; Professor and Research Director, Department of Anesthesiology, University of Washington School of Medicine, Seattle, Washington Volatile Anesthetics: Organ Toxicity

M. Sean Kincaid, MD Resident, Department of Anesthesiology, University of Washington Medical Center, Seattle, Washington Head Injury

Kathryn P. King, MD Associate Clinical Professor, Department of Anesthesiology, Duke University School of Medicine, Durham, North Carolina Methylmethacrylate

Kai T. Kiviluoma, MD, PhD Associate Professor, Department of Anaesthesiology, University of Oulu Faculty of Medicine; Head of the Department, Paediatric Anaesthesia, Oulu University Hospital, Oulu, Finland Disorders of Potassium Balance

Jerome M. Klafta, MD Associate Professor and Associate Chair for Education, Department of Anesthesia and Critical Care, University of Chicago Pritzker School of Medicine, Chicago, Illinois Mediastinal Masses

Pattricia S. Klarr, MD Paul E. Kazanjian, MD Clinical Assistant Professor, Department of Anesthesiology, University of Michigan Medical School, Ann Arbor, Michigan Fires in the Operating Room; Pulmonary Artery Pressure Monitoring

Clinical Assistant Professor, Department of Anesthesiology, University of Michigan Medical School; Associate Clinical Director, Department of Anesthesiology, University of Michigan Medical Center, Ann Arbor, Michigan Laser Complications

Jeffrey S. Kelly, MD

Sandra L. Kopp, MD

Associate Professor of Anesthesiology, Section of Critical Care, Wake Forest University School of Medicine, Winston-Salem, North Carolina Complications from Toxic Ingestion

Kevin J. Kelly, MD Professor and Chair, Department of Pediatrics; Associate Dean, School of Medicine, Children’s Mercy Hospital and Clinics, University of Missouri, Kansas City, Missouri Latex Reactions in Health Care Personnel

Instructor, Department of Anesthesiology, Mayo Clinic College of Medicine, Rochester, Minnesota Supraclavicular and Infraclavicular Block: Pneumothorax

Donald A. Kroll, MD, PhD Staff Anesthesiologist, Department of Surgery, Veterans Affairs Medical Center, Biloxi, Mississippi Quality Assurance; Cost Containment; Adverse Outcomes: Withheld Information or Misinformation

Robert E. Kettler, MD

Kenneth Kuchta, MD

Associate Professor, Department of Anesthesiology, Medical College of Wisconsin, Froedtert Memorial Lutheran Hospital East, Milwaukee, Wisconsin Patients with Seizure Disorders; Latex Reactions in Health Care Personnel

Assistant Clinical Professor, Department of Anesthesiology, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California Misidentification of a Patient

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C. Dean Kurth, MD

Ray P. Liao, MD

Professor of Anesthesia and Pediatrics, University of Cincinnati College of Medicine, Anesthesiologist-in-Chief; Chair, Institute for Pediatric Research; Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio Postoperative Apnea in Infants

Acting Assistant Professor, Department of Anesthesiology, University of Washington School of Medicine, Seattle, Washington Inotropic Drugs

Spencer S. Liu, MD Arthur M. Lam, MD, FRCPC Professor of Anesthesiology, Department of Anesthesiology, University of Washington School of Medicine; Head of Neuroanesthesia, Harborview Medical Center, Seattle, Washington Head Injury

Jeffrey L. Lane, MD Assistant Professor of Clinical Anesthesia and Director, Human Simulation Laboratory, Department of Anesthesia, Indiana University School of Medicine; Staff Anesthesiologist, Clarian Health Partners, Indianapolis, Indiana Postoperative Respiratory Insufficiency

Clinical Professor of Anesthesiology, Department of Anesthesiology, Virginia Mason Medical Center, Seattle, Washington Spinal Anesthesia: Post–Dural Puncture Headache

Emilio B. Lobato, MD Professor of Anesthesiology, Department of Anesthesiology, University of Florida College of Medicine; Chief, Cardiovascular Anesthesia, Department of Anesthesia Service, Malcom Randall Veterans Affairs Hospital, Gainesville, Florida Digitalis

Robert G. Loeb, MD Paul B. Langevin, MD Associate Professor, Department of Anesthesiology, Veterans Affairs–West Haven, West Haven, Connecticut Chemotherapeutic Agents

Associate Professor of Anesthesiology, University of Arizona College of Medicine, Tucson, Arizona Flowmeters

Celeste M. Lombardi, MD Melissa A. Laxton, MD Assistant Professor of Anesthesiology, Wake Forest University School of Medicine, Winston-Salem, North Carolina Pituitary Tumors: Diabetes Insipidus

Fellow in Interventional Pain Medicine, Department of Anesthesiology, University of Florida College of Medicine, Gainesville, Florida Chronic Nonsteroidal Anti-inflammatory Drug Use

Prashant Lotlikar, MD Marcia M. Lee, MD, MBA Assistant Chief, Department of Anesthesiology, Kaiser Permanente–South Bay, Harbor City, California Awareness under Anesthesia

Clinical Assistant Professor, Department of Anesthesiology, University of Texas Health Science Center, Texas Heart Institute, Houston, Texas Troubleshooting Common Problems during Cardiopulmonary Bypass

Mijin Lee, MD Assistant Clinical Professor, Department of Anesthesiology, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California Anesthesia for Electroconvulsive Therapy

Peter J. Lee, MD, MPH Formerly, Assistant Professor, Department of Anesthesiology, University of Michigan Medical School, Ann Arbor, Michigan Central Venous Pressure Monitoring

Philip Levin, MD Associate Professor, Department of Anesthesiology, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California Postoperative Delirium

Jerrold H. Levy, MD Professor and Department Chair/Research, Department of Anesthesiology, Emory University School of Medicine, Atlanta, Georgia Perioperative Hypertension

Ian Lewis, MB,BS, MRCP, FRCA Associate Professor, Department of Anesthesiology, University of Michigan Medical School, Ann Arbor, Michigan Surgical Diathermy and Electrocautery

Michelle L. Lotto, MD Assistant Professor of Anesthesiology, Department of General Anesthesiology and Critical Care Medicine, Cleveland Clinic Lerner College of Medicine; Associate Staff Anesthesiologist, Cleveland Clinic Foundation, Cleveland, Ohio Complications of Spinal Surgery

Katarzyna Luba, MD Assistant Professor of Clinical Anesthesiology, Department of Anesthesia and Critical Care, University of Chicago Pritzker School of Medicine, Chicago, Illinois Perioperative Management of Patients with Muscular Dystrophy

Stewart J. Lustik, MD Associate Professor of Anesthesiology, University of Rochester School of Medicine and Dentistry, Rochester, New York Proportioning Systems; Patient Warming Systems

Vinod Malhotra, MD Professor and Vice Chair for Clinical Affairs, Department of Anesthesiology, Weill Medical College of Cornell University, New York–Presbyterian Hospital, New York, New York Complications of Transurethral Surgery

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Christina M. Matadial, MD

Terri G. Monk, MD

Assistant Professor, Department of Anesthesiology, Leonard M. Miller School of Medicine at the University of Miami; Staff Physician, Department of Anesthesiology, Jackson Memorial Hospital, Miami, Florida Surgery in the Morbidly Obese

Professor, Department of Anesthesiology, Duke University Medical Center, Durham, North Carolina Intraoperative Penile Erection; Complications of Radical Urologic Surgery

Lisa M. Montenegro, MD Viktoria D. Mayr, MD Resident in Anesthesiology and Critical Care Medicine, Department of Anesthesiology and Critical Care Medicine, Medical University Innsbruck, Innsbruck, Austria Vasopressors: Vasoconstrictor Drugs

Assistant Professor of Anesthesiology, University of Pennsylvania School of Medicine and Children’s Hospital of Philadelphia; Attending Anesthesiologist, Department of Anesthesiology, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania Complications of Massive Transfusion

Deborah A. McClain, MD Chief, Anesthesiology Section, Veterans Affairs Medical Center, Biloxi, Mississippi Delayed Emergence

Thomas McCutchen, MD Assistant Professor, Department of Anesthesiology, Wake Forest University School of Medicine, Winston-Salem, North Carolina Epidural Anesthesia: Unintended Intrathecal Injection; Epidural Anesthesia: Unintended Subdural Injection

David L. McDonagh, MD Resident, Department of Anesthesiology, Duke University School of Medicine, Durham, North Carolina Autonomic Dysreflexia

Susan B. McDonald, MD Staff Anesthesiologist, Department of Anesthesiology, Virginia Mason Medical Center, Seattle, Washington Side Effects of Neuraxial Opioids

Lynda J. Means, MD Professor of Anesthesia and Surgery, Department of Anesthesia, Indiana University School of Medicine, Indianapolis, Indiana Postobstruction Pulmonary Edema in Pediatric Patients

Mark Meyer, MD Assistant Professor of Clinical Anesthesia, Department of Anesthesia, University of Cincinnati College of Medicine; Assistant Professor, Clinical Pediatrics, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio Perioperative Aspiration Pneumonitis

Mohammed Minhaj, MD Assistant Professor, Department of Anesthesia and Critical Care, University of Chicago Pritzker School of Medicine, Chicago, Illinois Adverse Neurologic Sequelae: Peripheral Nerve Injury

Vivek Moitra, MD Assistant Professor of Anesthesiology, Department of Anesthesiology, College of Physicians and Surgeons of Columbia University, New York, New York Carotid Endarterectomy

Timothy E. Morey, MD Associate Professor of Anesthesiology, Department of Anesthesiology, University of Florida College of Medicine, Gainesville, Florida Magnesium; Antibiotics

Lucille A. Mostello, MD Assistant Professor of Anesthesiology and Pediatrics, Department of Anesthesiology, George Washington University School of Medicine; Staff Anesthesiologist, Department of Anesthesiology, Children’s National Medical Center, Washington, DC Latex Allergy

Isobel Muhiudeen-Russell, MD Professor, Department of Anesthesia, University of California, San Francisco, San Francisco, California Postoperative Pulmonary Hypertension

J. Thomas Murphy, MD, FRCPC Associate Professor, Department of Anesthesiology, University of Kentucky College of Medicine, Lexington, Kentucky Disorders of Water Homeostasis: Hyponatremia and Hypernatremia

Catherine Friederich Murray Research Associate, Department of Anesthesiology, Mayo Clinic College of Medicine, Jacksonville, Florida Parkinson’s Disease; Alzheimer’s Disease

Michael J. Murray, MD, PhD Professor of Anesthesiology and Chair, Department of Anesthesiology, Mayo Clinic College of Medicine, Jacksonville, Florida Parkinson’s Disease; Alzheimer’s Disease

David Muzic, MD Fellow in Cardiac Anesthesia, Department of Anesthesia and Critical Care, University of Chicago Pritzker School of Medicine, Chicago, Illinois Adverse Neurologic Sequelae: Central Neurologic Impairment

Nader D. Nader, MD Constance L. Monitto, MD Assistant Professor of Anesthesiology, Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institute, Baltimore, Maryland Muscle Relaxants

Associate Professor of Anesthesiology, Surgery and Pathology, State University of New York at Buffalo School of Medicine, Buffalo, New York Uncontrolled Pain; Hemodynamic Instability; Cardioversion

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Contributors

Carsten Nadjat-Haiem, MD

Hector F. Nicodemus, MD

Assistant Professor, Department of Anesthesiology, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California Syringe Swaps

Pediatric Anesthesiologist, Department of Anesthesiology, Holy Cross Hospital, Silver Spring, Maryland Delayed Emergence in Pediatric Patients

Susan C. Nicolson, MD Mohamed Naguib, MB,Bch, MSc, FFARCSI, MD Professor, Department of Anesthesia, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, Iowa Myasthenic Disorders

Professor of Anesthesia, Department of Anesthesia, University of Pennsylvania School of Medicine; Division Director, Cardiothoracic Anesthesia, Department of Anesthesiology and Critical Care Medicine, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania Upper Respiratory Tract Infection

Bhiken Naik, MD Fellow, Department of Anesthesiology, University of Florida College of Medicine, Gainesville, Florida Intrathecal Opiates; Ketamine; Steroids

David A. Nakata, MD Associate Clinical Professor and Vice Chair, Residency Development, Department of Anesthesia, Indiana University School of Medicine, Indianapolis, Indiana Postoperative Peripheral Neuropathy; Intractable Nausea and Vomiting

Charles A. Napolitano, MD, PhD Associate Professor; Director, Division of Cardiothoracic Anesthesia; Co-Director, Residency Program, Department of Anesthesiology, University of Arkansas for Medical Sciences, Little Rock, Arkansas Class II Antiarrhythmic Drugs: β-Blockers—Heart Block or Bradycardia

Susan H. Noorily, MD Clinical Professor, Department of Anesthesiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas Laryngoscopy and Microlaryngoscopy

Mark Nunnally, MD Assistant Professor, Department of Anesthesia and Critical Care, University of Chicago Pritzker School of Medicine, Chicago, Illinois Postoperative Acute Renal Failure; Metabolic Acidosis and Alkalosis

Christopher J. O’Connor, MD Associate Professor, Department of Anesthesiology, Rush University Medical Center, Chicago, Illinois Abdominal Aortic Aneurysm Repair

Michael F. O’Connor, MD Bradly J. Narr, MD Associate Professor and Chair, Department of Anesthesiology, Mayo Clinic College of Medicine, Rochester, Minnesota Porphyrias

Associate Professor, Department of Anesthesia and Critical Care, University of Chicago Pritzker School of Medicine, Chicago, Illinois Thermally Injured Patients

Jerome F. O’Hara, Jr., MD Krishna M. Natrajan, MB,BS, FRCA Assistant Professor of Adult and Pediatric Cardiothoracic Anesthesiology, Department of Anesthesiology, University of Washington School of Medicine; Attending Anesthesiologist, Department of Anesthesiology, University of Washington Medical Center, Seattle, Washington Inotropic Drugs

Norah Naughton, MD Associate Professor of Anesthesiology and Associate Professor of Obstetrics and Gynecology, University of Michigan Medical School, Ann Arbor, Michigan Intracranial Pressure Monitoring

Patrick Neligan, MD Assistant Professor, Department of Anesthesia, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania Metabolic Acidosis and Alkalosis

Philippa Newfield, MD Assistant Clinical Professor of Anesthesia and Neurosurgery, University of California, San Francisco, School of Medicine; Attending Anesthesiologist, Department of Anesthesiology, California Pacific Medical Center, San Francisco, California Intracranial Aneurysms: Rebleeding; Intracranial Aneurysms: Vasospasm and Other Issues

Associate Professor, College of Medicine, Case Western Reserve University; Vice Chairman, Department of General Anesthesiology; Section Head of Anesthesia, Glickman Urological Center, Urology Department, Cleveland Clinic Foundation, Cleveland, Ohio Complications of Lithotripsy ..

Maria A. K. Ohrn, MD Anesthesiology Associates of North Florida, PA, North Florida Regional Medical Center, Gainesville, Florida Nondepolarizing Neuromuscular Relaxants

Nollag O’Rourke, MD Fellow in Obstetric Anesthesia, Department of Anesthesia, Brigham and Women’s Hospital, Boston, Massachusetts Pulmonary Aspiration in the Parturient

Sheela S. Pai, MD Assistant Professor, Department of Anesthesiology, Baylor College of Medicine; Staff Anesthesiologist, Department of Anesthesiology and Critical Care, Michael E. DeBakey Veterans Affairs Medical Center, Houston, Texas Mechanical Assist Devices

Craig M. Palmer, MD Professor of Clinical Anesthesiology; Director, Obstetric Anesthesia, University of Arizona College of Medicine, Tucson, Arizona Preterm Labor

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C. Lee Parmley, MD, JD

William Prince, MD

Professor of Anesthesiology, Department of Anesthesiology, Vanderbilt University Medical Center, Nashville, Tennessee Autonomic Hyperreflexia

Department of Anesthesiology, Kaiser Permanente Oakland Medical Center, Oakland, California Central Venous Pressure Monitoring

Lester T. Proctor, MD Komal Patel, MD Fellow in Cardiac Anesthesia, Department of Anesthesia and Critical Care, University of Chicago Pritzker School of Medicine, Chicago, Illinois Hypercoagulable States: Thrombosis and Embolism

D. Janet Pavlin, MD Professor, Department of Anesthesiology, University of Washington School of Medicine; Head of Teaching and Research in Ambulatory Anesthesia, Department of Anesthesia, University of Washington Medical Center, Seattle, Washington Postoperative Urinary Retention

Padmavathi Perala, MD Anesthesiologist, Department of Anesthesiology, Veterans Affairs Medical Center, Buffalo, New York Hemodynamic Instability

Patricia H. Petrozza, MD Professor of Anesthesiology, Associate Dean for Graduate Medical Education, Wake Forest University School of Medicine, Winston-Salem, North Carolina Pituitary Tumors: Diabetes Insipidus

Linda S. Polley, MD

Professor, Departments of Anesthesiology and Pediatrics, University of Wisconsin Medical School, Madison, Wisconsin Blood and Blood Products: Transfusion Reaction

Donald S. Prough, MD Professor and Chair, Department of Anesthesiology, University of Texas Medical Branch, Galveston, Texas Perioperative Fluid Management; Posterior Fossa Surgery

M. J. Pekka Raatikainen, MD Division of Cardiology, Oulu University Central Hospital, Oulu, Finland Adenosine; Class III Antiarrhythmic Drugs: Potassium Channel Blockers

Lee M. Radke, DDS Assistant Professor, Oral and Maxillofacial Surgery, Medical College of Wisconsin, Froedtert Memorial Lutheran Hospital, Milwaukee, Wisconsin Dental Injuries

Sivam Ramanathan, MD

Associate Professor, Department of Anesthesiology, University of Michigan Medical School, Ann Arbor, Michigan Postpartum Hemorrhage

Professor of Anesthesiology, University of Pittsburgh School of Medicine, Magee-Womens Hospital, Pittsburgh, Pennsylvania Humidifiers; Peripartum Neurologic Complications

David Porembka, FCCM

James G. Ramsay, MD

Professor of Anesthesia, Surgery and Internal Medicine (Cardiology), Department of Anesthesiology; Associate Director of Surgical Intensive Care; Director of Perioperative Echocardiography, University of Cincinnati College of Medicine, Cincinnati, Ohio Postoperative Respiratory Failure

Professor of Anesthesiology, Program Director, Anesthesiology Critical Care Medicine, Department of Anesthesia, Emory University School of Medicine; Anesthesiology Service Chief, Department of Anesthesiology, Emory University Hospital, Atlanta, Georgia Central Venous Pressure Monitoring

Claudia Praetel, MD

Monica N. Riesner, MD

Research Fellow, Department of Anesthesiology, College of Physicians and Surgeons of Columbia University, New York, New York Nitrous Oxide: Neurotoxicity

Joseph Previte, MD Associate Professor of Pediatrics and Anesthesiology, Project Leader of Anesthesia Centricity IS, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio Anesthetic Complications of Fetal Surgery: EXIT Procedures; Perioperative Aspiration Pneumonitis

Lecturer, Obstetric Anesthesia, Department of Anesthesiology, University of Michigan Medical School, Ann Arbor, Michigan Postpartum Hemorrhage

Edward T. Riley, MD Associate Professor, Department of Anesthesia, Stanford University School of Medicine, Stanford, California Antihistamines: H1- and H2-Blockers

Pamela R. Roberts, MD, FCCM, FCCP Richard C. Prielipp, MD, FCCM JJ Buckley Professor and Chair, Department of Anesthesiology, University of Minnesota Medical School, Minneapolis, Minnesota Hypothyroidism: Myxedema Coma; Hyperthyroidism: Thyroid Storm

Professor and Division Chief, Critical Care Medicine, John A. Moffitt Endowed Chair, Department of Anesthesiology, University of Oklahama Health Science Center, Oklahoma City, Oklahoma Hypothyroidism: Myxedema Coma; Hyperthyroidism: Thyroid Storm

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Kerri M. Robertson, MD

Ramachandran Satya-Krishna, MD, FRCA

Associate Clinical Professor of Anesthesiology; Chief, General, Vascular, High-Risk Transplant and Surgical Critical Care Medicine Division; Chief, Transplant Services, Duke University School of Medicine, Department of Anesthesiology, Durham, North Carolina Postoperative Hepatic Dysfunction; Complications of Carcinoid Tumors; Complications of Deliberate Hypotension: Visual Loss

Lecturer, Department of Anesthesiology, University of Michigan Medical School, Ann Arbor, Michigan; Consultant, Department of Anaesthesia, John Radcliffe Hospital, Oxford, United Kingdom Anesthesia Circuit

Marnie Robinson, MD Assistant Professor of Anesthesiology and Pediatrics, Department of Anesthesiology, University of Cincinnati College of Medicine, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio Anesthetic Complications of Fetal Surgery: EXIT Procedures

John B. Rose, MD Director, Pain Management Service, Department of Anesthesiology and Critical Care Medicine, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania Delayed Emergence in Pediatric Patients

Mark I. Rossberg, MD Assistant Professor of Anesthesiology, Department of Anesthesia and Critical Care Medicine, Johns Hopkins Medical Institute, Baltimore, Maryland Postintubation Croup

Scott R. Schulman, MD Associate Professor of Anesthesiology and Pediatrics, Division of Pediatric Anesthesia and Critical Care Medicine, Duke University Medical Center, Durham, North Carolina Malignant Hyperthermia

Annette Schure, MD Anesthesiologist and Pediatric Anesthesiologist, Department of Anesthesia, Tufts-New England Medical Center, Boston, Massachusetts Thoracic Aortic Aneurysm

Jeffrey J. Schwartz, MD Associate Professor, Department of Anesthesiology, Yale University School of Medicine; Attending Physician, Department of Anesthesiology, Yale-New Haven Hospital, New Haven, Connecticut Electrical Safety

Christian Seefelder, MD David M. Rothenberg, MD Professor of Anesthesiology; Associate Dean, Academic Affiliations; Co-Medical Director, Surgical Intensive Care Unit, Rush University Medical Center, Chicago, Illinois Acute Pancreatitis

Assistant in Anaesthesia, Harvard Medical School; Instructor in Anaesthesia, Department of Anaesthesiology, Perioperative and Pain Medicine, Children’s Hospital, Boston, Massachusetts Air Emboli

Daniel D. Rubens, MB,BS, FANZCA

Rajamani Sethuraman, MD, FRCA

Assistant Professor, Department of Anesthesia, University of Washington School of Medicine, Children’s Hospital and Regional Medical Center, Seattle, Washington Intraoperative Cardiac Arrest

Consultant Anaesthetist, Department of Anaesthesia, Princess Alexandra Hospital, Essex, United Kingdom Intravenous Drug Delivery Systems

Christoph N. Seubert, MD Senthilkumar Sadhasivam, MD Assistant Professor in Anesthesia and Pediatrics, Department of Anesthesia, University of Cincinnati College of Medicine, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio Postoperative Nausea and Vomiting

Tetsuro Sakai, MD, PhD Resident, Department of Anesthesiology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania Complications in Orthopedic Outpatients Not Receiving Peripheral Nerve Blocks

Francis V. Salinas, MD Clinical Assistant Professor, Department of Anesthesiology, University of Washington School of Medicine; Staff Anesthesiologist, Department of Anesthesiology, Virginia Mason Medical Center, Seattle, Washington Local Anesthetic Systemic Toxicity

Theodore J. Sanford, Jr., MD Clinical Professor of Anesthesiology, Department of Anesthesiology, University of Michigan Medical School, Ann Arbor, Michigan Difficult Airway: Opiate-Induced Muscle Rigidity

Assistant Professor, Department of Anesthesiology, University of Florida College of Medicine, Gainesville, Florida Barbiturates: Porphyrias

Jack S. Shanewise, MD Chief, Division of Cardiothoracic Anesthesiology, Department of Anesthesiology, College of Physicians and Surgeons of Columbia University, New York, New York Transesophageal Echocardiography

Kelly T. Shannon, MD Associate Professor of Anesthesiology, University of Pittsburgh School of Medicine; Associate Chief, Department of Anesthesiology, Magee-Womens Hospital, Pittsburgh, Pennsylvania Humidifiers

Gauhar Sharih, MD, FRCA Formerly, Visiting Instructor, Department of Anesthesiology, University of Michigan Medical School, Ann Arbor, Michigan; Specialist Registrar, Department of Anaesthetics, City Hospital, Birmingham, West Midlands, United Kingdom Inspiratory and Expiratory Gas Monitoring

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Aarti Sharma, MD, DA(UK)

Mark D. Stoneham, MD, FRCA

Assistant Professor of Anesthesiology, Department of Anesthesiology, Weill Medical College of Cornell University; Attending Anesthesiologist, Department of Anesthesiology, New York–Presbyterian Hospital, New York, New York Complications of Deliberate Hypotension: Visual Loss

Honorary Senior Clinical Lecturer, Nuffield Department of Anaesthesia, John Radcliffe Hospital, Oxford, United Kingdom Pulse Oximetry

Robert N. Sladen, MD Professor and Vice Chair, Department of Anesthesiology; Chief, Division of Critical Care, College of Physicians and Surgeons of Columbia University, New York, New York Postoperative Acute Renal Failure; Hypothermia

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E. Price Stover, MD* Clinical Assistant Professor, Department of Anesthesia, Stanford University Medical Center, Stanford, California Nonbarbiturate Anesthetics

Laura Stover, MD, MASc, FRCP(C)

Professor of Anesthesia, Department of Anesthesiology, Toronto General Hospital, Toronto, Ontario, Canada One-Lung Ventilation

Acting Instructor, Department of Anesthesiology, University of Washington School of Medicine; Acting Instructor, Department of Cardiothoracic Anesthesiology, University of Washington Medical Center, Seattle, Washington; Assistant Professor of Anesthesiology, Hamilton Health Sciences, Hamilton, Ontario, Canada Drugs Affecting the Renin-Angiotensin System

Tod B. Sloan, MD

Vijayendra Sudheendra, MD

Professor of Anesthesiology, University of Colorado Health Sciences Center, Denver, Colorado Spinal Cord Injury

Clinical Instructor, Department of Surgery and Anesthesiology, Brown University School of Medicine; Staff Anesthesiologist, Miriam Hospital, Providence, Rhode Island; Chief of Anesthesia, East Bay Surgery Center, Swansea, Massachusetts Complications of Transurethral Surgery

Peter D. Slinger, MD

Jonathan H. Slonin, MD Chief Resident, Department of Anesthesiology, Leonard M. Miller School of Medicine at the University of Miami, Miami, Florida Surgery in the Morbidly Obese

Paul Smythe, MD Assistant Professor of Anesthesiology, University of Michigan Medical School; Adjunct Clinical Lecturer in Dentistry, Department of Oral and Maxillofacial Surgery/Hospital Dentistry, University of Michigan School of Dentistry, Ann Arbor, Michigan Intracranial Pressure Monitoring

Jennifer E. Souders, MD Clinical Associate Professor, Department of Anesthesiology, University of Washington School of Medicine, Seattle, Washington Venous Air Embolism

Scott R. Springman, MD Professor, Departments of Anesthesiology and Surgery, University of Wisconsin Medical School, Madison, Wisconsin Preanesthetic Evaluation: False-Positive Tests; Preanesthetic Evaluation: Inadequate or Missing Test Result

James M. Steven, MD Associate Professor of Anesthesia and Pediatrics, Department of Anesthesia, University of Pennsylvania School of Medicine; Chief Medical Officer, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania Upper Respiratory Tract Infection

Robert K. Stoelting, MD Emeritus Professor and Chair, Department of Anesthesia, Indiana University School of Medicine, Indianapolis, Indiana Postoperative Peripheral Neuropathy; Intractable Nausea and Vomiting

Kevin J. Sullivan, MD Assistant Professor of Anesthesiology, Mayo Clinic College of Medicine; Clinical Assistant Professor of Pediatrics, University of Florida College of Medicine, Jacksonville; Staff Member, Department of Anesthesiology, Nemours Children’s Clinic; Staff Pediatric Anesthesiologist and Intensivist, Department of Anesthesia and Critical Care Medicine, Wolfson Children’s Hospital, Jacksonville, Florida Anticholinergics; Hypothermia in Pediatric Patients

Christer H. Svensén, MD Associate Professor, Department of Anesthesiology, University of Texas Medical Branch, Galveston, Texas Perioperative Fluid Management

James F. Szocik, MD Associate Professor, Department of Anesthesiology, University of Michigan Medical School; Chair, Technical Support Committee, Department of Anesthesiology, University of Michigan Medical Center, Ann Arbor, Michigan Pipeline Source Failure

Kenichi A. Tanaka, MD Assistant Professor, Department of Anesthesiology, Emory University School of Medicine, Atlanta, Georgia Perioperative Hypertension

Mark D. Tasch, MD Associate Professor of Clinical Anesthesia, Department of Anesthesia, Indiana University School of Medicine, Indianapolis, Indiana Pulmonary Aspiration

*Deceased

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Peter Tassani-Prell, MD

Karen M. Van Tassel, MD

Professor of Cardiac Anesthesia, Department of Anesthesia, German Heart Center Munich, München, Germany Anticoagulation Initiation and Reversal for Cardiac Surgery; Bleeding after Cardiac Surgery

Chief Resident, Department of Anesthesiology, Duke University Medical Center, Durham, North Carolina Malignant Hyperthermia

Lisa Thannikary, MD

Gurinder M. S. Vasdev, MB,BS

Adjunct Assistant Professor, Department of Anesthesiology, University of Florida College of Medicine, Gainesville, Florida Intrathecal Opiates; Ketamine; Steroids

Klaus D. Torp, MD Assistant Professor of Anesthesiology, Department of Anesthesiology, Mayo Clinic College of Medicine, Jacksonville, Florida Perioperative Management of Dialysis-Dependent Patients

Laurence C. Torsher, MD Assistant Professor of Anesthesiology, Department of Anesthesiology, Mayo Clinic College of Medicine, Rochester, Minnesota Perioperative Care for Patients with Hepatic Insufficiency (Cirrhosis)

Mark F. Trankina, MD Staff Anesthesiologist, Carraway Methodist Medical Center and University of Alabama Hospital at Birmingham, Birmingham, Alabama Class I Antiarrhythmic Drugs: Ventricular Proarrhythmia

Kenneth W. Travis, MD Associate Professor Emeritus, Department of Anesthesiology, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire Postobstruction Pulmonary Edema

Lawrence C. Tsen, MD Associate Professor of Anesthesia, Department of Anesthesia, Harvard Medical School; Director of Anesthesia, Center for Reproductive Medicine, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women’s Hospital, Boston, Massachusetts Antepartum Hemorrhage

Avery Tung, MD Associate Professor, Department of Anesthesia and Critical Care, University of Chicago Pritzker School of Medicine, Chicago, Illinois Major Organ System Dysfunction after Cardiopulmonary Bypass; Mechanical Assist Devices; Thermally Injured Patients

Manuel C. Vallejo, MD, DMD Associate Professor, Department of Anesthesiology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania Peripartum Neurologic Complications

Gail A. Van Norman, MD Clinical Associate Professor of Anesthesiology, Affiliate Associate Professor of Medical History and Ethics, University of Washington School of Medicine, Seattle, Washington; Physician, Department of Anesthesiology, St. Joseph Medical Center, Tacoma, Washington Patient Confidentiality; Do-Not-Resuscitate Orders in the Operating Room; The Jehovah’s Witness Patient

Assistant Professor of Anesthesiology, Department of Anesthesiology, Mayo Clinic College of Medicine, Rochester, Minnesota Cardiopulmonary Bypass in Pregnancy

Melissa M. Vu, MD Instructor of Anesthesiology, Department of Anesthesiology, Mayo Clinic College of Medicine, Jacksonville, Florida Hyperthermia

Mehernoor F. Watcha, MD Associate Professor of Anesthesia, Department of Anesthesiology and Critical Care Medicine, University of Pennsylvania School of Medicine, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania Postoperative Nausea and Vomiting

Eileen Watson, MD Clinical Assistant Professor, Department of Anesthesiology, State University of New York at Buffalo; Attending Anesthesiologist, Children’s Hospital of Buffalo, Buffalo, New York Hemodynamic Instability

B. Craig Weldon, MD Associate Professor, Department of Anesthesiology and Pediatrics, Duke University School of Medicine, Durham, North Carolina Cardiomyopathies; Emergence Agitation

Robert S. Weller, MD Associate Professor of Anesthesiology, Department of Anesthesiology, Wake Forest University School of Medicine; Staff Anesthesiologist, Department of Anesthesiology, North Carolina Baptist Hospitals, Inc., Winston-Salem, North Carolina Psoas Compartment Block: Potential Complications

Lynda Wells, MD Associate Professor of Anesthesiology, University of Virginia Health System, Charlottesville, Virginia Pediatric Neurosurgery

Volker Wenzel, MD, MSc Associate Professor of Anesthesiology and Critical Care Medicine, Department of Anesthesiology and Critical Care Medicine, Medical University of Innsbruck, Innsbruck, Austria Vasopressors: Vasoconstrictor Drugs

Harshdeep Wilkhu, MD Clinical Assistant Professor, Department of Anesthesiology, University of Florida College of Medicine, Gainesville, Florida Nonbarbiturate Anesthetics

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Contributors

Brian A. Williams, MD

Brian J. Woodcock, MD

Associate Professor, Department of Anesthesiology, University of Pittsburgh School of Medicine; Director of Outpatient Regional Anesthesia Service, Department of Anesthesiology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania Complications in Orthopedic Outpatients Not Receiving Peripheral Nerve Blocks

Assistant Professor of Anesthesiology, Department of Anesthesiology, University of Michigan Medical School, Ann Arbor, Michigan Mechanical Ventilators

Glyn D. Williams, MB,ChB, FFA Associate Professor, Department of Anesthesia, Stanford University School of Medicine, Lucile Packard Children’s Hospital, Palo Alto, California Catheter Ablation for Arrhythmias

xxiii

Christopher C. Young, MD, FCCM Assistant Clinical Professor of Surgery, Associate Clinical Professor of Anesthesiology, Chief of Critical Care Medicine Division, Department of Anesthesiology, Duke University School of Medicine, Durham, North Carolina Hypothermia

William L. Young, MD

Assistant Professor, Departments of Anesthesiology and Pediatrics, University of Colorado School of Medicine, Denver, Colorado Antidepressants; Air Emboli

James P. Livingston Professor and Vice Chair, Department of Anesthesia and Perioperative Care, University of California, San Francisco, San Francisco General Hospital, San Francisco, California Arteriovenous Malformation: Normal Perfusion Pressure Breakthrough

Eric P. Wittkugel, MD

Christine M. Zainer, MD

Associate Professor of Clinical Anesthesia and Critical Care; Staff Anesthesiologist; Director, Preoperative Services, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio Pediatric Laryngospasm

Assistant Professor of Anethesiology, Department of Anesthesiology, Medical College of Wisconsin, Froedtert Memorial Lutheran Hospital East, Milwaukee, Wisconsin Herbals and Alternative Medicine

Lisa Wise-Faberowski, MD

Mark A. Zakowski, MD David J. Wlody, MD Clinical Associate Professor of Anesthesiology and Vice Chair for Clinical Affairs, Department of Anesthesiology, State University of New York-Downstate Medical Center; Interim Chair, Department of Anesthesiology, Long Island College Hospital, Brooklyn, New York Postpartum Headache Other Than Post–Dural Puncture Headache

Gilbert Y. Wong, MD Assistant Professor of Anesthesiology and Consultant Physician, Division of Pain Medicine, Department of Anesthesiology, Mayo Clinic College of Medicine, Rochester, Minnesota Celiac Plexus Block: Side Effects and Complications

Chief, Section of Obstetric Anesthesia, Department of Anesthesiology, Cedars-Sinai Medical Center, Los Angeles, California Peripartum Neurologic Complications

Paul B. Zanaboni, MD, PhD Anesthesiologist, St. John’s Mercy Health Care, St. Louis, Missouri Bradyarrhythmias

R. Victor Zhang, MD, PhD Assistant Professor, Department of Anesthesiology, University of Florida College of Medicine, Gainesville, Florida a2-Adrenoreceptor Agonists

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Acknowledgments First, I wish to acknowledge the contributions to this work of my wife Barbara, my in-house administrative and editorial assistant. Thank you, Barbara! Your literary skills (you did major in English and minor in Philosophy) were much needed and greatly appreciated! I am deeply indebted to the Section Editors for this edition of Complications in Anesthesia, some of whom were Section Editors for the first edition as well. Organizing the topics for their sections or subsections, recruiting contributors, and seeing to it that the chapter manuscripts were submitted and pre-edited in a timely fashion were some of their tasks. Special appreciation goes to Natasha Andjelkovic (Executive Publisher), Jean Nevius (Senior Developmental Editor), and Amy Norwitz (Senior Project Manager). Once again, I salute Lewis Reines (former President of WB Saunders) and Leslie Day (former Medical Editor at WB Saunders), who in 1996-1997 convinced me of the need for this conceptually new work as a resource for busy practitioners in anesthesia and critical care. Finally, I express my sincere appreciation to John P. Kampine, MD, PhD, former Professor and Chair of the Department of Anesthesiology at the Medical College of Wisconsin, and to my colleagues in that department (some of whom have contributed to this work) for providing me the time and encouragement for yet again undertaking this work. John L. Atlee, MD

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PHARMACOLOGY

VASOACTIVE DRUGS

1

Vasodilator Drugs Jörg Dziersk Case Synopsis A 90-year-old man with severe aortic stenosis, stable angina, and pulmonary hypertension has surgery under general anesthesia for a femoral neck fracture. Owing to the associated cardiac morbidities, the anesthesiologist inserts a pulmonary artery catheter. Despite maintenance of normoxemia and mild hypocapnia, the patient’s pulmonary artery pressure rises from 60/25 to 70/35 mm Hg and is associated with signs of right ventricular strain. A nitroglycerin infusion is started at 0.2 μg/kg per minute. The pulmonary artery pressure returns to near baseline values, and the systemic blood pressure decreases from 125/90 to 75/30 mm Hg.

PROBLEM ANALYSIS Definition Left-sided heart disease (e.g., mitral valve disease, aortic stenosis, left ventricular failure) often causes significant pulmonary venous pressure elevation and leads to compensatory pulmonary artery (PA) hypertension. Chronic elevation of PA pressure promotes compensatory right ventricular (RV) hypertrophy and pulmonary vascular remodeling. This, in turn, results in increased pulmonary vascular resistance (PVR). For such patients, acute (or acute-on-chronic) increases in PA pressure are often poorly tolerated. The consequences are RV dilatation, significant tricuspid regurgitation, and reduced cardiac output secondary to reduced venous return and impaired left ventricular filling. Together, they may lead to a “downward spiral.” When RV systolic pressure exceeds aortic blood pressure, RV coronary perfusion is limited to diastole, which may further impair RV performance. Vasodilating drugs act by reducing the contraction of vascular smooth muscle cells through a reduction in cytoplasmic Ca2+ concentration [Ca2+]. Vascular smooth muscle relaxation may be mediated by the following: ●

●

●

● ●

●

Increased intracellular cyclic adenosine monophosphate (e.g., β2-adrenoceptor agonists, epoprostenol) Increased intracellular cyclic guanosine monophosphate (e.g., nitric oxide, nitroglycerin, sodium nitroprusside, brain natriuretic peptide) KATP channel-opening-related hyperpolarization (e.g., diazoxide) α1-Adrenoceptor antagonism (e.g., phentolamine) Ca2+ channel blockade (e.g., diltiazem, nicardipine, verapamil) Reduction of central sympathetic tone (e.g., clonidine)

Properties of an ideal vasodilator for perioperative use include (1) short onset time, (2) short to intermediate duration of action, (3) elimination independent of organ function (i.e., renal or hepatic), and (4) lack of serious side

effects or toxicity. At this time, there is no single drug that meets all these criteria. Clinical actions, mechanisms of action, and side effects of vasodilators currently available for intravenous or inhalational administration are listed in Table 1-1.

Recognition Systemic vasodilatation causes a decline in systemic blood pressure, the extent of which depends on circulating blood volume and venous return (cardiac preload), the adequacy of compensatory mechanisms (i.e., reflex increase in heart rate and contractility), and the cardiac ejection fraction (normal or reduced). The skin appears warm and may be flushed, with a shortened capillary refill time. Organ dysfunction may occur if systemic blood pressure is below the respective autoregulation threshold or if flow in a vascular territory is pressure dependent (e.g., in the presence of coronary artery disease, renal artery stenosis, head injury). Myocardial injury, acute renal failure, or neurologic deficits are typical examples of complications of systemic hypotension. Computation of systemic vascular resistance quantifies the average degree of vasodilatation (or vasoconstriction) in the whole body, but it requires a precise measurement of mean arterial pressure and central venous pressure, as well as a determination of cardiac output. A PA catheter equipped for thermodilution cardiac output is necessary. In the presence of PA hypertension, systemic vasodilatation may allow right-to-left shunting of blood through a patent foramen ovale, leading to a diminished arterial oxygen saturation. Reduced RV preload due to venous pooling and RV myocardial perfusion pressure may compromise RV performance and result in a low cardiac output state.

Risk Assessment Vasodilator therapy has an increased potential to cause complications in patients with the following conditions: ● ● ●

Hypovolemia Stenotic valvular lesions (especially severe aortic stenosis) Hypertrophic-obstructive cardiomyopathy 3

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Vasodilators Available for Intravenous or Inhalational Administration

Drug Class and Drug*

Terminal Half-life

α1-Antagonists Labetalol

5-8 hr

Phentolamine

19 min (IV)

Urapidil†

2.7 hr

α2-Adrenoceptor Agonists Clonidine

8-16 hr

Donors Nitric oxide

6 sec

Nitroglycerin

2-8 min

Sodium nitroprusside

3-4 min

Blockers Diltiazem

3-6 hr

Nicardipine

8.6 hr (infusions ≥48 hr)

Verapamil

2-8 hr

Angiotensin-Converting 11 hr

Venous > arterial vasodilatation NO or S-nitrosothiol release by metabolism ⇒ activation of guanylyl cyclase Arterial ª venous vasodilatation NO release by red cell metabolism ⇒ activation of guanylyl cyclase

Bradycardia Drug fever Reflex tachycardia Hypoglycemia

Bradycardia Potentiates anesthetic/narcotic sedation Slow IV onset (30-60 min)

Arterial vasodilatation Vascular remodeling Inhibits generation of angiotensin II Stimulates kallikrein-kinin system

18 min

Cyanide toxicity, especially with higher doses and lengthy infusions Thiocyanate toxicity (lengthy infusions) Methemoglobinemia Reflex tachycardia

Vasodilatation unpredictable Little effect in PA HTN

Possibly severe (first dose) Acute renal failure ↑ K+, especially with renal failure No effect on PA HTN (given acutely) Slow IV onset (>15 min)

Severe systemic hypotension with IV dosing (common) Inhibition of platelet aggregation and adhesion Stimulates coughing (inhalational use)

5-10 min 3-5 min 13-30 min

Natriuretic Peptides

Inhibits platelet aggregation Pulmonary edema secondary to contaminants (NO2) and metabolites (peroxynitrite) Methemoglobinemia Tachyphylaxis Methemoglobinemia

Moderate negative inotrope AV conduction blockade Does not block L-type cardiac Ca2+ channels (little or no effect on contractility or AV conduction) Significant negative inotrope Depresses sinus node Blocks AV node conduction Longer half-life with chronic use

Activation of adenylyl cyclase ⇒↑cAMP

Prostaglandins with VSM Relaxing Effect

Brain natriuretic peptide

↓ Central sympathetic vasomotor tone Inhibits peripheral NE release

Block L-type Ca2+ channels Primary arterial dilators (no venodilatation at therapeutic doses)

Calcium Channel

Alprostadil (PGE1) Epoprostenol (PGI2) Iloprost

Arterial > venous vasodilatation Competitive adrenoceptor blockade (α1:β = 1:7) Competitive α1- = α2-adrenoceptor blockade Direct action on VSM Competitive α1-adrenoceptor blockade Competitive α2-adrenoceptor block

Side Effects and Problems

Activation of guanylyl cyclase ⇒↑cGMP

Nitric Oxide and

Enzyme Inhibitors Enalaprilat

Principal Action and Mechanism of Action

Arterial and venous vasodilatation Stimulation of natriuretic peptide receptor A ⇒ activation of guanylyl cyclase domain ⇒ ↑cGMP Inhibits renin-aldosterone axis

Miscellaneous Agents Adenosine

7.5) may produce further pulmonary vasorelaxation but adversely affects oxygen delivery and enzyme function. High endogenous catecholamine levels cause pulmonary vasoconstriction through the stimulation of α1adrenoceptors. These high levels can be avoided or treated by providing adequate anesthetic depth and postoperative analgesia. Finally, it should be remembered that lung inflation above functional residual capacity causes a progressive increase in PVR. Ventilator settings should be adjusted, based on the patient’s pulmonary function, to provide adequate oxygenation and carbon dioxide elimination while keeping mean intrathoracic pressure to a minimum. Pharmacologic pulmonary vasodilatation without concomitant systemic vasodilatation, as was required in the case described here, can be attained in two ways: 1. Inhalation of a short-acting vasodilator, such as nitric oxide (NO) or prostacyclin (epoprostenol) 2. Coadministration of an intravenous pulmonary vasodilator (e.g., nitroglycerin, nitroprusside, epoprostenol) and a pulmonary vasculature-sparing vasoconstrictor (e.g., vasopressin or its synthetic analogue terlipressin). NO activates soluble guanylyl cyclase to increase cyclic guanosine monophosphate levels in vascular smooth muscle. It is inactivated by the heme moiety of hemoglobin and superoxide anions and has a blood half-life of approximately 6 seconds. Therefore, inhaled NO affects predominantly

PHARMACOLOGY

Table 1–1

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the tone of pulmonary vessels in ventilated lung areas but has negligible effects on systemic vascular resistance. Broader application is currently limited by its very high cost and the special equipment required for its administration. Prostacyclin (PGI2, epoprostenol) and its synthetic analogue iloprost are the most potent pulmonary vasodilators known. Their main application is continuous infusion in cases of severe pulmonary hypertension. Their vasodilator action is mediated by cyclic adenosine monophosphate. Intravenous administration frequently causes prohibitive systemic hypotension, but when administered via inhalation, the effectiveness is comparable to that of inhaled NO. Arginine vasopressin is a vasoactive nonapeptide produced in the hypothalamus. It is an agonist at three specific receptor types. Stimulation of the V1a receptor results in contraction of systemic vascular smooth muscle by means of an intracellular activation pathway shared with angiotensin II. Successful use of arginine vasopressin in vasodilatory shock after cardiopulmonary bypass and in hyperdynamic septic shock has been reported. The advanced cardiovascular life support guidelines of 2000 recommend vasopressin as an alternative to epinephrine in patients with refractory ventricular fibrillation. In contradistinction to the pulmonary vascular effects of other vasoconstrictors (e.g., α1adrenoceptor agonists, angiotensin II), vasopressin has been shown to cause pulmonary and cerebral artery vasodilatation, possibly through receptor-mediated local NO release. It may be the vasopressor drug of choice in patients with significantly elevated PVR or RV failure.

PREVENTION Preventing the complications of vasodilator use is based on an understanding of the patient’s pathophysiology and the pharmacology of available drugs. Vasodilators are used to advantage based on their specific profiles, always keeping in mind any undesired or dangerous side effects. For instance, in a patient with aortic stenosis and coronary artery disease, both systemic hypotension and tachycardia must be avoided. In the case described in this chapter, nitroglycerin would be a reasonable choice for treatment of

pulmonary hypertension, because it produces less relaxation of systemic resistance vessels than do other pulmonary vasodilators and does not cause a reflex tachycardia. Use of vasodilators in the perioperative period should take into account the common occurrence of hypovolemia due to preoperative fluid restriction, intraoperative fluid shifts or blood loss, and globally or regionally reduced sympathetic tone in anesthetized patients. Careful dose titration of vasodilators is advisable and is facilitated by using drugs with short half-lives. Vasodilator therapy for pulmonary hypertension coincides with the appropriate manipulation of physiologic factors known to affect PVR. Inhalational administration of NO or epoprostenol, if feasible, may help avoid unwanted systemic venodilatation or arterial vasodilatation effects. Finally, always keep in mind that adrenoceptor antagonists and vasodilators attenuate sympathetic responses, possibly masking the clinical signs of inadequate depth of anesthesia. The use of a depth-of-anesthesia monitor is encouraged, especially when neuromuscular blockers are used.

Further Reading Balser JR, Butterworth J: Cardiovascular drugs. In Hensley FA Jr, Martin DE, Gravlee GP (eds): A Practical Approach to Cardiac Anesthesia, 3rd ed. Philadelphia, JB Lippincott–Williams & Wilkins, 2003. Barnes PJ, Liu SF: Regulation of pulmonary vascular tone. Pharmacol Rev 47:87-131, 1995. Eagle KA, Berger PB, Calkins H, et al: ACC/AHA Guideline Update on Perioperative Cardiovascular Evaluation for Noncardiac Surgery, 2002. American College of Cardiology Web site available at http://www.acc.org/ clinical/ guidelines/perio/dirIndex.htm Frishman WH, Sonnenblick EH, Sica DH (eds): Cardiovascular Pharmacotherapeutics, 2nd ed. New York, McGraw-Hill, 2003. Katzung BG (ed): Basic & Clinical Pharmacology, 9th ed. New York, Lange Medical Books/McGraw-Hill, 2004. Malouf JF, Enriquez-Sarano M, Pellikka PA, et al: Severe pulmonary hypertension in patients with severe aortic valve stenosis: Clinical profile and prognostic implications. J Am Coll Cardiol 40:789-795, 2002. Olschewski H, Rose F, Schermuly R, et al: Prostacyclin and its analogues in the treatment of pulmonary hypertension. Pharmacol Ther 102:139-153, 2004. Reich DL, Bodian CA, Krol M, et al: Intraoperative hemodynamic predictors of mortality, stroke, and myocardial infarction after coronary artery bypass surgery. Anesth Analg 89:814-822, 1999.

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REGIONAL ANESTHESIA & PAIN PHARMACOLOGY MANAGMENT

Vasopressors: Vasoconstrictor Drugs

2

Viktoria D. Mayr, Volker Wenzel, and Martin W. Dünser Case Synopsis A 73-year-old woman with a history of chronic arterial hypertension and coronary heart disease undergoes surgery for an infected hip prosthesis. Etomidate, fentanyl, and rocuronium are used to induce anesthesia. After induction, the patient’s arterial blood pressure (BP) suddenly drops to 60/40/30 mm Hg (systolic/mean/diastolic). Infusion of 1 L normal saline and two 5-mg intravenous bolus injections of ephedrine have no significant effect on BP. Continuous infusion of norepinephrine restores BP to a more normal range (105/74/58 mm Hg); however, simultaneously, the patient develops tachycardia with ventricular ectopic beats. After norepinephrine is increased to 0.35 μg/kg per minute, atrial fibrillation with a rapid ventricular response develops and results in a sustained reduction in arterial BP.

PROBLEM ANALYSIS Definition The first priority of perioperative cardiovascular care is to maintain adequate perfusion of vital organs. In addition to sufficient cardiac output, mean arterial BP must be maintained to secure organ perfusion pressure. Accordingly, arterial hypotension is either a mean arterial pressure (MAP) less than 60 mm Hg or a drop in MAP of more than 30% from preoperative values. Below a MAP of about 60 mm Hg, vascular autoregulation1 declines in the brain, kidneys, and parts of the gastrointestinal tract. For the heart, autoregulation is lost below a diastolic BP of 50 to 55 mm Hg, presuming a normal left ventricular end-diastolic pressure. With loss of autoregulation, vital organ perfusion becomes compromised. Fluids, inotropes, and vasopressors are used to treat hypotension in perioperative and critical care settings. After restoration of normovolemia and adequate cardiac output with intravenous fluids and inotropes, ongoing hypotension may require the use of vasopressors. Commonly used vasopressors in the perioperative setting are dopamine, norepinephrine, epinephrine, phenylephrine, ephedrine, and vasopressin (Table 2-1). All these drugs exert their effects by stimulating α-adrenergic and β-adrenergic receptors. These receptors are found not only in vascular and cardiac smooth muscle but also in the liver, platelets, leukocytes, bronchiolar smooth muscle, fat, and muscle.

1 The autoregulatory (AR) curve is shifted upward and to the right in chronic hypertension. In normotensives, flow is constant over the MAP range of 60 to 160 mm Hg. With chronic hypertension, the AR range is 80 to 180 mm Hg or higher. Below or above this, flow is directly proportional to MAP: flow increases for MAP values above the upper AR setpoint, and it decreases for values below the lower setpoint. For the heart, the AR curve is a diastolic BP of 50 to 150 mm Hg, presuming a normal left ventricular end-diastolic pressure (0 to 3 mm Hg). If the left ventricular enddiastolic pressure increases, the AR curve shifts upward and to the right.

Systemic inflammation or sepsis leads to high cytokine concentrations, with overproduction of nitric oxide. In turn, both membranous and cytosolic adrenergic receptor complexes are quantitatively and qualitatively down-regulated. These pathophysiologic adaptive mechanisms lead to reduced effects of endogenous or exogenous catecholamines, often necessitating the infusion of even higher catecholamine doses to ensure adequate vital organ perfusion. However, such high-dose catecholamine infusions may adversely affect the risk-benefit ratio of adrenergic vasopressor therapy beyond clinically acceptable ranges.

Recognition Institution of vasopressor therapy may have a number of untoward effects on major organ systems. Among the more common side effects of catecholamines are α1- and primarily β-adrenergic-mediated ventricular ectopy and tachyarrhythmia.2 High-dose vasopressor therapy with primary α-adrenergic agonists may increase pulmonary artery pressure. Aside from these effects, some catecholamine derivatives have specific side effects that may have an adverse impact on patient outcomes. For example, dopamine is known to reduce mucosal perfusion in the gastrointestinal tract. Although mesenteric blood flow significantly increases during therapy with dopamine, mucosal oxygenation deteriorates. This paradoxical effect is likely due to an intervillus shunt (i.e., shift of intestinal wall blood flow to the submucosa). Dopamine also influences the production and release of several hormones. Lengthy infusions may lead to reduced serum concentrations of prolactin, human growth hormone, and thyroid hormones.

2 A synergistic interaction between α1- and β-adrenoceptors has been implicated in the genesis of catecholamine-anesthetic ventricular arrhythmias: a1A-mediated slowing of Purkinje fiber conduction, with enhanced conduction at the Purkinje fiber–ventricular muscle fiber junction.

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Effects of Vasopressor Drugs

Drug

Negative Effects

Positive Effects

Dopamine

Tachycardia Tachyarrhythmia Pulmonary artery vasoconstriction ↓ PaO2 (↑ O2 demand) ↑ Systemic vascular resistance Tachycardia Tachyarrhythmias ↑ O2 consumption Tachycardia Tachyarrhythmias ↑ O2 consumption Hyperglycemia ↑ Systemic vascular resistance ↑ O2 consumption

↑ Myocardial contractility ↑ Glomerular filtration rate

Norepinephrine

Epinephrine

Phenylephrine

Ephedrine

Tachycardia Indirectly mediated effects†

Vasopressin

Ischemic skin lesions Gut ischemia

↑ Myocardial contractility

↑ Cardiac index ↑ Stroke volume ↑ O2 delivery ↑ Cardiac index* ↑ Stroke volume* ↑ Cardiac output* ↑ O2 delivery ↑ Heart rate ↑ Cardiac output ↑ Mean arterial pressure ↑ O2 delivery ↑ Mean arterial pressure Heart rate‡ ↑ Mean pulmonary artery pressure ↑ Catecholamine requirements

*Venous constriction in venous capacitance bed augments venous return and cardiac preload, thereby increasing cardiac output. † Effects largely mediated by endogenous catecholamine release. ‡ No effect, or decrease due to baroreceptor stimulation caused by increased blood pressure.

Apart from reduced gastrointestinal blood flow, phenylephrine may reduce cardiac output. Although this is not a consistent finding, it may be explained by a baroreceptormediated reduced heart rate and possibly reduced contractility. Aside from substantial tachycardia and proarrhythmia potential, both epinephrine and norepinephrine may have significant metabolic side effects, including sustained hyperglycemia due to β-adrenergic stimulation of hepatic gluconeogenesis and down-regulation of peripheral insulin receptors. Further, epinephrine may lead to significant hyperlactatemia via the stimulation of muscular β receptors. Consequently, excessive stimulation of glycoclysis leads to the overproduction of lactate. Epinephrine is also known to cause a significant reduction in the hepatosplanchnic oxygen supply. Catecholamines stimulate α receptors to activate platelets and induce a hypercoagulable state. Such hypercoagulability may be aggravated by α-adrenergic-mediated vasoconstriction. Consequent thrombosis or vasoconstriction could further impair vital organ perfusion. Also, adrenergic receptor stimulation exerts several immune-modulating effects. Whereas α receptors mediate immune-suppressive effects by increasing tumor necrosis factor α, stimulation of β receptors improves immune function by releasing interleukin-10 to reduce dendritic cell migration. This influences antigen expression and contact hypersensitivity responses. Thus, a number of complications involving multiple organ systems may occur when administering catecholamines to support BP.

Risk Assessment The occurrence of adverse effects during vasopressor therapy with catecholamines depends not only on the doses used but

also on individual patient characteristics. Patients with coronary heart disease or congestive heart failure are more prone to develop tachyarrhythmias, myocardial ischemia, or myocardial infarction during therapy with catecholamine vasopressors. Owing to a reduced arrhythmogenic threshold in the elderly, catecholamine-induced tachyarrhythmias occur at much lower doses in older patients than in younger ones. Moreover, the α-receptor-mediated increase in pulmonary vascular resistance may significantly impair right heart function in patients suffering from chronic pulmonary hypertension or right ventricular failure. If fluids and inotropic therapy fail to restore normovolemia and sufficient cardiac output, complications caused by catecholamine vasopressor therapy may occur sooner and with greater severity than would otherwise be the case. In this circumstance, catecholamine vasopressors may produce tissue hypoxia by aggravating peripheral vasoconstriction and significantly interfering with vital organ perfusion. Thus, ensuring adequate cardiac output with fluids and inotropic support is the mainstay of cardiovascular therapy, before initiating any vasopressor treatment.

Implications Adverse effects of high-dose catecholamine therapy substantially alter the risk-benefit ratio of any vasopressor therapy. Further, they increase the risk for adverse perioperative outcomes. Especially in elderly patients and those with cardiac dysfunction, catecholamine-induced tachycardia may significantly increase myocardial oxygen demand, thereby causing ischemia or myocardial infarction. Vasopressor-induced increased myocardial oxygen consumption not only compromises oxygen availability but also significantly reduces cardiac output and systemic oxygen delivery.

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Chapter 2

Vasopressors: Vasoconstrictor Drugs

9

of new tachyarrhythmias (8.3%) compared with high-dose norepinephrine alone (54.3%). Although arginine vasopressin has no antiarrhythmic activity by itself, adding it to high-dose norepinephrine in patients with advanced vasodilatory shock after cardiopulmonary bypass can significantly reduce norepinephrine needs and facilitate spontaneous conversion of about 50% of new-onset tachyarrhythmias independent of antiarrhythmic therapy. In contrast to high-dose norepinephrine, the significantly lower heart rates after arginine vasopressin therapy in patients with advanced vasodilatory shock can substantially reduce myocardial oxygen demand. There is now evidence of improved myocardial performance with norepinephrine–arginine vasopressin, likely owing to the reduced need for norepinephrine. Adverse effects of arginine vasopressin include possible deterioration of hepatic function and reduced platelet counts; however, reduced platelet counts do not appear to lead to increased clinical bleeding. Effects of arginine vasopressin on gastrointestinal blood flow have been inadequately studied. Although some authorities fear gastrointestinal hypoperfusion, there is evidence that arginine vasopressin may actually improve gastrointestinal perfusion when given continuously at doses of 4 units/hour in patients with advanced vasodilatory shock. At present, because there are no data supporting a beneficial effect on patient outcomes with the administration of supplementary arginine vasopressin in cases of advanced vasodilatory shock, its use with catecholamine vasopressors to reduce the latter’s toxicity can be advised only as a last resort.

MANAGEMENT If vasopressors are not necessary, do not use them. However, do assure normovolemia and adequate inotropic therapy. If cardiac output is still inadequate, administer catecholamine vasopressors in the lowest possible doses. In patients with significant cardiovascular dysfunction, even this may not be possible. If this is the case, symptomatic therapy, such as that for new-onset tachyarrhythmias, is the only therapy for catecholamine-induced complications. Striking recent evidence suggests that supraphysiologic doses of hydrocortisone (200 to 300 mg/day) not only significantly improve cardiovascular function and reduce catecholamine requirements but also reduce mortality in patients with septic shock. Possible mechanisms include relief of relative adrenal insufficiency as well as unspecific, permissive effects leading to up-regulation of adrenergic receptors. Also, hydrocortisone may favorably alter several pathophysiologically relevant inflammatory pathways that contribute to cardiovascular failure. Adverse hydrocortisone effects appear to occur independent of the dosage used and include hypernatremia and hyperglycemia. It is unknown whether hydrocortisone-mediated immune modulation or aggravation of catabolic metabolism is clinically relevant. Arginine vasopressin is used as a supplementary vasopressor in the treatment of advanced vasodilatory shock. Several studies show that continuous arginine vasopressin (4 units/hour) significantly improves hemodynamic variables and reduces catecholamine vasopressor requirements. In these cases, combined arginine vasopressin–norepinephrine infusion leads to a significant reduction in the incidence

PREVENTION Assurance of adequate volume and inotropic therapy to guarantee sufficient cardiac output are the most important preventive measures to avoid catecholamine vasopressormediated complications. Infusion of high dosages of hydrocortisone may reduce the need for high-dose norepinephrine therapy and thus reduce catecholamine-associated complications. Also, recent evidence suggests that a supplementary continuous infusion of arginine vasopressin (4 units/hour) might contribute to improved hemodynamic stability, fewer norepinephrine-related complications, and higher survival rates, but only when started before norepinephrine doses exceed 0.6 μg/kg per minute.

Further Reading Annane D, Sebille V, Charpentier C, et al: Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. JAMA 288:862-871, 2002. Dellinger RP: Cardiovascular management of septic shock. Crit Care Med 31:946-955, 2003. Dunser MW, Mayr AJ, Ulmer H, et al: Arginine vasopressin in advanced vasodilatory shock: A prospective, randomized, controlled study. Circulation 107:2313-2319, 2003. Heyndrickx GR, Boettcher DH, Vatner SF: Effects of angiotensin, vasopressin, and methoxamine on cardiac function and blood flow distribution in conscious dogs. Am J Physiol 231:1579-1587, 1976. James JH, Luchette FA, McCarter FD, Fischer JE: Lactate is an unreliable indicator of tissue hypoxia in injury or sepsis. Lancet 354:505-508, 1999.

PHARMACOLOGY

Catecholamine-induced tachyarrhythmias may further aggravate myocardial ischemia. In particular, the development of atrial fibrillation with a rapid ventricular response—the most common tachyarrhythmia with catecholamine therapy— exacerbates cardiovascular dysfunction due to a loss of atrial transport function and reduced ventricular filling. This can cause a substantial reduction in cardiac output, with a subsequent backward increase in pulmonary vascular resistance, leading to right ventricular failure and further deterioration of cardiovascular function. Reduced hepatic, splanchnic, or intestinal mucosal oxygen delivery with prolonged epinephrine or dopamine infusions can increase organ damage, facilitate endotoxin production, and exacerbate systemic inflammation and multiple organ dysfunction. Arterial lactate concentrations correlate with patient outcome, because hyperlactatemia may increase perioperative mortality irrespective of metabolic acidosis. Moreover, elevated serum glucose concentrations significantly contribute to adverse patient outcomes, especially among the critically ill. Theoretically, catecholamine-induced hypercoagulability may facilitate thrombus formation at the microcirculatory level, thus precipitating multiorgan system damage; however, there is no clinical evidence of this. Such hypercoagulability may also facilitate the evolution of perioperative myocardial infarction. Further, it is unknown whether adrenergic vasopressor-mediated immune modulation influences immune responses in the perioperative setting.

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Lorton D, Lubahn C, Bellinger DL: Potential use of drugs that target neuralimmune pathways in the treatment of rheumatoid arthritis and other autoimmune diseases. Curr Drug Targets Inflamm Allergy 2:1-30, 2003. Luckner G, Dunser MW, Jochberger S, et al: Arginine vasopressin in 316 patients with advanced vasodilatory shock. Crit Care Med 33:2659-2666, 2005. Maestroni GJ, Mazzola P: Langerhans cells beta 2-adrenoceptors: Role in migration, cytokine production, Th priming and contact hypersensitivity. J Neuroimmunol 144:91-99, 2003. Marik PE, Varon J: The hemodynamic derangements in sepsis: Implications for treatment strategies. Chest 114:854-860, 1998. Meier-Hellmann A, Reinhart K, Bredle DL, et al: Epinephrine impairs splanchnic perfusion in septic shock. Crit Care Med 25:399-404, 1997. Practice parameters for hemodynamic support of sepsis in adult patients in sepsis. Task Force of the American College of Critical Care

Medicine, Society of Critical Care Medicine. Crit Care Med 27: 639-660, 1999. Rudis MI, Basha MA, Zarowitz BJ: Is it time to reposition vasopressors and inotropes in sepsis? Crit Care Med 24:525-537, 1996. Schutz W, Anhaupl T, Gauss A: Principles of catecholamine therapy. 1. Characterization of clinically relevant sympathomimetics. Anasthesiol Intensivmed Notfallmed Schmerzther 35:67-81, 2000. Trager K, DeBacker D, Radermacher P: Metabolic alterations in sepsis and vasoactive drug-related metabolic effects. Curr Opin Crit Care 9:271-278, 2003. van den Berghe G, Wouters P, Weekers F, et al: Intensive insulin therapy in the critically ill patient. N Engl J Med 345:1359-1367, 2001. Zhang H, De Jongh R, DeBacker D, et al: Effects of alpha- and beta-adrenergic stimulation on hepatosplanchnic perfusion and oxygen extraction in endotoxic shock. Crit Care Med 29:581-588, 2001.

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Krishna M. Natrajan and Ray P. Liao

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3

Inotropic Drugs Case Synopsis A 72-year-old man with mitral regurgitation has mitral valve replacement. His preoperative transesophageal echocardiogram (TEE) reveals reduced left ventricular function and moderate pulmonary hypertension. Just before separation from cardiopulmonary bypass (CPB), a 50 μg/kg bolus of milrinone is given, followed by an infusion at 0.5 μg/kg per minute, along with epinephrine at 0.03 μg/kg per minute. The TEE reveals good left ventricular function with adequate filling after release of the aortic cross-clamp, but the patient cannot be weaned from CPB owing to low mean arterial pressure. Pulmonary artery catheter data show a cardiac index of 2.8 L/min/m2 and systemic vascular resistance of 550 dyne . sec . cm–5. The addition of vasopressin (4 units/hour) enables weaning from CPB, after which the heart rate is 94 beats per minute and the mean arterial pressure is 72 mm Hg.

PROBLEM ANALYSIS Definition Inotropic drugs (Table 3-1) are classified as (1) naturally occurring catecholamines (e.g., dopamine, epinephrine, norepinephrine), (2) synthetic catecholamines (e.g., dobutamine, isoproterenol), or (3) phosphodiesterase-3 inhibitors (e.g., amrinone, milrinone). They are commonly administered solely or used in combination to treat low-output syndromes that are frequently encountered in congestive heart failure and myocardial infarction and following openheart surgery. The primary effect of inotropic drugs is to increase contractility, which ultimately increases cardiac output and promotes tissue perfusion.

Recognition The case synopsis illustrates the need to tailor appropriate therapy. Depressed left ventricular function with elevated pulmonary artery pressure suggests the need for inotropic

Table 3–1

■

Inotropic Drugs

Digitalis Digoxin Digitoxin Ouabain Catecholamines Natural Epinephrine Norepinephrine Dopamine Synthetic Dobutamine Dopexamine Isoproterenol Synthetic noncatecholamines Indirect acting Ephedrine

Mephentermine Amphetamines Metaraminol Direct acting Phenylephrine Methoxamine Phosphodiesterase-3 inhibitors Amrinone Milrinone Enoximone Miscellaneous Calcium Glucagon Thyroid hormone

support, but with a drug that does not increase pulmonary vascular resistance (PVR). Milrinone is one option because it increases cardiac output and lowers PVR. However, it also significantly lowers systemic vascular resistance (SVR), which can jeopardize perfusion of the heart and other vital organs. Reduced SVR with milrinone may require therapy with a vasopressor, such as norepinephrine, epinephrine, phenylephrine, or vasopressin. Notably, vasopressin increases SVR without increasing pulmonary artery pressure.

Risk Assessment The primary goal of inotropic drugs is to improve myocardial contractility and increase cardiac output, vital organ perfusion, and tissue oxygen delivery (Table 3-2). However, these drugs have other effects that can be useful or problematic, depending on the circumstances. Their effects on SVR are important and can be used to divide the drugs into two groups: vasoconstrictors (epinephrine, norepinephrine, dopamine) and vasodilators (dobutamine, isoproterenol, milrinone). Epinephrine and norepinephrine are naturally occurring catecholamines used in cardiac emergencies. The inotropic and vasoconstrictive responses are mediated by the activation of adrenergic receptors. The effects of these drugs can be titrated to the desired level owing to their linear dose response, rapid (almost immediate) onset of action, and fast elimination. Dopamine is another inotrope with vasoconstrictive properties. Its positive inotropic effect is mediated by the release of norepinephrine from nerve terminals. Dopamine’s pharmacodynamic effect is dose dependent, and the hemodynamic profile with low, medium, and high doses can vary greatly among individuals, with higher doses commonly producing an increase in SVR. Dopamine has the theoretical advantage of selective renal and mesenteric vascular dilatation, thus enhancing renal blood flow and natriuresis while preventing mesenteric ischemia in low cardiac output states. However, the clinical value of this effect remains uncertain. Isoproterenol and its chemical derivative dobutamine are vasodilators. They act directly on β-adrenergic receptors 11

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Hemodynamic Profile of Inotropic Drugs

Drug

CO

HR

MAP

VR

SVR

PVR

MCO

Epinephrine Norepinephrine Dopamine Dobutamine Isoproterenol Milrinone

↑↑↑ ↑↑ ↑↑ ↑↑ ↑↑ ↑↑

↑↑↑ ↑↑ ↑↑ ↑↑ ↑↑↑ ←→

↑ ↑↑ ↑ ↓ ↓↓ ↓↓

↑ ↑↑↑ ↑ ↓ ↓ ↓↓

↑↑↑ ↑↑↑ ↑↑ ↓ ↓↓↓ ↓↓↓

↑ ↑↑ ↑↑ ↓↓ ↓↓ ↓↓↓

↑↑↑ ↑↑↑ ↑↑ ↑↑ ↑↑↑ ←→

CO, cardiac output; HR, heart rate; MAP, mean arterial pressure; MCO, myocardial oxygen consumption; PVR, pulmonary vascular resistance; SVR, systemic vascular resistance; VR, venous return (preload). ↑, increase; ↓, decrease; ←→, unchanged.

to cause a positive inotropic response while decreasing SVR. Hypotension resulting from their use may require treatment with vasoconstrictors. Milrinone is a phosphodiesterase-3 inhibitor and prevents cyclic adenosine monophosphate (cAMP) degradation. It increases myocardial contractility in a linear doseresponse relationship without increasing myocardial oxygen consumption. The onset of action is slower than that of catecholamines, and its elimination half-life is longer, causing a prolonged duration of effect. Rapid administration produces vascular smooth muscle relaxation to reduce SVR and venous return. This can lead to hypotension, especially in hypovolemic patients. Concomitant use of volume loading and vasoconstrictors (e.g., phenylephrine, epinephrine, norepinephrine, vasopressin) attenuates milrinone’s potential for vasodilatation and hypotension. These inotropes are routinely used to treat the low cardiac output states often seen after CPB. The unique hemodynamic profile of each agent needs to be considered when deciding which inotrope, alone or in combination, will best facilitate a particular patient’s separation from CPB.

Implications Low cardiac output and hypotension following separation from CPB can reduce tissue perfusion and lead to vital organ dysfunction. The use of hemodynamic parameters and TEE identifies its cause. Treatment must be prompt and may require the administration of combined inotropes. The use of inotropes with vasodilator properties may necessitate the addition of a vasoconstrictor. Of the available vasoconstricting agents, vasopressin has the advantage of not increasing PVR. Arrhythmias resulting from inotropes can occur and should be monitored closely.

CPB is often complicated by post-CPB low cardiac output states that require inotropic support. Combined epinephrine and milrinone, which have different actions, increase cardiac contractility better than either agent alone. Epinephrine increases the formation of cAMP by activating adrenergic receptors, while milrinone reduces the rate of cAMP degradation by inhibiting the phosphodiesterase-3 enzyme. The cardiovascular actions and other effects of each of these drugs must be taken into consideration. At low doses, epinephrine has predominant β-adrenergic actions: positive inotropy and chronotropy. Milrinone is also a positive inotrope, and a systemic and pulmonary arterial vasodilator as well. A reduction in PVR may benefit patients with pulmonary artery hypertension. However, reduced SVR and systemic hypotension may require substantial volume loading and use of a vasoconstrictor, such as vasopressin, which has minimal effects on the pulmonary and splanchnic vasculature. Also, a reduction in either PVR or SVR may lead to a reflex increase in heart rate, mediated by pulmonary mechanoreceptors or aortic barorecptors, respectively. Phosphodiesterase-3 inhibitors (e.g., amrinone) have been associated with thrombocytopenia, possibly due to a metabolite-mediated toxic effect on platelets. However, milrinone appears to have a better safety profile. Further, like all positive inotropic agents, milrinone and epinephrine have the potential to initiate or aggravate troublesome arrhythmias. Causative or provocative factors, such as a concurrent physiologic imbalance and (perhaps) even the inotrope itself, must be quickly identified and corrected before significant hemodynamic compromise occurs.

PREVENTION ● ●

MANAGEMENT ●

●

●

●

TEE to assess left ventricular filling and function and maintain adequate preload and afterload Careful titration of inotropes to achieve adequate cardiac output and arterial pressure Vasoconstrictors as needed for low perfusion pressure due to vasodilator effects of inotropes Prompt correction of acid-base and electrolyte abnormalities

●

Ensure adequate preload and afterload Normalize metabolic parameters Titrate inotropic drugs precisely

TEE to assess left ventricular filling and function, preload, and afterload is often useful when weaning patients from CPB. Volume depletion should be corrected by the judicious use of fluids or blood products. It is also important to correct metabolic abnormalities, especially acidosis and hypokalemia. Inotropic support is commonly necessary for separation from CPB. The choice of inotropic agent or agents depends on surgical and patient factors. Precise titration of

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Further Reading Lehtonen LA, Antila S, Pentikainen PJ: Pharmacokinetics and pharmacodynamics of intravenous inotropic agents. Clin Pharmacokinet 43: 187-203, 2004.

Inotropic Drugs

13

Levy JH, Bailey JM, Deeb GM: Intravenous milrinone in cardiac surgery. Ann Thorac Surg 73:325-330, 2002. Stoelting RK: Sympathomimetics: Pharmacology and Physiology in Anesthetic Practice, 3rd ed. Philadelphia, JB Lippincott, 1999, pp 259-277. Tisdale JE, Patel R, Webb CR, et al: Electrophysiologic and proarrhythmic effects of intravenous inotropic agents. Prog Cardiovasc Dis 38: 167-180, 1995.

PHARMACOLOGY

inotropic drugs is needed, especially when several drugs are used in combination.

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Chronotropic Drugs Cyrus DeSouza

4

Case Synopsis Five years after heart transplantation, a 44-year-old man has laparoscopic cholecystectomy. After induction of anesthesia, the electrocardiogram (ECG) rhythm strip shows absent P waves and a wide QRS rhythm at a rate of 38 beats per minute (Fig. 4-1). Neither intravenous (IV) atropine (1.0 mg) nor ephedrine (10 mg) affects the rhythm or increases its rate. IV bolus epinephrine (200 μg) is given, followed by an IV infusion at 0.25 μg/kg per minute. The heart rate increases to 130 beats per minute, accompanied by frequent ventricular ectopic beats.

PROBLEM ANALYSIS Definition Epinephrine and other positive chronotropes, especially when given in large doses, can have deleterious effects in patients with cardiovascular disease. These effects include the following: ● ● ●

Untoward tachycardia and hypertension Generation of new or worse atrial or ventricular arrhythmias Increased myocardial oxygen consumption and ischemia due to increased heart rate and contractility and left ventricular wall stress

As the case synopsis illustrates, the effects in cardiac transplant patients are even more unpredictable or may be nonexistent owing to cardiac denervation. Consequently, only drugs that act directly on cardiac receptors should be used. Drugs such as atropine and ephedrine may be ineffective or unpredictable because they act indirectly to increase heart rate. Moreover, coronary atherosclerosis can occur in transplant recipients, with an incidence of up to 50% at 5 years. Without cardiac afferent innervation, ischemia in heart transplant recipients may be silent.

Recognition Bradycardia with absent P waves on the ECG can have many causes, including the following: ●

● ● ●

Sinoatrial (SA) exit block, sinus arrest, or sick sinus syndrome Atrioventricular (AV) junctional rhythm Idioventricular rhythm Slow atrial fibrillation or flutter

Also, P waves may be “buried” within the QRS complex with AV dissociation, such as in advanced second degree or third degree (complete) AV heart block. With third degree SA exit block, P waves are absent or have an altered morphology if a subsidiary atrial pacemaker has usurped atrial control. If so, they will be bifid, inverted, or flattened in leads with SA node origin (upright) P waves. On the surface ECG, third degree SA exit block is indistinguishable from sinus arrest. A subsidiary atrial, junctional, or ventricular pacemaker usually usurps ventricular control. Third degree SA exit block is distinguished from third degree AV block, which has the following features on ECG: ● ●

●

P waves present but with no relation to QRS complexes QRS complexes wide (ventricular origin or with ventricular aberration) or of normal width (AV junctional origin above bifurcation of bundle of His [common]) Slow ventricular escape rate (≈30 to 45 beats per minute)

Intraoperative bradycardia that is severe or that compromises the patient’s cardiac output or blood pressure must be treated aggressively. Assessment for reversible causes is important (Fig. 4-2) and must occur simultaneously with treatment. Temporary pacing and drug therapy are the two main options. Two different classes of drugs are commonly used to increase the heart rate: anticholinergics (e.g., atropine, glycopyrrolate) and adrenergic receptor agonists (e.g., ephedrine, epinephrine, isoproterenol, dopamine). Direct adrenergic agonists are more reliable than ephedrine. Isoproterenol is a nonselective β agonist with chronotropic, inotropic, and vasodilatory effects. It is usually recommended to treat bradycardia after heart transplantation, but care must be exercised in the presence of coronary artery disease. Isoproterenol increases myocardial osygen consumption and may reduce coronary perfusion pressure, worsening ischemia. Thus, isoproterenol is no longer part of

Figure 4–1 ■ Bradycardia and absent P waves with ventricular escape rhythm. (From Conover MB: Understanding Electrocardiography, 8th ed. St. Louis, Mosby, 2003.)

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Chronotropic Drugs

15 PHARMACOLOGY

Figure 4–2 ■ Algorithm for the management of intraoperative bradycardia. AV, atrioventricular. (Modified from Guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care. Part 6: Advanced cardiovascular life support. Section 7: Algorithm approach to ACLS emergencies. 7C: A guide to the international ACLS algorithms. Circulation 102 [8 Suppl]: I142-I157, 2000.)

the advanced cardiovascular life support algorithms for the emergency treatment of bradycardia. The side effects of atropine are as follows: ● ● ● ●

Excessive tachycardia; arrhythmias Pupillary dilatation, blurred vision, dry mouth Difficulty in micturition; decreased intestinal peristalsis Central anticholinergic crisis (e.g., ataxia, restlessness, delirium, coma) (This cannot occur with glycopyrrolate because it does not cross the blood-brain barrier.)

Atropine is ineffective in heart transplant patients owing to the lack of vagal innervation. In fact, in some cases, it may provoke bradyarrhythmias. Ephedrine acts predominantly by a presynaptic mechanism (i.e., indirect release of catecholamines) and may be unpredictable or ineffective owing to cardiac sympathetic denervation in heart transplant recipients. However, it offers some protection against many reflex-mediated causes of bradycardia and produces a high resting heart rate. Bradyarrhythmias occurring late

after heart transplantation, without an obvious reversible cause, may be a sign of ischemia or chronic rejection.

Risk Assessment ●

●

●

Heart transplant patients have denervated hearts and are prone to accelerated coronary vasculopathy. Effects of chronotropic drugs are unpredictable or nonexistent owing to cardiac denervation in heart transient recipients. Epinephrine can exacerbate ischemia by causing tachycardia, hypertension, increased contractility, and arrhythmias in patients with intact hearts, whether diseased or not.

Epinephrine is given as an IV bolus or infusion in emergencies. Typical starting infusion rates are 0.03 to 0.2 μg/kg per minute, with titration to the desired effect. The goal should be to restore the heart rate to greater than 60 beats per minute while avoiding excess tachycardia.

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However, temporary pacing is often the preferred treatment for nontransient, severe bradycardia and can be rapidly instituted via the noninvasive transcutaneous or transesophageal (atrial pacing only; requires intact AV conduction) route. Pacing is more predictable (i.e., precision titration of rate, can be turned “on” or “off ” as needed) than treatment with positive chronotropic drugs, which have the following disadvantages: ● ●

● ●

May cause excess tachycardia or arrhythmias May cause myocardial ischemia or decompensation (i.e., heart failure) May take time or fail to produce the desired effect May produce adverse drug effects that are compounded by the drugs used to treat them

Implications Tachycardia associated with severe ventricular ectopy must be treated urgently, because it may degenerate into ventricular tachycardia-fibrillation. Also, the potential for myocardial ischemia exists if myocardial oxygen consumption exceeds demand.

MANAGEMENT ●

● ●

Cease the epinephrine infusion and allow its plasma concentration to decrease. Prepare for temporary pacing if the bradycardia recurs. Assess for reversible causes of intraoperative bradycardia (see Fig. 4-2).

Low-dose epinephrine infusions may restore the heart rate without adverse effects. If drug therapy is ineffective, is contraindicated, or causes complications, pacing should be instituted. Temporary transcutaneous pacing is a class I therapy for the emergency treatment of severe bradycardia. If available, transesophageal atrial pacing is useful (with intact AV conduction). Arrangements should be made for the insertion of a temporary pacing pulmonary artery catheter or transvenous pacing catheter.

PREVENTION ●

●

Suspect coronary artery disease in heart transplant recipients more than 2 years post transplant. Recognize the implications of cardiac denervation for treating bradycardia with drugs.

●

●

●

Anticipate and avoid common reversible causes of intraoperative bradycardia. Avoid high doses of chronotropic drugs by carefully titrating smaller doses to effect. Use temporary pacing for severe bradycardia or when drugs fail.

Careful preoperative evaluation is important to identify patients at increased risk for bradycardia. Pretreatment with a chronotrope and avoidance of known causes of bradycardia may prevent tachycardia or arrhythmias from occurring. In some cases, pacing therapy is required preoperatively, depending on the underlying rhythm (e.g., advanced second degree or complete AV heart block). There are special considerations for heart transplant recipients who develop intraoperative bradycardia.

Further Reading Atlee JL, Pattison CZ, Mathews EL, et al: Transesophageal atrial pacing for intraoperative sinus bradycardia or AV junctional rhythm: Feasibility as prophylaxis in 200 anesthetized adults and hemodynamic effects of treatment. J Cardiothorac Vasc Anesth 7:436-441, 1993. Bernheim A, Fatio R, Kiowski W, et al: Atropine often results in complete atrioventricular block or sinus arrest after cardiac transplantation: An unpredictable and dose-independent phenomenon. Transplantation 77:1181-1185, 2004. Brawn JH, Taylor P: Muscarinic receptor agonists and antagonists. In Hardman JG, Limbird LE (eds): Goodman and Gilman’s The Pharmacological Basis of Therapeutics, 10th ed. New York, McGrawHill, 2001, pp 155-174. Conover MB: Understanding Electrocardiography, 7th ed. St. Louis, Mosby, 1996. Gao SZ, Schroeder JS, Alderman EL, et al: Prevalence of accelerated coronary artery disease in heart transplant survivors: Comparison of cyclosporine and azathioprine regimens. Circulation 80:100-105, 1989. Guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care. Part 6: Advanced cardiovascular life support. Section 5: Pharmacology. I: Agents for arrhythmias. Circulation 102 (8 Suppl): I112-I128, 2000. Guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care. Part 6: Advanced cardiovascular life support. Section 7: Algorithm approach to ACLS emergencies. 7C: A guide to the international ACLS algorithms. Circulation 102(8 Suppl):I142-I157, 2000. Hoffman BB: Catecholamines, sympathomimetic drugs, and adrenergic receptor antagonists. In Hardman JG, Limbird LE (eds): Goodman and Gilman’s The Pharmacological Basis of Therapeutics, 10th ed. New York, McGraw-Hill, 2001, pp 215-268. Quinlan JJ, Firestone S, Firestone LL: Anesthesia for heart, lung, and heartlung transplantation. In Kaplan JA, Reich DL, Konstadt SN (eds): Cardiac Anesthesia, 4th ed. Philadelphia, WB Saunders, 1999. Weinfeld MS, Kartashov A, Piana R, et al: Bradycardia: A late complication following cardiac transplantation. Am J Cardiol 78:969-971, 1996.

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5

Drugs Affecting the Renin-Angiotensin System Laura Stover Case Synopsis A 95-kg, 70-year-old man is scheduled to have left internal carotid endarterectomy. He takes nicardipine (50 mg/day) and irbesartan (150 mg/day), an angiotensin II receptor antagonist, for hypertension. He took his usual doses of both medications on the morning of surgery. Preoperative tests included a transthoracic echocardiogram that showed normal left ventricular systolic function and septal hypertrophy. Blood pressure and heart rate immediately before induction of anesthesia were 150/70 mm Hg and 56 beats per minute, respectively. After receiving 900 mL of crystalloid, he was induced slowly with sufentanil (45 μg), propofol (140 mg), and vecuronium (7 mg), with subsequent endotracheal intubation and anesthetic maintenance with oxygen and nitrous oxide (50:50) and a propofol infusion. Three minutes after induction, his blood pressure fell to 92/44 mm Hg. Despite repeated intravenous boluses of ephedrine (20 mg total), his blood pressure was 47/30 mm Hg 5 minutes after induction.

PROBLEM ANALYSIS Definition Renin-angiotensin system (RAS) antagonists include both angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor antagonists. These drugs are used with increasing frequency to treat hypertension and heart failure in selected patients. ACE inhibitors and angiotensin II receptor antagonists cause a blockage of the RAS that can adversely affect hemodynamics during anesthesia and surgery. Although anesthesia is not invariably associated with hemodynamic instability in RAS-blocked patients, unexpected episodes of refractory hypotension have been reported. Also, RAS antagonists, specifically ACE inhibitors, have been associated with potentially life-threatening angioedema of the head and neck. The RAS plays an essential role in the regulation of vascular tone and extracellular fluid volume. As shown in Figure 5-1, sympathetic stimulation via β1-adrenergic receptors, renal artery hypotension, and decreased sodium delivery to the distal tubules stimulate the release of renin by the kidney. Renin is a proteolytic enzyme that cleaves to the circulating substrate angiotensinogen to form angiotensin I, which has little intrinsic pharmacologic activity. Angiotensin I is converted immediately to angiotensin II via a reaction catalyzed by ACE, which is present in vascular endothelium and lung tissue. In the short term (e.g., intraoperatively), angiotensin II contributes to vascular homeostasis by increasing vascular (especially arteriolar) tone. It acts directly on angiotensin II receptors and indirectly by enhancing sympathetic adrenergic function to increase vascular tone, which is necessary to maintain adequate perfusion pressure in patients with hypovolemia or reduced cardiac output. In the longer term (e.g., hours to days), angiotensin II contributes to vascular

homeostasis by its effect on extracellular fluid volume. It causes the adrenal cortex to release aldosterone, a hormone that acts on the kidneys to increase sodium and fluid retention. Angiotensin II also stimulates the release of vasopressin (i.e., antidiuretic hormone) from the posterior pituitary, which causes the kidneys to increase fluid retention. Blocking angiotensin II–mediated increased vascular tone and relative reductions in intravascular volume in patients receiving RAS antagonists chronically may cause refractory hypotension following the induction of anesthesia. Angioedema of the oropharynx or larynx has been recognized as an unusual complication of ACE inhibitor therapy. ACE-induced angioedema usually manifests spontaneously within hours to days of the initiation of treatment and has been described in association with anesthesia and Sympathetic stimulation Hypotension Decreased sodium delivery Angiotensinogen

Kidneys

Renin

Angiotensin I

Cardiac and vascular hypertrophy

ACE

Adrenal cortex

Angiotensin II

Pituitary

Aldosterone

ADH Thirst Systemic vasoconstriction

Renal sodium and fluid retention

Increased blood volume

Figure 5–1 ■ The renin-angiotensin system. ACE, angiotensin-converting enzyme; ADH, antidiuretic hormone.

17

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endotracheal intubation. Edema of the tongue is commonly the presenting symptom, with involvement of the face, lips, floor of the mouth, pharynx, glottis, or larynx frequently observed. The precise mechanism of angioedema formation is uncertain. Because it is likely mediated by the kallikreinbradykinin system, it is probably a biochemical rather than an immunologic phenomenon. Bradykinin is a potent vasodilator that increases vascular permeability and produces tissue edema. Kinase II (which is identical to ACE) is the major tissue enzyme responsible for the breakdown of bradykinin. ACE inhibitors inhibit kinase II to prevent bradykinin breakdown. Angioedema associated with ACE inhibitor therapy may therefore be a result of inhibition of bradykinin inactivation by kinase II.

Recognition HYPOTENSION Recognition of RAS antagonist therapy as a contributor to hypotension relies on the exclusion of other intraoperative events that may produce hypotension. A heightened index of suspicion in patients chronically treated with these drugs, especially those with a history of severe hypotension or left ventricular diastolic dysfunction, is justified. The temporal relationship between cardiovascular instability and induction of anesthesia in patients chronically treated with RAS antagonists, along with the failure of ephedrine in usual doses (10 to 20 mg IV in adult patients) to resolve the hypotension, makes RAS antagonism a likely cause of hypotension. ANGIOEDEMA Recognition of ACE inhibition as the cause of angioedema relies on the exclusion of other perioperative events associated with swelling of the head and neck (e.g., allergy, anaphylaxis), as well as the knowledge that angioedema can occur (though infrequently) with ACE inhibitors. When it does occur, angioedema is usually temporally related to the initiation of ACE inhibitor therapy.

Risk Assessment HYPOTENSION A number of patient factors modify the risk of severe hypotension with the induction of anesthesia in those treated with RAS antagonists. Patients treated with other antihypertensive agents in combination with a RAS antagonist are more likely to have refractory hypotension on induction. Likewise, the combination of RAS antagonists and other vasodilator drugs (e.g., amiodarone) increases the risk for hypotension. Patients with “complete” RAS blockade, which is associated with high doses and recent administration, are more likely to be unstable on induction. Patients with a history of severe hypertension, especially those with left ventricular diastolic dysfunction (which amplifies the dependence of blood pressure on intravascular volume in patients receiving ACE inhibitors), are also at increased risk for refractory hypotension. Short-term preoperative RAS inhibition (1 to 2 days) in normotensive or mildly hypertensive subjects

is less likely to result in refractory hypotension on induction. Patients who continue therapy until the day of surgery are also at increased risk. One review found that the incidence of hypotension on induction of anesthesia in patients with a history of severe hypertension was 75% to 100% when ACE inhibitors were continued until the day of surgery. ANGIOEDEMA Angioedema involving the oropharynx or larynx is an unusual complication of ACE inhibitor therapy, occurring on average in 0.1% of patients taking captopril, lisinopril, or enalapril; the incidence in patients taking enalapril may be slightly higher (0.2%) than in those taking the other two drugs. Patients are at highest risk within the first week of starting an ACE inhibitor; a retrospective study of 36,000 patients receiving enalapril showed that 60% to 70% of cases of angioedema occurred within this period. However, angioedema has occurred suddenly after months to years of therapy, and about 20% of known cases of angioedema occurring in this context may involve severe symptoms (e.g., dyspnea, stridor, laryngospasm). Unfortunately, there are no characteristics to predict which patients will progress to lifethreatening airway compromise.

Implications Concerning the risk for refractory hypotension on induction of anesthesia in patients taking RAS antagonists, there is no consensus on continuing or discontinuing the drug in the immediate preoperative period. For this class of drugs, the elimination half-life does not necessarily predict the duration of action, making recommendations with respect to perioperative dosing difficult.

MANAGEMENT Hypotension If RAS blockade contributes significantly to refractory hypotension after induction of anesthesia, therapy relies on the prompt restoration of adequate systemic vascular resistance and venous tone1 with phenylephrine or vasopressin, as well as increased intravenous fluid administration. Remedial actions for managing hypotension related to RAS antagonists include discontinuing or reducing the dose of other agents that might contribute to hypotension. Advanced cardiovascular life support protocols should be invoked in the event of cardiovascular collapse.

Angioedema Most occurrences of ACE inhibitor–induced angioedema are mild and resolve spontaneously or with discontinuation of the drug. However, swelling may progress rapidly to include the posterior pharynx or larynx, causing partial or complete 1 Venoconstriction (venous capacitance bed) indirectly increases venous return and preload.

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time to allow the return of RAS activity. However, any risk reduction might be at the expense of optimal therapy for hypertension or heart failure. Identifying patients at the greatest risk for severe hypotension (those with severe hypertension or those receiving high doses of RAS antagonists, RAS antagonists in combination with other antihypertensives, or RAS antagonists chronically), along with intravenous fluid loading before the induction of anesthesia, may reduce the risk for refractory hypotension. Such pretreatment combined with the early use of vasopressors for hypotension believed to be caused by RAS blockade will shorten the duration of hypotension. Consistent with the foregoing, frequent blood pressure measurement immediately after induction (direct arterial pressure monitoring may be necessary) contributes to the earlier detection of severe hypotension.

Further Reading PREVENTION As noted earlier, there is no consensus regarding the management of patients receiving RAS antagonist therapy in the immediate preoperative period. Discontinuation of RAS antagonists during this period reduces the risk for hypotension with anesthesia induction, provided there is sufficient

Colson P, Ryckwaert F, Coriat P: Renin angiotensin antagonists and anesthesia. Anesth Analg 89:1143-1155, 1999. Dean DE, Schultz DL, Powers RH: Asphyxia due to angiotensin converting enzyme (ACE) inhibitor mediated angioedema of the tongue during the treatment of hypertensive heart disease. J Forensic Sci 46: 1239-1243, 2001. Kharash ED: Angiotensin-converting enzyme inhibitor–induced angioedema associated with endotracheal intubation. Anesth Analg 74:602-604, 1992.

PHARMACOLOGY

upper airway obstruction. The symptoms may progress despite aggressive therapy and may recur hours after apparent resolution. Angioedema caused by ACE inhibitors can be fatal. Management ranges from simply stopping the ACE inhibitor to endotracheal intubation or tracheostomy. Mild cases confined to the anterior tongue or lips generally resolve with discontinuation of the drug and administration of intravenous diphenhydramine and corticosteroids. More severe cases involving the pharynx and associated with dysphagia may require subcutaneous epinephrine, tracheal intubation, or both. As with any evolving process involving the airway, the potential for life-threatening airway obstruction dictates close observation and prompt intervention. Following resolution of the acute process, a note should be made in the patient’s medical record of this potentially lifethreatening adverse reaction to ACE inhibitor therapy, and the patient should receive appropriate counseling.

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CARDIAC DRUGS

Phosphodiesterase Inhibitors

6

Gregory M. Janelle Case Synopsis A 56-year-old man presents for emergent repair of an open olecranon fracture sustained in a motorcycle accident. There are no other signs of trauma. His past medical history is significant for hypertension, dyslipidemia, gastroesophageal reflux disease, and a 40-pack-year history of tobacco use. His father died from a myocardial infarction at age 60. He has no allergies and denies alcohol or other illicit drug use. Medications prior to admission include atorvastatin, ramipril, and esomeprazole. Baseline vital signs include blood pressure, 148/74 mm Hg; heart rate, 86 beats per minute; and respiration, 18 breaths per minute and nonlabored. An electrocardiogram (ECG) in the emergency room shows normal sinus rhythm with no evidence of ischemic changes. The patient refuses regional anesthesia. Preoperative medications include midazolam 2 mg and sodium bicitrate 30 mL. After uneventful induction of general anesthesia (thiopental, fentanyl, and succinylcholine), anesthesia is continued with isoflurane. After surgical stimulation, the patient has hypertension (180/100 mm Hg) and tachycardia (115 beats per minute). Concomitantly, there is 2-mm downsloping ST depression in lead V5 of a calibrated, monitored ECG. The end-tidal isoflurane concentration is increased from 0.8% to 1.2%, and intravenous esmolol (20 mg) and sublingual nitroglycerin spray (0.4 mg × 2) are also given. Within minutes, the patient’s blood pressure drops to 60/40 mm Hg and his heart rate increases to 90 beats per minute. While treating this, the anesthesiologist has the circulating nurse call the patient’s wife to inquire about unreported drug use. He learns that the patient was taking sildenafil for erectile dysfunction along with his other medications.

PROBLEM ANALYSIS Definition Intraoperative myocardial ischemia is potentially life threatening, especially if it is not recognized and promptly treated. It demands utmost vigilance on the part of the anesthesiologist. Intraoperative ischemia is defined as ST deviation, relative to the preoperative, reference ECG, of 0.2 mV or greater in one lead or 0.1 mV or greater in two contiguous leads and lasting at least 10 minutes. Once ischemia is diagnosed, the anesthesiologist must identify and aggressively treat the cause. Based on this definition of intraoperative myocardial ischemia, the patient described in the case synopsis had at least demand ischemia and likely significant underlying coronary artery disease (CAD) as well. The case synopsis also illustrates that aggressive treatment of hypertension, tachycardia, and myocardial ischemia by increasing the end-tidal concentration of isoflurane, along with esmolol and sublingual nitroglycerin, can lead to profound hypotension in patients also taking phosphodiesterase-5 (PDE-5) inhibitors. This hypotension may further aggravate myocardial ischemia by reducing coronary perfusion pressure. In this case, the anesthesiologist was not expecting 20

the sudden, profound hypotension that resulted from his treatment, which was quite reasonable given the ECG evidence, the circulatory changes, and the patient’s past medical history. Unfortunately, the patient had failed to report his use of sildenafil. Only further (indirect) inquiry by an astute and knowledgeable anesthesiologist led to the discovery of the likely proximate cause of the patient’s hypotension. Sildenafil citrate is a highly selective PDE-5 inhibitor that interacts with organic nitrates such as nitroglycerin to potentiate vascular smooth muscle relaxation, with the potential to cause profound blood pressure reduction. For this reason, organic nitrates are contraindicated if sildenafil has been taken in the preceding 24 hours.

Recognition PDE-5 breaks down cyclic guanosine monophosphate (cGMP). Therefore, PDE-5 inhibitors such as sildenafil are expected to increase available cGMP. The formation of cGMP is stimulated by guanylate cyclase, which in turn is stimulated by nitric oxide (NO). Nitroglycerin is a potent NO donor, although its effects are more prominent in the venous capacitance bed, except in very high doses. Nonetheless, nitroglycerin does dilate epicardial coronary

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Risk Assessment Although the intraoperative hypotension experienced by the patient described in the case synopsis was probably due to an adverse interaction between nitroglycerin and the PDE-5 inhibitor sildenafil, intraoperative hypotension has many other causes unrelated to this interaction (Table 6-1) that are discussed elsewhere in this book. In addition, for this patient, increasing the end-tidal isoflurane concentration and giving intravenous esmolol compounded his hypotension. Refractory hypotension is also associated with angiotensin-converting enzyme (ACE) inhibitors and selective antagonists of angiotensin II receptors, such as olmesartan (see Chapter 5). Patients with preoperative sympathetic blockade or volume depletion due to fasting, blood loss, or diuretic therapy have a reduced venous capacitance. This reduces venous return and cardiac output and often compounds hypotension with the induction of anesthesia. For patients on ACE inhibitors, angiotensin II (a potent vasoconstrictor) does not counter such hypotension.

Table 6–1

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Causes of Intraoperative Hypotension Unrelated to Phosphodiesterase-5 and Nitroglycerin Interactions

Anesthetics (IV and volatile agents) Central neuraxial anesthesia (spinal, epidural) Myocardial ischemia and reperfusion injury Heart failure (systolic or diastolic) Cardiac rhythm disturbances Chronic adrenocortical insufficiency Overly aggressive use of diuretics Recent hemo- or peritoneal dialysis Volume depletion related to third-space loss Inadequate fluid resuscitation Severe hemorrhage; hemorrhagic shock Hemothorax; hemopericardium Reduced venous return secondary to caval compression Restrictive pericarditis; pericardial effusion Tumors compressing or restricting heart Tumors compressing or restricting great vessels Severe bronchospasm; pneumothorax Increased intrathoracic pressure Excessive tidal volumes or airway pressures Sepsis and septic shock Anaphylactic and anaphylactoid reactions Carcinoid syndrome Monitoring artifacts Angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers

Phosphodiesterase Inhibitors

21

However, the timing of this patient’s hypotension makes it less likely that ramipril (an ACE inhibitor) was the primary agent that precipitated the profound decrease in blood pressure. The patient also had multiple risk factors for CAD: ● ● ● ● ●

Hypertension Age older than 50 years Dyslipidemia Tobacco abuse Strongly positive family history

Further, erectile dysfunction disproportionately affects patients with cardiovascular disease. Thus, one must consider that these patients may be receiving sildenafil or similar potent PDE inhibitors. As the case synopsis illustrates, patients may fail to report the use of these drugs. Finally, this patient had objective evidence of CAD: ECG changes consistent with ischemia associated with tachycardia and hypertension with surgical stimulation.

Implications The clinical effects of sildenafil and other PDE-5 inhibitors (e.g., tidalafil, vardenafil) are mediated by a local increase in available cGMP. This, in turn, leads directly to smooth muscle relaxation in the arteries, arterioles, and sinusoids of the corpus cavernosum. The net result with sildenafil alone is vasodilatation and enhanced erectile function. The reduction in systolic and diastolic blood pressure is modest (≈8 and 5.5 mm Hg, respectively). When given to healthy volunteers, sildenafil had no apparent orthostatic effects. Sildenafil has also been investigated as a potential treatment for pulmonary hypertension. In patients with severe congestive heart failure, sildenafil reduces mean pulmonary artery pressure and arteriolar resistance by 20% and 45%, respectively. However, the drug has no significant effect on the cardiac index, ejection fraction, or pulmonary capillary wedge pressure. The safety of sildenafil in patients with documented CAD has been the subject of numerous reports. In one recent controlled trial, patients with CAD receiving sildenafil reported improved erections and sexual performance but experienced more side effects (e.g., transient headache, hypertension, flushing, dyspepsia) compared with placebo. However, there were no serious drug-related cardiovascular effects. An American College of Cardiology–American Heart Association consensus statement asserts that the available evidence supports the general safety of sildenafil in patients with CAD. Patients should not receive PDE-5 inhibitors and nitrates concomitantly. In fact, the current sildenafil product label states that the use of nitrates with sildenafil is strictly contraindicated. The simultaneous administration of nitric oxide donors (e.g., nitroglycerin) results in a marked accumulation of cGMP. This occurs because nitrates increase the production of cGMP, whereas sildenafil prevents its breakdown. The net result is a pronounced reduction in blood pressure with symptomatic hypotension. Other drugs that attenuate or block compensatory hemodynamic responses, including β- or α-adrenergic blockers, ACE inhibitors, and angiotensin II receptor antagonists, can also dramatically

PHARMACOLOGY

arteries; also important to the anti-ischemic action of nitroglycerin are reduced venous return and decreased cardiac preload, which lessen myocardial wall stress and reduce oxygen consumption. Sildenafil is prescribed for erectile dysfunction because sexual stimulation normally results in the release of NO from nerves and endothelial cells in the corpus cavernosum and systemic blood vessels, and NO stimulates guanylate cyclase to promote the formation of cGMP. Both aging and peripheral vascular disease interfere with this process; hence, the rationale for prescribing sildenafil or other PGE-5 inhibitors.

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exaggerate the adverse drug interaction between organic nitrates and PDE-5 inhibitors, especially when there is preexisting cardiovascular compromise. Twenty-one PDE genes have been cloned and belong to 11 PDE families based on their homology sequence and biochemical and pharmacologic properties. Table 6-2 depicts both experimental and clinical PDE inhibitors and their relative selectivity as inhibitors of PDE-1 through -11. Among these families, the PDE-3 inhibitors (e.g., enoximone, amrinone, milrinone, imazodan) are the most extensively studied group. By blocking the breakdown of cyclic adenosine monophosphate (cAMP), PDE-3 inhibitors reduce systemic and pulmonary arterial pressures. They also increase cardiac cAMP and Ca2+-induced Ca2+ release to increase myocardial contractility and the cardiac index, but without increasing myocardial oxygen consumption. Thus, PDE-3 inhibitors are considered positive inotropes and vasodilator agents. They have been used successfully in patients with advanced heart failure (both acutely and chronically) and as a bridge to cardiac transplantation. Thrombocytopenia limits the long-term use of amrinone, and the chronic use of milrinone has been associated with increased mortality in patients with New York Heart Association class III and IV heart failure. This mortality increase may be due to QTc prolongation with intravenous milrinone. The addition of a β-adrenergic blocking agent to low-dose milrinone therapy has been shown to reduce QTc prolongation and is associated with an improvement in patients’ functional status; however, sudden death was a relatively uncommon occurrence. Also, milrinone has been used to treat cerebral vasospasm associated with subarachnoid hemorrhage.

Table 6–2

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Experimental and Clinical Inhibitors of Phosphodiesterase and Their Relative Selectivity

Phosphodiesterase Inhibitor

Phosphodiesterase Selectivity (IC50)

IBMAX Papaverine EHNA Rolipram Dipyridamole

Nonselective (2-50 μM) Nonselective (5-25 μM) PDE-2 (1.0 μM) PDE-4 (2.0 μM) PDE-5 (0.9 μM) PDE-6 (0.38 μM) PDE-7 (9.0 μM) PDE-8 (4.5 μM) PDE-10 (1.1 μM) PDE-1 and -5 (0.1 μM) PDE-7 (35 μM) PDE-9 (1.15 μM) PDE-10 (1.0 μM) PDE-3 (1.0 μM) PDE-5 (3.9 nM) PDE-5 (0.76 μM) PDE-6 (0.15 μM) Nonselective (45-150 nM)

SCH51866

Enoximone Sildenafil Zaprinast Pentoxifylline

EHNA, erythro-9-[3-(2-hydroxynonyl)]adenine; IBMAX, 3-isobutyl-1-methylxanthine; IC50, concentration of PDE inhibitor with 50% activity against PDE; PDE, phosphodiesterase; SCH, succinylcholine. Adapted from Hetman JM, Robas N, Baxendale R, et al: Cloning and characterization of two splice variants of human phosphodiesterase 11A. Proc Natl Acad Sci U S A 97:12891-12895, 2000.

Inhibition of PDE-3 and PDE-4 may have therapeutic utility in reactive airway disease and for ameliorating pulmonary hypertension. PDE-4 inhibitors, such as compound A, cilomilast, and rolipram, also have anti-inflammatory and uterorelaxant effects. Finally, several commonly used drugs (e.g., papaverine, dipyridamole, pentoxifylline) appear to have significant nonselective PDE-inhibiting properties. Clinical effects of inhibition of the various PDE subtypes require further elucidation.

MANAGEMENT The management of perioperative myocardial ischemia and infarction is discussed in Chapter 76. Treatment for perioperative hypotension includes correction of the underlying pathophysiology and the administration of vasopressors if needed. For the patient described in the case synopsis, knowledge of all his preoperative medications would have permitted the recognition of potential drug-drug interactions (i.e., sildenafil-nitroglycerin) and prevented his profound hypotension. Therapy to counter nitroglycerin’s potentiation of sildenafil’s vasodilatory effect includes restoring intravascular volume by fluid resuscitation and increasing blood pressure with a vasoconstrictor such as phenylephrine, vasopressin, norepinephrine, epinephrine, or ephedrine. All are systemic arterial and venous vasoconstrictors, but phenylephrine and vasopressin have no β-adrenergic effects and would be the most judicious primary therapy in light of the patient’s predisposition for developing demand myocardial ischemia. Further, and importantly, by constricting the venous capacitance bed, α1 agonists such as phenylephrine and vasopressin increase venous return to augment preload and cardiac output. Refractory hypotension may necessitate the use of an intraaortic balloon counterpulsation device (see Chapter 98). Finally, administration of subsequent nitroglycerin doses is absolutely contraindicated.

PREVENTION Awareness is the key factor in preventing potentially lifethreatening drug-drug interactions. Unfortunately, erectile dysfunction still represents a social stigma in many cultures, which may prevent patients from reporting the problem and its treatment to their physicians and sexual partners. Sildenafil use increased by approximately 84% between 1998 and 2002. It was estimated that more than 14 million patients in the United States were taking sildenafil by 2001. With the advent of novel formulations of PDE-5 inhibitors and the reported growth in use among females and males between 18 and 45 years of age, it is likely that this number will well exceed 20 million patients by 2006. Although sildenafil is safe when taken by healthy patients, it should be administered with extreme caution in patients with cardiovascular disease. It is absolutely contraindicated in patients taking organic nitrates and those with hemodynamically significant aortic stenosis or hypertrophic obstructive cardiomyopathy. The cytochrome P-450 2C9 and 3A4

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Further Reading Cheitlin MD, Hutter AM Jr, Brindis RG, et al: Use of sildenafil (Viagra) in patients with cardiovascular disease: ACC/AHA expert consensus document. Circulation 99:168-177, 1999. Hermann HC, Chang G, Klugherz BD, et al: Hemodynamic effects of sildenafil in men with severe coronary artery disease. N Engl J Med 342:1622-1626, 2000.

Phosphodiesterase Inhibitors

23

Hetman JM, Robas N, Baxendale R, et al: Cloning and characterization of two splice variants of human phosphodiesterase 11A. Proc Natl Acad Sci U S A 97:12891-12895, 2000. Jaski BE, Fifer MA, Wright RF, et al: Positive inotropic and vasodilator actions of milrinone in patients with severe congestive heart failure: Dose-response relationships and comparison to nitroprusside. J Clin Invest 75:643-649, 1985. Kulkarni SK, Patil CS: Phosphodiesterase 5 enzyme and its inhibitors: Update on pharmacological and therapeutical aspects. Methods Find Exp Clin Pharmacol 26:789-799, 2004. Landesberg G, Mosseri M, Wolf Y, et al: Perioperative myocardial ischemia and infarction: Identification by continuous 12-lead electrocardiogram with online ST-segment monitoring. Anesthesiology 96:264-270, 2002. Viagra (sildenafil citrate): US prescribing information. In Physicians’ Desk Reference, 57th ed. Montvale, NJ, Medical Economics, 2003, pp 2653-2656. Zusman RM, Morales A, Glasser DB, et al: Overall cardiovascular profile of sildenafil citrate. Am J Cardiol 83(Suppl):35C-44C, 1999.

PHARMACOLOGY

pathways are the primary pathways for the metabolism of sildenafil. Thus, potent inhibitors of the these cytochromes (e.g., cimetidine, erythromycin, digoxin, some statins) may increase sildenafil’s plasma concentration. In such patients, and in those with severely compromised renal or hepatic function, reduced starting doses of sildenafil have been advocated to reduce the incidence of significant untoward effects.

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7

Digitalis Emilio B. Lobato Case Synopsis A 70-year-old man is scheduled for a subtotal colectomy under general anesthesia. He has a history of anterior myocardial infarction and intermittent atrial fibrillation and is receiving digoxin. His preoperative serum digoxin and potassium concentrations are 1.5 ng/dL and 3.9 mEq/L, respectively. Preparation for surgery includes colonic enemas (given until clear). His digoxin is withheld. Soon after the patient is placed on mechanical ventilation, he develops atrioventricular junctional tachycardia (AVJT) at 95 to 100 beats per minute (Fig. 7-1). Pulse oximetry reveals an arterial blood oxygen saturation of 100%. The end-tidal carbon dioxide partial pressure is 22 mm Hg, and the serum potassium concentration is 3.0 mEq/L. Digitalis toxicity is the suspected cause of the AVJT. Intravenous potassium chloride is given, and ventilation is reduced. Eventually, AVJT gives way to sinus rhythm, and the surgical procedure continues uneventfully.

PROBLEM ANALYSIS

●

●

Definition The use of digitalis to treat congestive heart failure (CHF) has been eclipsed by the current widespread use of angiotensinconverting enzyme (ACE) inhibitors and β-blockers to treat this condition. Prospective, randomized clinical trials have shown conclusively that both ACE inhibitors and β-blockers reduce mortality, whereas digoxin does not. However, one meta-analysis of available clinical trials (2001) showed that digoxin had beneficial effects, even in patients treated with ACE inhibitors; these findings may extend to β-blockers, but specific data were lacking. The results of this meta-analysis strengthen the concept that digoxin still has beneficial clinical effects in symptomatic patients with CHF, including the ability to reduce hospitalizations. Further, most patients in these reviewed trials were also receiving diuretics. Thus, clinicians still offer digoxin to symptomatic patients or those at appreciable risk for hospitalization for CHF, with a reasonable expectation of some benefit. Digitalis increases myocardial contractility in patients with heart failure and reduces the ventricular rate in those with atrial fibrillation. Cardiac complications can result from therapeutic or toxic effects of digitalis, primarily due to inhibition of membrane Na+,K+-ATPase. Extracardiac complications usually involve the central nervous system and gastrointestinal tract. Monitoring serum concentrations of digoxin (normally, 0.9 to 2.0 ng/dL) may help prevent toxic effects; however, there is considerable overlap between digoxin’s toxic and therapeutic effects, especially with hypokalemia or increased sensitivity to its effects (e.g., patients with severe cardiac disease or hypothyroidism). To avoid sampling errors due to slow digoxin equilibration, blood must be drawn at least 4 hours after intravenous dosing or 12 hours after oral dosing. Elevated serum digoxin concentrations may be due to the following: ● ●

Overdose or increased bioavailability (e.g., digitalis gel caps) Reduced volume of distribution (especially in elderly patients)

24

Reduced excretion (e.g., renal failure, patients receiving quinidine) Displacement from binding sites (e.g., with calcium channel blockers)

Recognition Digitalis toxicity may be immediately apparent or difficult to recognize, especially if cardiac manifestations are due to underlying heart disease. The presenting signs and symptoms depend on whether the digitalis toxicity is acute or chronic. If acute, gastrointestinal symptoms may be prominent. If chronic, patients may present with nonspecific symptoms (e.g., weakness and malaise). However, the sole evidence of chronic toxicity may be new arrhythmias. CARDIAC MANIFESTATIONS Cardiac manifestations of digitalis toxicity (primarily arrhythmias) include the following: ● ● ● ● ● ● ●

Sinus bradycardia Ventricular premature beats Nonparoxysmal AVJT Wenckebach atrioventricular (AV) block Atrial tachycardia with varying AV block Bidirectional ventricular tachycardia Ventricular fibrillation

When interpreting electrocardiogram (ECG) findings in patients receiving digitalis, one must distinguish between

Figure 7–1 ■ Nonparoxysmal atrioventricular junctional tachycardia at 100 beats per minute. Negative P waves after each QRS complex indicate retrograde atrial capture.

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●

● ●

●

T-wave changes (often the earliest sign), ranging from flattening to inversion or peaking of the terminal portion of the T wave Shortening of the Q-T interval ST-T segment flattening or depression, resulting in the classic concave (“scooped”) appearance (often more pronounced in ECG leads with tall R waves) Increased U-wave amplitude

Also, a slowed but irregular ventricular rate in atrial fibrillation implies a therapeutic digitalis effect. Regularization of the ventricular rate suggests toxicity and is usually due to the development of AV junctional rhythm (rate ≤70 beats per minute) or AVJT (rate >70 beats per minute). Cardiac complications can also result from the therapeutic effects of digitalis and include the following: ●

●

●

Increased risk for ventricular tachycardia and ventricular fibrillation in patients with Wolff-Parkinson-White syndrome and atrial fibrillation. Digitalis shortens refractoriness and speeds conduction in accessory AV conducting pathways. This may lead to preferential accessory pathway conduction and a greatly increased ventricular rate with atrial fibrillation (see Chapter 80). The latter can exceed 300 beats per minute and is limited solely by accessory pathway refractoriness. If this rate is sustained, there is a strong potential for early degeneration into ventricular tachycardia or ventricular fibrillation. Increased ventricular outflow tract obstruction in patients with asymmetrical ventricular septal hypertrophy, due to the positive inotropic effects of digitalis. Aggravation of myocardial ischemia in patients with coronary artery disease; this is “demand” ischemia due to digitalis-increased myocardial oxygen consumption.

Digitalis is ill-advised in any of these circumstances. The associated risks outweigh any potential benefits. ECG signs of toxicity occur in 5% to 20% of patients receiving digitalis. Almost any arrhythmia can result from the direct toxic or neurally mediated electrophysiologic effects of digitalis on cardiac muscle or the specialized conducting tissues (Table 7-1). The most common arrhythmia

Table 7–1

■

Digitalis

in patients with sinus rhythm is the appearance of ventricular extrasystoles. With atrial fibrillation, regularization of the ventricular rate occurs due to the development of AV junctional rhythm or AVJT; this may be the first manifestation of digitalis toxicity. In fact, the development of accelerated AV junctional rhythm or idioventricular rhythm in patients with AV heart block is highly suggestive of digitalis toxicity. Two other arrhythmias are characteristically identified with digitalis toxicity: 1. Paroxysmal atrial tachycardia with AV heart block. This is due to increased atrial conduction time and reduced refractoriness, along with AV node conduction block. 2. Bidirectional ventricular tachycardia. In this case, QRS complexes alternate between two distinctly different morphologies. In some leads, distinct R and S waves alternate between each other. Table 7-2 lists arrhythmias associated with digitalis toxicity in decreasing order of frequency. Worsening of preexisting CHF is often the first symptom of digitalis-induced arrhythmias and should alert the clinician to possible toxicity. EXTRACARDIAC MANIFESTATIONS Extracardiac manifestations of digitalis toxicity include the following: ●

●

●

Gastrointestinal symptoms, including nausea, vomiting, diarrhea, and increased salivation, from stimulation of central vagal nuclei Central nervous system manifestations (more common in the elderly), including blurred vision, abnormal color perception (e.g., green halos), hallucinations, and frank delirium Acute life-threatening hyperkalemia, occurring with severe digitalis overdose and caused by paralysis of the Na+-K+ pump and outward intracellular K+ leak

Risk Assessment Knowledge of factors that may alter digitalis pharmacokinetics or myocardial sensitivity and thus predispose patients to digitalis toxicity is of paramount importance (Table 7-3). Elderly patients are at greater risk than younger ones, and

Electrophysiologic Effects of Therapeutic and Toxic Digitalis

Tissue

Therapeutic Effects

Clinical Manifestations

Toxic Effects

Clinical Manifestations

Sinus node

Slows sinus rate

Sinus bradycardia

Sinus pause; SA conduction block

Atrium

None

None

AV node/AVJ

↓ Conduction time

Purkinje fibers

↓ Refractoriness; ↑ repolarization ↓ Refractoriness

↓ Ventricular rate; ↑ P-R interval None; ST-T segment depression ↓ Q-T interval

Sinus pause or arrest; SA conduction block ↑ Conduction; ↓ refractoriness AV heart block; ↑ AVJ automaticity ↑ Automaticity; DADtriggered activity ↑ Automaticity; DADtriggered activity

Ventricle

25

↑ Atrial rate (atrial flutter/fibrillation) Mobitz type I-II second or third degree heart block; AVJR or AVJT VPB; VT VPB; VT

AV, atrioventricular; AVJ, atrioventricular junction; AVJR, atrioventricular junctional rhythm; AVJT, atrioventricular junctional tachycardia; DAD, delayed after depolarization; SA, sinoatrial; VPB, ventricular premature beats; VT, ventricular tachycardia.

PHARMACOLOGY

normal and toxic effects. Normal ECG changes with therapeutic levels of digitalis include the following:

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Table 7–2

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Digitalis-Caused Arrhythmias in Decreasing Order of Frequency

Premature ventricular beats Accelerated AV junctional rhythm or tachycardia Wenckebach (Mobitz type I) AV block Sinus bradycardia or arrest Atrial tachycardia with variable AV block* Bidirectional ventricular tachycardia* Atrial flutter Ventricular fibrillation *Almost always due to the toxic effects of digitalis. AV, atrioventricular.

reduced body mass lowers the volume of distribution for digitalis. Other drugs administered concomitantly may interact with digoxin and affect serum concentrations. Also, a progressive decline in renal function and reduced serum albumin may elevate serum digoxin concentrations, as does reduced creatinine clearance if no adjustment in dosage is made. Importantly, dialysis is not effective for clearing digoxin. In hypothyroidism, the activity of membrane Na+,K+ATPase is reduced, which means that lower digoxin doses are needed to achieve a therapeutic effect, and toxicity can occur with usual doses. Hypoxemia enhances digitalis’s acceleration of lower pacemaker activity and may trigger arrhythmias from delayed afterpotentials. In patients receiving digitalis, ectopic beats or tachycardia can be exacerbated by the concomitant use of β-adrenergic agonists and diuretics. Hypokalemia potentiates the effects of digitalis owing to impaired Na+-K+ pump function. Low serum K+ concentrations increase the binding of digitalis to myocardium. Hypomagnesemia reduces the activity of membrane Na+,K+ATPase and may increase kaliuresis and cause hypokalemia. Hypercalcemia increases digitalis activity by increasing intracellular Ca2+. In addition, many drugs and other factors interact with digoxin to alter its pharmacokinetics, displace it from tissue binding sites, or reduce its clearance to increase serum drug concentrations (see Table 7-3).

Table 7–3

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Factors that Predispose to Digitalis Toxicity

Older age Electrolyte imbalance (hypokalemia, hypomagnesemia, hypercalcemia) Renal insufficiency Severity of heart disease Hypoxemia Hypothyroidism Drug interactions Angiotensin-converting enzyme inhibitors Benzodiazepines Quinidine or quinine Calcium channel blockers Erythromycin Cyclosporine Amiodarone

Implications Digitalis toxicity constitutes a serious condition that merits hospitalization. Hemodynamic deterioration with associated arrhythmias in patients with significantly impaired cardiac function may cause acute hemodynamic decompensation. In addition to hemodynamic compromise, some arrhythmias themselves are life threatening. Therefore, early recognition of the toxic effects of digitalis is imperative. Some extracardiac manifestations may be debilitating and may, in fact, precipitate arrhythmias. In surgical candidates, all but the most urgent procedures should be postponed until the digitalis toxicity has been resolved.

MANAGEMENT The treatment of digitalis toxicity depends on the severity of the clinical manifestations (Table 7-4). However, all patients suspected of digitalis intoxication should have an assessment of serum electrolytes, potassium, magnesium, and calcium, as well as a determination of serum digoxin concentration. For patients with mild symptoms, temporary discontinuation of the drug, cardiac monitoring, and supportive measures are sufficient. For patients with severe or lifethreatening arrhythmias (complete heart block, ventricular tachyarrhythmias), in addition to discontinuing digitalis, the administration of potassium chloride (in the absence of hyperkalemia) and magnesium sulfate should be considered. For heart block, 1 mg of atropine is usually effective in counteracting the vagal effects of digoxin. For ventricular arrhythmias, in addition to monitoring serum levels, lidocaine is the drug of choice, with a loading dose of 1 to 2 mg/kg, followed by an infusion of 1 to 2 mg/minute. Phenytoin was used in the past but, owing to its myocardial depressant properties and its tendency to produce hypotension when given intravenously, has largely been replaced by digoxin-specific antibodies (Digibind). There is no evidence to support the use of amiodarone to treat ventricular tachycardia or to prevent recurrences of ventricular fibrillation in patients with digitalis toxicity. At least in theory, the complementary electrophysiologic actions of amiodarone and digitalis to promote sinus bradycardia and increase sinoatrial and AV node conduction times and refractoriness might promote or precipitate asystole. More important is that amiodarone is known to

Table 7–4

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Management of Digitalis Toxicity

Withhold further digitalis Assess electrolytes (K+, Ca2+, Mg2+) Administer potassium chloride in the absence of hyperkalemia Administer magnesium sulfate Treat bradyarrhythmias Atropine Temporary or (possibly) permanent artificial pacing Treat ventricular arrhythmias Lidocaine Phenytoin (diphenylhydantoin) Digoxin-specific antibodies (Digibind)

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PREVENTION Knowledge of the multiple factors that affect digoxin pharmacokinetics and pharmacodynamics is important to avoid

Digitalis

27

its toxic effects. Regular determination of serum digoxin concentrations and dose adjustments in patients with conditions that increase the risk of digitalis toxicity are important measures, especially in the elderly.

Further Reading Antman EM, Wenger TL, Butler VP Jr, et al: Treatment of 150 cases of life-threatening digitalis intoxication with specific Fab antibody fragments: Final report of a multicenter study. Circulation 81:1744-1750, 1990. Fenster PE, White NW Jr, Hanson CD: Pharmacokinetic evaluation of the digoxin-amiodarone interaction. J Am Coll Cardiol 5:108-112, 1985. Hauptman PJ, Kelly RA: Digitalis. Circulation 99:1265-1270, 1999. Hood WB Jr, Dans AL, Guyatt GH, et al: Digitalis for treatment of congestive heart failure in patients in sinus rhythm. Update of Cochrane Database Syst Rev 3:CD002901, 2001; PMID: 11687032. Kelly RA, Smith TW: Recognition and management of digitalis toxicity. Am J Cardiol 69:108G-119G, 1992. Ma G, Brady WJ, Pollack M, et al: Electrocardiographic manifestations: Digitalis toxicity. J Emerg Med 20:145-152, 2000. Ooi H, Colucci WS: Pharmacological treatment of heart failure. In Hardman JG, Limbird LE (eds): Goodman and Gilman’s The Pharmacological Basis of Therapeutics, 10th ed. New York, McGrawHill, 2001, pp 901-932. Spratt KA, Doherty JE: Principles and practice of digitalis. In Messerli FH (ed): Cardiovascular Drug Therapy, 2nd ed. Philadelphia, WB Saunders, 1996, pp 1136-1146.

PHARMACOLOGY

increase serum digoxin levels. Systemic clearance of digoxin is significantly prolonged owing to reduced renal and nonrenal clearance, which lengthens its half-life of elimination by approximately 20%. However, amiodarone does not appear to affect the volume of distribution for digoxin. Electrical countershock (direct-current cardioversion) is contraindicated because it can exacerbate the severity of arrhythmias. Administration of digoxin-specific antibodies (Digibind) is the treatment of choice for life-threatening arrhythmias and for digoxin-induced refractory hyperkalemia. The use of an antibody rapidly reduces the percentage of unbound digoxin in the serum from 75% to less than 5%. The antibody-digoxin complex then undergoes renal excretion. Side effects are infrequent but include allergic reactions and rebound toxic digoxin effects in patients treated with inadequate doses of Digibind. Importantly, conventional serum assays for digoxin cannot distinguish between free and bound digoxin; thus, serum digoxin concentrations appear markedly elevated following Digibind treatment. The results of treatment are monitored by manifestations of clinical improvement; however, free digoxin determinations can be obtained in patients who show a poor response to treatment.

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Anticholinergics Kevin J. Sullivan Case Synopsis A 1-year-old child weighing 10 kg is in the pediatric intensive care unit with respiratory failure and a difficult airway. Prior attempts at laryngoscopy and endotracheal intubation have been unsuccessful, and mask ventilation is difficult. The infant, who becomes hypoxic and bradycardic during resuscitation efforts, is unintentionally given 4 mg of intravenous atropine, instead of the 0.2 mg that was ordered. Endotracheal intubation is performed to reverse the respiratory failure and hypoxia. Shortly thereafter, the patient is noted to be tachycardic (225 beats per minute), with warm, red, dry skin and fever (39°C). He appears disoriented, agitated, and inconsolable.

PROBLEM ANALYSIS Definition Because infants and young children have a relatively enhanced vagal tone compared with adults, vagotonic physiologic perturbations, such as airway instrumentation, can result in bradycardia. Thus, in pediatric anesthesia and critical care settings, bradycardia can be seen during laryngoscopy and induction of anesthesia with volatile inhalational agents (most commonly halothane), as well as with hypoxemia and elevated intracranial pressure. Bradycardia and the consequent reduced cardiac output can be prevented by premedication with oral, intravenous, or intramuscular anticholinergic drugs. In the case synopsis, an inadvertently high dose of atropine (about 20-fold too high) was given to increase the patient’s heart rate during bradycardia. Anticholinergic (antimuscarinic) toxicity is commonly seen in infants and young children after the accidental ingestion of belladonna alkaloids and their synthetic congeners, antiparkinson medications, histamine receptor antagonists, tricyclic antidepressants, and phenothiazines. For persons of all ages, the ingestion of plants that contain large quantities of belladonna alkaloids can cause anticholinergic toxicity. Such plants include deadly nightshade (Atropa belladonna), jimsonweed (Datura stramonium), and angel’s trumpet (Brugmansia candida). Anticholinergics used in anesthesia include atropine, glycopyrrolate, and scopolamine. They compete with neurally released acetylcholine to attach to muscarinic cholinergic receptors and block the effects of acetylcholine, and they antagonize muscarinic agonist actions at noninnervated muscarinic cholinergic receptors. Further, presynaptic muscarinic receptors on adrenergic nerve terminals inhibit norepinephrine release. Thus, muscarinic antagonists (anticholinergics) can enhance sympathetic activity. Except for the fact that quaternary ammonium compounds (glycopyrrolate) do not readily cross the blood-brain barrier to exert central nervous system (CNS) actions, there is little difference in the qualitative actions of atropine, glycopyrrolate, and scopolamine. However, some quantitative differences in effect may be seen. For example, both atropine and scopolamine have a shorter duration of action than glycopyrrolate. Further, the 28

antisialagogue effects of glycopyrrolate and scopolamine are greater than those of atropine. In addition, heart rate is most increased by atropine, then by glycopyrrolate, and least by scopolamine. Finally, although both atropine and scopolamine are tertiary amines that readily cross the blood-brain barrier, they differ in CNS effects: atropine causes CNS stimulation, whereas scopolamine produces sedation and amnesia. Human tissues vary with respect to both the density and the type of muscarinic receptors present. Five subtypes of muscarinic receptors have been identified (M1, M2, M3, M4, M5), each with a different location and function. For example, M1 receptors are found in the cerebral cortex, sympathetic ganglia and postganglionic neurons, and some presynaptic sites. M2 receptors are present in myocardium, smooth muscle cells, and some presynaptic sites. M3 receptors are found in exocrine glands, and M4 receptors in heart. M5 receptors are found mostly in brain. All muscarinic receptor subtypes interact with heterotrimeric, guanine nucleotide-binding regulatory proteins (G proteins) linked to cellular effectors. Although selectivity is not absolute, stimulation of M1 or M3 receptors causes hydrolysis of polyphosphoinositides and mobilization of intracellular Ca2+, which is due to interaction with a G protein (Gq) that activates phospholipase C. The latter causes a variety of Ca2+-mediated events, either directly or via phosphorylation of target proteins. In contrast, M2 and M4 muscarinic receptors inhibit adenylyl cyclase and regulate specific ion channels (e.g., enhancement of K+ conductance in cardiac atrial tissue) through subunits released from pertussis toxinsensitive G proteins (G1 and G0). These are distinct from the G proteins used by the M1 and M3 receptors. Finally, M5 receptors may inhibit M-type (KCNQ2/KCNQ3) K+ channels via the activation of a common G protein.

Recognition Table 8-1 lists the effects of anticholinergics in various organ systems. Appreciation of the range of organ systems affected by anticholinergic drugs is required to maximize their benefits while minimizing side effects. Drugs in common use (atropine, scopolamine, glycopyrrolate) are nonselective muscarinic receptor antagonists. They have similar side effects, but to a varying extent. As stated earlier, atropine and

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Clinical Effects of Anticholinergic Drugs

Cardiovascular effects (observed at moderate doses) Increased rate of sinoatrial (SA) node discharge Decreased rate of SA node discharge (low doses of atropine) Enhanced atrioventricular node conduction Little or no effect on ventricular function Little effect on peripheral vasculature Cutaneous vasodilatation in high doses Respiratory effects (observed at low doses) Drying of respiratory secretions Relaxation of bronchial smooth muscle Increased anatomic dead space Central nervous system effects (observed at larger doses) Wide range of symptoms, from sedation and depression to agitation and delirium Gastrointestinal effects (observed at larger doses) Decreased salivation Reduced gastric secretions and motility Decreased lower esophageal sphincter tone Ophthalmic effects (observed at moderate doses) Mydriasis Cycloplegia Genitourinary effects (observed at larger doses) Decreased ureter and bladder tone Urinary retention Thermoregulation effects (observed at small doses) Inhibition of sweat gland secretions (function most sensitive to anticholinergics) Elevated temperature

scopolamine cross the blood-brain barrier, whereas glycopyrrolate does not. Scopolamine is more sedating than atropine but causes less of a heart rate increase; similar to atropine, it is a moderately potent antisialagogue. Glycopyrrolate is the most potent antisialagogue, causes moderate tachycardia, and is nonsedating. The pharmacologic effects of anticholinergics used in anesthesia are summarized in Table 8-2. Another anticholinergic agent, ipratropium (Atrovent), is used primarily in pulmonary care. This drug was introduced

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Pharmacologic Effects of Anticholinergics Used in Anesthesia

Atropine Causes greater vagolysis than glycopyrrolate Increases heart rate and enhances atrioventricular node conduction Paradoxical slowing of heart rate at low doses Little sedation Moderately potent antisialagogue Glycopyrrolate Moderate vagolytic effect on heart, but less than that of atropine No sedation (charged quaternary amine; does not cross blood-brain barrier) Highly potent antisialagogue Scopolamine Marked sedation-amnesia (tertiary amine structure; lipid soluble; crosses blood-brain barrier) Most likely to cause central anticholinergic syndrome (easily reversed with physostigmine) Moderately potent antisialagogue

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29

in the 1980s and reestablished anticholinergics as a therapy for bronchospastic disorders. Although ipratropium is structurally similar to atropine and has similar actions if given parenterally, it is a quaternary ammonium compound. Ipratropium is poorly absorbed when inhaled and has few extrapulmonary effects, even with very large inhaled doses. When inhaled, 90% of ipratropium is swallowed, and only 1% of the total dose is absorbed systemically. When given to normal volunteers, the drug provides almost complete protection against bronchospasm induced by a variety of provocative agents. However, in asthmatics, the results can vary. Whereas the bronchospastic effects of some agents (e.g., methacholine, sulfur dioxide) are completely blocked, there is little blocking of leukotriene-induced bronchoconstriction. Also, unlike atropine, ipratropium has no negative effect on ciliary clearance. In general, this drug and other anticholinergics are more effective in chronic obstructive pulmonary disease, especially when cholinergic tone is high. The development of new drugs that affect specific muscarinic receptor subtypes will provide more effective therapy with fewer adverse or troublesome side effects than the drugs used today. The child in the case synopsis displayed many of the signs and symptoms of anticholinergic toxicity, which can be divided into two types: CNS and peripheral antimuscarinic. CNS toxicity can manifest as agitation, delirium, seizures, or coma. Systemic anticholinergic effects are most prominent in tissues or organs with dense parasympathetic innervation and include tachycardia; dry mucous membranes; urinary retention; dry, flushed skin; dilated pupils with cycloplegia; fever; and ileus. The child in the case illustrated the typical findings accompanying anticholinergic overdose in pediatric patients. Although the cause of his condition was known, the differential diagnosis includes other potentially lifethreatening conditions (Table 8-3). Physical examination and the natural history of the disease process should allow the clinician to differentiate among these conditions. Physical and laboratory findings of anticholinergic toxicity that help exclude other conditions are summarized in Table 8-4. Although the conditions in the differential diagnosis share overlapping features with anticholinergic toxicity, the combination of abolition of pupillary responses and sweating is very specific for anticholinergic toxicity. Many clinicians confuse anticholinergic toxicity with the diametrically opposed toxidrome associated with anticholinesterase poisoning, which results in excessive cholinergic tone. Physician familiarity with toxic syndromes due to anticholinesterase poisoning has increased dramatically with the proliferation of chemical weapons of mass destruction. In contrast to the symptoms and signs of anticholinergic

Table 8–3

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Differential Diagnosis of Anticholinergic Toxicity

Hypoxemia and/or hypercarbia Sepsis Malignant hyperthermia Thyroid storm (crisis) Pheochromocytoma Carcinoid syndrome

PHARMACOLOGY

Table 8–1

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Distinguishing Features of Anticholinergic Toxicity*

Relatively normal arterial O2 and CO2 tensions (rules out hypoxemia and hypercarbia) Cycloplegia (pupillary light reflexes remain intact for most other conditions) Mydriasis (pupils may also be dilated in MH due to elevated circulating catecholamines) Anhidrosis; warm, red skin (sweating is preserved in other disorders within the differential diagnosis; see Table 8-3) Lack of muscle rigidity (commonly seen with MH) No ventricular arrhythmias (not characteristic of carcinoid syndrome, but common with MH, pheochromocytoma, and thyrotoxicosis) Minimal to modest increase in end-tidal CO2 due to hyperthermia (usually far greater with MH or thyrotoxicosis) Mild (or no) hypertension (as in MH), or paroxysmal, severe hypertension (thyroid storm, pheochromocytoma, or carcinoid tumor†), especially with gland or tumor manipulation Mild to no metabolic acidosis (far more severe in MH) *In anesthetized patients, the modulatory effects of anesthesia must be considered. † Serotonin released by carcinoid tumors has little if any direct effect on the heart. However, positive chronotropic and inotropic effects, and possibly arrhythmias, may occur with the release of norepinephrine. Effects of serotonin on the peripheral vasculature include both vasoconstriction and vasodilatation. MH, malignant hyperthermia.

overdose, poisoning with carbamate insecticides or organophosphates leads to CNS excitation and excessive nicotinic and muscarinic receptor activation. CNS signs include ataxia, restlessness, agitation, convulsions, and coma. Muscarinic signs include excessive salivation, perspiration, vomiting, diarrhea, abdominal cramps, tenesmus, bradycardia or heart block, pupillary constriction, lacrimation, wheezing, hypotension, blurred vision, and urinary and fecal incontinence. Nicotinic signs include muscle twitching, fasciculations, cramping, paralysis, respiratory compromise, and subsequent cardiac arrest.

Risk Assessment Patients with heart disease are at far greater risk for anticholinergic complications. In this respect, atropine and glycopyrrolate produce more vagolysis than scopolamine does, causing a much greater increase in the sinus rate and speed of atrioventricular (AV) node conduction. An increased heart rate is more dangerous in patients with coronary artery disease and valvular or subvalvular restrictive cardiac lesions (e.g., aortic and mitral valve stenosis, idiopathic hypertrophic subaortic stenosis). Further, in patients with functional accessory AV pathways and a history of AV reciprocating tachycardia or atrial flutter or fibrillation (e.g., WolffParkinson-White syndrome), atropine or glycopyrrolate (especially in a relative overdose) may precipitate dangerously fast tachyarrhythmias (see Chapter 80). Also, because both drugs facilitate AV node conduction, they are contraindicated in patients with supraventricular tachyarrhythmias, especially atrial flutter or fibrillation.

Implications Anticholinergics exert their effects in many organ systems (see Table 8-1). Therapeutic effects in one organ system may be accompanied by undesirable side effects in others. Careful selection of the anticholinergic agent and its dose allows the clinician to target the appropriate organ system and simultaneously minimize undesirable side effects in other organ systems (see Table 8-2). Although atropine is considered relatively safe and benign in adults, an atropine overdose is very dangerous in pediatric

patients, especially infants. Deaths due to anticholinergic poisoning have been reported with doses as low as 2 mg of atropine in infants. Anticholinergics have complex gastrointestinal actions. Salivary gland secretions are reduced and are the most sensitive to cholinergic block. Gastric secretions are also reduced, but this requires larger doses. Both gastrointestinal motility and lower esophageal sphincter tone are reduced. However, it is important to remember that anticholinergic premedication does not confer protection against aspiration of gastric contents and chemical or bacterial pneumonitis. Also, the function of a number of other organs can be impaired by anticholinergic therapy. In the eye, anticholinergic drugs can precipitate narrow-angle glaucoma. Individuals with a shallow anterior chamber can suffer acute increased intraocular pressure due to impaired drainage via the canal of Schlemm. Postsurgical patients, especially elderly men with prostatic hypertrophy, are at risk for severe urinary retention after taking anticholinergics. Further, confusion, agitation, and delirium are CNS side effects of anticholinergics that cross the blood-brain barrier (scopolamine, atropine). Patients at greatest risk for mental status changes are those at the extremes of age, those with preexisting abnormalities of mental status, and those taking drugs with significant anticholinergic properties (e.g., antiparkinson drugs, phenothiazines, tricyclic antidepressants, butyrophenones, antihistamines, cycloplegics, antispasmodics). Impaired thermoregulation due to the inability to sweat can result in hyperpyrexia. Children and infants are especially vulnerable owing to their high metabolic rate and immature thermoregulatory mechanisms. It is clear that hyperpyrexia involves an impaired ability to dissipate heat through sweating. Whether there is a central effect on thermal regulation remains unclear. Finally, atropine and glycopyrrolate are commonly given with or prior to anticholinesterase drugs to reverse nondepolarizing neuromuscular blockade. Because of similarities in onset of drug action, atropine is commonly administered with edrophonium, which has a very rapid onset. Similarly, glycopyrrolate is often administered with neostigmine because both have a slower onset and a longer duration of action. By selecting an anticholinergic that matches the anticholinesterase drug’s onset and duration of action, heart

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MANAGEMENT Most complications related to anticholinergic drugs are self-limited and can be effectively treated with supportive care. For example, urinary retention in elderly men may require short-term or intermittent bladder catheterization. However, some complications, such as fast sinus or nonparoxysmal atrial tachycardias in patients with myocardial ischemia or infarction, aortic or mitral valve stenosis, or idiopathic hypertrophic subaortic stenosis, require prompt treatment. Therapeutic options include β-blockers and calcium channel antagonists. If paroxysmal supraventricular tachycardia is likely, adenosine is useful. However, the current advanced cardiovascular life support guidelines advise early cardioversion for most hemodynamically disadvantageous tachyarrhythmias, rather than a trial of drugs (see Chapter 79). Likewise, severe hyperthermia should be treated aggressively with cooling blankets and, if needed, immersion in ice water and irrigation of body cavities with cold saline. With careful consideration of the underlying medical history and the pharmacodynamics of the various anticholinergics, it is possible to maximize the benefits of this class of medications while minimizing undesirable side effects of therapy.

PREVENTION Prevention of the side effects of anticholinergic drugs begins with an appreciation of the fact that they affect different

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organ systems with different intensities (see Tables 8-1 and 8-2) but do so in a predictable, dose-related fashion. To avoid complications, it is most important to recognize that certain subsets of patients are at greater risk for morbidity related to the use of anticholinergic drugs. Therefore, it is crucial to evaluate the specific vulnerabilities of the patient, delineate the goals of anticholinergic therapy, and select a drug with a pharmacodynamic profile that most closely suits the goals of therapy.

Further Reading Brown JH, Taylor P: Muscarinic receptor agonists and antagonists. In Hardman JG, Limbird LE (eds): Goodman and Gilman’s The Pharmacological Basis of Therapeutics, 10th ed. New York, McGrawHill, 2001, pp 155-173. Das G: Therapeutic review: Cardiac effects of atropine in man: An update. Int J Clin Pharmacol 27:473-477, 1989. Feldman MD: The syndrome of anticholinergic intoxication. Am Fam Physician 34:113-116, 1986. Friesen RH, Lichtor JL: Cardiovascular depression during halothane anesthesia in infants: A study of three induction techniques. Anesth Analg 61:42-45, 1982. Goyal RK: Muscarinic receptor subtypes: Physiology and clinical implications. N Engl J Med 321:1022, 1989. Gross NJ: Ipratropium bromide. N Engl J Med 319:486-494, 1988. Guo J, Schofield GG: Activation of muscarinic M5 receptors inhibits recombinant KCNQ2/KCNQ3 K+ channels expressed in HEK293T cells. Eur J Pharmacol 462:25-32, 2003. Mirakhur RK: Antagonism of the muscarinic effects of edrophonium with atropine or glycopyrrolate. Br J Anaesth 57:1213-1216, 1985. Moss J, Glick D: The autonomic nervous system. In Miller RD (ed): Miller’s Anesthesia, 6th ed. Philadelphia, Churchill Livingstone, 2005, pp 617-677. Patton WDM: The principles of drug action. Proc R Soc Med 53:815-820, 1965. Polak RL: Effects of hyoscine on the output of acetylcholine into preferred cerebral ventricles on cats. J Physiol 181:317-323, 1965.

PHARMACOLOGY

rates that are too fast or too slow can be avoided. It also appears that lower doses of anticholinergics are required to antagonize the weaker and shorter-lived muscarinic effects of edrophonium compared with those of neostigmine.

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9

Adenosine M. J. Pekka Raatikainen and John L. Atlee Case Synopsis A 63-year-old man with a history of transient ischemic attacks is admitted to the hospital for elective surgery. His medications include aspirin 250 mg/day orally and dipyridamole 75 mg orally three times a day. During the operation under regional anesthesia, a regular supraventricular tachycardia (SVT) is observed. The tachycardia terminates after intravenous bolus adenosine (12 mg) and is followed by a long sinus pause and angina-like pain (Fig. 9-1).

PROBLEM ANALYSIS Definition The first step is to determine whether the signs or symptoms are due to tachycardia. If they are, the existing advanced cardiovascular life support guidelines advise immediate cardioversion rather than a trial of antiarrhythmic drugs. If cardioversion is not indicated (e.g., ectopic atrial tachycardia), the guidelines stress making a specific diagnosis and identifying patients with impaired cardiac function (ejection fraction 55 yr History of Smoking Supraglottic, Glottic, and Subglottic Pathology or Stridor Consider prospective placement of translaryngeal jet ventilation catheter Strongly consider awake airway management Avoid sedation if stridor is present

Bronchospasm (active or at risk for) Nebulize with bronchodilator before induction

Recognition The cause of the majority of difficult endotracheal intubations is limited oropharyngeal space, decreased atlantooccipital extension, decreased pharyngeal space, or decreased submandibular compliance. Recognition of potentially difficult direct laryngoscopy and endotracheal intubation is facilitated by a systematic search for abnormalities during the preoperative airway examination (Table 40-4). Unfortunately, airway examination findings have low and variable sensitivity and marginal specificity; however, worrisome findings, particularly in combination, suggest a difficult intubation. A Mallampati class higher than II (Fig. 40-3) in association with other airway findings signifies potential difficulty during traditional direct laryngoscopy. Reviewing the patient’s prior anesthetic history and previous records of airway management (if available) is extremely helpful when formulating the airway management plan. Anesthesiologists must accurately document the ease or difficulty of facemask ventilation, laryngoscopy attempts and blades used, the laryngoscopic view obtained (see Fig. 40-2), how intubation was ultimately achieved, and any special maneuvers or devices used. Assume high reliability if the patient selfreports a difficult airway. Consider any systemic diseases or congenital abnormalities that require special attention during airway management.

GENERAL ANESTHESIA

Inaccurate or incomplete preoperative airway assessment Incorrect prediction of: Easy mask airway Routine direct laryngoscopy-guided intubation Uncomplicated extubation Unwillingness to abandon failed airway management plan Failure to call for help early, when difficult airway is first apparent Incomplete preparation of backup plan Deterioration of performance under stress Failure in judgment

Difficult Airway: Cannot Ventilate, Cannot Intubate

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Figure 40–2 ■ Laryngoscopic view grading systems. A, Cormack-Lehane system: grade 1, visualization of the entire laryngeal aperture; grade 2, visualization of only the posterior portion of the laryngeal aperture; grade 3, visualization of only the epiglottis; grade 4, visualization of only the soft palate. B, Modified grading system of view at direct laryngoscopy: grade 1, most of cords visible (direct intubation); grade 2A, posterior cord visible (direct intubation); grade 2B, only arytenoids visible (indirect intubation); grade 3A, epiglottis visible and liftable (indirect intubation); grade 3B, epiglottis adherent to pharynx (specialist required for intubation); grade 4, no laryngeal structures seen (specialist required for intubation). (A, From Cormack RS, Lehane J: Difficult tracheal intubation in obstetrics. Anaesthesia 39:1105, 1984. B, From Cook TM: A new practical classification of laryngeal view. Anaesthesia 55:274-279, 2000.)

Laryngoscope

Epiglottis

A

1

2

3

4

Grade 1

B

Grade 2A

Grade 2B

Easy

Grade 3A

Restricted

ENDOTRACHEAL INTUBATION INTRODUCERS AND INTUBATING CATHETERS A malleable tracheal tube introducer (gum-elastic bougie [GEB], length 60 cm) or an intubating catheter can be placed blindly and gently under the epiglottis (or directed through partially visible, posterior vocal cords) into the trachea during one of the laryngoscopic attempts. The anesthesiologist will not see the GEB entering the larynx with a grade 3 or 4 laryngoscopic view. Tactile “clicking” may be felt as the angled (about 60 degrees), anteriorly directed tip of the GEB passes over (hits against) the tracheal rings. If clicks are not perceived, the GEB should be gently advanced to a maximum depth of 45 cm (in an adult patient). If distal hold-up is sensed, such as slight resistance to further advancement, the GEB is likely “caught up” in the bronchial tree, and the patient may cough if not completely paralyzed. If neither clicks, hold-up, nor coughing is evoked, the GEB is probably in the esophagus and should be removed. A second attempt at passing the GEB blindly into the trachea can be considered, unless there is a grade 4 laryngeal view or the epiglottis

Grade 3B

Grade 4

Difficult

cannot be elevated (the epiglottis is “adherent” to the pharynx). If the GEB is believed to be in the trachea, an internally lubricated endotracheal tube (ETT) is advanced (“railroaded”) over the GEB. Leaving the laryngoscope blade in the mouth and rotating the ETT 90 degrees counterclockwise facilitates ETT advancement (orientation of the Murphy eye at the 12 o’clock position prevents the ETT tip from hanging up on the right vocal cord or arytenoids during passage). Tracheal location is confirmed by auscultation of equal bilateral breath sounds and sustained end-tidal carbon dioxide waveforms. The rule is, “if in doubt, take the ETT out,” unless immediate flexible bronchoscopy via the ETT confirms a tracheal location. Optimal results achieving intubation with the GEB are dependent on experience and regular use. DIFFICULT EXTUBATION The risks for difficult facemask ventilation and difficult intubation, as well as other events, herald difficult extubation. Patients with a difficult airway should meet the usual criteria for extubation and be fully awake. They also should cough

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Airway Examination Predictors of Difficult Direct Laryngoscopy and Endotracheal Intubation

Interincisor Gap

Length of Upper Incisors Long incisors impede alignment of oral and pharyngeal axes during direct laryngoscopy Relatively long, protruding upper incisors are worrisome Mallampati Oropharyngeal Classification (see Fig. 40-3) With Mallampati class I or II, tongue should be easily retracted from the line of site during direct laryngoscopy Mallampati class >II is worrisome

Mandibular Space With hyomental and thyromental distances (estimates of mandibular space) >6 and 7 cm, respectively, larynx should be sufficiently posterior for favorable line of sight with direct laryngoscopy Distance II are worrisome

Head and Neck Range of Motion Atlanto-occipital (AO) extension or neck flexion on chest of 72 hours after admission) are most often associated with multidrug-resistant microorganisms such as Acinetobacter, Pseudomonas, and MRSA. Yeasts such as Candida albicans or other Candida species are an infrequent cause of nosocomial pneumonia (2 hr

Erythema; scalded or parched appearance; chapped, cracked, fissured, or scaling skin; possibly vesicles or blisters Swelling, pruritus, urticaria, rhinoconjunctivitis, asthma, hypotension, anaphylaxis

Delayed contact hypersensitivity reaction (type IV)

6-48 hr after contact

Acute: erythema, pruritus, vesicles, blisters, cracking, crusting, desquamation Chronic: dryness, scaling, fissures, thickening or darkening of skin

IgE release of mast cell mediators; antigens are natural latex proteins Delayed or cell-mediated immunity; T-cell response to small rubber chemicals acting as haptens

From Ownby DR: Manifestations of latex allergy. Immunol Allergy Clin North Am 15:34, 1995.

TYPE I IGE-MEDIATED REACTION Type I reactions are mediated by IgE and usually occur within minutes of contact with latex proteins. The allergen binds to IgE, resulting in the release of vasoactive substances from mast cells (i.e., histamine, bradykinin, leukotrienes, prostanoids). There are several potential manifestations of IgE-mediated reactions, including urticaria, pruritus, bronchospasm, rhinoconjunctivitis, flushing, hypotension, angioedema, and anaphylaxis. TYPE IV DELAYED HYPERSENSITIVITY REACTION Type IV reactions to latex gloves are cell-mediated reactions to chemicals retained in the glove. The symptoms are apparent within several days and include erythema, pruritus, vesicles, fissuring, scaling, and thickening. The rash usually extends beyond the site of contact. Natural rubber latex is usually not the cause of type IV reactions; additives from the manufacturing process, such as thiuram and mercaptobenzathiazole, are more likely causes.

Risk Assessment There are few studies on the natural history and clinical course of natural rubber latex reactions; in addition, owing

Table 53–3

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to differences in their methodology, there is variation in the reported prevalence. Even so, the prevalence of latex allergy in the general population has been consistently reported as less than 1%. Although a study of blood donors revealed detectable antibody in 6.5% of subjects, this does not indicate the presence of clinical allergy. The pediatric spina bifida population has been estimated to have a prevalence of 28% to 67%. The prevalence of latex allergy in health care workers is 5% to 17%, but its prevalence in health care workers with a history of atopy is 24% to 36%. Latex reaction risk factors include a history of environmental allergy, food allergy (especially to banana, kiwi, or avocado), hay fever, eczema, asthma, and chronic latex exposure (either occupational or as a result of repeated therapeutic procedures, with both frequency and exposure intensity being factors). The skin is relatively impermeable to latex proteins. However, disruption of the skin by irritant or contact reactions may predispose subjects to the development of IgE-mediated disease and subsequent systemic reactions. Cornstarch powder lubricant, which binds latex protein, and any activity that disperses these particles in the atmosphere can increase the quantity of respiratory exposure. If a patient’s history indicates a risk of latex allergy, a serum level of IgE reactive to latex allergens or skin testing from an allergist may be obtained. Further workup can be performed as outlined in Table 53-3.

Manifestations of Irritant, Immediate, and Delayed Reactions to Latex

Negative

Positive

Patient at Risk of Latex Allergy* No symptoms; no latex allergy; no testing needed

Symptomatic; possible latex allergy; perform diagnostic tests

Serum Test Negative; do further testing

Positive; no further testing needed (latex allergy confirmed)

Latex Use Test Negative; do further testing

Positive; no further testing needed (latex allergy confirmed)

Skin Test Negative; no latex allergy

Positive; no further testing needed (latex allergy confirmed)

*Some investigators have advocated latex testing in all patients with spina bifida. This approach would identify asymptomatic patients who have positive serum test results. Until further studies are performed, this patient group should be considered to be allergic to latex. From Kelly KJ, Kurup VP, Reijula KE, et al: The diagnosis of natural rubber latex allergy. J Allergy Clin Immunol 93:814, 1994.

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Implications

MANAGEMENT The mainstays of management are as follows: ● ● ●

Avoidance of allergens Topical therapy Systemic therapy (see Chapter 27)

Antigen avoidance can be difficult because of the ubiquitous presence of natural rubber products, especially in the health care environment. However, steps can be taken, such as wearing nonlatex gloves or using some type of barrier between the latex gloves and the skin (e.g., vinyl gloves). Using gloves only when necessary can also reduce exposure. Individuals who suffer severe reactions and cannot avoid allergens may have to change their specialty or profession. Airborne exposure can be eliminated or reduced to levels that are clinically insignificant by the exclusive use of powder-free, low-allergen latex gloves or synthetic gloves. Topical therapy with steroids and moisturizers can relieve the symptoms of irritant and type IV reactions. Therapy for systemic IgEmediated reactions includes airway management, ventilatory and circulatory support if necessary (including the use of epinephrine), antihistamines, and bronchodilators.

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PREVENTION Susceptible individuals should be advised to avoid latex products, but as already noted, this can be difficult. They should wear allergy-alert identification and carry an autoinjectable device for the emergency administration of epinephrine. Institutions should consider managing prevention through a multidisciplinary committee that develops guidelines for patients, health care workers, and other employees. This committee should provide guidelines for the identification of latex-containing medical products, the identification and purchase of latex-free substitutes, the establishment of latex-free treatment areas for susceptible individuals, and the use of powder-free gloves.

Further Reading Garabrant DH, Schweitzer S: Epidemiology of latex sensitization and allergies in health care workers. J Allergy Clin Immunol 110:S82-S95, 2002. Kelly KJ: Management of the latex-allergic patient. Immunol Allergy Clin North Am 15:139-157, 1995. Kelly KJ, Kurup VP, Reijula KE, et al: The diagnosis of natural rubber latex allergy. J Allergy Clin Immunol 93:813-816, 1994. Landwehr LP, Boguniewicz M: Current perspectives on latex allergy. J Pediatr 128:305-312, 1996. Ownby DR: Manifestations of latex allergy. Immunol Allergy Clin North Am 15:31-43, 1995. Ranta PM, Owenby DR: A review of natural-rubber latex allergy in health care workers. Clin Infect Dis 38:252-256, 2004. Sussman GL, Beezhold DH: Allergy to latex rubber. Ann Intern Med 122: 43-46, 1995. Truscott W: The industry perspective on latex. Immunol Allergy Clin North Am 15:89-121, 1995.

GENERAL ANESTHESIA

The severity of a latex reaction can range from a minor annoyance to life-threatening anaphylaxis and can include disabling symptoms (e.g., asthma). In addition to these medical complications, there are social implications, such as the need to change responsibilities or careers and the cost of disability payments. Institutions and individuals may have to change aspects of their medical practice to reduce the risk of latex reactions in others.

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Spinal Anesthesia: Post–Dural Puncture Headache

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Matthew P. Feuer and Spencer S. Liu REGIONAL ANESTHESIA & PAIN MANAGEMENT

Case Synopsis A 25-year-old woman undergoes spinal anesthesia with a 25-gauge Quincke needle for outpatient knee arthroscopy. The following day, she complains of a severe frontaloccipital headache in the upright position that resolves when she is supine.

PROBLEM ANALYSIS Definition

●

●

Presence of less common associated symptoms: shoulder pain, cranial nerve dysfunction, auditory complaints Spontaneous resolution between 1 and 6 weeks after dural puncture

Post–dural puncture headache (PDPH) is a well-known complication of spinal anesthesia. It commonly occurs 24 to 48 hr after dural puncture (in 92% of affected patients), but the presentation can be delayed for as long as 5 days. Current evidence from laboratory and clinical imaging studies strongly supports the theory that loss of cerebrospinal fluid (CSF) from the puncture site is the key initiating factor (Fig. 54-1). Reduction in CSF fluid and pressure allows sagging of the brain and supporting structures when the patient assumes the upright position. Sagging of the brain places direct traction on pain-sensitive structures and can also cause painful reflex vasodilatation of cerebral blood vessels. This theory is also supported by PDPH’s pathognomonic feature of occurrence or exacerbation in the upright position and resolution in the supine position. Typically, 70% of PDPHs resolve spontaneously by 1 week after dural puncture, and 95% resolve by 6 weeks.

Recognition PDPH should be considered a diagnosis of exclusion. Medical conditions that have been misdiagnosed as PDPH include hypothalamic tumors, eclampsia, spinal meningitis, and superior sagittal sinus thrombosis. Clinical features of PDPH include the following: ● ●

●

● ●

History of dural puncture Delayed presentation of headache (usually 24 to 48 hours after dural puncture) Positional nature of headache (exacerbated when upright and resolved when supine) Headache that is typically frontal or occipital in nature Presence of common associated symptoms: neck ache (57%), backache (35%), nausea (22%)

Figure 54–1 ■ Lumbar spine magnetic resonance image in a patient with post–dural puncture headache before the administration of an epidural blood patch. The static collection of fluid at L2-L3 (arrows) corresponds to leakage of cerebrospinal fluid from the dural puncture site. (From Vakharia SB, et al: Magnetic resonance imaging of cerebrospinal fluid leak and tamponade effect of blood patch in postdural puncture headache. Anesth Analg 84:585, 1997.)

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Risk Assessment With current anesthetic practice, the incidence of PDPH typically ranges from 1% to 7% after spinal anesthesia. Both patient characteristics and anesthetic technique have been implicated as risk factors for the subsequent development of PDPH. Patient factors that increase the risk include the following: ●

● ●

Younger age, probably owing to changes in the elastic properties of the dura with aging Female gender Previous history of PDPH

Anesthetic factors that reduce the risk of PDPH are the following: ●

●

●

Smaller-diameter spinal needles, probably owing to smaller dural punctures (Figs. 54-2 and 54-3) Use of pencil-point rather than cutting-tip spinal needles— the former result in less CSF leakage in vitro (see Figs. 54-2 and 54-3) Orientation of the bevel of cutting-tip needles parallel to the long axis of the dura, which may produce a smaller rent in the dura because of the longitudinal splitting of fibers, as opposed to direct transection (cutting)

Figure 54–2 ■ From the left: Atraucan, Quincke, Gertie Marx, Sprotte, and Whitacre needles. Note the cutting points on the Atraucan and Quincke needles. Also, note the differences in the configuration of the lateral eyes of the pencil-point needles. The eye of the Gertie Marx needle is the smallest and situated closest to the needle tip. The left horizontal markings are in 2-mm increments. (From Vallejo MC, et al: Postdural puncture headache: A randomized comparison of five spinal needles in obstetric patients. Anesth Analg 91:916, 2000.)

MANAGEMENT Implications PDPH can result in significant discomfort and limitation of activity owing to its positional nature. Approximately 60% of affected patients can be treated with mild analgesics until spontaneous resolution occurs. Of these patients, approximately 18% will have slight restriction of physical activity, 31% will be partially bedridden with restricted physical activity, and 51% will be entirely bedridden.

Both systemic and invasive therapies have been advocated for the treatment of PDPH. It is reasonable to try systemic treatments before instituting more invasive therapies (Fig. 54-4).

Systemic Therapy Because the proposed pathophysiology of PDPH includes reflex vasodilatation of cerebral blood vessels, systemic

mL/5 hr 140

120 116 100

80

60 54.6 40 40.3 31.2 25.5

20

22.5 17.2

16.2

11.8

9.4

27 W

26 A

0 22 Q

25 Q

24 S

27 Q

25 W

25 S

26 W

29 Q

Needle type

Figure 54–3 Relationship between needle size and bevel type and leakage of cerebrospinal fluid after dural puncture in a laboratory model. (From Holst D, et al: In vitro investigation of cerebrospinal fluid leakage after dural puncture with various spinal needles. Anesth Analg 87:1331, 1998.) ■

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Signs and symptoms of PDPH

12–24 hr PO fluids Mild analgesics Caffeine 300 mg PO Caffeine 500 mg IV 12–24 hr

Figure 54–4 headache.

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12–24 hr

Epidural blood patch 20 mL blood

Suggested treatment algorithm for post–dural puncture

therapies generally focus on the administration of vasoconstrictive agents or adrenocorticotropic hormone (ACTH). Caffeine. The intravenous administration of caffeine (500 mg) has been observed to decrease cerebral blood flow by 22% in patients suffering from PDPH. Success rates with intravenous caffeine therapy range from 40% to 80%, with mild side effects (dizziness, flushing). Oral caffeine can also be an effective therapy, with an approximately 50% success rate after 300 mg of oral caffeine.

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225

after “bloody” dural punctures. Epidural blood patch (EBP) is currently the gold standard for PDPH treatment, with a success rate ranging from 90% to 99%. Its mechanisms of action are thought to involve increased intracranial CSF pressure due to mass effect and sealing of the dural puncture site with fibrin clot (Fig. 54-5). Injection of blood into the epidural space results in an immediate mass effect persisting for at least 3 hours. Mature clot formation and sealing of the dural rent occurs by 7 hours after injection. Initial reports of EBP used small volumes of blood (2 to 3 mL), but recent recommendations are for larger volumes (15 to 20 mL). These larger volumes provide greater spread of clot (five to nine spinal segments), greater mass effect, and a higher incidence of successful treatment. Although safe and effective, the use of EBP is not risk free. Contraindications to EBP include systemic infection, localized infection of the back, and active neurologic disease. Reported complications of EBP include transient backache (35% to 100% incidence), mild temperature elevation (5%), sudden bradycardia, and radicular pain. Prolonged sequelae from EBP may also occur. Less successful epidural analgesia after prior EBP has been reported. Epidural Injection of Other Solutions. Both saline and dextran have been injected into the epidural space for the treatment of PDPH. Highly variable success rates have been reported, ranging from no effect to 90% success. The variable and often temporary nature of relief from saline or dextran,

Sumatriptan. This serotonin type 1d receptor agonist is a potent cerebral vasoconstrictor that is an effective treatment for migraine and cluster headaches. Sumatriptan can be administered intranasally, orally, or by subcutaneous injection. Case reports on the use of sumatriptan to treat PDPH are conflicting, and the sole available small randomized trial showed no benefit. Adrenocorticotropic Hormone. ACTH and its synthetic analogues have been administered intravenously for the treatment of PDPH. Proposed mechanisms of action include increased CSF production, dural edema secondary to aldosterone production, and increased β-endorphin production. Anecdotal evidence suggests a success rate of 70% to 95%, but the sole randomized controlled trial to date showed no benefit. There have been case reports of seizures in obstetric patients treated with ACTH analogues.

Invasive Therapy Loss of CSF pressure due to leakage of CSF from the dural puncture site has prompted investigators to inject substances into the epidural space to try to return CSF pressure to normal: Epidural Blood Patch. Epidural injection of autologous blood was first proposed as a treatment for PDPH in 1960, after anecdotal observations of a reduced incidence of PDPH

Figure 54–5 ■ Magnetic resonance image of 20-mL epidural blood patch demonstrating sealing of the dural leak and spread from L4 to T12 (arrowheads). (From Vakharia SB, et al: Magnetic resonance imaging of cerebrospinal fluid leak and tamponade effect of blood patch in postdural puncture headache. Anesth Analg 84:585, 1997.)

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Sumatriptan 6 mg SQ? Cosyntropin 0.5 mg IV?

12–24 hr

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coupled with the inherent risk of an epidural injection, makes their use questionable. A recent case report documented the successful use of 3 mL of fibrin glue to treat a PDPH resistant to three EPBs.

PREVENTION The cornerstone of preventing PDPH is the selection of small, non-cutting-tipped needles for dural puncture. The prophylactic administration of systemic therapies has not been well studied, and results are disappointing. The prophylactic administration of EBP is controversial. Because not all patients undergoing dural puncture will develop PDPH, many experts recommend EBP only after the development of symptoms. Another argument against the prophylactic use of EBP is its questionable efficacy when administered early (50% to 60% methemoglobin) may cause confusion, seizures, arrhythmias, hemodynamic instability, and death. The diagnosis is suggested by the presence of “chocolate-colored” blood that does not change color when exposed to air and an arterial percentage of oxygen saturation gap when analyzed by pulse oximetry and arterial blood gases. The diagnosis is confirmed by qualitative measures of methemoglobin concentrations by co-oximetry.

Local Anesthetic Systemic Toxicity

doses of local anesthetics than the latter does. In contrast, the frequency of cardiac arrest is low with either technique. Although the systemic toxic effects of local anesthetics are dose dependent, the rate of change in plasma levels is also an important factor. In the absence of intravascular injection, local anesthetics are absorbed into the systemic circulation by uptake and distribution from the surrounding perineural tissue. Subsequent plasma levels are governed by the following factors: ●

METHEMOGLOBINEMIA

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Table 56–2

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Lidocaine

Mepivacaine

Ropivacaine

Levobupivacaine

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Typical Maximal Plasma Concentrations of Common Local Anesthetics, by Regional Technique

Local Anesthetic Bupivacaine

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Technique Brachial plexus Epidural Intercostal Sciatic/femoral Brachial plexus Epidural Intercostal Sciatic/femoral* Brachial plexus Epidural Intercostal Sciatic/femoral Brachial plexus Epidural Intercostal Femoral† Psoas compartment† Brachial plexus‡ Epidural

Dose (mg) 150 50 140 400 400 400 400 650 500 500 500 500 190 150 140 150 150 250 150

Cmax (μg/mL) 1.00 1.50 1.26 1.89 4.00 4.27 6.80 2.39 3.68 4.95 8.06 3.59 1.30 1.07 1.10 0.65 1.19 1.20 1.02

Tmax (min) 20 1.7 20 15 25 20 15 30 24 16 9 31 53 40 21 30 15 55 2

Toxic Plasma Concentration (μg/mL) 3 3 3 3 5 5 5 5 5 5 5 5 4 4 4 4 4 >4 >4

*Data from Elmas C, Atanassoff PG: Combined inguinal paravascular (3-in-1) and sciatic nerve blocks for lower limb surgery. Reg Anesth 18:88-92, 1993. † Data from Kaloul I, Guay J, Cote C, et al: Ropivacaine plasma concentrations are similar during continuous lumbar plexus block using the anterior three-in-one and the posterior psoas compartment techniques. Can J Anaesth 51:52-56, 2004. ‡ Data from Crews JC, Weller RS, Moss J, James RL: Levobupivacaine for axillary brachial plexus block: A pharmacokinetic and clinical comparison in patients with normal renal function or renal disease. Anesth Analg 95:219-223, 2002. Cmax, maximal plasma concentration; Tmax, maximal time. From Salinas FV: Ion channel ligands/sodium channel blockers/local anesthetics. In Evers AS, Maze M (eds): Anesthetic Pharmacology: Physiologic Principles and Clinical Practice, 1st edition. Philadelphia, Churchill Livingstone, 2004, pp 507-537.

depression and peripheral vasodilatation occur only with extremely high levels of either lidocaine or mepivacaine. Conversely, more potent amide local anesthetics, such as bupivacaine, have a significantly narrower margin of CVS safety, expressed as the ratio of the dosage or plasma concentration required to produce irreversible cardiovascular collapse (CC) to that required to produce CNS toxicity (generalized seizures). In contrast to lidocaine, the CC/CNS ratio for bupivacaine can result in nearly simultaneous progression from CNS toxicity to cardiovascular collapse, in large part owing to bupivacaine’s ability to cause malignant ventricular arrhythmias. Bupivacaine’s enhanced ability to precipitate ventricular arrhythmias is thought to be related primarily to differences in the recovery of sodium channel block between bupivacaine and lidocaine. Both drugs rapidly block sodium channels during systole; however, bupivacaine dissociates from the sodium channel receptor much more slowly than lidocaine during diastole. Thus, within the physiologic range of heart rate, lidocaine dissociates rapidly (fast on–fast off) from the sodium channel, whereas bupivacaine remains avidly bound to it during diastole (fast on–slow off). The net electrophysiologic effect is slowed ventricular conduction and prolonged refractoriness, both of which are conducive to reentry ventricular arrhythmias. Although bupivacaine has the advantage of prolonged duration of block, with enhanced sensory-motor dissociation, concerns about its potent cardiotoxicity led to the development of alternative long-acting amide local anesthetics with the same beneficial properties but an enhanced margin of safety.

Ropivacaine is the propyl homologue of mepivacaine and bupivacaine. In contrast to older amide local anesthetics, which exist as racemic mixtures, ropivacaine is an enantiomerically pure (levorotatory isomer) local anesthetic. In general, the levorotatory isomer has less potential for systemic toxicity than the dextrorotatory isomer of the same local anesthetic. Animal and human volunteer studies have confirmed that ropivacaine is approximately 30% to 40% less cardiotoxic than racemic bupivacaine. Ropivacaine causes less prolongation of cardiac conduction and less direct negative inotropic effects than equivalent doses of bupivacaine. During cardiac resuscitation after incremental overdosage in anesthetized dogs, free plasma concentrations of ropivacaine causing cardiac arrest were more than twice those of bupivacaine. Further, the inability to resuscitate dogs with bupivacaine was higher than with ropivacaine (50% versus 10%). Recent case reports attest to ropivacaine’s lower cardiotoxicity, even after the injection of large doses sufficient to cause cardiac arrest. Although the incidence of severe systemic toxicity from local anesthetics appears to be decreasing, the potential catastrophic outcomes from cardiotoxicity cannot be underestimated. In the most recent ASA closed claims analysis of injuries associated with regional anesthesia, unintentional intravascular injections were the second largest category of neuraxial anesthesia claims that were block related and resulted in high-severity outcome (death or brain damage). Of 12 such cases, 11 occurred in the 1980s and only 1 in the 1990s; 75% of these were associated with cardiac arrest. Clinically significant methemoglobinemia can occur when large doses of prilocaine (>600 mg) are administered.

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MANAGEMENT Management of systemic toxicity depends on the severity of the event. Because plasma levels of local anesthetics associated with minor reactions fall rapidly, as long as normal metabolic processes are functional, such events can be allowed to terminate spontaneously, provided attention is paid to maintaining airway patency and providing supplemental oxygen and hemodynamic support. Seizures can be terminated with small doses of intravenous midazolam (0.05 to 0.1 mg/kg), sodium thiopental (1 to 2 mg/kg), or propofol (0.5 to 1.5 mg/kg). If generalized tonic-clonic seizures are not aborted with these doses of intravenous anesthetics, administration of succinylcholine followed by endotracheal intubation is indicated. Prompt termination of seizure activity is important to prevent the rapid development of severe metabolic acidosis associated with tonic-clonic muscular contractions.

Table 56–3

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Local Anesthetic Systemic Toxicity

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Cardiovascular depression should be treated by fluid resuscitation and vasopressors, if required. Because hypotension is usually due to a combination of direct myocardial depression and peripheral vasodilatation, agents with both β1 and α1 activity are recommended: ephedrine or phenylephrine or both (even epinephrine or norepinephrine) in incremental doses until the desired response is obtained. With cardiovascular collapse refractory to these drugs, vasopressin should be considered. Malignant ventricular arrhythmias should be managed with direct-current cardioversion and amiodarone if needed to prevent recurrences. If CVS toxicity is not responsive to any of these measures, intravenous lipid infusion or cardiopulmonary bypass should be considered. Recent animal models have demonstrated that intravenous lipid emulsion can facilitate resuscitation from acute bupivacaine overdose.

PREVENTION Because the vast majority of systemic toxic reactions to local anesthetics are the result of either inadvertent intravascular injection or systemic absorption of excessive doses, efforts should be made to minimize that potential. The anesthesiologist must be aware of the risk factors associated with both the regional technique and physiologic status of the patient that predispose to clinically significant systemic toxic reactions. Proper patient preparation includes appropriate monitoring of heart rate, blood pressure, and oxygenation; recent data indicate the added value of continuous electrocardiography. Resuscitative drugs and equipment should be immediately available. Sedatives may increase the seizure threshold but also attenuate the patient’s ability to report subjective symptoms of CNS toxicity, as well as reducing the heart rate’s response to the traditional 15-μg epinephrine “test dose.” Techniques that reduce the likelihood of direct intravascular injection should be used. Although no single measure is 100% reliable in preventing severe systemic toxicity, the following measures are recommended: ●

●

●

Inject local anesthetics in small, fractionated doses, with frequent aspiration of the syringe to assess for intravascular placement of either the needle or catheter. In the absence of contraindications, add epinephrine to local anesthetic solutions to aid in the identification of intravascular injections (“test dose”) and to decrease systemic absorption from the injection site. Be aware of the different criteria for a positive epinephrine test dose during different clinical scenarios (Table 56-3).

Criteria for Positive Epinephrine (15 μg) Test Dose in Adults

Clinical Scenario

Heart Rate Increase (bpm)

Systolic Blood Pressure Increase (mm Hg)

>20

>15

Decrease ≥25%

NA >9 >8

>15 >15 >15

NA Decrease ≥25% Decrease ≥25%

Age 60 yr General anesthesia bpm, beats per minute; NA, not applicable.

T-Wave Amplitude

REGIONAL ANESTHESIA & PAIN MANAGEMENT

After several cases reports of methemoglobinemia after intravenous prilocaine was used for regional anesthesia, it was withdrawn for such use. However, it is still available as a eutectic mixture of prilocaine 2.5% and lidocaine 2.5% (EMLA cream), commonly used as a topical anesthetic. Neonatal patients have immature reductase enzyme pathways that may predispose them to methemoglobinemia with the application of EMLA cream. Benzocaine is an ester-type local anesthetic commonly used for topical anesthesia before fiberoptic intubation, bronchoscopy, transesophageal echocardiography, and upper gastrointestinal endoscopy procedures. The Food and Drug Administration’s adverse event reporting system described 132 cases of methemoglobinemia secondary to benzocaine between 1997 and 2002. These resulted in two deaths (1.5%) and 55 (42%) life-threatening complications. Potential risk factors include concomitant use of other oxidizing agents and excessive absorption from either breaks in the mucosal barrier or delivery of excessive dosages. Clinically significant toxicity is effectively treated with intravenous methylene blue (1 mg/kg). Immunologic-mediated (allergic) reactions to preservative-free amide local anesthetics are extremely rare. However, ester local anesthetics may produce allergic reactions due to their metabolism to para-aminobenzoic acid (PABA), a known allergen. Amide local anesthetics are not metabolized to PABA unless preservatives (e.g., methylparaben) are used in their formulation; methylparaben is metabolized to PABA. Patients with true allergic reactions to ester local anesthetics should be treated with preservative-free local anesthetics.

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Although the scientific basis for maximum recommended doses is tenuous, and actual plasma levels vary with the site of injection, always administer the minimum effective dose. For blocks with a higher risk of intravascular injection or systemic absorption, consider using ropivacaine. During the administration of the local anesthetics, be vigilant for symptoms and signs of toxicity. Early intervention can reduce the complications of local anesthetic–induced toxicity.

Further Reading Albright GA: Cardiac arrest following regional anesthesia with etidocaine or bupivacaine [editorial]. Anesthesiology 51:285-287, 1979. Auroy Y, Benhamou D, Barguues L, et al: Major complications of regional anesthesia in France: The SOS regional anesthesia hotline service. Anesthesiology 97:1274-1280, 2002. Auroy Y, Narchi P, Messiah A, et al: Serious complications related to regional anesthesia: Results of a prospective survey in France. Anesthesiology 87:479-486, 1997. Berkum Y, Ben-Zvi A, Levy Y, et al: Evaluation of adverse reactions to local anesthetics: Experience with 236 patients. Ann Allergy Asthma Immunol 91:342-345, 2003. Bernards CM, Carpenter RL, Rupp SM, et al: Effects of midazolam and diazepam premedication on the central nervous system and cardiovascular toxicity of bupivacaine in pigs. Anesthesiology 70:318-323, 1989. Braid DP, Scott DB: The effect of adrenaline on the systemic absorption of local anaesthetic drugs. Acta Anaesthesiol Scand Suppl 23:334-346, 1996. Brown DL, Ransom DM, Hall JA, et al: Regional anesthesia and local anesthetic-induced systemic toxicity: Seizure frequency and accompanying cardiovascular changes. Anesth Analg 81:321-328, 1995. Butterworth JF, Brownlow RC, Leith JP, et al: Bupivacaine inhibits cyclic-3′, 5′-adenosine monophosphate production: A possible contributing factor to cardiovascular toxicity. Anesthesiology 79:88-95, 1993. Butterworth JF, Strichartz GR: Molecular mechanisms of local anesthesia: A review. Anesthesiology 72:711-734, 1990. Chazalon P, Tourtier JP, Villevielle T, et al: Ropivacaine-induced cardiac arrest after peripheral nerve block: Successful resuscitation. Anesthesiology 99:1449-1451, 2003. Clarkson CW, Hondeghem LM: Mechanism for bupivacaine depression of cardiac conduction: Fast block sodium channels during the action potential with slow recovery during diastole. Anesthesiology 62: 396-405, 1985. Dernedde M, Furlan D, Verbesselt R, et al: Grand mal convulsions after accidental intravenous injection of ropivacaine. Anesth Analg 98:521-523, 2004. Gall H, Kaufmann R, Kalveram CM: Adverse reactions to local anesthetics: Analysis of 197 cases. J Allergy Clin Immunol 97:933-937, 1996. Groban L: Central nervous system and cardiac effects from long-acting amide local anesthetic toxicity in the intact animal model. Reg Anesth Pain Med 28:3-11, 2003. Groban L, Butterworth J: Lipid reversal of bupivacaine toxicity: Has the silver bullet been identified? [editorial] Reg Anesth Pain Med 28:167-169, 2003.

Groban L, Deal DD, Vernon JC, et al: Cardiac resuscitation after incremental overdosage with lidocaine, bupivacaine, levobupivacaine, and ropivacaine in anesthetized dogs. Anesth Analg 92:37-43, 2001. Heavner JE: Cardiac toxicity of local anesthetics in the intact isolated heart model: A review. Reg Anesth Pain Med 27:545-555, 2002. Huet O, Eyrolle LJ, Mazoit JX, Ozier YM: Cardiac arrest after injection of ropivacaine for posterior lumbar plexus blockade. Anesthesiology 99:1451-1453, 2003. Knudsen K, Suurkula MB, Blomberg S, et al: Central nervous and cardiovascular effects of IV infusions of ropivacaine, bupivacaine, and placebo in volunteers. Br J Anaesth 78:507-514, 1997. Lee LA, Posner KL, Domino KB, et al: Injuries associated with regional anesthesia in the 1980s and 1990s: A closed claims analysis. Anesthesiology 101:143-152, 2004. Liu PL, Feldman HS, Giasi R, et al: Comparative CNS toxicity of lidocaine, etidocaine, bupivacaine, and tetracaine in awake dogs following rapid intravenous administration. Anesth Analg 62:375-379, 1983. Lofstrom JB: 1991 Labat lecture: The effects of local anesthetics on the peripheral vasculature. Reg Anesth 17:1-11, 1992. Moore JM, Liu SS, Neal JM: Premedication with fentanyl and midazolam decreases the reliability of intravenous lidocaine test dose. Anesth Analg 86:1015-1017, 1998. Moore TJ, Walsh CS, Cohen MR: Reported adverse event cases of methemoglobinemia associated with benzocaine products. Arch Intern Med 164:1192-1196, 2004. Mulroy MF: Systemic toxicity and cardiotoxicity from local anesthetics: Incidence and preventative measures. Reg Anesth Pain Med 27:556-561, 2002. Orringer CE, Eustace JC, Wunsch CD, Gardner LB: Natural history of lactic acidosis after grand-mal seizures. N Engl J Med 297:796-799, 1977. Salinas FV: Ion channel ligands/sodium channel blockers/local anesthetics. In Evers AS, Maze M (eds): Anesthetic Pharmacology: Physiologic Principles and Clinical Practice, 1st ed. Philadelphia, Churchill Livingstone, 2004, pp 507-537. Scott DB: Evaluation of the toxicity of local anesthetic agents in man. Br J Anaesth 47:56-59, 1975. Soltesz EG, van Pelt F, Byrne JG: Emergent cardiopulmonary bypass for bupivacaine cardiotoxicity. J Cardiothorac Vasc Anesth 17:357-358, 2003. Stewart J, Kellett N, Castro D: The central nervous system and cardiovascular effects of levobupivacaine and ropivacaine in healthy volunteers. Anesth Analg 97:412-416, 2003. Szocik JF, Gardener CA, Webb RC: Inhibitory effects of bupivacaine and lidocaine on adrenergic neuroeffector junctions in rat-tail artery. Anesthesiology 78:911-917, 1993. Tanaka M, Nishikawa T: T-wave amplitude as in indicator for detecting intravascular injection of epinephrine test dose in awake and anesthetized elderly patients. Anesth Analg 93:1332-1337, 2001. Tanaka M, Sato M, Nishikawa T: The efficacy of simulated intravascular test dose in sedated patients. Anesth Analg 93:1612-1617, 2001. Weinberg GL: Current concepts in resuscitation of patients with local anesthetic cardiac toxicity. Reg Anesth Pain Med 27:568-575, 2002. Weinberg GL, Ripper R, Feinstein DL, Hoffman W: Lipid emulsion infusion rescues dogs from bupivacaine-induced cardiac toxicity. Reg Anesth Pain Med 28:198-202, 2003. Xuecheng J, Xiaobin W, Bo G, et al: The plasma concentration of lidocaine after slow versus rapid administration of an initial dose of epidural anesthesia. Anesth Analg 84:570-573, 1997.

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Spinal Hematoma Terese T. Horlocker Case Synopsis A 75-year-old man undergoes total knee replacement under continuous epidural anesthesia. The epidural catheter is left indwelling to provide postoperative analgesia with 0.125% bupivacaine. Thromboprophylaxis with low-molecular-weight heparin (LMWH), 30 mg twice daily, is initiated 24 hours after surgery. Forty-eight hours later, the epidural catheter is removed 1 hour after a dose of LMWH. The patient’s sensory and motor block progresses, however, despite discontinuation of the local anesthetic infusion. A magnetic resonance image reveals an epidural hematoma at T12. Immediate surgical decompression results in complete neurologic recovery.

Definition The actual incidence of neurologic dysfunction resulting from hemorrhagic complications associated with neuraxial blockade is unknown; however, estimates in the literature are less than 1 in 150,000 for epidural anesthesia and less than 1 in 220,000 for spinal anesthesia. In a review of the literature between 1906 and 1994, Vandermeulen and colleagues reported 61 cases of spinal hematoma associated with epidural or spinal anesthesia. In 42 of the 61 patients (69%) with spinal hematomas associated with central neural blockade, there was evidence of hemostatic abnormality. Twenty-five of the patients had received intravenous or subcutaneous (unfractionated or low-molecular-weight) heparin, and an additional five patients were presumably administered heparin during vascular surgical procedures. In addition, 12 patients had evidence of coagulopathy or thrombocytopenia or were treated with antiplatelet drugs (aspirin, indomethacin, ticlopidine), oral anticoagulants (phenprocoumon), thrombolytics (urokinase), or dextran 70 immediately before or after the spinal or epidural anesthetic. Needle and catheter placement

Table 57–1

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was difficult in 15 patients (25%) and bloody in 15 patients (25%). Overall, in 53 of 61 cases (87%), either a clotting abnormality or difficult needle placement was noted. A spinal anesthetic was administered in 15 patients. The remaining 46 patients received an epidural anesthetic, including 32 patients with indwelling catheters. In 15 of the latter, spinal hematoma occurred immediately after removal of the epidural catheter. These results suggest that catheter removal is not entirely atraumatic and that the patient’s coagulation status should be optimized at the time of both catheter placement and removal.

Recognition In Vandermeulen’s series, neurologic compromise presented as progression of sensory or motor block (68% of patients) or bowel or bladder dysfunction (8% of patients), rather than severe radicular back pain. Spinal hematoma should be ruled out in patients exhibiting early signs of cord compression in the postoperative period. The differential diagnosis includes cauda equina syndrome, epidural abscess, and anterior spinal artery syndrome (Table 57-1). If spinal hematoma is suspected, radiographic confirmation must be sought immediately,

Differential Diagnosis of Epidural Abscess, Epidural Hemorrhage, and Anterior Spinal Artery Syndrome

Finding

Epidural Abscess

Epidural Hemorrhage

Anterior Spinal Artery Syndrome

Age of patient Previous history Onset Generalized symptoms

Any age Infection* 1-3 days Fever, malaise, back pain

Elderly Arteriosclerosis, hypotension Sudden None

Sensory involvement Motor involvement Segmental reflexes Myelogram/CT scan Cerebrospinal fluid Blood data

None or paresthesias Flaccid paralysis, later spastic Exacerbated*; later obtunded Signs of extradural compression Increased cell count Rise in sedimentation rate

50% >50 yr Anticoagulants Sudden Sharp, transient back and leg pain Variable, late Flaccid paralysis Abolished Signs of extradural compression Normal Prolonged coagulation time*

Minor, patchy Flaccid paralysis Abolished Normal Normal Normal

*Infrequent findings. CT, computed tomography. From Wedel DJ, Horlocker TT: Risks of regional anesthesia—infectious, septic. Reg Anesth 21:57-61, 1996.

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PROBLEM ANALYSIS

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because delay can lead to irreversible cord ischemia. Although spontaneous recovery has been reported, the treatment of choice is decompressive laminectomy. Complete neurologic recovery is unlikely if surgery is postponed for more than 8 hours.

Risk Assessment The risk of spinal hematoma depends on the timing of needle or catheter placement and removal and the degree of anticoagulation with the following drugs: ● ● ● ●

Standard heparin (intravenous and subcutaneous) Low-molecular-weight heparin (LMWH) Oral anticoagulants Antiplatelet medications

STANDARD HEPARIN Ruff and Dougherty reported spinal hematomas in 7 of 342 patients (2%) who underwent diagnostic lumbar puncture with subsequent heparinization. Three factors were associated with increased risk: less than 60 minutes between the administration of heparin and the lumbar puncture, traumatic needle placement, and concomitant use of other anticoagulants (aspirin). These findings have been used to define safe practice protocols for patients undergoing neuraxial blockade during systemic heparinization, particularly in the case of vascular surgery. Intrathecal and epidural anesthesia and analgesia, along with complete heparinization and cardiopulmonary bypass, have been reported without neurologic sequelae. However, at this time, there are insufficient data and experience to quantify the risk of spinal hematoma among this patient population. Low-dose subcutaneous, unfractionated heparin is administered for thromboprophylaxis in patients undergoing major thoracoabdominal surgery and in those at increased risk for hemorrhage with oral anticoagulant or LMWH therapy. A review by Schwander and Bachmann noted no spinal hematomas in more than 5000 patients who received subcutaneous heparin with spinal or epidural anesthesia. There were five cases of spinal hematoma associated with neuraxial blockade in patients receiving low-dose heparin. This confirms the limited risk associated with the use of epidural and spinal anesthesia in the presence of subcutaneous heparin treatment. LOW-MOLECULAR-WEIGHT HEPARIN Despite a notable safety record in Europe, in the first 5 years after the release of LMWH in North America, there were 40 cases of spinal hematoma associated with LMWH and neuraxial anesthesia. The risk of spinal hematoma, based on LMWH sales, prevalence of neuraxial techniques, and reported cases, was estimated to be approximately 1 in 3000 continuous epidural anesthetics, compared with 1 in 40,000 spinal anesthetics. However, this risk was later found to be much higher. Similar to the Vandermeulen series, severe radicular back pain was not the presenting symptom. Most patients complained of new-onset numbness, weakness, or bowel and

bladder dysfunction. About half of patients undergoing a continuous technique reported neurologic deficits 12 hours or more after catheter removal. The median interval between initiation of LMWH therapy and neurologic dysfunction was 3 days, and the median time to onset of symptoms and laminectomy was more than 24 hours. Less than one third of patients reported fair or good neurologic recovery. Over the past 5 years, the number of reported cases of spinal hematoma associated with LMWH therapy has declined markedly. This may be a result of decreased reporting, improved management, or simple avoidance of all neuraxial techniques in patients receiving LMWH. Continued monitoring is necessary. Indications and labeled uses for LMWH continue to evolve, including for thromboprophylaxis and the treatment of deep venous thrombosis. In addition, several off-label applications of LMWH are of special interest to the anesthesiologist and warrant discussion. LMWH has been shown to be efficacious as “bridge therapy” for patients chronically anticoagulated with warfarin, including parturients and patients with prosthetic cardiac valves, a history of atrial fibrillation, or preexisting hypercoagulable conditions. The patient is therapeutically anticoagulated with LMWH while the warfarin effect is allowed to resolve before surgery. Doses of LMWH are two- to threefold higher than those used for thromboprophylaxis. At least 24 hours is required for normal hemostais following this level of LMWH anticoagulation. ORAL ANTICOAGULANTS Few data exist regarding the risk of spinal hematoma in patients with indwelling epidural catheters who are anticoagulated with warfarin. The optimal duration of an indwelling catheter and the timing of its removal in an anticoagulated patient are also controversial. A combined series of 651 patients reported no spinal hematomas in those receiving neuraxial block in conjunction with low-dose warfarin therapy. The mean international normalized ratio (INR) at the time of catheter removal was 1.4. However, marked variability in patient response to warfarin was noted. ANTIPLATELET MEDICATIONS Several large studies have demonstrated the relative safety of neuraxial blockade in obstetric, surgical, and ambulatory pain clinic patients receiving antiplatelet medications. In a prospective study involving 1000 patients, Horlocker and colleagues reported that preoperative antiplatelet therapy did not increase the incidence of blood present at the time of needle or catheter placement or removal, suggesting that trauma during needle or catheter placement is neither increased nor sustained by these medications. The paucity of case reports among these patients is notable, given the prevalence of aspirin and other nonsteroidal anti-inflammatory drug (NSAID) use among patients with acute, chronic, or cancer pain who receive interventional therapy. No series involving the performance of neuraxial blockade in the presence of thienopyridine derivatives (clopidogrel and ticlopidine) or platelet glycoprotein IIb/IIIa receptor antagonists has been reported. Although case reports are inconsistent, increased perioperative bleeding has been noted in patients undergoing cardiac and vascular surgery after

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receiving ticlopidine, clopidogrel, and glycoprotein IIb/IIIa antagonists. This suggests that these medications may increase the risk of regional anesthesia–related hemorrhagic complications.

●

Low-molecular-weight heparin ● Proceed cautiously. ● For preoperative LMWH, administer spinal anesthesia 12 to 24 hours after the administration of LMWH, depending on dose (i.e., treatment versus thromboprophylaxis). ● Epidural catheters may remain indwelling with oncedaily dosing of LMWH. Place or remove catheters in the morning; administer LMWH in the evening. ● Epidural catheters should not remain indwelling with twice-daily dosing of LMWH. Remove the epidural catheter 2 hours before the initiation of twice-daily LMWH therapy.

●

Oral anticoagulants ● Preoperative administration does not preclude regional technique. ● Monitor the prothrombin time postoperatively; there is marked variability in patient response. ● Remove the catheter when the INR is less than 1.5.

●

Antiplatelet agents ● NSAIDs do not represent significant risk. ● Allow the antiplatelet effects of clopidogrel, ticlopidine, and glycoprotein IIb/IIIa inhibitors to resolve before neuraxial block.

Intravenous heparin ● Administer heparin 60 minutes after needle placement. ● Monitor the effect of the heparin. ● Remove the catheter when heparin activity is low or completely reversed.

Table 57–2

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PREVENTION The patient’s coagulation status should be optimized at the time of spinal or epidural needle or catheter placement, and

Pharmacologic Activities of Anticoagulants, Antiplatelet Agents, and Thrombolytics Effect on Coagulation Variables

Time to Normal Hemostasis after Discontinuation

Agent

PT

aPTT

Time to Peak Effect

Intravenous heparin Subcutaneous heparin Low-molecular-weight heparin Warfarin

↑ — — ↑↑↑

↑↑↑ ↑ — ↑

Minutes 40-50 min 3-5 hr 4-6 days (less with loading dose)

4-6 hr 4-6 hr 12-24 hr 4-6 days

Antiplatelet agents Aspirin Other NSAIDs Ticlopidine, clopidogrel Platelet glycoprotein IIb/IIIa receptor inhibitors Fibrinolytics

—

— Hours Hours Hours Minutes

5-8 days 1-3 days 1-2 wk 8-48 hr

Minutes

24-36 hr

↑

↑↑

aPTT, activated partial thromboplastin time; NSAID, nonsteroidal anti-inflammatory drug; PT, prothrombin time; —, no effect; ↑, clinically insignificant increase; ↑↑, possibly clinically significant increase; ↑↑↑, clinically significant increase.

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●

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Subcutaneous heparin ● Consider delaying administration until after needle or catheter placement in patients with anticipated technical difficulties. ● Monitor platelet count in patients receiving heparin for more than 4 days.

MANAGEMENT Before surgery, the patient’s history should be reviewed for medical conditions associated with bleeding tendencies, and the patient should be questioned about previous episodes of sustained bleeding after trauma or surgery. Because patients respond to anticoagulants with varying sensitivities, it may be helpful to verify the reversal of heparin’s or warfarin’s effects before the performance of epidural or spinal blockade (Table 57-2). The following guidelines will assist in the management of patients with altered hemostasis undergoing regional anesthetic techniques. Except in the most extraordinary circumstances, spinal and epidural blockade should be avoided in fully anticoagulated patients or those who have received thrombolytic therapy.

Spinal Hematoma

●

Implications Whether to perform spinal or epidural anesthesia or analgesia and the timing of catheter removal in a patient receiving thromboprophylaxis should be decided on an individual basis, weighing the small but definite risk of spinal hematoma against the benefits of regional anesthesia for the particular patient. Alternative anesthetic and analgesic techniques exist for patients considered to be at an unacceptably high risk.

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the level of anticoagulation must be carefully monitored during the period of epidural catheterization. It is important to note that patients respond with variable sensitivities to anticoagulant medications. Indwelling catheters should not be removed in the presence of therapeutic anticoagulation, because this appears to significantly increase the risk of spinal hematoma. In addition, communication among clinicians involved in the perioperative management of patients receiving anticoagulants for thromboprophylaxis is essential to decrease the risk of serious hemorrhagic complications.

Further Reading Bergqvist D, Lindblad B, Matzsch T: Low molecular weight heparin for thromboprophylaxis and epidural/spinal anaesthesia: Is there a risk? Acta Anaesthesiol Scand 36:605-609, 1992. Chaney MA: Intrathecal and epidural anesthesia and analgesia for cardiac surgery. Anesth Analg 84:1211-1221, 1997. CLASP (Collaborative Low-Dose Aspirin Study in Pregnancy): A randomized trial of low-dose aspirin for the prevention and treatment of preeclampsia among 9364 pregnant women. Lancet 343:619-629, 1994. Ho AM, Chung DC, Joynt GM: Neuraxial blockade and hematoma in cardiac surgery: Estimating the risk of a rare adverse event that has not (yet) occurred. Chest 117:551-555, 2000. Horlocker TT, Bajwa ZH, Ashraft Z, et al: Risk assessment of hemorrhagic complications associated with nonsteroidal antiiflammatory

medications in ambulatory pain clinic patients undergoing epidural steroid injection. Anesth Analg 95:1691-1697, 2002. Horlocker TT, Wedel DJ, Benzon H, et al: Regional anesthesia and anticoagulation—defining the risk. The Second ASRA consensus conference on neuraxial anesthesia and anticoagulation. Reg Anesth Pain Med 28:172-197, 2003. Horlocker TT, Wedel DJ, Offord KP, et al: Preoperative antiplatelet therapy does not increase the risk of spinal hematoma associated with regional anesthesia. Anesth Analg 80:303-309, 1995. Odoom JA, Sih IL: Epidural analgesia and anticoagulant therapy. Anaesthesia 38:254-259, 1983. Rao TLK, El-Etr AA: Anticoagulation following placement of epidural and subarachnoid catheters: An evaluation of neurologic sequelae. Anesthesiology 55:618-620, 1981. Ruff RL, Dougherty JH: Complications of lumbar puncture followed by anticoagulation. Stroke 12:879-881, 1981. Schroeder DR: Statistics: Detecting a rare adverse drug reaction using spontaneous reports. Reg Anesth Pain Med 23:183-189, 1998. Schwander D, Bachmann F: Heparin and spinal or epidural anesthesia: Decision analysis [review]. Ann Fr Anesth Reanim 10:284-296, 1991. Tryba M: Epidural regional anesthesia and low molecular heparin: Pro [German]. Anasth Intensivmed Notfallmed Schmerzther 28:179-181, 1993. Vandermeulen EP, Van Aken H, Vermylen J: Anticoagulants and spinalepidural anesthesia. Anesth Analg 79:1165-1177, 1994. Wu CL, Perkins FM: Oral anticoagulant prophylaxis and epidural catheter removal. Reg Anesth 21:517-524, 1996.

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James C. Crews Case Synopsis

PROBLEM ANALYSIS Definition Infectious complications of central neuraxial anesthetic and analgesic procedures occur rarely but may be associated with significant patient morbidity, including sepsis, epidural or paravertebral abscess formation, meningitis, and paraplegia. A high index of suspicion, early diagnosis, and prompt intervention with appropriate therapy are important for achieving optimal outcomes. Infectious complications of central neuraxial block techniques may range from superficial infection at the percutaneous puncture site to more consequential infections, such as epidural abscess or meningitis. Most consequential infectious complications are associated with percutaneous catheter techniques, although epidural abscess and meningitis have been reported after single-injection epidural anesthesia or corticosteroid injections. Potential mechanisms for infection associated with central neuraxial block include (1) direct inoculation during needle or catheter placement; (2) infection at the catheter exit site, with spread along the catheter track; (3) contamination of the injectate; and (4) hematogenous spread (“bacteremic seeding”) from a distant site of infection. Progressive neurologic impairment of bowel and bladder function or lower extremity sensory and motor function may result from epidural or paravertebral abscess with spinal cord or nerve root compression. The specific pathogenesis underlying spinal cord dysfunction with spinal epidural abscess is thought to be related to direct mechanical

REGIONAL ANESTHESIA & PAIN MANAGEMENT

A 63-year-old woman with a history of diabetes mellitus, hypertension, and chronic low back pain underwent a small bowel resection for obstruction secondary to metastatic colon cancer. A thoracic epidural catheter was placed for perioperative analgesia, and the patient received an epidural infusion of bupivacaine and morphine for 3 days postoperatively. At the time of epidural catheter removal, the insertion site was surrounded by a small area of erythema, with a scant amount of serosanguineous drainage. The patient was followed by the Acute Pain Service for an additional 2 days, at which time she reported severe thoracolumbar back pain, low-grade fever, and heaviness in her legs. Examination of the back revealed a small erythematous area at the previous epidural catheter insertion site with a small amount of purulent drainage. The neurologic examination was unremarkable. Laboratory studies demonstrated leukocytosis. Owing to the patient’s history and complaints, a magnetic resonance imaging (MRI) scan with and without gadolinium contrast was obtained of the thoracic, lumbar, and sacral spine. MRI demonstrated an extensive posterior spinal epidural abscess from T10 to L2. The patient underwent a laminotomy drainage procedure and culture-directed antibiotic therapy for Staphylococcus aureus. The remainder of her hospital recovery was uneventful, and she was discharged home without neurologic sequelae.

compression or vascular damage, with resultant spinal cord hypoxia.

Recognition Superficial infectious complications usually present with localized erythema and drainage at the needle or catheter insertion site. Deep infections may present with local symptoms at the needle or catheter insertion site in addition to the following: ● ● ● ●

Back pain Fever Localized tenderness Leukocytosis

Neurologic impairment due to deep tissue abscess and spinal cord or nerve root compression may present with the following: ● ● ●

Radicular irritation Progressive sensory or motor neurologic deficit Bowel and bladder incontinence The clinical features of meningitis include the following:

● ● ● ●

Nuchal rigidity Headache Leukocytosis and fever Photophobia

Patients with evidence of superficial infection should be evaluated and monitored for the development of symptoms associated with deep infection. Culture of purulent drainage at the site of infection or epidural catheter tip may 239

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be important to direct appropriate antibiotic therapy. Before hospital discharge, patients must be instructed to notify appropriate health care personnel or to seek emergency medical evaluation in the event of any of the following: ● ● ● ●

New onset of back pain Fever Redness or soreness at the needle or catheter insertion site Subtle signs or symptoms of neurologic impairment

Patients with signs or symptoms suggestive of spinal or epidural abscess should be urgently evaluated for fever and leukocytosis and have a thorough neurologic evaluation. Radiographic diagnosis of spinal epidural abscess is best made by gadolinium-enhanced MRI scan of the spine (Figs. 58-1 and 58-2). Diagnosis and treatment of epidural abscess should not be delayed until neurologic deficits become apparent.

Risk Assessment In a meta-analysis of 915 patients with spinal epidural abscess reported in the world literature between 1954 and 1997, neuraxial anesthesia or analgesia had been performed in 5.5% of them; other invasive procedures as diverse as vascular access and spinal surgery accounted for 16.5%. Estimates of the incidence of spinal epidural abscess after central neuraxial block range from 1 in1930 for continuous epidural catheter techniques to 1 in 100,000 for single-injection and short-term techniques. For patients with chronically implanted epidural catheter systems, infectious risk has been reported as 1 per 1702 catheter-days. Although the specific incidence is unclear, the presence of any of the following factors suggests a higher risk for infection following central neuraxial block: ●

● ●

Immunocompromised state (e.g., acquired immunodeficiency syndrome [AIDS], cancer chemotherapy, organ transplantation, chronic dialysis, intravenous drug abuse, chronic alcoholism) Diabetes mellitus Concomitant steroid treatment

Figure 58–2 ■ Sagittal T1-weighted magnetic resonance image of the spine following intravenous administration of gadolinium. There is a large gadolinium-enhanced mass (arrow) in the posterior epidural space extending from T9 to L3. The area of low signal density within the abscess represents a poorly perfused area of liquefaction. (From Rathmell JP, Garahan MB, Alsofrom GF: Epidural abscess following epidural analgesia. Reg Anesth Pain Med 25:79-82, 2000.)

● ● ● ●

Localized infection at insertion site Sepsis Long-term catheter use Bacteremia

Implications Both meningitis and epidural abscess can be life threatening or result in permanent neurologic sequelae if not treated immediately. A high index of clinical suspicion, early diagnosis, and prompt treatment before massive neurologic symptoms occur are key to optimizing patient outcomes.

MANAGEMENT

Figure 58–1 ■ Axial T2-weighted magnetic resonance image of the spine at the level of L1. There is a large, high-signal fluid collection in the posterior epidural space. The abscess is causing anterior displacement of the dural sac (arrowheads), producing approximately 30% reduction in the anteroposterior diameter of the spinal canal. (From Rathmell JP, Garahan MB, Alsofrom GF: Epidural abscess following epidural analgesia. Reg Anesth Pain Med 25:79-82, 2000.)

Patients with superficial infectious complications can be managed by local drainage and antibiotic therapy. However, even these patients, especially those at increased risk for more serious infectious complications, should be carefully instructed and monitored for the development of any signs or symptoms of epidural or spinal abscess or meningitis. They should also be advised to seek immediate medical attention for progressive back pain, fever, or the development of subtle neurologic changes. This will facilitate timely detection, diagnosis, and therapy. Patients with a history of central neuraxial block who present with back pain and fever should undergo a thorough evaluation for serious infectious complications as part of the differential diagnosis. Epidural abscess following

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PREVENTION As with any invasive procedure, the risks associated with a planned central neuraxial block must be weighed against its potential benefits. Although infectious complications are rare, patients who might benefit most from such blocks are often those with associated morbidities or other factors that increase the risk for serious infectious complications. If central neuraxial blocks are used in patients at increased risk for complications, especially if the extended use of indwelling catheters is anticipated for postoperative or post-traumatic injury pain relief, a higher index of suspicion is required when evaluating these patients for potential infectious complications. Meticulous attention to sterile technique is vital for reducing infectious complications associated with central neuraxial blocks or catheters. Thorough hand washing, sterile gloves, surgical caps or hoods and masks, and sterile block techniques are all important considerations. A wide area of skin should be prepared with povidone-iodine, iodophor-inisopropyl alcohol, or chlorhexidine. Adequate time must be given for the solution to dry before the central neuraxial block is performed. Also, use of a “no-touch” technique (i.e., landmarks identified and marked, if necessary, before skin preparation) helps reduce the risk of central neuraxial infectious complications. Chlorhexidine and iodophor-in-isopropyl alcohol reportedly provide better antimicrobial skin disinfection and prevention of bacterial regrowth compared with povidone-iodine. Use of clear plastic surgical drapes offers the advantage of being able to visualize landmarks during the block procedure. Further, covering epidural catheters with clear sterile dressings allows daily assessment of the insertion site. Sterile technique should be maintained for dosing catheters and when changing infusion connections for continuous epidural infusions. Maintaining a tightly closed infusion system throughout therapy should help reduce catheter contamination during line or infusate changes. Infusion solutions should be prepared by pharmacy personnel with sterile technique and under a laminar flow hood. Central neuraxial block in patients with bacteremia remains controversial. If such blocks are deemed necessary or appropriate in patients with bacteremia, one should consider performing the block only after appropriate antibiotic

241

coverage has been provided. For patients with indwelling epidural catheters who become bacteremic, it is my practice to remove the catheter, provide indicated antibiotic therapy, and then replace the catheter at a different level if continuous epidural therapy is still desired. Both for cost considerations and because of its low predictive value in identifying contamination and infection, routine culture of epidural catheter tips is not advised. However, if the epidural catheter insertion site is surrounded by an area of localized inflammation or drainage, bacteriologic examination of the epidural catheter tip may suggest appropriate antibiotic therapy. Although preventive measures are important, they cannot entirely eliminate the risk of infectious complications of central neuraxial block. A high index of suspicion for the development of infectious complications, prompt diagnosis, and immediate therapy are paramount for reducing patient morbidity and permanent neurologic injury.

Further Reading Aota Y, Onari K, Suga Y: Iliopsoas abscess and persistent radiculopathy: A rare complication of continuous infusion techniques of epidural anesthesia. Anesthesiology 96:1023-1025, 2002. Birnbach DJ, Meadows W, Stein DJ, et al: Comparison of povidone iodine and DuraPrep, an iodophor-in-isopropyl alcohol solution, for skin disinfection prior to epidural catheter insertion in parturients. Anesthesiology 98:164-169, 2003. Dawson S: Epidural catheter infections. J Hosp Infect 47:3-8, 2001. Du Pen SL, Peterson DG, Williams A, Bogosian AJ: Infection during chronic epidural catheterization: Diagnosis and treatment. Anesthesiology 73:905-909, 1990. Hooten WM, Kinney MO, Huntoon MA: Epidural abscess and meningitis after epidural corticosteroid injection. Mayo Clin Proc 79:682-686, 2004. Huang RC, Shapiro GS, Lim M, et al: Cervical epidural abscess after epidural steroid injection. Spine 29:E7-E9, 2004. Kindler CH, Seeberger MD, Staender SE: Epidural abscess complicating epidural anesthesia and analgesia: An analysis of the literature. Acta Anaesthesiol Scand 42:614-620, 1998. Kinirons B, Mimoz O, Lafendi L, et al: Chlorhexidine versus povidone iodine in preventing colonization of continuous epidural catheters in children: A randomized, controlled trial. Anesthesiology 94:239-244, 2001. Koka VK, Potti A: Spinal epidural abscess after corticosteroid injections. South Med J 95:772-774, 2002. Lee BB, Kee WD, Griffith JF: Vertebral osteomyelitis and psoas abscess occurring after obstetric epidural anesthesia. Reg Anesth Pain Med 27: 220-224, 2002. Leys D, Lesoin F, Viaud C, et al: Decreased morbidity from acute bacterial spinal epidural abscesses using computed tomography and nonsurgical treatment in selected patients. Ann Neurol 17:350-355, 1985. Rathmell JP, Garahan MB, Alsofrom GF: Epidural abscess following epidural analgesia. Reg Anesth Pain Med 25:79-82, 2000. Reihsaus E, Waldbaur H, Seeling W: Spinal epidural abscess: A meta-analysis of 915 patients. Neurosurg Rev 23:175-204, 2000. Sorensen P: Spinal epidural abscesses: Conservative treatment for selected subgroups of patients. Br J Neurosurg 17:513-518, 2003. Steffen P, Seeling W, Essig A, et al: Bacterial contamination of epidural catheters: Microbiological examination of 502 epidural catheters used for postoperative analgesia. J Clin Anesth 16:92-97, 2004. Trautmann M, Lepper PM, Schmitz FJ: Three cases of bacterial meningitis after spinal and epidural anesthesia. Eur J Clin Microbiol Infect Dis 21:43-45, 2002. Wang LP, Hauerberg J, Schmidt JF: Incidence of spinal epidural abscess after epidural analgesia: A national 1-year survey. Anesthesiology 91: 1928-1936, 1999. Wittum S, Hofer CK, Rolli U, et al: Sacral osteomyelitis after single-shot epidural anesthesia via the caudal approach in a child. Anesthesiology 99:503-505, 2003.

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central neuraxial block has been diagnosed days, weeks, and even months after the intervention. Although more conservative treatment approaches have been reported, surgical drainage and antibiotic therapy for epidural abscess are still the definitive treatment of choice. Epidural abscess with neurologic signs or symptoms requires urgent surgical intervention to prevent progressive and possibly permanent neurologic injury. Antibiotic therapy should be initiated promptly. The initial agent used should be effective against Staphylococcus aureus and able to penetrate bone. Ultimately, antibiotic therapy should be directed by specific culture and sensitivity determinations, as well as by clinical or institutional considerations. Depending on the nature and severity of the infection, antibiotic therapy may be required for 4 to 6 weeks or longer.

Infectious Complications of Central Neuraxial Block

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Thomas McCutchen and J. C. Gerancher Case Synopsis A frail, 55-kg, 79-year-old woman is admitted for elective hip replacement as the first surgery of the day in a busy ambulatory surgery center. An epidural catheter is placed for surgical anesthesia and postoperative analgesia. With the patient sitting on the operating room table, catheter placement is uneventful. Fifteen milliliters of a slightly hypobaric solution (2% lidocaine with 5 μg/mL of both fentanyl and epinephrine) is administered via the catheter in three 5-mL doses over 3 minutes. Pain in the arthritic hip is immediately relieved, and the patient’s lower extremities become insensate. Five minutes later, she complains of weakness and experiences difficulty breathing. She then becomes apneic and unconscious, with subsequent oxygen desaturation and hypotension. She is ventilated with a mask and then intubated. Blood pressure is maintained with ephedrine and intravenous fluid.

PROBLEM ANALYSIS Definition When local anesthetic in volumes typically used for epidural analgesia or anesthesia is unintentionally administered into the subarachnoid (intrathecal) space, morbidity and mortality may result due to high spinal anesthesia. Such injection may occur if local anesthetic is delivered through a needle or catheter that has fully or partially penetrated the dura and arachnoid membranes.

Recognition The clinical consequences of unintended intrathecal injection depend on the amount of local anesthetic introduced into the cerebrospinal fluid (CSF). Small amounts result in numbness of the lower extremities; larger amounts result in extensive spread and possibly unconsciousness and respiratory arrest secondary to brainstem anesthesia.

Risk Assessment: Anatomic Considerations The epidural space lies outside the dura mater. This tough outer layer of the meninges fuses with periosteum at the foramen magnum. The epidural space extends laterally to the spinal nerve roots, where it fuses with epineurium in the intervertebral foramina, caudad to the sacrococcygeal ligament and anterior to the posterior longitudinal ligament, ligamentum flavum, and laminae. It communicates with the paravertebral space via intervertebral foramina. The contents of the epidural space consist of fat, which is found predominantly posteriorly and laterally. Valveless veins are found predominantly in the lateral and anterior epidural space. 242

The arachnoid membrane is a delicate membrane that abuts the inner surface of the dura mater. It consists of layers of flattened cells with connective tissue fibers running between these layers. The cells are interconnected by tight junctions, which likely accounts for the fact that the arachnoid is the principal physiologic barrier for drugs diffusing from the epidural space to the intrathecal space. In the region of the foramina, where spinal nerve roots traverse both the arachnoid and the dura mater, the arachnoid membrane herniates through the dura to form granulations. Both spinal and intracranial arachnoid granulations serve as portals for CSF and its constituents to exit the central nervous system. The pia mater is an even more delicate layer of the meninges that is adherent to the spinal cord. The intrathecal space lies between the arachnoid membrane and the pia mater and contains CSF. Spinal CSF directly communicates with intracranial CSF.

Implications The epidural space is a potential space, as the majority of the dura is in contact with the walls of the vertebral canal. It is also a discontinuous series of compartments that become continuous only when liquid or air is injected. Thus, a larger dose of local anesthetic is required for epidural anesthesia or analgesia compared with spinal anesthesia. This anatomy also explains the bandlike block that develops in dermatomes just above and below the level of epidural local anesthetic injection, with further spread directly related to the volume of local anesthetic injected. In contrast, when local anesthetic is introduced into and diffuses throughout CSF within the intrathecal space to produce spinal anesthesia, it can produce block well above and below the level of injection. In addition to the volume of drug delivered and its concentration, spread

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MANAGEMENT Early recognition of unintentional spinal injection is paramount to prevent further injections and limit the potential for morbidity. If the patient is in pain as the epidural is being dosed (e.g., an obstetric patient in active labor), the first sign of an unintended intrathecal injection may be almost immediate, total cessation of all pain after injection of a small test dose. This may be followed by motor and sensory block that develops more rapidly and extensively than expected with epidural injection. Treatment for unintended spinal injection is supportive and consists of ensuring a patent airway, oxygenating and ventilating the patient, and supporting blood pressure with fluids (volume) and vasopressors (if needed) until the high block resolves. In any setting where neuraxial anesthesia is used, basic airway equipment must be readily available, along with a wellthought-out plan for managing unconscious and apneic patients with possible complete cardiovascular collapse.

PREVENTION Prevention requires a high index of suspicion during epidural needle and catheter placement, with careful aspiration and appropriate test dosing of the needle and catheter before the administration of the planned epidural volume of local anesthetic. With obvious free flow of CSF via the epidural needle or catheter during attempts to locate the epidural space, epidural-strength doses and volumes of local anesthetic should not be administered. Often, inadvertent intrathecal needle or catheter placement is not obvious. For example, a dural rent or small tear may be made by the tip of the needle intended for epidural placement. This rent or tear may be large enough to admit an epidural catheter, but there would be no CSF return from the needle because its tip resides mostly in the epidural space. In this case, slow, deliberate aspiration of the catheter before injection might identify CSF.

If saline is used for the loss-of-resistance technique or an epidural catheter is being replaced after recent dosing via a previously placed epidural catheter, it may be difficult to determine whether the clear fluid aspirated from the supposed epidural space is previously injected saline or local anesthetic or CSF. Several maneuvers have been suggested to distinguish CSF from other fluids, including measurement of pH, temperature, glucose, and turbidity when mixed with thiopental. Unfortunately, none of these methods has broad clinical utility. If bubbles are aspirated along with the clear fluid and the total amount of clear fluid that can be aspirated is less than 3 to 5 mL, the catheter is not likely to be in the intrathecal space. However, the catheter should not be used until it has been adequately tested. Epidural test doses consist of a small amount of local anesthetic. The rationale is that such small amounts injected into the intrathecal space would produce an easily recognizable motor and sensory spinal block without producing unacceptably high spinal anesthesia; if the same test dose were injected epidurally, it should produce minimal or no obvious effects. A typical test dose might be 40 to 60 mg of lidocaine, which would quickly produce signs and symptoms of relatively low-level spinal block if injected intrathecally. One must also keep in mind that if combined spinal-epidural anesthesia is performed and the patient has received sufficient spinal local anesthetic for high- or low-level surgical anesthesia, any subsequent epidural test dose might result in an unacceptably high level of spinal anesthesia. In all instances, repeat dosing of an in situ epidural catheter should be incremental. Case reports have noted catheter migration into the intrathecal space. Providing an appropriate time interval between incremental dosing to assess for intrathecal injection should allow for the detection of migrated catheters. Finally, intrathecal catheters left in place intentionally should be clearly labeled as such, to prevent accidental dosing with epidural volumes of local anesthetic.

Further Reading Bernards CM: Epidural and spinal anesthesia. In Barash PG, Cullen BF, Stoelting RK (eds): Clinical Anesthesia, 4th ed. Philadelphia, Lippincott Williams & Wilkins, 2001, pp 689-713. Bernards CM, Hill H: The spinal nerve root sleeve is not a preferred route for redistribution of drugs from the epidural space to the spinal cord. Anesthesiology 75:827, 1991. Calimaran AL, Strauss-Hoder TP, Wang WY, et al: The effect of epidural test dose on motor function after a combined spinal-epidural technique for labor analgesia. Anesth Analg 96:167-172, 1996. Hogan Q: Epidural catheter tip position and distribution of injectate evaluated by computed tomography. Anesthesiology 90:964-970, 1994. Poblete B, Van Gessel EF, Gaggero G, Gamulin Z: Efficacy of three test doses to detect epidural catheter misplacement. Can J Anaesth 46:34-39, 1999. Reisner LS: Epidural test solution or spinal fluid? Anesthesiology 44:451, 1976. Tessler MJ, Wiesel S, Wahba RM, Quance DR: A comparison of simple identification tests to distinguish cerebrospinal fluid from local anaesthetic solution. Anaesthesia 49:821-822, 1994. Visser WA: Delayed subarachnoid migration of an epidural catheter. Anesthesiology 88:1414-1415, 1998. Waters JH, Rizzo VL, Ramanathan S: A re-evaluation of the ability of thiopental to identify cerebrospinal fluid in epidural catheter aspirate. J Clin Anesth 7:224-227, 1995.

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of an intrathecally administered local anesthetic is related to the patient’s position, depending on whether a hypotonic or hypertonic local anesthetic solution is injected. If the solution is isotonic, spread of the block is more dependent on the volume and concentration of the local anesthetic injected intrathecally, regardless of whether vasoconstrictors are used to prolong the block. The C3-C5 spinal nerve roots, which contribute to the phrenic nerves, may be anesthetized with “high” epidural blocks. Thus, phrenic nerve paralysis may result from high epidural anesthesia. This can lead to respiratory paralysis with complete awareness. However, because intracranial and vertebral spinal fluid are continuous, spinal anesthetics can reach and anesthetize the brainstem. Finally, direct communication between the epidural and paravertebral spaces may result in a one-sided epidural block, especially if the epidural catheter is placed near, or the majority of local anesthetic is deposited into, a nerve root foramen laterally or the posterior longitudinal ligament anteriorly.

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Thomas McCutchen and J. C. Gerancher Case Synopsis A healthy, 80-kg primigravida (38 weeks’ gestation) is admitted in active labor, with a cesarean section (C-section) planned for breech presentation. Because of an anticipated 1-hour delay before the C-section can begin, a lumbar epidural block is requested for analgesia and anesthesia. This is placed without incident. The patient experiences a significant amount of pain with injection of the 3-mL test dose (1.5% lidocaine with 1:200,000 epinephrine). There are no signs of intrathecal or intravenous administration. The catheter is pulled back 1 cm, and 10 mL of 2% lidocaine is injected in 5-mL increments, with less pain. Her contraction pain resolves completely, and she develops a T6-level block to temperature. Fifteen minutes before the C-section, an additional 15 mL of 2% lidocaine is administered through the epidural catheter, with total loss of sensation below T6 5 minutes after arrival in the operating room. Fifteen minutes later, the patient complains of difficulty breathing; her hand grip and biceps strength are weak. The patient becomes lethargic, followed by a loss of consciousness and finally apnea. She is successfully intubated, and the case proceeds under general anesthesia. She is mechanically ventilated in the operating room and postanesthesia care unit for 3 hours after the initial epidural dosing. She then begins to awaken, gains strength, and is successfully extubated. Later that day, radiopaque contrast material is injected through the epidural catheter and reveals cephalad, parallel, “train-tracking” of the contrast medium.

PROBLEM ANALYSIS Definition If local anesthetic in volumes typically used for epidural analgesia or anesthesia are unintentionally administered into the subdural space, considerable morbidity and mortality may result. Also, such injections may result in inadequate blockade.

Recognition Classically, subdural injection has been described as an unexpectedly high block 15 to 35 minutes after intended lumbar epidural injection. When investigated with radiographic contrast material, a stereotypical cephalad “railroad tracking” of contrast material (outlining the subdural space circumferentially around the thecal sac) has been seen (Figs. 60-1 to 60-3). Since 1975, there have been 30 reports of unusually extensive blocks with subdural injection that were confirmed by radiocontrast radiography. Because the subdural space extends above the foramen magnum, some cases presented as unconsciousness with centrally mediated apnea. Recent work, mainly by Collier, suggests that cases with the latter presentation are merely one subset of the possible clinical manifestations of subdural injection. Other presentations, including low block, unilateral block, and dermatomal block, are usually not investigated with radiographic contrast 244

material and thus are not recognized as attributable to local anesthetic subdural injection. The myriad possible presentations of subdural injection have not been identified owing to the dearth of investigation. Collier recently used radiography to investigate 35 cases of atypical or inadequate epidural blocks for cesarean delivery and found four instances (11.4%) of subdural radiocontrast injection. Each patient had severe pain with injection of less than 5 mL of “epidural” local anesthetic. Three had low blocks, and one had a one-sided block. With time (25 to 50 minutes), and after the injection of 10 to 20 mL of additional local anesthetic, all patients eventually achieved surgical anesthesia. Depending on the volume injected and the force and direction of injection, local anesthetic may track cephalad, caudad, or laterally toward a nerve root or form a well-localized “pocket” of local anesthetic. Further, use of multiple orifice catheters may facilitate multicompartment (e.g., subduralepidural or subdural-intrathecal) injections. Collier further speculates that several potential tissue planes exist within the arachnoid membrane and the arachnoid-dura interface,“with each plane having its own radiographic findings and clinical significance.”

Risk Assessment Subdural injections are not injections into a potential space, as epidural injections are. Rather, the injectate produces

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A

B

Figure 60–1 ■ Anteroposterior (A) and lateral (B) views of the lumbar spine after radiocontrast injection through a lumbar catheter (dotted line) reveal a focal collection of contrast material in the subdural space anterior to the thecal sac. (From Collier CB: Accidental subdural injection during attempted lumbar epidural block may present as failed or inadequate block: Radiographic evidence. Reg Anesth Pain Med 29:45-51, 2004.)

A

B

Figure 60–2 ■ Anteroposterior (A) and lateral (B) views of the lumbar spine after contrast injection through a lumbar catheter (dotted line) reveal multicompartment spread of radiocontrast around the thecal sac in the subdural space of L3-L5 (S), and anterior-caudad spread of radiocontrast into the sacral canal (E). (From Collier CB: Accidental subdural injection during attempted lumbar epidural block may present as failed or inadequate block: Radiographic evidence. Reg Anesth Pain Med 29:45-51, 2004.)

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A

B

Figure 60–3 ■ Anteroposterior (A) and lateral (B) views of the lumbar spine after radiocontrast injection through a lumbar catheter reveal multicompartment subdural spread of radiocontrast (S), including localized extension along the L4 nerve root (visible in A) and into the epidural space (E) of L3. (From Collier CB: Accidental subdural injection during attempted lumbar epidural block may present as failed or inadequate block: Radiographic evidence. Reg Anesth Pain Med 29:45-51, 2004.)

a disruptive dissection between two tissue planes. Both Collier and Reina and colleagues describe the subdural space as the dura-arachnoid interface formed by a cellular junction between the two membranes. This junction is composed of neuroepithelial cells surrounded by an amorphous substance. There is no subdural space in nontraumatized tissues. Both groups hypothesize that a subdural space may appear if the neuroepithelial cells break up as a result of pressure exerted by mechanical shear forces, air, or injected fluids. Any of these have the potential to create fissures within the amorphous substance of the dura-arachnoid interface. Such fissures could readily expand toward weaker areas, especially laterally, where the amorphous substance is more prolific. Unintended subdural injection occurs when local anesthetic is injected through a needle or catheter that has created a disruption in the subdural space large enough to accommodate local anesthetic. Subdural injections are unpredictable. Given the flimsy nature of the arachnoid and its intimate relationship with the dura, it is remarkable that subdural injections are even possible. Indeed, the most skilled neurosurgeons have difficulty incising the dura under direct vision without disrupting the arachnoid membrane. The reported rate of unintended subdural injection during epidural anesthesia is about 0.8%. However, it is now believed that subdural injections are more common than previously thought. Indeed, the radiology literature reports a 10% rate of subdural injection during attempted spinal myelography. A likely explanation for this discrepancy is that radiologists have readily available radiocontrast materials for detecting subdural injections. Thus, unusual blocks following

epidural injection that are not investigated radiographically may be the result of subdural injection.

Implications Patients may have transient pain with the injection of small volumes of local anesthetic. This is uncommon with epidural or intrathecal injection of similar volumes. This pain is thought to be caused by either cleaving of meningeal tissues or nerve root compression due to the mass effect of subdural injectates. Pain is short-lived and without sequelae. Additional doses cause little if any pain. Subdural local anesthetic injection can present in multiple ways, depending on the spread and direction of the dissecting injectate and the amount that enters the epidural, subdural, or intrathecal compartment. Subdural and multicompartment injections may present as a high block, low block, radicular block, “patchy” block, or one-sided block. High blocks caused by subdural injections have a clinical presentation similar to that of high spinal blockade (unconsciousness, centrally mediated apnea, hypotension). High subdurals may be difficult to distinguish from high epidurals, because both blocks mature over a relatively long period (15 to 30 minutes). With additional local anesthetic and time, inadequate blocks may eventually resemble a normal epidural block, or they may require catheter manipulation and replacement. Attempted intrathecal block after subdural injection may be difficult, because the needle and injectate tend to reenter the newly created subdural space. This may occur even several months after suspected subdural injection, suggesting

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that a permanent defect may be formed that predisposes the patient to subsequent subdural injections. Indeed, two of Collier’s most recent cases involved one patient who experienced subdural injection during what appeared to be uncomplicated epidural catheter placements for two cesarean deliveries.

MANAGEMENT Treatment of extensive blockade is supportive, as for unintended high intrathecal injection. Inadequate subdural blockade may be overcome with additional doses of local anesthetic, but there is the associated risk of more extensive block.

Unlike the situation with intrathecal needle or catheter placement, aspiration and incremental dosing do not prevent

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subdural injection. However, removing a needle or catheter through which small injections of local anesthetic produced pain may prevent subdural blockade.

Further Reading Bernards CM: Epidural and spinal anesthesia. In Barash PG, Cullen BF, Stoelting RK (eds):Clinical Anesthesia, 4th ed. Philadelphia, Lippincott Williams & Wilkins, 2001, pp 689-713. Collier CB: Accidental subdural block: Four more cases and a radiographic review. Anesth Intensive Care 20:215-232, 1992. Collier CB: Accidental subdural injection during attempted lumbar epidural block may present as a failed or inadequate block: Radiographic evidence. Reg Anesth Pain Med 29:45-51, 2004. Jones M, Newton T: Inadvertent extra-arachnoid injections in myelography. Radiology 80:818, 1963. Lubenow T, Keh-Wong E, Kristof K, et al: Inadvertent subdural injection: A complication of epidural block. Anesth Analg 67:175, 1988. Reina MA, De Leon Casasola O, Lopez A, et al: The origin of the spinal subdural space: Ultrastructure findings. Anesth Analg 94:991-995, 2002. Schultz GH, Brogden BG: The problem of subdural placement in myelography. Radiology 79:91-95, 1962.

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PREVENTION

Epidural Anesthesia: Unintended Subdural Injection

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Alain Borgeat and Steffan Blumenthal Case Synopsis A 25-year-old man presents for rotator cuff repair and has an interscalene block and catheter placed. The block is performed using Winnie’s landmarks and with the aid of a nerve stimulator. A triceps response is obtained at a depth of 2.5 cm. The catheter is threaded 6 cm past the tip of the stimulating needle. The procedure is uneventful, except for transient resistance encountered during catheter placement. After negative aspiration for blood and cerebrospinal fluid, 0.5% bupivacaine is slowly injected through the catheter. After 10 mL is injected, the patient becomes drowsy, then unresponsive and apneic, with loss of muscle tone in all extremities; his pupils are widely dilated. The patient is given oxygen with manual assisted ventilation, followed by tracheal intubation.

PROBLEM ANALYSIS Definition Total spinal anesthesia is one of the most severe complications that can occur during the performance of an interscalene block. Other severe complications include injection of the local anesthetic into the vertebral artery, high epidural anesthesia, subdural injection, pneumothorax, and neuropathy.

Recognition The signs and symptoms of total spinal anesthesia result from blockade of the cervicothoracic segments of the central neuraxis. Symptoms of central nervous system involvement are virtually always present and range from the inability to phonate to unconsciousness and the rapid development of bilateral flaccid paralysis. Bilateral dilated, nonreactive pupils are frequently observed, consistent with a block of parasympathetic efferent activity from the Edinger-Westphal nucleus. The latter sign demonstrates that some amount of local anesthetic entered the cranium. Apnea is usually (but not always) present, due to the close proximity of the phrenic nerve roots (C3-C5) to the site of interscalene injection (C6-C7). The development of bradycardia and hypotension is explained by either cervicothoracic spinal block of the cardiac accelerator fiber (T1-T4) or penetration of local anesthetic into the medullary region of the central nervous system. The application of local anesthetic in this structure results in hypotension, bradycardia, and ventricular arrhythmias. The differential diagnosis includes injection of local anesthetic into the vertebral artery. When this occurs, seizures and unconsciousness are almost immediate. Hypotension and bradycardia may also be due to the cardiotoxic effects of local anesthetics. After epidural injection, such signs and symptoms develop more slowly. Moreover, the epidural 248

space does not extend intracranially. Therefore, signs and symptoms related to intracranial spread of local anesthetic are unlikely. Subdural injection is also part of the differential diagnosis. In this case, the development of clinical block is even slower and usually asymmetrical and incomplete. Intravascular injection or rapid reabsorption of the local anesthetic should always be considered with both central nervous system toxicity and hemodynamic instability. However, the presence of bilateral flaccid paralysis makes this diagnosis very unlikely. Different mechanisms may be implicated in the occurrence of total spinal anesthesia following interscalene block (Table 61-1). Direct injection into the subdural or epidural space may be the consequence of incorrect needle placement through an intervertebral foramen. A perineural or intraneural injection may lead to secondary migration of the drug into the subdural space. Finally, long dural sleeves have been shown in autopsy studies, extending as far as 3 to 5 cm beyond the intervertebral foramen. Placement of a needle into an abnormally long dural root sleeve may explain the spread of local anesthetic into the intrathecal space.

Risk Assessment Total spinal anesthesia following interscalene block, either with or without a perineural catheter, is a rare but serious complication. Such events are often documented as case

Table 61–1

■

Proposed Mechanisms of Intrathecal Migration of Local Anesthetics

Injection through intervertebral foramen Direct intraneural injection Injection into dural root sleeve

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Advantages/ Disadvantages Spinal injection Epidural injection Vertebral artery injection Intravenous injection Pneumothorax Discomfort Ease of catheter placement

Winnie ++ ++ + + + +/− −

Posterior ++ ++ +/– + + ++ +

Modified Lateral – – − + + +/− ++

reports. Thus, there is no way to estimate the specific risk for this complication. The only identifiable factor that increases risk is the approach used to perform the block. Three main techniques are used: the Winnie approach, the posterior approach, and the modified lateral approach. The relative advantages and disadvantages of each technique are given in Table 61-2.

Implications Total spinal anesthesia is a rare complication following interscalene block. However, its diagnosis should be prompt. The differential diagnoses of vertebral artery or intravenous injection should be rapidly ruled out so that the appropriate remedial measures can be instituted. Spontaneous breathing often ceases promptly, so assisted manual or mechanical ventilation will be necessary. Bradycardia and hypotension may occur as a result of vasodilatation and block of the cardiac accelerator fibers, which may lead to cardiac arrest if not treated urgently.

Figure 61–1 ■ Winnie’s technique. The needle is directed medially, caudad, and slightly posteriorly toward the transverse process of C6. The needle is close to the spinal structures. C, clavicle; MC, cricothyroid membrane; MS, clavicular head of sternocleidomastoid muscle; dotted line, interscalene groove.

intra-arterial, or intrathecal drug administration is still possible. The choice of approach for performing the interscalene block has implications in the occurrence of complications. Winnie’s approach (Fig. 61-1) directs the needle more toward the spine and therefore increases the risk of injection through an intervertebral foramen, especially if the needle is directed too horizontally. The posterior approach is a paravertebral block. All paravertebral blocks carry at least some risk of puncturing the dural cuff (whether abnormally long or not) that accompanies spinal nerves distal to the intervertebral foramina. The modified lateral approach (Fig. 61-2) directs the needle away from spinal structures and is likely the safest technique for avoiding intervertebral or inadvertent dural puncture Advancing the catheter more than 2 to 3 cm past the tip of the stimulating needle carries no advantage. In fact, by threading it

MANAGEMENT The first step is to immediately cease the local anesthetic injection. Further management includes the following: ●

●

●

●

●

Provide assisted manual or mechanical ventilation with 100% oxygen. Tracheal intubation is often necessary but not always mandatory. Consider the patient’s mental status, drugs administered, and surgical procedure. Volume expansion may be required to treat or prevent hemodynamic instability. Vasopressors, positive chronotropic drugs, or temporary pacing may be required to treat bradycardia or hypotension. Monitor the patient in the intensive care unit or recovery room until the block wears off.

PREVENTION The most important precaution is to administer the drug slowly, with repeated aspiration; however, intravenous,

Figure 61–2 ■ Modified lateral approach. The needle is inserted toward the plane of the interscalene space at an angle of between 45 and 60 degrees. The needle avoids the spinal structures. C, clavicle; MC, cricothyroid membrane; MS, clavicular head of sternocleidomastoid muscle; dotted line, interscalene groove.

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++, most likely/easiest; +, less likely/easy; +/−, possible; − unlikely/difficult.

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farther, the anesthesiologist loses control over its position (e.g., interscalene catheters have been placed within the pleura). Last, an important precaution is to perform the interscalene block only in awake or lightly sedated patients. This allows the patient to report paresthesia (needle encounters a nerve root) or pain due to intraneural injection, and it allows the operator to more promptly recognize early signs of central nervous system toxicity.

Further Reading Borgeat A, Dullenkopf A, Ekatodramis G, Nagy L: Evaluation of the lateral modified approach for continuous interscalene block after shoulder surgery. Anesthesiology 99:436-442, 2003.

Borgeat A, Ekatodramis G, Kalberer F, Benz C: Acute and nonacute complications associated with interscalene block and shoulder surgery: A prospective study. Anesthesiology 95:875-880, 2001. Brown AR: Regional anesthesia for shoulder surgery. Tech Reg Anesth Pain Manage 3:64-78, 1999. Iocolano CF: Total spinal anesthesia after an interscalene block. J Perianesth Nurs 12:163-170, 1997. Long TR, Wass CT, Burkle CM: Perioperative interscalene blockade: An overview of its history and current clinical use. J Clin Anesth 14:546-556, 2002. Norris D, Klahsen A, Milne B: Delayed bilateral spinal anaesthesia following interscalene brachial plexus block. Can J Anaesth 43:303-305, 1996.

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Supraclavicular and Infraclavicular Block: Pneumothorax Sandra L. Kopp Case Synopsis

PROBLEM ANALYSIS Definition Pneumothorax is an accumulation of air or gas in the space between the lung and the chest wall (pleural space). With the supraclavicular approach, the brachial plexus is blocked at the level of its three trunks, where it is most compactly arranged (Fig. 62-1). There are several advantages to the supraclavicular brachial plexus technique, including neutral position of the arm, quick onset of blockade, and a very homogeneous block. Limitations of this approach include difficulty describing or teaching the technique and the risk of pneumothorax. This block is best avoided in uncooperative patients or those with unclear landmarks. Special consideration must be given to patients who could not tolerate the respiratory distress that may accompany a pneumothorax or phrenic nerve block, such as those with severe respiratory disease. The infraclavicular approach to brachial plexus block allows local anesthetic injection above the level where the musculocutaneous and axillary nerves branch off the plexus. This approach is more proximal than the axillary technique and more distal than the supraclavicular approach, thus leading to blockade of all the nerves derived from the plexus, but with a lower incidence of pneumothorax (Fig. 62-2). As with the supraclavicular approach, the arm can remain in a neutral position. This approach has recently gained favor for use in patients requiring a continuous catheter technique, because maintaining an aseptic dressing at this site is much more practical than in the axilla.

Recognition Recognition of a pneumothorax is based largely on the clinical presentation. A pneumothorax may occur immediately during block placement, or it may present hours later. The diagnosis of pneumothorax should be suspected if air is aspirated through the needle during performance of the block, or if a patient becomes acutely dyspneic after block placement.

Unilateral phrenic nerve paralysis and concomitant elevation of the hemidiaphragm must be ruled out, as this is very common after proximal brachial plexus blocks (e.g., interscalene blocks). Although the incidence of hemidiaphragmatic paresis is significantly lower in patients having supraclavicular block compared with interscalene block, it is still estimated to occur in approximately 50% of all patients. Infraclavicular block is rarely associated with changes in pulmonary function. If a patient’s clinical condition suddenly deteriorates during mechanical ventilation, pneumothorax must be considered.

Middle and anterior scalene muscles

Brachial plexus

A

First rib

Brachial plexus

B

Subclavian artery

Figure 62–1 ■ A, Supraclavicular block. The needle is systematically walked anteriorly and posteriorly along the rib until the brachial plexus is located. B, Trunks of the brachial plexus are compactly arranged at the level of the first rib. (From Miller RD [ed]: Anesthesia, 5th ed. Philadelphia, Churchill Livingstone, 2000, p 1524.)

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A 42-year-old man complains of shortness of breath and mild right-sided chest pain in the outpatient recovery area, shortly after a right wrist fusion. A preoperative brachial plexus block was placed using the supraclavicular approach. Upon examination, the patient’s respiratory rate is 20 breaths per minute, and his room-air saturation is 94%. His blood pressure and heart rate are normal. A chest radiograph is positive for a small, right-sided pneumothorax.

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Chassaignac's tubercle C6

B 2.5 cm Insertion site

A Figure 62–2 ■ A, Surface markings for the infraclavicular approach to brachial plexus block. B, Cephalocaudad arc of needle redirection. (From Brown DL: Atlas of Regional Anesthesia, 2nd ed. Philadelphia, WB Saunders, 1999, p 47.)

Patients who are being ventilated with volume-controlled ventilators present with increased peak and plateau pressures; those ventilated with pressure-controlled ventilators have reduced tidal volumes with a new pneumothorax. The chest may have a hyperresonant or tympanitic sound during percussion. There may also be absent breath sounds on the affected side. These signs are most notable when there is at least a 25% reduction in lung volume. Although a computed tomography (CT) scan is the most sensitive study, a chest radiograph is usually diagnostic. Radiographs obtained at the end of expiration allow easier visualization because the pneumothorax takes up a greater proportion of the hemithorax during this part of the respiratory cycle. The main radiographic feature of a pneumothorax is a white visceral pleural line, separated from the parietal pleura by an avascular collection of gas. In most cases, no pulmonary vessels are visible beyond the visceral pleural edge (Fig. 62-3).

Implications Normally, the pressure in the pleural space is negative with respect to the alveolar pressure during the entire respiratory cycle. If the needle punctures the chest wall during block placement, it creates a communication between the atmosphere and the pleural space. Air begins to enter the pleural space until

Risk Assessment The incidence of pneumothorax during supraclavicular block ranges from 0.5% to 6.1%. There is an inverse relationship between the incidence of pneumothorax and the experience of the anesthesiologist performing the block. Relatively new techniques, such as the “plumb-bob” approach, have been used to reduce the risk of pneumothorax. Routine chest radiography following a supraclavicular block is not justified because of the low incidence of pneumothorax and the fact that the onset of symptoms may take up to 24 hours.

Figure 62–3 ■ Right-sided 40% pneumothorax. Arrows mark the visceral pleural line.

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MANAGEMENT If the patient has minimal symptoms and the pneumothorax is less than 15% of the lung volume, simple observation is advised. It is also necessary to provide the patient with supplemental oxygen, which will increase the rate of absorption of the pneumothorax. Because nitrogen is the primary gas in the pleural space, the gradient for nitrogen absorption into the blood is the main factor in determining the rate of reabsorption of a pneumothorax. Reabsorption can be accelerated by breathing 100% oxygen, which lowers the partial pressure of nitrogen in the blood, thereby increasing the gradient for nitrogen absorption from the pleural space. If the patient has more than minimal symptoms or if the pneumothorax occupies more than 15% of the hemithorax, aspiration with a plastic catheter is the treatment of choice. If aspiration does not prevent expansion of the pneumothorax, tube thoracostomy should be performed. Treatment of patients who are undergoing positivepressure mechanical ventilation should include tube thoracostomy to prevent the development of a tension pneumothorax.

Most often, the chest tube is inserted via an incision at the fourth or fifth intercostal space in the anterior axillary or midaxillary line and directed apically. A tension pneumothorax is a medical emergency. When it is suspected, the patient should immediately receive 100% oxygen to alleviate hypoxia. A large-bore angiocatheter should be inserted into the pleural space through the second intercostal space, along the midclavicular line. If the diagnosis is confirmed by the aspiration of air through the catheter, the patient should undergo immediate tube thoracostomy.

PREVENTION Many modifications have been made to supraclavicular and infraclavicular blocks to decrease the complication rate. In 1949 Bonica and colleagues first recommended a careful, gentle technique; thorough familiarity with anatomic relationships; use of the first rib as a protective shield over the lung; and use of a short, fine needle to help prevent complications, including pneumothorax. Although many years have passed, and several reviews have been published since then, this careful approach is still the best advice for any anesthesiologist planning to perform these techniques.

Further Reading Bonica JJ, Moore DC, Orlov M: Brachial plexus block anesthesia. Am J Surg 65, 1949. Brown DL, Bridenbaugh LD: The upper extremity: Somatic block. In Cousins MJ, Bridenbaugh PO (eds): Neural Blockade in Clinical Anesthesia and Management of Pain, 3rd ed. Philadelphia, Lippincott-Raven, 1998, pp 345-371. Brown DL, Cahill DR, Bridenbaugh LD: Supraclavicular nerve block: Anatomic analysis of a method to prevent pneumothorax. Anesth Analg 76:530-534, 1993. Light RW, Broaddus VC: Pneumothorax, chylothorax, hemothorax, and fibrothorax. In Murray JF, Nadel JA (eds): Textbook of Respiratory Medicine, 3rd ed. Philadelphia, WB Saunders, 2000, pp 2043-2066. Neal JM, Moore JM, Kopacz DJ, et al: Quantitative analysis of respiratory, motor, and sensory function after supraclavicular block. Anesth Analg 86:1239-1244, 1998. Rodriquez J, Barcena M, Rodriguez V, et al: Infraclavicular brachial plexus block effects on respiratory function and extent of the block. Reg Anesth Pain Med 23:564-568, 1998.

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the pressure gradient is eliminated or the communication is repaired. The main physiologic changes associated with a pneumothorax are decreased arterial partial pressure of oxygen (PO2) and decreased vital capacity. The consequences are much more pronounced in patients with poor lung function, because a decrease in vital capacity can lead to respiratory insufficiency, which manifests as hypoventilation and ultimately respiratory acidosis. Although a tension pneumothorax is unlikely in a spontaneously breathing patient, those who have positive-pressure mechanical ventilation are at significantly increased risk. A tension pneumothorax occurs when the positive pressure of inspiration forces more air into the pleural space than exits during expiration. A sudden decline in the patient’s cardiopulmonary status should raise suspicions of the presence of a tension pneumothorax. The deterioration in cardiopulmonary status is likely due to the combination of decreased cardiac output secondary to decreased venous return and extreme hypoxia due to ventilation-perfusion mismatching.

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Gilbert Y. Wong and David L. Brown Case Synopsis A 55-year-old woman presents with epigastric abdominal pain of several months’ duration and a recent diagnosis of pancreatic cancer. To manage her pain, a neurolytic celiac plexus block is performed using the classic posterior percutaneous approach. Soon after injection of the neurolytic solution, she notices sensory loss and impaired motor control of her lower extremities.

PROBLEM ANALYSIS Definition Neurolytic celiac plexus block (CPB) is an effective analgesic technique used primarily for pain management in patients with intra-abdominal malignancies, especially pancreatic cancer. Neurolytic solutions are injected in the area of the celiac plexus or splanchnic nerves, which are the neural structures transmitting the majority of visceral pain from the abdomen. Because the targeted area of neurolysis is in close proximity to vascular and other neurologic structures (Fig. 63-1), neurologic side effects and complications are the primary concerns associated with CPB. Neurologic side effects such as orthostatic hypotension or bowel hypermotility often occur after an effective neurolytic CPB. The celiac plexus and splanchnic nerves are primarily sympathetic nervous system structures. Neurolysis of these structures results in sympatholysis and a relative increase in parasympathetic tone in the splanchnic region. As a result, vasodilatation of the splanchnic vasculature, especially the venous capacitance bed (which effectively reduces venous return and cardiac preload), can result in orthostatic hypotension. In addition, the relative increase in parasympathetic outflow to the viscera can result in increased peristalsis and bowel hypermotility. Neurologic complications are the most serious concerns associated with neurolytic CPB. Although they are rare, these complications can include sensory and motor deficits of the lower trunk and lower extremities, loss of bladder or bowel control or both, and impotence in males. Neurolysis of sensory or motor nerves can occur from direct contact of the neurolytic solution, such as alcohol or phenol, spreading to the intrathecal or epidural space or thoracic or lumbar nerve roots (see Fig. 63-1). In a separate mechanism, alcohol has been shown to cause arterial spasm of feeding arteries to the spinal cord, which can result in ischemia and permanent neurologic deficits (Fig. 63-2).

Recognition Neurologic side effects, such as orthostatic hypotension and bowel hypermotility, are not appreciated until after the 254

neurolytic procedure is completed. Patients with intraabdominal malignancies often have decreased oral intake owing to pain or nausea. Decreased intravascular volume can potentiate the hypotensive effects of neurolytic CPB. Symptoms associated with orthostatic hypotension include syncope or dizziness in the upright position, which may be exacerbated during a rapid shift from the supine position. These symptoms may occur immediately after the CPB. Orthostatic hypotension can be diagnosed based on blood pressure measurements performed before and after the neurolytic CPB with the patient in the supine and upright positions. Bowel hypermotility effects may not be noticed until hours after the neurolytic CPB. Because patients experiencing pain associated with intra-abdominal malignancies are frequently treated with opioid medications, and because constipation is a common side effect of opioid medications, such patients often consider increased bowel motility to be beneficial. Neurologic complications, such as sensory and motor changes of the lower trunk and extremities, must be carefully evaluated both during and after the CPB procedure. Although not completely reliable, needle aspiration for cerebrospinal fluid or blood should occur both before and during the incremental injections of neurolytic solution. If cerebrospinal fluid or blood is aspirated, no additional injections should occur until the needle position is reevaluated. Before the injection of a neurolytic agent, a functional test consisting of local anesthetic injection is important to rule out incorrect needle placement. Neurologic deficits occurring as a result of local anesthetic injection into the intrathecal or epidural space or in contact with the thoracolumbar nerve roots confirm incorrect needle positioning. Radiographic guidance, such as fluoroscopy or CT, can also be used to recognize grossly inaccurate needle placement.

Risk Assessment The risks of neurologic side effects and complications must be carefully considered and weighed against the benefits of neurolytic CPB in patients with intra-abdominal malignancies and limited life expectancy. Meta-analysis of the literature regarding patients undergoing neurolytic CPB found that hypotension occurred in

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Aorta Retrocrural spread

L1

Splanchnic nerves Celiac plexus

REGIONAL ANESTHESIA AND PAIN MANAGEMENT

Ao

Anterocrural spread

Diaphragmatic crura Figure 63–1 ■ The spread of neurolytic solution in a celiac plexus block occurs in anterocrural or retrocrural regions. The neurolytic solution is in close proximity to vital structures associated with the spine, including the intrathecal and epidural spaces, thoracic and lumbar nerve roots, and major feeding arteries of the spinal cord.

Ant. sulcal a.

Ant. radicular a. A. of Adamkiewicz Ant. spinal a. T – 12

L–1

L–2

Lumbar a. Aorta

Figure 63–2 ■ Arterial supply of the spinal cord at low thoracic and high lumbar vertebral levels. The largest feeding artery to the spinal cord is the artery of Adamkiewicz (anterior radicular artery), which branches from the lumbar artery (in this case).

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38% of cases and bowel hypermotility occurred in 31% to 44% of cases. A case series of 136 patients who had neurolytic CPB reported that 8 patients (6%) with symptomatic orthostatic hypotension required treatment. Another study (61 patients) that prospectively compared different CPB techniques reported a 38% incidence of transient decreases in systolic blood pressure greater than 33% compared with baseline measurements. Bowel hypermotility also occurred in 31% of these patients. In the largest series (2730 patients) evaluating neurologic complications associated with neurolytic CPB, four cases (0.15%) of permanent paraplegia were identified. In three of these cases, there was also loss of anal and bladder sphincter function. Radiographic guidance with radiocontrast dye was used for CPB in all four cases. In a case series by Brown and coworkers, there were no cases of permanent paraplegia in 136 patients undergoing neurolytic CPB. Meta-analysis of the literature revealed a 1% incidence of neurologic complications, including lower extremity weakness, paresthesia, epidural anesthesia, and lumbar puncture, after neurolytic CPB.

Implications Benign neurologic side effects can occur in patients receiving neurolytic CPB. These side effects can usually be treated in a symptomatic manner with no significant impact on the patient. Orthostatic hypotension typically improves shortly after equilibration of the intravascular volume. Bowel hypermotility is usually transient and may actually be desirable in many patients. The potential for neurologic side effects should be discussed with the patient and family before the procedure. Neurologic complications are very uncommon but can have a significant impact. In patients with intra-abdominal malignancies, these neurologic deficits are likely to continue for the remainder of their lives.

MANAGEMENT The management of neurologic side effects is directed toward symptomatic relief. Orthostatic hypotension, if symptomatic, can be treated by increasing oral fluid intake or intravenous fluids. Leg wrappings with elastic bandages or support stockings can also decrease venous capacitance and improve hypotension. Antihypertensive medications, if any, should be discontinued until equilibration of intravascular volume is reached. If symptoms are sustained and not responsive to conservative therapy, pharmacologic treatment with an α1-agonist, such as midodrine, can be considered. Bowel hypermotility can be treated symptomatically with antihypermotility medications such as diphenoxylate with atropine.

The management of neurologic complications is more complicated. If neurologic deficits occur during neurolytic CPB, the procedure should be terminated immediately. Aspiration of the injectate can be attempted but is unlikely to be effective. Emergency consultation with a neurologist is recommended. If ischemia of the spinal cord is suspected as a result of spasm of a lumbar radicular artery, the immediate involvement of an interventional radiologist for arterial vasodilatation should be considered.

PREVENTION The neurologic side effects of orthostatic hypotension and bowel hypermotility are not preventable; they are merely the result of a successful CPB. The ability to prevent neurologic complications with the use of radiographic guidance is controversial. Traditionally, the CPB procedure relies on anatomic landmarks rather than radiographic guidance. Needle position is confirmed with a functional test of injected local anesthetic. If the patient notes an appropriate improvement in preexisting pain with no neurologic deficits, the needle position is considered to be correct. This approach requires that the patient not be oversedated, so that he or she can provide reliable responses. The large case series of 2730 patients undergoing neurolytic CPB revealed four cases of permanent paraplegia, all of which involved the use of radiography and radiocontrast dye to confirm final needle placement. Thus, radiographic guidance cannot ensure the prevention of neurologic complications. Despite these observations, the use of radiographic guidance provides the advantage of confirming needle position and the spread of injectate, as traced by the radiocontrast dye, before the injection of neurolytic solution.

Further Reading Brown DL, Bulley CK, Quiel EL: Neurolytic celiac plexus block for pancreatic cancer pain. Anesth Analg 66:869-873, 1987. Davies DD: Incidence of major complications of neurolytic coeliac plexus block. J R Soc Med 86:264-266, 1993. Eisenberg E, Carr DB, Chalmers TC: Neurolytic celiac plexus block for treatment of cancer pain: A meta-analysis. Anesth Analg 80:290-295, 1995. Goudas L, Carr DB, Bloch R, et al: Management of Cancer Pain: Evidence Report/Technology Assessment No. 35 (AHCPR Publication No. 02E002). Rockville, Md, Agency for Healthcare Research and Quality, 2001. (Prepared by the New England Medical Center Evidence-Based Practice Center under Contract No. 290-97-0019.) Ischia S, Ischia A, Polati E, et al: Three posterior percutaneous celiac plexus block techniques. Anesthesiology 76:534-540, 1992. Wong GY, Brown DL: Transient paraplegia following celiac plexus block. Reg Anesth 20:352-355, 1995. Wong GY, Schroeder DR, Carns PE, et al: Effect of neurolytic celiac plexus block on pain relief, quality of life, and survival in patients with unresectable pancreatic cancer—a randomized controlled trial. JAMA 291:1092-1099, 2004.

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64

Robert S. Weller Case Synopsis

PROBLEM ANALYSIS Definition Retroperitoneal hemorrhage after psoas compartment block (PCB) results from arterial bleeding into the retroperitoneal space. Signs and symptoms of PCB depend on the rate and extent of bleeding and whether the hematoma compresses adjacent structures. The most rapid and dramatic bleeding occurs with aortic rupture, which is often fatal. However, bleeding from smaller arteries after PCB can also cause morbidity or mortality. Numerous cases of retroperitoneal hemorrhage have been reported following interventional radiology procedures requiring femoral artery cannulation, especially if the artery is injured proximal to the inguinal ligament. The incidence following cardiac catheterization is reportedly 0.12%. Only a few cases of retroperitoneal hemorrhage have been reported after PCB or lumbar sympathetic block; anticoagulant therapy at the time of or after the block was involved in each of those cases. Spontaneous retroperitoneal hematoma may also occur in patients on chronic anticoagulant therapy. The risk of this complication increases as the degree of anticoagulation increases. Finally, spontaneous iliopsoas hemorrhage with femoral nerve palsy is the most common nerve palsy caused by spontaneous bleeding in hemophiliacs.

Recognition Retroperitoneal bleeding is deep, concealed, and rarely obvious until significant blood loss has occurred. The most common signs of retroperitoneal hemorrhage are hypotension and tachycardia due to intravascular volume depletion, and

REGIONAL ANESTHESIA & PAIN MANAGEMENT

A 76-year-old man with a mechanical aortic valve was scheduled for left above-knee amputation. Chronic warfarin (Coumadin) was stopped, and a heparin infusion was begun on admission but stopped 4 hours before surgery. On arrival in the preoperative area, his prothrombin time, international normalized ratio, and activated partial thromboplastin time were normal; hemoglobin was 13 g/dL. A posterior approach to the lumbar plexus block (psoas compartment block) was performed, in combination with a subgluteal sciatic block. His vital signs remained stable, and the surgery and recovery room stay were uneventful. The estimated blood loss was 300 mL. The patient was returned to the floor, and heparin was restarted 8 hours postoperatively at 1200 units/hour. His blood pressure gradually declined overnight from his usual 140/90 to 95/55 mm Hg, and he became confused and oliguric. He received several 500-mL normal saline fluid challenges. The blood pressure improved, but urine output remained low. The next morning, his hemoglobin was 7.3 g/dL. Two units of packed red blood cells were given. Hemoglobin was 7.7 g/dL. He was moved to the intensive care unit, heparin was discontinued, and a computed tomography (CT) scan of the abdomen showed a large left retroperitoneal hematoma.

anemia (Table 64-1). In one series, 64% of patients had hypotension (systolic blood pressure 800 sec during CPB, or fixed heparin dosing should be used

Dose

CARDIOTHORACIC & VASCULAR SURGERY

ACT, activated clotting time; CABG, coronary artery bypass graft; CPB, cardiopulmonary bypass; DIC, disseminated intravascular coagulation; FDA, Food and Drug Administration; TF, tissue factor.

Binds to plasmin, inhibiting fibrinolysis

∈-aminocaproic acid (EACA)

Aprotinin (half-dose regimen)

Mechanism of Action

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30 minutes. The principal adverse side effect is hypotension. A similar beneficial effect, but without hypotension, can be achieved by giving 4 μg/kg of DDAVP intranasally. Platelet transfusion should consist of an appropriate number of units, preferably obtained by apheresis from a single donor. During cardiac transplantation, blood from the organ donor can be acquired during cardiac explantation, from which platelet-rich plasma is derived by separation plasmapheresis. Such platelet-rich plasma is then transfused into the organ recipient. This can substantially reduce the need for perioperative blood transfusion in cardiac transplant recipients.

Coagulation Factor Deficiencies When the prothrombin time is greater than 16 seconds or the aPTT is greater than 57 seconds, coagulation factor deficiencies are treated with fresh frozen plasma. Although the amount needed varies, depending on initial factor concentrations and circulating blood volume, 1 mL/kg of fresh frozen plasma usually increases coagulation factor concentrations by 1% to 2%. Cryoprecipitate provides a concentrated source of fibrinogen, which is beneficial when deficiencies of this coagulation factor are documented. A prothrombin complex concentrate may be useful when liver function is compromised or liver-generated coagulation factors have been chemically reduced by warfarin. Substitution or supplementation of native antithrombin III leads to higher ACT values and reduced concentrations of fibrin monomer and D-dimer. Substitution of antithrombin III is essential when its activity is less than 60%, because the heparin effect is dependent on it. Several case reports have described using recombinant activated factor VII in cases of life-threatening hemorrhage after cardiac surgery. Randomized, controlled trials to assess the efficacy and safety of such therapy are under way.

PREVENTION Measures to prevent bleeding after cardiac surgery include the following: ● ●

● ●

Minimal CPB duration Autologous blood procurement before CPB to provide a source of fresh whole blood with functioning platelets and coagulation factors for use after heparin neutralization Maintenance of normothermia Judicious postoperative blood pressure control

The fibrinolytic system is known to be up-regulated during CPB owing to the activation of multiple physiologic systems. This results in clot dissolution, coagulation factor

consumption, and platelet dysfunction. Multiple clinical studies indicate that the prophylactic administration of antifibrinolytic drugs reduces blood loss and the number of transfusions in patients after cardiac surgery, particularly reoperations (Table 75-1).

Further Reading Cammerer U, Dietrich W, Rampf T, et al: The predictive value of modified computerized thromboelastography and platelet function analysis for postoperative blood loss in routine cardiac surgery. Anesth Analg 96:51-57, 2003. Caputo M, Bryan AJ, Calafiore AM, et al: Intermittent antegrade hyperkalaemic warm blood cardioplegia supplemented with magnesium prevents myocardial substrate derangement in patients undergoing coronary artery bypass surgery. Eur J Cardiothorac Surg 14:596-601, 1998. Despotis GJ, Filos KS, Zoys TN, et al: Factors associated with excessive postoperative blood loss and hemostatic transfusion requirements: A multivariate analysis in cardiac surgical patients. Anesth Analg 82:13-21, 1996. Hekmat K, Zimmermann T, Kampe S, et al: Impact of tranexamic acid vs aprotinin on blood loss and transfusion requirements after cardiopulmonary bypass: A prospective, randomized, double-blind trial. Curr Med Res Opin 20:121-126, 2004. Herbertson M: Recombinant activated factor VII in cardiac surgery. Blood Coagul Fibrinolysis 15(Suppl 1):S31-S32. 2004. Levi M, Cromheecke ME, de Jonge E: Pharmacological strategies to decrease excessive blood loss in cardiac surgery: A meta-analysis of clinically relevant endpoints. Lancet 354:1940-1947, 1999. Levy JH, Despotis GJ, Szlam F, et al: Recombinant human transgenic antithrombin in cardiac surgery: A dose-finding study. Anesthesiology 96:1095-1102, 2002. Mongan PD, Hosking MP: The role of desmopressin acetate in patients undergoing coronary artery bypass surgery: A controlled clinical trial with thromboelastographic risk stratification. Anesthesiology 77:38-46, 1992. Nuttall GA, Fass DN, Oyen LJ, et al: A study of a weight-adjusted aprotinin schedule during cardiac surgery. Anesth Analg 94:283-289, 2002. Nuttall GA, Oliver WC, Santrach PJ, et al: Efficacy of a simple intraoperative transfusion algorithm for nonerythrocyte component utilization after cardiopulmonary bypass. Anesthesiology 94:773-781, 2001. Ohata T, Sawa Y, Kadoba K, et al: Effect of cardiopulmonary bypass under tepid temperature on inflammatory reactions. Ann Thorac Surg 64:124-128, 1997. Remadi JP, Marticho P, Butoi I, et al: Clinical experience with the miniextracorporeal circulation system: An evolution or a revolution? Ann Thorac Surg 77:2172-2175, 2004. Richter JA, Meisner H, Tassani P, et al: Drew-Anderson technique attenuates systemic inflammatory response syndrome and improves respiratory function after coronary artery bypass grafting. Ann Thorac Surg 69:77-83, 2000. Spiess BD, Gillies BS, Chandler W, et al: Changes in transfusion therapy and reexploration after institution of a blood management program in cardiac surgical patients. J Cardiothorac Vasc Anesth 9:168-173, 1995. Tassani P, Otto D, Szekely A, et al: Transfusion of platelet-rich plasma from the organ donor during cardiac transplantation. J Clin Anesth 9:409-414, 1997. Woodman RC, Harker LA: Bleeding complications associated with cardiopulmonary bypass. Blood 76:1680-1697, 1990.

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Mark A. Chaney Case Synopsis A 62-year-old man is scheduled for elective coronary artery bypass grafting. Immediately after uneventful induction of general anesthesia and tracheal intubation, new ST segment depression is observed on the electrocardiogram (ECG) tracing.

PROBLEM ANALYSIS Definition

Recognition Ischemia Anginal symptoms and hemodynamic alterations are not necessarily reliable indicators of myocardial ischemia. Reliance on increased pulmonary artery wedge pressure for the detection of ischemia is controversial at best. In fact, acutely increased pulmonary artery wedge pressure probably signifies only global ischemia. Detection of regional wall motion abnormalities with transesophageal echocardiography is the most sensitive of the currently available, clinically useful techniques for detecting myocardial ischemia. In addition to wall motion abnormalities, decreased systolic wall thickening or abnormal diastolic filling patterns, detected by Doppler interrogation across the left ventricular

INFARCTION The ECG is the most commonly used modality to detect myocardial ischemia and acute MI. Transmural MI presents initially with prominent T waves, hyperacute ST segment elevation, or both. This evolves over minutes, hours, or even days to a pattern of significant Q waves (i.e., >40 msec duration, >30% of QRS amplitude) or persistent ST-T wave changes. Subendocardial (non-Q-wave) MI is less clearly defined because it may present only as subtle ST-wave or T-wave changes. Detection of non-Q-wave MI often relies on other modalities (e.g., CK, cardiac-specific troponins, transesophageal echocardiographic radionuclide imaging) to confirm the diagnosis. Most perioperative MIs are subendocardial in nature. Serum CK exceeds the normal range within 4 to 8 hours following acute MI and declines to normal by 2 to 3 days. Three isoenzymes of CK (BB, MM, MB) have been identified. Brain and kidney contain predominantly BB, skeletal muscle MM (with 1% to 3% MB), and myocardium both MM and MB (isoforms MB1 and MB2). One study found 59% and 92% sensitivity for the diagnosis of acute MI at 2 to 4 and 4 to 6 hours, respectively, for CKMB2 greater than 1 unit/L or CKMB2/CKMB1 ratio greater than 1.5. Cardiac troponins are highly sensitive and specific chemical markers for myocardial necrosis and predict increased risk of mortality and reinfarction in patients presenting with acute coronary syndrome. The troponin (Tn) complex consists of three subunits (TnC, TnI, TnT) that regulate calciummediated contraction in striated muscle. TnC binds to calcium, TnI binds to actin, and TnT binds to tropomyosin. Both TnI and TnT are present in skeletal and cardiac muscle, but they are encoded by different genes and have different amino acid sequences. This permits the production of specific antibodies for cardiac Tn (cTn) and the development of 309

CARDIOTHORACIC & VASCULAR SURGERY

Myocardial ischemia results from an imbalance between myocardial oxygen supply and demand. If this persists, ischemia eventually leads to myocardial infarction (MI). Patients in whom perioperative ischemia develops are at increased risk for subsequent cardiac morbidity and mortality. Postoperative MI and major cardiac complications occur in more than 4% of patients who have either an established diagnosis of coronary artery disease or risk factors for it and who undergo major noncardiac surgery. In the United States alone, 1.5 to 2 million patients are at such risk for postoperative MI each year. There is marked variability in the reported short-term mortality (5 mg/dL Serum calcium level 6 L From Ranson JHC: Etiological and prognostic factors in human acute pancreatitis: A review. Am J Gastroenterol 77:633-638, 1982.

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Acute Pancreatitis

APACHE II Severity of Disease Classification System High Abnormal Range

Physiologic Variable

+4

+3

+2

Low Abnormal Range +1

0

+1

+2

+3

+4

APS, APACHE score. From Knaus WA, Draper EA, Wagner DP, et al: APACHE II: A severity of disease classification system. Crit Care Med 13:818-829, 1985.

Implications Although the majority of patients with acute pancreatitis have an uncomplicated course, 20% to 25% develop sequelae that may be life threatening, requiring either ICU support or surgical intervention. Local complications include sterile or infected tissue necrosis, pseudocysts, abscesses, colonic fistulas, gastrointestinal hemorrhage, and splenic rupture. Systemic complications include shock, acute renal failure, acute lung injury, coagulopathy, hyperglycemia, hypocalcemia, retinopathy, and psychosis.

MANAGEMENT The treatment of uncomplicated acute pancreatitis is primarily supportive, with the judicious use of intravenous fluids and parenteral analgesia. Nasogastric suctioning is beneficial only in patients with documented ileus. Recent randomized, controlled trials have confirmed the benefits of early enteral feedings in patients with severe acute pancreatitis, noting

less end-organ failure, a diminished systemic inflammatory response, and shorter length of hospital stay compared with parenteral feedings. The use of prophylactic antibiotics for severe acute pancreatitis remains controversial. A 1998 metaanalysis of eight prospective, randomized, controlled trials found that reduced mortality was limited to patients who were administered broad-spectrum antibiotics that could penetrate pancreatic tissue. However, a more recent study cited an increase in the incidence of fungal infections and higher perioperative mortality. Also, controlled trials investigating the use of H2-antagonists, protease inhibitors, and peritoneal lavage were unable to document improved outcomes. Early use of endoscopic retrograde cholangiopancreatography (ERCP) and papillotomy for biliary pancreatitis is also controversial. One prospective multicenter study in the late 1990s failed to show a benefit from ERCP. In more severe forms of acute pancreatitis, ICU support with mechanical ventilation for respiratory failure, dialysis for acute renal failure, and infusions of vasoactive drugs may be required. Urgent surgery is indicated only in cases of deteriorating condition or evidence of pancreatic sepsis. The diagnosis of

PHYSIOLOGIC IMBALANCE & COEXISTING DISEASE

Temperature, rectal (°C) ≥41 39-40.9 38.5-38.9 36-38.4 34-35.9 32-33.9 30-31.9 ≤29.9 Mean arterial pressure (mm Hg) ≥180 130-179 110-129 70-109 50-69 ≤49 Heart rate (ventricular response) ≥180 140-179 110-139 70-109 55-69 40-54 ≤39 Respiratory rate (nonventilated or ≥50 35-49 25-34 12-24 10-11 6-9 ≤5 ventilated) Oxygenation: PAO2 – PaO2, or PaO2 (mm Hg) a. FiO2 ≥0.5: 500 350-499 200-349 2 SD above normal value Plasma procalcitonin >2 SD above normal value

Hemodynamic Variables Arterial hypotension (SBP 1 mmol/L) Decreased capillary refill or mottling MAP, mean arterial pressure; SBP, systolic blood pressure; SD, standard deviations; SvO2, venous oxygen saturation; WBC, white blood cell. Adapted from Levy MM, Fink MP, Marshall JC, et al: 2001 SCCM/ESICM/ ACCP/ATS/SIS International Sepsis Definitions Conference. Intensive Care Med 29:530-538, 2003.

released by leukocytes. The resultant hyperglycemia is associated with an increased release of insulin. Finally, substrate delivery is facilitated by vasodilatation, fluid retention, increased cardiac output, and capillary leak, all of which appear to be essential, because damaged tissue is avascular. The hypermetabolic phase of the stress response can evolve via two possible pathways; one is normal, and the other is pathologic. In the normal pathway, completion of angiogenesis by postinjury day 4 leads to the resolution of inflammation, hypermetabolism, and the hyperendocrine state. This is the more common scenario and is normal. Although it meets all the criteria for SIRS, it is clearly not what the 1991 consensus conference participants had in mind when they coined the term “systemic inflammatory response syndrome.” In some patients, however, inflammation becomes pathologic. The mechanism of such transformation is unknown. These patients have SIRS or, with infection, sepsis. Either of these is characterized by important changes in metabolism and regulation: ●

●

●

In contrast to simple stress, the ability to extract and use oxygen is diminished, despite increased cellular demand. The increased demand for energy by white blood cells, coupled with an inability to use molecular oxygen, leads to aerobic glycolysis. That is, oxygen delivery is adequate, but the inability to use oxygen increases lactate production. This causes persistent hyperglycemia, impaired glucose utilization, and a state of relative glucose intolerance. Endocrine abnormalities become prominent. The production and release of some hormones, notably vasopressin, are reduced, resulting in relative deficiency. Also, tissues become resistant to the effects of other hormones. This is exemplified by the development of insulin resistance or the diminished ability of catecholamines to modulate vascular tone.

Cellular dysfunction leads to biochemical abnormalities without overt organ failure. For example, hepatic dysfunction impairs gluconeogenesis, which prevents the conversion of lactate to pyruvate. Also, oxidation of long-chain triglycerides and the expression of key β-oxidative enzymes are decreased. As a result, amino acids become an increasingly important fuel source, despite the fact that hepatic dysfunction compromises ureagenesis. Importantly, contractile dysfunction is often observed in patients with MODS. In each case, compensatory mechanisms (increased substrate delivery to the liver, vasodilatation, and increased diastolic volume in the heart) may mask organ dysfunction.

MANAGEMENT AND PREVENTION There is no “magic bullet” to cure SIRS, sepsis, or MODS. It is not known what causes a controlled inflammatory response to become pathologic. In the absence of a specific target for therapy, management is based on source control, supportive care, and prevention of further complications.

Source Control The patient history, physical examination, and laboratory or diagnostic studies are used to identify infectious causes of continuing inflammation.

PHYSIOLOGIC IMBALANCE & COEXISTING DISEASE

Table 119–3

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Criteria for Organ Dysfunction Severity of Dysfunction

Body System

Mild

Severe

Pulmonary

Hypoxia or hypercarbia requiring assisted ventilation for ≥ 3-5 days Bilirubin ≥ 2-3 mg/dL; prothrombin time or other liver function tests ≥2 times normal Oliguria (5 days

ARDS requiring PEEP ≥10 cm H2O and FiO2 ≥0.5

Hepatic Renal Gastrointestinal Hematologic Central nervous system Peripheral nervous system Cardiovascular

Partial thromboplastin time ≥125% of normal, platelets < 50,000-80,000 Confusion Mild sensory neuropathy Decreased ejection fraction, persistent capillary leak

Jaundice with bilirubin ≥8-10 mg/dL Need for dialysis Stress ulceration with need for transfusion; acalculous cholecystitis Disseminated intravascular coagulation Coma Combined motor and sensory deficit Hypodynamic state not responsive to pressors

ARDS, acute respiratory distress syndrome; FiO2, fraction of inspired oxygen; PEEP, positive end-expiratory pressure.

Supportive Care Supportive care includes the following. Fluid Resuscitation. The goal of fluid resuscitation is to maintain intravascular volume despite ongoing capillary leak. This can be accomplished with colloid-based fluids such as albumin or hetastarch, crystalloid (use of a balanced salt solution is preferred to saline, to avoid the development of hyperchloremic metabolic acidosis), or blood or blood products if appropriate. The Canadian Transfusion Trial suggests that a hemoglobin of 7 mg/dL is sufficient for most critically ill patients. Goals for appropriate fluid resuscitation vary with the patient’s underlying disease and premorbid cardiac, pulmonary, and renal status. A study by Rivers and colleagues indicated that early goal-directed therapy designed to achieve a central venous pressure of 8 to 12 mm Hg, mean arterial pressure greater than 65 mm Hg, urine output greater than 0.5 mL/kg per hour, and mixed venous oxygen saturation greater than 70% improved outcomes. Vasopressors and Inotropes. In cases of severe sepsis or septic shock, fluid resuscitation may not be sufficient to restore organ perfusion. Clinically, it is difficult to distinguish between vasodilatation and myocardial depression. Consequently, vasoactive drugs are an important treatment adjuvant. Most recent studies favor the use of norepinephrine. If cardiac output is severely depressed, primary inotropes, such as dobutamine, may be useful. Dopamine administration is of historical interest only. This agent is arrhythmogenic and can cause maldistribution of splanchnic flow; putative renal sparing effects have been disproved in myriad studies, although stimulation of D1 receptors on the distal renal tubule does cause a diuretic effect. Mechanical Ventilation. Respiratory control is best viewed as having two components: hypoxia or, as in severe sepsis, acute respiratory distress syndrome (ARDS). Either may require an increase in the fraction of inspired oxygen (FiO2), although it is customary to try to keep FiO2 less than 0.5 to

0.6 to prevent “oxygen toxicity.” However, there are no human data to indicate that higher levels of FiO2 at one atmosphere of pressure are truly damaging. One recent trial indicated that keeping plateau pressures below 30 cm H2O or tidal volumes less than 6 mL/kg in patients with ARDS limits secondary lung injury and improves outcomes. Positive endexpiratory pressure (PEEP) is useful both to improve pulmonary compliance and to maintain recruitment of alveoli. We strongly advocate the “open lung” strategy of Amato. This somewhat controversial approach involves titrating PEEP to a level above the “lower inflection point” in the pressurevolume curve, increasing functional residual capacity and recruiting collapsed alveoli. Additional ventilatory adjuvants include the use of sighs and other recruitment maneuvers (e.g., tiltable and rotating posturing beds to improve ventilation/ perfusion mismatch). Keeping the head of the patient’s bed elevated above 30 degrees limits aspiration and decreases the incidence of nosocomial pneumonia. Broad-Spectrum Antibiotics. Early use of broad-spectrum antibiotics improves the outcome in septic patients. If cultures reveal a causative organism, antibiotic therapy is directed at that organism. This reduces the risk of resistant organisms or superinfections. Endocrine Support. Recent studies indicate that sepsis can rapidly progress to a state of relative endocrine insufficiency. For example, data by Landry and coworkers convincingly show a loss of vasopressin stores from the posterior pituitary, which is problematic. Vasopressin is most active in controlling tone in the splanchnic circulation, and the major component of sepsis-associated vasodilatation arises in this bed. Infusion of replacement vasopressin (0.01 to 0.04 unit/minute) restores normotension and may help wean the patient from other vasoactive substances. However, the use of corticosteroids in sepsis remains controversial. The debate centers on the inability to determine what constitutes a “normal” hypothalamic-pituitary-adrenal response in severe sepsis. Nonetheless, recent studies indicate that low doses of

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exogenous corticoids (hydrocortisone 50 mg/day) may improve refractory hypotension and facilitate weaning of exogenous catecholamines. Early Dialysis. Recent studies support the use of dialysis early in sepsis. Continuous dialysis is favored because it is associated with less hemodynamic instability. High flows seem to offer better solute clearance. When conventional hemodialysis is used, daily dialysis appears to be more effective than the more standard every-other-day approach.

Prevention of Further Complications Activated Protein C. In 2001, one multicenter, randomized trial examined the effects of activated protein C (APC) infusion started within 24 hours of the diagnosis of sepsis associated with major organ dysfunction. This was continued for 96 hours and led to a 6% reduction in 28-day mortality. However, protocol concerns and the risk of serious bleeding led the Food and Drug Administration to limit the indications for APC. Thus, APC has been approved for use in patients with severe sepsis and APACHE II scores greater than 25. However, newer data suggest that the improvement seen at 28 days is not sustained. In addition, APC is quite expensive. Thus, this drug is rarely used.

A New Syndrome The incidence of SIRS, sepsis, and MODS is difficult to quantify. This reflects both the diverse group of entities giving rise to these conditions and confusion about what does and does not constitute SIRS. However, recent studies indicate

that while mortality from sepsis has declined, the incidence of sepsis is steadily increasing. Indeed, the natural history of these conditions is rapidly evolving. Initial descriptions of what we now call SIRS, sepsis, and MODS arose when our ability to treat these conditions was dismal (with almost certain early mortality). We now have the ability to support most forms of major organ dysfunction, and this has led to the emergence of a new syndrome. There is no consensus name or definition for this new entity, which is characterized by a stable but highly abnormal state involving endocrine and inflammatory exhaustion. The failure of multiple components of the neuroendocrine system in the chronically, critically ill has been well described, and the concept of immune incompetence has recently been reviewed by Hotchkiss and Karl. More often than not, modern medical technology can maintain survival in this state. Reversal of the disorder, however, is difficult. What is increasingly clear is that mortality from SIRS, sepsis, or MODS most often occurs when exogenous life support is discontinued.

Further Reading Angus DC, Wax S: Epidemiology of sepsis: An Update. Crit Care Med 29:S109-S116, 2001. Bernard GR, Vincent JL, Laterre PF, et al: Recombinant Human Protein C Worldwide Evaluation in Severe Sepsis (PROWESS) study group: Efficacy and safety of recombinant human activated protein C for severe sepsis. N Engl J Med 344:699-709, 2001. Bone RC, Balk RA, Cerra FB, et al: Definition for sepsis and organ failure and guidelines for use of innovative therapies in sepsis: American College of Chest Physicians/Society of Critical Care Medicine. Chest 101:1644-1655, 1992. Deitch EA: Multiple organ failure: Pathophysiology and potential future therapy. Ann Surg 216:117-134, 1992. Dellinger RP, Carlet JM, Masur H, et al: Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock. Crit Care Med 32:858-873, 2004. Deutschman CS: The systemic inflammatory response syndrome and the multiple organ dysfunction syndrome. In Fishman AP (ed): Pulmonary Diseases and Disorders. New York, McGraw-Hill, 1997. Hotchkiss RS, Karl IE: The pathophysiology and treatment of sepsis. N Engl J Med 348:138-150, 2003. Landry DW, Levin HR, Gallant EM, et al: Vasopressin deficiency contributes to the vasodilation of septic shock. Circulation 95:1122-1125, 1997. Rivers E, Nguyen B, Havstad S, et al: Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 345:1368-1377, 2001. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med 342:1301-1308, 2000.

PHYSIOLOGIC IMBALANCE & COEXISTING DISEASE

Tight Glucose Control. Another single-center study examined tight glucose control (>80 but 60%) burns, and patients remain at high risk until wound closure. Burn wound sepsis can have an extremely rapid onset and an unusually severe course. Infected burn wounds require immediate debridement to maximize the chances for survival.

MANAGEMENT AND PREVENTION Severely burned patients may require rapid application of the basic ABCs (airway, breathing, circulation) during initial

Classification of Smoke Inhalation

Mechanism of Injury

Clinical Symptoms and Effects

Heat injury to glottis and upper larynx

Soot on face or in mouth and nose Redness or blistering of mouth, nose, or hard palate Difficulty phonating or swallowing Resuscitation edema may cause airway to swell dramatically Prophylactic tracheal intubation should be strongly considered if thermal injury to glottis is suspected Tachypnea, tachycardia, headache, dyspnea May progress to frank seizure, hypotension, malignant arrhythmias Cyanide poisoning acts synergistically with carbon monoxide to cause vital organ injury Although carbon monoxide can be readily detected on blood gas analysis, there is no rapid assay for cyanide; empirical therapy with sodium thiosulfate should be started if suspicion is high Toxicity of smoke depends on its temperature and the nature of burning materials and cannot be easily predicted There is no ready test for this component of inhalation thermal injury Unusually high fluid resuscitation volumes strongly suggest pulmonary involvement Symptoms usually manifest within 48 hr after thermal injury, including: Tachypnea Sputum production Fever Leukocytosis Hypoxemia Atelectasis Tracheal intubation to maintain oxygenation is often required; recovery occurs over a period of 2-3 wk

Ingested toxins (cyanide and carbon monoxide)

Irritant damage from contact with chemicals contained in smoke

PHYSIOLOGIC IMBALANCE & COEXISTING DISEASE

require to survive extensive burn injuries (Table 121-1). Patients burned in an indoor environment or closed space are at risk for inhalation injury. Smoke inhalation can manifest as laryngeal or glottal swelling, metabolic poisoning caused by carbon monoxide or cyanide, or sloughing of lung mucosa due to direct toxin exposure (Table 121-2). Patients at risk for such complications commonly have a supportive history, such as soot on their faces or in the nares or oropharnyx or blistering of the mouth and hard palate. Carbon monoxide poisoning commonly manifests as neurologic symptoms (ranging from agitation and confusion to frank seizures) and cardiovascular symptoms (including malignant arrhythmias and hypotension). Hypovolemia is due to fluid translocation caused by capillary leak and possibly blood loss if there is associated trauma. Electrolyte abnormalities due to thermal injury and resuscitation include hyponatremia, acidosis, and hypocalcemia. The aggressive fluid administration required may cause pulmonary and peripheral edema. Increased intra-abdominal pressure may also result from edema formation and may reduce urine output or compromise ventilation. Finally, compartment syndromes are common in patients with circumferential burns. If unrecognized, these may be associated with

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resuscitation, followed by other indicated management and preventive measures. There are two indications for emergent surgery: 1. Burn wound sepsis. This condition is diagnosed by positive quantitative wound cultures and signs of systemic sepsis. Although wound infection without systemic sepsis can be treated topically, severe wound sepsis with associated systemic changes often requires aggressive operative debridement to maximize survival. 2. Peripheral edema. Increased extremity compartment pressures, circumferential chest burns, or increased intraabdominal pressures (bladder pressure >25 mm Hg) require emergent surgical intervention to reduce compression injury. Because of large protein losses with thermal injury, patients with severe burns are often fed aggressively via an enteral route. Therefore, preoperative NPO orders should strive to minimize periods when patients are not being fed.

Fluid Requirements Fluid requirements for burn-injured patients are difficult to estimate, even for experienced practitioners. Underresuscitation may worsen injury, increase circulatory instability, and lead to end-organ dysfunction. Conversely, overresuscitation worsens edema and may increase the risk of abdominal compartment syndrome. Fluid replacement guidelines for the first 24 hours are provided in Table 121-3. These guidelines represent only starting fluid infusion rates. Because of the risk of edema formation, infusion rates should be titrated to the minimum amount needed to keep urine output at 0.5 mL/kg per hour. The “rule of nines” is used to estimate burn surface area (Table 121-4).

Intraoperative Care The intraoperative care of burn-injured patients undergoing debridement or grafting procedures can be extremely challenging. Wounds are typically debrided down to briskly bleeding tissue, with partial hemostasis achieved using topical phenylephrine. Because of the large wound surface and topical vasopressor use, blood loss may be difficult to assess.

Table 121–3 ■ Burn Life Support Guidelines for Initial Volume Resuscitation (First 24 Hours) Adults: 2-4 mL × body weight (kg) × burn area (%) Children: 3-4 mL × body weight (kg) × burn area (%) First half of volume to be infused over the first 8 hr, with remainder over next 16 hr Example: A 70-kg man with 50% BSA partial- and full-thickness burns: 2-4 mL × (70) × (50) = 7000-14,000 mL of lactated Ringer’s solution in the first 24 hr, with 3500-7000 mL given in the first 8 hr. Note that these are initial estimates only and that fluid therapy should be titrated to no more than 0.5 mL/kg/hr of urine output to minimize edema-related complications. BSA, body surface area. Adapted from Sheridan RL, et al: ABLS Provider’s Manual. Chicago, American Burn Association, 2001.

Table 121–4

■

Rule of Nines for Calculating Percentage of Body Surface Area Burned Body Surface Area

Body Part Arm Head and neck Leg Anterior trunk Posterior trunk

Adult 9 9 (and 1) 18 18 18

Child 9 18 14 18 18

Although tourniquets can be used on the extremities to reduce blood loss, they cannot be used for debridement involving the head, face, neck, chest, or back. Further, due to the greater vascularity of the head and face, blood loss can be especially severe during debridement of these areas. Careful attention to intravascular volume status and avoidance of the adverse consequences of overly aggressive fluid administration (acidosis, hypothermia, coagulopathy, pulmonary edema) are the cornerstones of intraoperative care. Preplanning, adequate intravenous (IV) access, and ongoing communication among members of the burn care team are essential to avoid hypovolemia in the perioperative period. Because of the risk of infection, burn patients usually have only the minimum necessary IV access on arrival to the operating room. Establishment of large-bore IV access is mandatory for debridement involving the head or if it is likely to be extensive. Alternating debridement with grafting can spread the requirement for transfusions over a longer time, allowing the anesthesia team greater opportunity to maintain adequate fluid balance. Surgical debridement should stop if the patient develops a coagulopathy, refractory hypotension, hypothermia (temperature 10 kg 1500 + 20 mL·kg−1 >20 kg

≥20

*4-2-1 rule. † 100-50-20 rule.

MANAGEMENT The goals of intraoperative fluid management are to provide an appropriate amount of parenteral fluids (water plus electrolytes) to maintain adequate intravascular volume, cardiac output, and urine output and, in some instances, to provide sufficient glucose to prevent hypoglycemia or minimize the risk of perioperative hyperglycemia. To avoid both hypoglycemia and hyperglycemia during surgical procedures, some have suggested administering 2.5% dextrose in lactated Ringer’s (LR) solution at maintenance rates, along with a glucose-free fluid (e.g., LR or normal saline) for replacement of blood and third-space losses. Because 2.5% dextrose-LR solution is not commercially available, either the practitioner or a pharmacist must prepare it. Blood obtained from central venous or arterial catheters or from finger or heel sticks is used to monitor glucose concentrations. Glucose testing is usually available at the point of care. If not, concentrations are measured in the blood gas laboratory. Serial blood glucose determinations can be made, with the amount of intravenous glucose adjusted accordingly.

PREVENTION Prevention of hypoglycemia and hyperglycemia requires a case-specific risk-benefit analysis. Some caveats deserve special mention: ●

●

● ●

Be aware of patients at increased risk for hypoglycemia or hyperglycemia. Be judicious when administering glucose-containing solutions to patients at risk for hypoglycemia. Withhold glucose-containing solutions when appropriate. Frequently monitor blood glucose concentrations.

Further Reading Aun CD, Panesar NS: Paediatric glucose homeostasis during anaesthesia. Br J Anaesth 64:413-418, 1990. Bazaes RA, Salazar TE, Pittaluga E, et al: Glucose and lipid metabolism in small for gestational age infants at 48 hours of age. Pediatrics 111: 804-809, 2003. Ferranti SD, Gaureau K, Hickey PR, et al: Intraoperative hyperglycemia during infant cardiac surgery is not associated with adverse neurodevelopmental outcomes at 1, 4, and 8 years. Anesthesiology 100: 1345-1352, 2004. Leelanukrom R, Cunliffe M: Intraoperative fluid and glucose management in children. Paediatr Anaesth 10:353-359, 2000. Nishima K, Mikawa K, Maekawa N, et al: Effects of exogenous intravenous glucose on plasma glucose and lipid homeostasis in anesthetized infants. Anesthesiology 83:258-263, 1995. Pereira GR: Nutrition care of the extremely premature infant. Clin Perinatol 22:61-75, 1995. Welborn LG, Hannallah RS, McGill WA, et al: Glucose concentration in routine intravenous infusion in pediatric outpatient surgery. Anesthesiology 67:427-430, 1987. Welborn LG, McGill WA, Hannallah RS, et al: Perioperative blood glucose concentrations in pediatric outpatients. Anesthesiology 65:545-547, 1986.

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Pulmonary Hypertension Deborah A. Davis

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Case Synopsis A 4-month-old, formerly preterm infant with bronchopulmonary dysplasia presents for closure of a ventricular septal defect after failing to wean from mechanical ventilation. The surgical procedure is not difficult, but after weaning from cardiopulmonary bypass, the patient has suprasystemic pulmonary artery pressures.

PROBLEM ANALYSIS Definition Elevated pulmonary artery pressure (PAP) is due to increased pulmonary vascular resistance (PVR) or pulmonary blood flow. Pressure, resistance, and flow are related by Poiseuille’s adaptation of Ohm’s law: Ohm’s law: R = PAP − Pv/Q, where R is pulmonary vascular resistance, Pv is pulmonary venous pressure (approximately equal to left atrial pressure), and Q is flow. Poiseuille’s law: R = 8L/πr4,

Recognition The workup for secondary PAH entails serial physical examinations and laboratory and diagnostic testing (Table 164-3). In children without a predisposing condition,

Risk Assessment In lesions that involve a communication between the systemic and pulmonary circulations, some proportion of the systemic pressure is transmitted to the pulmonary circulation. Associated high pressure and increased blood velocities produce shear stress, causing structural and functional damage to the pulmonary vascular endothelium. In lesions with reduced pulmonary blood flow, there may be hypoplasia of the arteries themselves. The risk of

Table 164–1

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Cardiac Causes of Secondary Pulmonary Hypertension

Cardiac lesions that increase pulmonary flow (left-to-right shunt) Patent ductus arteriosus Atrial septal defect Ventricular septal defect (VSD) Atrioventricular canal Aorta-pulmonary window Arterial-pulmonary collaterals Transposition of great vessels with VSD Systemic-to-pulmonary shunts Cardiac lesions that decrease pulmonary flow Tetralogy of Fallot Ebstein’s anomaly Pulmonary atresia Tricuspid atresia Cardiac lesions that cause pulmonary venous hypertension Cor triatriatum Mitral stenosis Mitral atresia Interrupted aortic arch Cardiomyopathy Hypoplastic left ventricle Critical aortic stenosis Coarctation of aorta Veno-occlusive disease Endocarditis

PEDIATRICS & NEONATOLOGY

where R is pulmonary resistance, L is length of resistor, and r is radius of resistor. The latter suggests that the length of the pulmonary bed (and blood viscosity) has a direct impact on resistance, and that the effect of altered arterial radius is exponential. With increased PVR, higher perfusion pressures are needed to maintain constant pulmonary flow; otherwise, flow diminishes. Normal values for mean PAP (i.e., pulmonary artery – left atrial pressure) and PVR are 10 to 20 mm Hg and 4 Wood units, respectively. Either primary or secondary pulmonary artery hypertension (PAH) can occur in children. To diagnose the former, all other causes must be excluded (see Chapter 78). Persistent PAH of the newborn is one cause of primary PAH. It may be due to underdevelopment of the lung, pulmonary vascular maladaptation to extrauterine life, or maldevelopment of the pulmonary vascular bed in utero. With primary PAH, lung pathologic examination reveals a reduced number of arteries relative to the number of bronchioles. Secondary PAH typically develops in response to specific types of cardiac or pulmonary disease (Tables 164-1 and 164-2). Within the context of congenital heart disease, secondary PAH may be due to increased pulmonary artery blood flow, resistance, or both. Secondary PAH can result from advanced pulmonary disease, as well as from nonrespiratory causes (see Chapter 78).

early signs of secondary PAH are those of right ventricular failure, exercise limitation, and, possibly, hypoxemia if a patent foramen ovale is present. Neonates with a patent ductus arteriosus may exhibit differential upper and lower body systemic oxygen saturation as desaturated blood shunts right to left across the ductus to perfuse the lower body.

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Noncardiac Causes of Secondary Pulmonary Hypertension

Table 164–4

Respiratory Obstructed lung disease (rare) Restrictive lung disease Collagen vascular disease Bronchopulmonary dysplasia Respiratory distress syndrome Interstitial disease Infiltrative disease Pleural adhesions Neuromuscular disease Other Upper airway obstruction Pickwickian syndrome

■

Classification of Structural Changes with Pulmonary Vascular Disease

Grade Structural Change

Status

I II III

Reversible Reversible

IV V VI

Medial hypertrophy Cellular intimal proliferation Intimal hyperplasia, luminal occlusion Pulmonary artery dilatation Pulmonary angiomatoid formation Pulmonary fibrinoid necrosis

Probably reversible Probably reversible Irreversible Irreversible

From Heath D, Edwards SE: The pathology of hypertensive pulmonary vascular disease. Circulation 18:533-547, 1958.

Nonrespiratory Juvenile rheumatoid arthritis Lupus erythematosus Pulmonary embolism (fat, thrombus, air, tumor) Sickle cell disease Scleroderma

developing increased PVR varies, depending on the cardiac malformation: ● ● ●

●

Ventricular septal defect, 15% Transposition of great arteries, 8% Transposition of great arteries with ventricular septal defect, 40% Complete atrioventricular canal defect, almost 100%

If the hematocrit is elevated, vascular thrombotic changes may exacerbate structural arterial changes. Secondary PAH

Table 164–3

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Workup for Secondary Pulmonary Hypertension

Physical examination Irregular heart rhythms Elevated jugular venous pressure Loud P2, systolic ejection click, wide split P2 Diastolic murmur Chest radiograph (may be normal) Prominent pulmonary artery; enlarged heart Increased pulmonary vascular markings (congestive heart failure) Decreased pulmonary vascular markings (severe disease) Echocardiogram Define anatomy; estimate shunt flows Estimate right ventricular and pulmonary artery pressures Catheterization Further define anatomy Calculate pulmonary vascular resistance Test response to oxygen, nitric oxide, vasodilators Wedge angiography (pulmonary artery tapering and filling; circulation time) Other Electrocardiogram (right ventricular hypertrophy) Lung biopsy Elevated hematocrit

also occurs if left-sided lesions cause pulmonary venous hypertension, with increased venous pressure transmitted back to the pulmonary arteries. Heath and Edwards classified the structural changes that occur with pulmonary vascular disease (Table 164-4). Several factors contribute to secondary PAH with severe parenchymal lung disease: (1) hypoxia and polycythemia, (2) pulmonary endothelial injury, and (3) structural pulmonary artery damage. For example, along with the proliferation of vascular muscularis into nonmuscular peripheral pulmonary arteries, infants with bronchopulmonary dysplasia have excessive pulmonary interstitial water. This compresses the arterioles and further elevates PVR. Treatment of the primary lung disease helps reduce the impact of contributory causes of secondary PAH, allowing regression of some of the associated structural changes. Nonrespiratory diseases can also cause secondary PAH via inflammation (arteritis) or occlusion (thrombosis). Either reduces the pulmonary vascular cross-sectional area and elevates PVR. Also, vasoactive substances (e.g., prostaglandins, thromboxanes, leukotrienes) cause pulmonary vascular changes that increase PAP: ●

●

●

Pulmonary endothelium-derived von Willebrand’s factor increases platelet adhesion and the formation of microaggregates, along with the release of vasoconstrictive factors. Endothelium-derived relaxing factor (i.e., nitric oxide) relaxes vascular smooth muscle and is reduced in patients with lung injury and after cardiopulmonary bypass. Primary pulmonary hypertension can be triggered by almost any neonatal stress (e.g., hypoxemia, hemorrhage, hypoglycemia, hypothermia, aspiration, acidosis) via some of the aforementioned cellular mediators.

Paroxysmal increased PVR occurs on occasion, even with normal baseline PAPs (e.g., post–cardiac surgery patients with large left-to-right shunts or pulmonary venous obstruction). Such pulmonary hypertensive crises can arise when vascular endothelial cells are triggered by a particular stimulant. Consequent acute PAH is poorly tolerated, and

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circulatory collapse can be immediate. The following are more common triggers: ● ●

●

Hypoxia, hypercarbia, acidosis Aggressive suctioning, noxious stimuli, bronchoscopic procedures Pleural effusion, hemothorax, pneumothorax

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Sildenafil is a phosphodiesterase inhibitor that shows promise as an effective intravenous agent for reducing PAP. However, its use may be limited because of its potential to increase intrapulmonary shunt and worsen ventilationperfusion mismatch.

Invasive Measures

Implications

ATRIAL SEPTOSTOMY

High PVR increases right ventricular impedance and may lead to acute or chronic right ventricular failure. As a result, pulmonary blood flow decreases. Without direct pulmonary-systemic connections that allow right-to-left shunting (e.g., a patent foramen ovale), the systemic cardiac output will also fall.

If tissue oxygen delivery is unsatisfactory despite ventilatory and pharmacologic management, more invasive measures may be necessary. In children with low cardiac output due to right ventricular failure but without intracardiac connections, atrial septostomy may prove beneficial. The creation of an atrial septal defect enables systemic venous blood return to bypass the pulmonary circulation and augment left ventricular output, albeit at the cost of systemic hypoxia.

MANAGEMENT MECHANICAL CIRCULATORY SUPPORT Because the management of PAH due to increased pulmonary blood flow is surgical elimination of the left-to-right shunt, only the management of increased PVR is discussed here. The goal is to provide adequate systemic oxygen delivery. Initial therapy should focus on lowering PVR to optimize right ventricular performance. If this fails, intervention to bypass the pulmonary circulation may be necessary.

If low cardiac output persists despite atrial septostomy, or if systemic hypoxemia becomes life threatening, extracorporeal circulatory support is the final option. Because the pathophysiology resides in the pulmonary microcirculation, selective right ventricular assist devices usually do not provide sufficient benefit, necessitating the interposition of a membrane oxygenator.

Ventilatory Strategies

LUNG

Ventilatory strategies represent the most effective measures for selectively influencing PVR. Maintenance of a normal functional residual capacity optimizes PVR, because lung overdistention or underinflation can result in compression and distortion of the pulmonary microcirculation. Reactive pulmonary vasculature dilates in response to enriched oxygen mixtures and local alkalosis. The latter is achieved by hyperventilation or with sodium bicarbonate. When conventional ventilation cannot achieve satisfactory gas exchange without deleterious levels of intrathoracic pressure, jet ventilation may prove beneficial. Inhaled nitric oxide is a selective pulmonary vasodilator that may be effective in cardiac or noncardiac PAH.

Unless the pulmonary hypertensive crisis can be attributed to a finite and reversible cause (e.g., persistent pulmonary hypertension of the newborn), extracorporeal circulatory support must be regarded as a bridge to heart or heart-lung transplantation. Given the limited availability of these organs for children, both the patient’s family and medical providers must have realistic expectations before embarking on such heroic therapy.

Pharmacologic Agents A variety of intravenous drugs, listed here, can have a salutary effect on PVR. They vary in efficacy from patient to patient, and none is selective for the pulmonary circulation: ● ●

● ● ● ● ● ● ● ●

HEART-LUNG TRANSPLANTATION

PREVENTION Therapeutic options for primary and secondary PAH are limited in both scope and efficacy; therefore, prevention is vital. Children with PAH or medical histories that predispose to pulmonary hypertensive crises require meticulous anesthesia care. Preoperative measures directed at optimizing right ventricular function (e.g., digoxin, arrhythmia control) and intravascular volume status deserve special consideration and may provide some benefit. Most critical are precautions to preserve optimal ventilation and provide sufficient analgesia to blunt endogenous, catecholaminemediated responses to noxious stimuli. Also, children with intracardiac shunts and the potential for right-to-left shunting should receive drugs that substantially reduce systemic vascular resistance, even though this promotes systemic hypoxemia. Assuming that cardiac reserve is sufficient to tolerate the requisite doses of anesthetic agents, children with PAH should be managed similarly to those with other conditions in which endogenous responses to noxious stimuli

PEDIATRICS & NEONATOLOGY

●

Prostacyclin Isoproterenol Angiotensin-converting enzyme inhibitors Adenosine Nitroprusside Amrinone Acetylcholine Tolazoline Prostaglandin E1 Nitroglycerin Sildenafil

OR

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have a deleterious impact on the underlying circulatory pathophysiology.

Further Reading Avery GB (ed): Neonatology: Pathophysiology and Management of the Newborn. Philadelphia, JB Lippincott, 1987, p 1399. Davis DA, Russo PA, Greenspan J, et al: High frequency jet versus conventional ventilation in infants undergoing Blalock-Taussig shunts. Ann Thorac Surg 57:846-849, 1994.

Fishman AP: Hypoxia as the pulmonary circulation: How and where it acts. Circ Res 38:221-231, 1976. Haworth SG: Primary pulmonary hypertension. Br Heart J 49:517-521, 1983. Heath D, Edwards SE: The pathology of hypertensive pulmonary vascular disease. Circulation 18:533-547, 1958. Rabinovitch M, Andrew M, Thom H, et al: Abnormal endothelial factor VIII associated with pulmonary hypertension and congenital heart defects. Circulation 76:1043-1052, 1987. Schulze-Neick I, Hartenstein P, Li J, et al: Intravenous sildenafil is a potent pulmonary vasodilator in children with congenital heart disease. Circulation 108(Suppl II):167-173, 2003.

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Hypothermia in Pediatric Patients Kevin J. Sullivan Case Synopsis A 1-month-old, formerly premature (28-week) infant undergoes general anesthesia for magnetic resonance imaging of the brain and spine. At the conclusion of the imaging study, the patient is noted to have a core body temperature of 34.5°C and demonstrates delayed emergence from anesthesia and increased severity of apnea and bradycardia in the neonatal intensive care unit.

PROBLEM ANALYSIS Definition Central (core) body temperature is one of the most tightly regulated parameters in human physiology. Normal core body temperature in infants, children, and adults is about 37°C and seldom fluctuates more than 0.5°C above or below this setpoint. However, mild hypothermia (1°C to 3°C below normal) is commonly seen perioperatively. Anesthetic medications, environmental exposure, and critical illness may result in altered thermoregulation and hypothermia.

Recognition The minimum basic monitoring standards of the American Society of Anesthesiologists require that temperaturemonitoring capabilities be readily available to anesthesiologists. Temperature monitoring is especially important for detecting hypothermia in infants and children, because they are very susceptible to this complication. Sites for temperature monitoring are classified as central (nasopharyngeal, esophageal, axillary, rectal, or bladder) or peripheral (skin): ● ●

● ● ● ●

Nasopharyngeal—posterior to the soft palate Esophageal—posterior to the heart below the level of the carina Rectal Urinary bladder (less accurate with reduced urine output) Axillary—near the axillary artery with the arm abducted Skin surface (poor correlation with core body temperature) HEAT LOSS

IN

ANESTHETIZED INFANTS

The four mechanisms of heat loss in anesthetized patients are conduction, evaporation, convection, and radiation. An understanding of these mechanisms leads to a better understanding of the strategies to minimize heat loss in anesthetized children. Conduction is the direct transfer of heat energy between objects, as occurs with direct patient contact with a cold

663

PEDIATRICS & NEONATOLOGY

MECHANISMS OF AND CHILDREN

metal surface, irrigation of wounds with cold saline, and the intravenous administration of cold fluids. Evaporation results in heat loss when the latent heat of vaporization is expended to convert a liquid to a gaseous state. Evaporative heat loss in anesthetized patients comes from the skin (evaporation of sweat or surgical preparation solutions from the skin), respiratory tract, and wounds (especially exposed thoracic and peritoneal cavities). Convection occurs when molecules at different temperatures cause the net transfer of heat between objects, such as when cool air circulates over the surface of the patient’s skin. The rate of convective heat loss is proportional to the temperature difference between ambient air and skin and to the surface area of the patient’s skin exposed to that air. Finally, radiation heat loss occurs when infrared energy is exchanged between two solid objects that are not in contact. The magnitude of heat exchange is proportional to the fourth power of the temperature difference between the two objects. Body temperature is monitored by the hypothalamus through afferent sensory input from the skin, neuraxis, and deep body tissues. Under normal conditions, core body temperature is tightly regulated by the hypothalamus and remains within a narrow interthreshold range of 0.5°C above or below a recognized normal body temperature, or setpoint. When the hypothalamus detects a change in core body temperature beyond the acceptable interthreshold range, effector mechanisms are activated to bring core body temperature back to normal (Figs. 165-1 and 165-2). Central regulation of temperature is present in infancy but may be impaired in the elderly, in the critically ill, and in children with severe damage to the central nervous system. In response to hypothermia, effector mechanisms are activated. These mechanisms are classified as those that reduce heat loss (behavioral changes, vasoconstriction) and those that increase heat production (behavioral changes, nonshivering thermogenesis, shivering). Behavioral changes are not relevant in anesthetized patients, so cutaneous vasoconstriction is the primary response to hypothermia in this setting. Cutaneous blood flow can be reduced via norepinephrine secreted at presynaptic adrenergic terminals. This results in a 25% to 50% decrease in heat loss.

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Hypothalmus Other parts of brain Skin surface Spinal cord Deep central tissues

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Hypothalmus

Warm responses

PERIOPERATIVE THERMOREGULATION

Active vasodilation Sweating

Predictable changes in body temperature occur in infants and children after the induction of general anesthesia (Fig. 165-3). The first phase of heat redistribution begins when volatile anesthetics cause peripheral vasodilatation, effectively reducing core body (central compartment) perfusion. Central temperature declines as heat is lost to the peripheral tissues. During the second phase, there is reduced endogenous heat production and increased heat loss to the environment. During the third phase, metabolic heat production exceeds heat loss, causing the core temperature to stabilize (adults) or increase (greater in infants than in children). General anesthesia widens the thermoregulatory interthreshold range (≥2.5°C below the setpoint). This leads to passive core body temperature changes over a wider range of hypothermic temperatures before effector mechanisms become activated (see Fig. 165-2). A lower temperature threshold for effector mechanism activation has been demonstrated with halothane, enflurane, desflurane, sevoflurane, isoflurane propofol, and nitrous oxide–opioid anesthesia. Regional anesthesia techniques produce hypothermia as readily as general anesthesia does. The vasodilatation induced by neuraxial local anesthetics causes rapid redistribution of core heat to the periphery in a manner similar to that seen with the induction of general anesthesia. Effector mechanisms of shivering and vasoconstriction are absent below the level of block but remain intact above the level of block. Also, the interthreshold range for effector mechanisms appears to be widened in a manner similar to that seen with general anesthesia. It is postulated that the absence of cold afferent input from the tissues below the level of the block is interpreted as warm afferent input, which leads to

Interthreshold Vasoconstriction Nonshivering thermogenesis Shivering

range

Cold responses Figure 165–1 ■ Thermoregulatory model. Thermal afferent input is integrated and compared with the threshold temperature for heat and cold. The interthreshold range is the temperature range over which no regulatory effector responses occur. On either side of this interthreshold range are triggered thermoregulatory respononses. (From Bissonnette B: Thermoregulation and pediatric anesthesia. Curr Opin Anesthesiol 6:537-542, 1993.)

Under anesthesia

Awake

Heat production is augmented in anesthetized patients by nonshivering thermogenesis (NST) and shivering. NST is the production of heat in skeletal muscle and brown fat due to the catabolism of brown fat around the blood vessels of the neck, mediastinum, adrenal glands, and axillae. NST can be inhibited by ganglionic blockade, β-blockade, and inhalational anesthetics. Preterm infants, term neonates, infants, and children are capable of NST; however, recent reports have questioned the importance of NST in infants and small mammals during general anesthesia. Shivering is characterized by high-frequency, irregular muscle activity that begins in upper body muscles when vasoconstriction and NST have failed to maintain an adequate mean body temperature. Shivering is an important mechanism for thermoregulation in adults, but it has not been observed in children younger than 6 years.

NST Shivering

Active vasodilatation

NST Shivering >6 years

Sweating

35

Infants Children Adults

Sweating

Vasoconstriction Children Infants

33

38

Active vasodilatation

Vasoconstriction

37

39

Central temperature (°C)

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37

A

36

B

35

41°C

Figure 165–2 ■ Thermoregulatory thresholds and gains in awake and anesthetized infants and children. Thermoregulation appears to be an allor-none phenomenon. The threshold temperature triggering a thermoregulatory response to hypothermia during anesthesia—nonshivering thermogenesis (NST)—is about 2.5°C below the setpoint (about 37°C), whereas during hyperthermia, the temperature must increase approximately 1.3°C above the setpoint to activate an effector response. Within this temperature range, thermoregulatory responses are absent. Consequently, the patient’s body temperature changes passively in proportion to the difference between metabolic heat production and environmental heat loss. (From Bissonnette B: Thermoregulation and pediatric anesthesia. Curr Opin Anesthesiol 6:537-542, 1993.)

C

34 0

80

160

240

Elapsed time (min)

Figure 165–3 ■ Typical pattern of hypothermia during anesthesia. This occurs in three distinct phases in infants, children, and adults: internal redistribution of heat (A), heat loss to the environment (B), and thermal steady state or rewarming (C). Slopes for each stage vary as a function of age. (From Bissonnette B: Thermoregulation and pediatric anesthesia. Curr Opin Anesthesiol 6:537-542, 1993.)

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suppression of vasoconstriction, despite the fact that core body temperature is reduced. When combined with general anesthesia, the additional effects of regional anesthesia on thermoregulatory thresholds appear to be minimal.

Risk Assessment Infants and neonates are more likely than adults to develop perioperative hypothermia. Infants and small children have an increased surface area relative to their body mass. The prominence of the head and trunk and the small extremities of infants prevent the pooling of heat content in the peripheral compartment during anesthesia-related vasodilatation, while the increased surface area–to–body mass ratio diminishes the effectiveness of cutaneous vasoconstriction. Infants lose more heat through their thin skin and have a higher minute ventilation, which increases evaporative heat loss from the respiratory tract. Finally, although vasoconstriction and NST are present in infants and young children, small infants’ inability to shiver effectively limits their ability to optimally generate endogenous heat. These innate limitations in the conservation and production of endogenous heat render infants and children particularly vulnerable to the development of hypothermia in cool ambient environments.

Implications

Hypothermia in Pediatric Patients

665

MANAGEMENT AND PREVENTION The simplest and most effective method to treat or prevent heat loss is to warm the operating room to at least 26°C, and often to temperatures greater than 30°C when caring for term or preterm infants. Likewise, maintenance of relative humidity in the operating room minimizes evaporative heat losses from infants. Use of other heat conservation methods may allow the operating room to be cooled to ambient temperatures that are more comfortable for the health care team. During anesthesia induction, passive patient warming is accomplished by insulating as much of the skin surface as is practical. The amount of skin surface covered is more important than which part is covered, and no one material is superior to others for reducing radiation and convective heat loss from the skin. Passive insulation of the peripheral compartment limits the transfer of heat from the central compartment to the peripheral compartment during general anesthesia. Active patient warming can be used to minimize ambient heat loss during general anesthesia. Infrared radiant heaters are commonly used during anesthesia induction and patient preparation and positioning. Once the patient has been positioned and draped, convective air warming blankets or circulating warm water blankets are commonly used. The former circulate warm air at variable temperatures over the body surface outside the surgical field. Circulating warm water blankets are usually placed underneath the patient, with layers of cotton sheets between the blanket and the patient to prevent thermal injury. Convective blankets are more effective than warm water blankets for the prevention and treatment of perioperative hypothermia in infants. Care must be exercised to (1) monitor the patient’s skin for thermal injury, (2) ensure that warming devices are properly applied, and (3) use the minimal temperature required for gradual rewarming. This is especially important if surface blood flow is reduced (e.g., low cardiac output states, regions of pressure necrosis, procedures involving skin grafting or the creation of muscle flaps). Significant burn injuries have been reported with the use of warming devices. Efforts to reduce respiratory tract evaporative losses are more effective heat conservation measures in children than in adults owing to their higher minute ventilation. Airway humidification, whether active or passive, minimizes heat loss from the respiratory tree. Active humidifiers nebulize water particles in inspired gas mixtures and are most commonly used on ventilators in critical care settings. Care must be taken to monitor the temperature of the inspired gases to prevent tracheal mucosal thermal injury. Passive humidifiers (“artificial noses”) condense water contained in exhaled gases and return it to the patient during inspiration. Care must be taken to place the heat and moisture exchanger in close proximity to the airway to prevent condensation and “rain-out” of free water in the cool gas in the inspiratory limb of the ventilator circuit. Finally, attention to the temperature of intravenous and irrigation fluids is critical to prevent rapid conductive cooling during pediatric anesthesia. If large amounts of crystalloid and blood products are

PEDIATRICS & NEONATOLOGY

The primary disadvantages of hypothermia in awake patients are shivering and discomfort. Shivering increases heat production at the expense of a pronounced increase in oxygen consumption (up to 600%). Cardiac output increases to match increased oxygen demands, and although this is easily tolerated in healthy patients, it may be poorly tolerated in those with cardiovascular disease. Neutral thermal environment is the term used to describe the range of ambient temperatures at which metabolic expenditures for heat production are minimal. The critical temperature is the temperature below which heat must be produced by the patient to prevent a decrease in body temperature. Term newborns have a critical temperature of about 33°C, whereas preterm infants can have critical temperatures as high as 35°C. Because oxygen consumption for NST increases with larger skin surface–to– environmental temperature gradients, infants in cool ambient environments may expend considerable metabolic energy in pursuit of a stable body temperature. Hypothermia has deleterious effects on platelet function, immune function, nitrogen balance, and blood flow to surgical wounds. Surgical blood loss is increased when hip arthroplasty is performed during hypothermia, and surgical wound infection and prolonged hospital stays have been noted in patients having procedures performed under hypothermic conditions. Hypothermia depresses drug metabolism, prolongs the duration of action of muscle relaxants, and reduces the minimum alveolar concentration for volatile anesthetics. Severe hypothermia may impair cognitive function, but there is conflicting evidence about whether it delays anesthetic emergence. Finally, hypothermia often occurs with metabolic aberrations known to exacerbate central apnea in preterm infants (e.g., hypoglycemia, hypocalcemia, hypoxemia, acidosis).

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administered, precipitous declines in body temperature can occur if they are not warmed beforehand. Likewise, irrigation fluids that are not warmed to body temperature can cause rapid declines in body temperature, especially when used to irrigate the peritoneal and thoracic cavities.

Further Reading Bissonnette B: Thermoregulation and pediatric anesthesia. Curr Opin Anesthesiol 6:537-542, 1993. Bissonnette B, Ryan JF: Temperature regulation: Normal and abnormal (malignant hyperthermia). In Cote CJ, Todres ID, Ryan JF, et al (eds): A Practice of Anesthesia for Infants and Children. Philadelphia, WB Saunders, 2001, pp 610-635. Bissonnette B, Sessler DI: The thermoregulatory thresholds for vasoconstriction in pediatric patients anesthetized with halothane or halothane and caudal bupivacaine. Anesthesiology 76:387-392, 1992. Bissonnette B, Sessler DI, LaFlamme P: Intraoperative temperature monitoring sites in infants and children and the effect of inspired gas warming on esophageal temperature. Anesth Analg 69:192-196, 1989.

Dicker A, Ohlson KB, Johnson L, et al: Halothane selectively inhibits nonshivering thermogenesis: Possible implications for thermoregulation during anesthesia of infants. Anesthesiology 82:491-501, 1995. Kurz A, Kurz M, Poeschl G, et al: Forced-air warming maintains intraoperative normothermia better than circulating-water mattresses. Anesth Analg 77:89-95, 1993. Kurz A, Sessler DI, Lenhardt R: Perioperative normothermia to reduce the incidence of surgical-wound infection and shorten hospitalization. Study of Wound Infection and Temperature Group. N Engl J Med 334:1209-1215, 1996. Plattner O, Semsroth M, Sessler DI, et al: Lack of non-shivering thermogenesis in infants anesthetized with fentanyl and propofol. Anesthesiology 86:772-777, 1997. Schmied H, Kurz A, Sessler DI, et al: Mild hypothermia increases blood loss and transfusion requirements during total hip arthroplasty. Lancet 347:289-292, 1996. Sessler D: Temperature disturbances. In Gregory GA (ed): Pediatric Anesthesia, 4th ed. Philadelphia, Churchill Livingstone, 2002, p 67. Truell KD, Bakerman PR, Teodori MF, et al: Third-degree burns due to intraoperative use of a Bair Hugger warming device. Ann Thorac Surg 69:1933-1934, 2000. Zukowski ML, Lord JL, Ash K: Precautions in warming light therapy as an adjuvant to postoperative flap care. Burns 24:374-377, 1998.

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Cardiomyopathies Stephanie S. F. Fischer and B. Craig Weldon Case Synopsis A 6-month-old boy with Pompe’s disease (glycogen storage disease type II) presents for muscle biopsy and central venous catheter placement under general anesthesia. Mask induction with sevoflurane is followed by a maintenance propofol infusion. The patient develops signs of ischemia on the electrocardiogram (ECG) and hypotension. This quickly leads to ventricular fibrillation and cardiac arrest. The return of spontaneous circulation is achieved with external cardiac massage and two intravenous doses of epinephrine, and the surgery is canceled.

PROBLEM ANALYSIS Definition The World Health Organization defines cardiomyopathies (CMs) as myocardial diseases associated with cardiac dysfunction. They are classified by the dominant pathophysiology or, if known, by causative factors. Thus, CM may be dilated, hypertrophic, restrictive, or a special type called arrhythmogenic right ventricular cardiomyopathy (or arrhythmogenic right ventricular dysplasia). If the cause of a CM is known (i.e., secondary CM), it may be ischemic, valvular, hypertensive, inflammatory, metabolic, or peripartum in origin. CMs can also be associated with systemic disease, neuromuscular disorders, or exposure to toxins.

Recognition Primary CM (not caused by some other organ system disease or pathophysiologic state) and secondary CM (proven cause) can be dilated, hypertrophic, restrictive, or arrhythmogenic right ventricular, based on functional and anatomic presentations. Unclassified CMs consist of cases that do not fit readily into any of these groups, such as the following: ● ● ●

Fibroelastosis Noncompacted myocardium Mitochondrial disorders

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PEDIATRICS & NEONATOLOGY

Dilated cardiomyopathy (DCM) is characterized by left ventricular chamber dilatation and impaired systolic function involving the left ventricle (LV), right ventricle (RV), or both. DCM may be viral or immunologic, idiopathic, or familial (genetic); it may be caused by alcohol or toxins or associated with other diseases involving the cardiovascular system. DCM may be asymptomatic or associated with severe functional impairment (New York Heart Association [NYHA] class III or IV heart failure). Patients with decompensated heart failure (NYHA class IV) present with low cardiac output and pulmonary edema (cor pulmonale). Also, all four cardiac chambers appear dilated on chest radiographs. The ECG in

acute cor pulmonale may resemble that of inferior myocardial infarction. However, differences include the following: (1) the pattern of lead II tends to follow that of lead I (no Q wave) as opposed to that of lead III (with Q waves); (2) the ECG changes may be fleeting or resolve over a period of hours or days, as opposed to weeks or months; (3) the ST-T abnormalities in the limb leads are slight, and those in the right precordial leads resemble the anteroseptal infarction pattern; (4) transient right bundle branch block may be present. In chronic cor pulmonale, the ECG is characterized by (1) a rightward shift of the QRS axis by greater than 30 degrees; (2) inverted, biphasic, or flattened T waves in leads V1 to V3; (3) ST segment depression in the inferior leads (II, III, aVF); and (4) right bundle branch block. Echocardiography confirms DCM as well as poor systolic function. Hypertrophic cardiomyopathy (HCM) may involve the LV, RV, or both and is often asymmetrical. Ventricular volumes may be normal or reduced. HCM is characterized by diastolic dysfunction, with preserved systolic function. HCM is a genetic condition and involves sarcomeric protein mutations. There is an autosomal dominant pattern of inheritance, with variable penetrance. Patients with HCM may be asymptomatic or present with exertional dyspnea, chest pain, and syncope. The ECG shows a progressive pattern, from septal hypertrophy to generalized left ventricular hypertrophy. A few other tendencies are also worth noting: (1) the ECG can be normal in up to 20% of cases; (2) many patients have ECG evidence of left ventricular hypertrophy; (3) some cases are associated with left axis deviation; (4) the pattern of bundle branch block (in reality, intraventricular conduction block) tends to be atypical, with notching and slurring of the QRS complex in the limb leads; (5) the P waves may be widened and notched, with evidence of left atrial enlargement; (6) in infants with HCM, the ECG pattern is commonly consistent with right ventricular hypertrophy; (7) possibly the most suggestive finding (25% to 30% of patients) is obviously abnormal Q waves, but dissimilar to those of myocardial infarction. Also, HCM is associated with an increased incidence of both supraventricular and ventricular arrhythmias. Finally, echocardiography reveals asymmetrical septal

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hypertrophy, with a septal–to–left ventricular wall ratio greater than 1.3. Restrictive cardiomyopathy (RCM) is characterized by restricted left or right (or both) ventricular filling due to reduced ventricular diastolic compliance. There may be normal or near-normal systolic function. RCM may be idiopathic, or it can be associated with endomyocardial fibrosis or the hypereosinophilic syndrome. Arrhythmogenic right ventricular cardiomyopathy (ARVCM) is characterized by fibrofatty replacement of right or left ventricular (or both) myocardium. ARVCM is a genetic cardiac disease with autosomal dominant inheritance and incomplete penetrance. Patients with ARVCM often present with dyspnea, fatigue, hepatomegaly, and ascites. The chest radiograph shows pulmonary venous congestion. The ECG may show impaired atrioventricular conduction. However, without histiologic confirmation (i.e., myocardial biopsy), ARVCM is diagnosed based on the presence of ventricular arrhythmias (most often sustained ventricular tachycardia) with a left bundle branch block configuration and wall motion abnormalities on echocardiography in the free wall of the RV. In addition, echocardiography may show atrial dilatation associated with near-normal ventricular dimensions and atrioventricular valve regurgitation.

Risk Assessment DCM is the most common form of CM in children; it has an equal prevalence in males and females. HCM usually does not present before adolescence. With HCM, morbidity and mortality are greatest in patients diagnosed at younger ages. Premature death is commonly due to ventricular fibrillation. RCM is uncommon in children but, when present, is often an end-stage finding with myocarditis or an infiltrative myocardial disease. ARVCM is uncommon but accounts for a high percentage of sudden cardiac deaths in children and adolescents. The prevalence in females is threefold grater than in males.

Implications In DCM, cardiac output is maintained by sympathetically mediated tachycardia and ventricular chamber dilatation with increased stroke volume. However, this leads to increased myocardial wall tension and oxygen utilization. In HCM, there is ventricular inflow obstruction secondary to diastolic dysfunction. Some 20% to 25% of patients also have dynamic obstruction of the left ventricular outflow tract. The systolic volume of the LV, the force of left ventricular contraction, and the transmural pressure gradient distending the outflow tract determine the severity of the obstruction. With RCM, the ejection fraction is maintained early in the process. However, as ventricular fibrosis progresses, left ventricular end-diastolic pressure increases, resulting in pulmonary hypertension and decreased stroke volume and cardiac output. With ARVCM, contractility is normal initially; however, the onset of ventricular arrhythmias (ventricular tachycardia) leads to slow deterioration of right ventricular function. Eventually, ventricular tachyarrhythmias (ventricular tachycardia or fibrillation) become resistant to antiarrhythmic therapy.

MANAGEMENT The perioperative management of children with known CM requires an understanding of normal cardiovascular physiology and an appreciation of the particular pathophysiology associated with the patient’s CM. Maintenance of cardiac output is the primary objective. As illustrated by the case synopsis, induction of anesthesia may cause myocardial depression or loss of systemic vascular tone, leading to abrupt circulatory collapse and, possibly, malignant arrhythmias and cardiac arrest. Two rather simple but crucial relationships illustrate the components that regulate cardiac output: 1. Cardiac output = Heart rate × Stroke volume. 2. Stroke volume is determined by preload, contractility, and afterload. Typically, the myopathic ventricle requires at least normal to increased preload to maintain adequate stroke volume. At the same time, intravenous volume loading may upset a delicate balance between sufficient preload and that which will dilate the ventricle and increase its end-diastolic pressure. The latter reduces endocardial perfusion to decrease rather than increase stroke volume. Invasive monitoring helps assess hemodynamic responses to intravenous fluid challenges, as well as intermittent positive-pressure ventilation. Patients who have been fluid-restricted preoperatively are most susceptible to severe hypotension in response to intermittent positive-pressure ventilation. Once preload has been optimized, contractility may need to be addressed. Except for patients with HCM, children with CM have compromised contractility and limited myocardial functional reserve. Anesthetic agents should be administered with this in mind. Inotropes (e.g., dopamine, dobutamine, epinephrine) or inodilators (e.g., milrinone) may be required perioperatively to maintain cardiac output. Augmented contractility improves stroke volume, but at the cost of increased myocardial oxygen consumption. Increased afterload, due to increased systemic or pulmonary vascular resistance, impedes the contraction of the LV and/or RV. Intramyocardial wall stress (a major determinant of afterload) increases directly with ventricular diameter according to Laplace’s principle. Thus, at the same level of arterial pressure, afterload encountered by an enlarged ventricle is higher than that for a ventricle of normal size. Children with end-stage CM may have pulmonary hypertension. Every effort should be made to avoid increases in pulmonary vascular resistance. This is done by minimizing mean airway pressures, maintaining normocapnea to hypocapnia, providing permissive metabolic alkalosis, and giving exogenous pulmonary vasodilator agents (e.g., nitric oxide, prostaglandins). Finally, a reduction in stroke volume often results in a sympathetically mediated increase in heart rate to compensate for the decrease in cardiac output. Maintenance of sinus or atrial-origin rhythms (e.g., wandering atrial pacemaker), and the associated atrial contribution to ventricular filling, is critical. Loss of sinoatrial rhythm with nonatrial, lower pacemaker escape rhythms (e.g., atrioventricular junctional or idioventricular rhythms or tachycardia) leads to inadequate diastolic filling and lower end-diastolic volumes. This aggravates any preexisting diastolic dysfunction.

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Management objectives for the specific CMs are as follows.

Dilated Cardiomyopathy ●

●

●

●

Preload: normovolemia ● Adequate fluids are required to maintain increased end-diastolic volume and cardiac output. Contractility: increase ● Inodilators (e.g., milrinone) are especially useful because they augment contractility and reduce afterload at the same time. Heart rate: normal or increase ● A mildly accelerated heart rate compensates for reduced stroke volume to help maintain cardiac output. Afterload: normal or decrease ● Afterload reduction helps unload a poorly contractile ventricle.

Hypertrophic Cardiomyopathy ●

●

● ●

Preload: increase ● Avoid hypovolemia due to inadequate fluid replacement or vasodilatation of the venous capacitance bed causing reduced venous return. Contractility: decrease ● Halothane is a useful anesthetic agent for reducing contractility and heart rate. ● Avoid light anesthesia and sympathetically mediated increases in contractility. ● β-Blockers can be used to control both the hyperdynamic myocardium and heart rate. Heart rate: normal or decrease Afterload: normal or increase ● Decreased systemic vascular resistance reduces coronary perfusion pressure. ● Reduced coronary perfusion pressure may lead to myocardial ischemia, with the potential to cause intraoperative cardiac arrest due to ventricular fibrillation or bradyasystole. ● Phenylephrine is the drug of choice to increase afterload.

Restrictive Cardiomyopathy ● ●

● ●

Preload: normovolemia Contractility: increase ● Inotropic support is frequently required. Heart rate: normal Afterload: do not increase or decrease

Arrhythmogenic Cardiomyopathy ● ●

●

Preload: normovolemia Contractility: normal Heart rate: normal ● Maintain sinus rhythm and place defibrillator pads before the induction of anesthesia. Afterload: do not increase or decrease

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PREVENTION To avoid a catastrophic reduction in cardiac output during anesthesia and surgery in pediatric patients with CM, one must have a thorough understanding of the pathophysiology of the particular CM present. Obviously, elective or less urgent surgery in a patient known to have a CM requires extensive discussion with the child’s cardiologist, surgeon, and parents. This should allow complete medical preparation of the patient before the day of surgery and help reduce the risk of perioperative deterioration. When more urgent surgery is required, it may not be possible to optimize the patient’s medical condition before his or her arrival in the operating room. If so, the cardiologist should be immediately available for consultation with the anesthesia team. In general, preoperative preparation should follow the management objectives outlined earlier.

Further Reading Antman EM: Cardiovascular Therapeutics, 2nd ed. Philadelphia, WB Saunders, 2002. Atlee JL III: Perioperative Cardiac Dysrhythmias, 2nd ed. Chicago, Year Book Medical Publishers, 1990. Atlee JL: Arrhythmias and Pacemakers. Philadelphia, WB Saunders, 1996. Carvahlo JS: Cardiomyopathies. In Anderson RH, Baker EJ, Macartney FJ (eds): Pediatric Cardiology. Philadelphia, JB Lippincott–Williams & Wilkins, 2002, pp 1595-1643. Denfield SW, Gajarski RJ, Towbin JA: Cardiomyopathies. In Garson A, Bricker JT, Fischer DJ (eds): The Science and Practice of Pediatric Cardiology. Philadelphia, WB Saunders, 1998. Ing RJ, Cook DR, Bengur RA, et al: Anesthetic management of infants with glycogen storage disease type II: A physiological approach. Paediatr Anaesth 14:514-519, 2004. Kishnani PS, Howell RR: Pompe disease in infants and children. J Pediatr 144:35-43, 2004. Lipschultz SE, Sleeper LA, Towbin JA, et al: The incidence of pediatric cardiomyopathy in two regions of the United States. N Engl J Med 348:1647-1655, 2003. McKenzie IM: Cardiomyopathies. In Lake CL, Booker PD (eds): Pediatric Cardiac Anesthesia. Philadelphia, JB Lippincott–Williams & Wilkins, 2005, pp 530-535. Nugent AW, Daubeney PE, Chondros P, et al: The epidemiology of childhood cardiomyopathy in Australia. N Engl J Med 348:1639-1646, 2003. Richardson P, McKenna W, Bristow M, et al: Report of the 1995 World Health Organization/International Society and Federation of Cardiology Task Force on the Definition and Classification of Cardiomyopathies. Circulation 93:841-842, 1996. Stockwell JA, Tobias JD, Greeley WJ: Noninflammatory, noninfiltrative cardiomyopathy. In Nichols DG, Cameron DE, Greeley WJ (eds): Critical Heart Disease in Infants and Children. St. Louis, Mosby, 1995, pp 1037-1051. Venugolapan P, Agarwal AK, Worthing EA: Chronic cardiac failure in children due to dilated cardiomyopathy: Diagnostic approach, pathophysiology and management. Eur J Pediatr 159:803-810, 2000. Weller RJ, Weintraub R, Addonizio LJ, et al: Outcome of idiopathic restrictive cardiomyopathy in children. Am J Cardiol 90:501-506, 2002.

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Anterior Mediastinal Mass Randall Flick

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Case Synopsis An 8-year-old, previously healthy girl is admitted with respiratory distress, wheezing, and stridor. Her symptoms have been slowly progressive over 2 weeks and are associated with nocturnal fever and exercise intolerance. The chest radiograph demonstrates a widened mediastinum and a retrosternal mass (Fig. 167-1). A computed tomography (CT) scan of the chest confirms the presence of an anterior mediastinal mass (Fig. 167-2). A biopsy of the mass is scheduled.

PROBLEM ANALYSIS Definition Anterior mediastinal masses affect many intrathoracic structures. Most significant are those that compress the heart or major vessels within their respective compartments. Many reports describe sudden, progressive cardiopulmonary compromise due to these masses. Commonly, they involve the anterior mediastinum and, to a lesser extent, the middle and posterior mediastinum. The mediastinum is defined as that portion of the thorax between the medial aspects of the pleura, above the diaphragm, and below the thoracic inlet. It is bound anteriorly by the sternum and posteriorly by the thoracic vertebrae. A line between the fourth thoracic vertebra and the sternal angle subdivides the mediastinal space into inferior and superior compartments. The inferior space is further subdivided by the pericardium into anterior, middle, and posterior regions. The location of a mediastinal mass, whether benign or malignant, is characteristic. It provides the clinician with clues to the origin of the mass and determines what physiologic effects it will have on surrounding mediastinal and other thoracic structures.

Risk Assessment The best approach for the anesthetic management of patients with anterior mediastinal masses is still subject to debate. Some reports describe sudden death or severe cardiopulmonary compromise with the induction of anesthesia and, in some cases, emergence from anesthesia. Some authors suggest that these masses should be biopsied under

Recognition Adult patients with anterior or middle mediastinal masses present with a variety of signs and symptoms. Most, however, either are asymptomatic or have minimal to moderate symptoms, including cough, dyspnea on exertion, chest pain, fatigue, and vocal cord paralysis. Severe symptoms in a minority of adults include orthopnea, stridor, cyanosis, jugular vein distention, or superior vena cava syndrome. The presenting signs and symptoms of anterior mediastinal masses in pediatric patients can include the following: ● ● ●

Orthopnea or cough in the supine position Superior vena cava syndrome with jugular vein distention Wheezing or stridor; dyspnea on exertion; increased work of breathing

In pediatric patients, most anterior mediastinal masses are malignant, with lymphomas, germ cell tumors, mesenchymal tumors, and thymic lesions found in decreasing order of frequency. 670

Figure 167–1 ■ Lateral chest film of an 8-year-old girl later determined to have lymphoma. A large mass is seen in the anterior mediastinum. Treatment was initiated before biopsy.

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Figure 167–2 ■ Chest computed tomography scan revealing near-complete compression of the distal trachea and main-stem bronchi by a large anterior mediastinal mass. The mass measured approximately 7 by 7 cm and involved not only the trachea but also the great vessels and pericardium.

local anesthesia or, if lymphoma is suspected, they should be treated with chemotherapeutic agents or radiation therapy before biopsy. Others suggest that, given the importance of obtaining early tissue diagnosis, most patients can safely undergo general anesthesia, assuming proper preparation and anesthetic care. To better predict which patients are likely to have significant cardiopulmonary compromise while under general anesthesia, there have been attempts to correlate preoperative symptoms and CT and spirometry findings with anesthetic outcomes. Patients with a peak expiratory flow rate and tracheal area greater than 50% of predicted for age on CT appear to tolerate general anesthesia without incident. However, even with CT and spirometry, it is often difficult to predict which patients are likely to experience difficulties. A large case series of adult patients suggested that the most reliable predictors of cardiopulmonary compromise are the following: ● ●

● ●

Presence of symptoms on presentation Combined obstructive and restrictive pattern on pulmonary function testing Presence of pericardial effusion Tracheal compression with greater than 50% reduction in cross-sectional area on CT

In addition, the presence of severe preoperative symptoms (e.g., supine dyspnea) has been emphasized as an indicator of high-risk status.

Cardiopulmonary compromise in patients with mediastinal masses results from direct compression or, occasionally, invasion of adjacent pulmonary or vascular structures. The effects of anesthesia increase the impact of airway or vascular compression due to the loss of intrinsic thoracic muscle tone, resulting in reduced thoracic diameter and increased compression of vascular and pulmonary structures.

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The location of such compression is critical, because if airway compression occurs distal to the trachea or mainstem bronchi, patients may not benefit from airway stenting with endotracheal or endobroncial tubes. CT scanning can help localize any airway compression. Still, it must be recognized that airway compression following the induction of anesthesia may be more extensive than that seen on CT. Cardiovascular compromise can take the form of the superior vena cava syndrome owing to compression of venous structures within the superior mediastinum. If so, cardiac output may be compromised by the resulting reduction in preload or by direct compression of the right ventricle by the anterior mediastinal mass. Also, echocardiography has shown that masses of the posterior mediastinum may compress the left atrium and, to a lesser extent, the left ventricle. Children given general anesthesia for surgery on an anterior mediastinal mass are at risk for developing significant respiratory compromise and complete airway collapse intraoperatively or postoperatively. Some patients may not be able to be extubated after surgery and will require intensive care for the initiation of radiation or chemotherapy. Cardiovascular collapse and death, though rare, are potential complications of general anesthesia in these patients. An inflatable balloon in the anterior mediastinum has been used in animal models to simulate anterior mediastinal masses. In such models, cardiac output is equally reduced during controlled or spontaneous ventilation in direct proportion to the volume of the mass. This cardiac output reduction is due to increased right ventricular afterload, leading to right ventricular dilatation and septal encroachment on the left ventricle.

MANAGEMENT Based on the available evidence, it is clear that children with mediastinal masses, especially anterior masses, are at increased risk for cardiopulmonary compromise during the induction of general anesthesia. The question is: Is the risk sufficient for anesthesiologists to request that biopsies of such masses be performed under local anesthesia with monitored anesthesia care, or that radiation or chemotherapy be used preoperatively to shrink these masses? This question is difficult to answer. However, some recommendations can be made regarding the safe management of most, if not all, children with anterior mediastinal masses. Rather than defining those patients expected to experience cardiopulmonary compromise, existing reports allow us to predict those who are unlikely to have a complicated perioperative course. The following factors allow the anesthesiologist to make that prediction: ●

●

Anterior mediastinal masses are most likely to produce significant cardiopulmonary compromise during general anesthesia. A chest radiograph can provide sufficient information about the location and size of most of these masses to ascertain actual risk. Patients without cardiopulmonary symptoms at rest are unlikely to experience related compromise. Most reassuring is the absence of postural cough, stridor, or dyspnea.

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On CT scans, patients with a tracheal cross-sectional area greater than 50% of predicted are less likely to experience cardiopulmonary compromise. CT scanning should be routine for the evaluation of all patients with anterior mediastinal masses. Peak expiratory flow rates greater than 50% of predicted are reassuring and should be obtained whenever possible.

Older, more cooperative children thought to be at high risk of cardiopulmonary compromise can have their masses biopsied under local anesthesia. Fine-needle aspiration is sufficient to make an accurate diagnosis in more than 80% of cases. More problematic are children in whom it is impossible to perform such procedures under local anesthesia. An alternative may be a procedure at another site (e.g., bone marrow or lymph node biopsy, aspiration of pleural fluid) conducted under local anesthesia, possibly with intravenous ketamine for sedation. In those (rare) high-risk cases for which general anesthesia is required, the available reports suggest the following: ●

● ●

●

●

●

Use inhalational induction with spontaneous ventilation to maintain airway patency. If possible, avoid muscle relaxants. The sitting, lateral, or prone position may reduce the risk of airway obstruction. Rigid bronchoscopy should be available for immediate distal airway access (i.e., beyond the distal tracheal lumen of an endotracheal tube). Cardiopulmonary bypass standby has been advocated by some for extremely high-risk patients, including cannulation of the femoral vessels before the induction of anesthesia. Fiberoptic bronchoscopy, advocated by some, offers little advantage over endotracheal intubation under deep general anesthesia (without muscle relaxants) in most patients.

PREVENTION Prevention of acute airway compromise in patients with symptomatic mediastinal masses is achieved by avoiding

general anesthesia or deep sedation. Instead, biopsies should be performed with local anesthesia, or radiation therapy or chemotherapy should be administered to reduce the size of the mass before biopsy or before anesthesia and surgery. Although debates are ongoing, it appears that the ability to make a molecular diagnosis has greatly improved, even after radiation or chemotherapy. For the rare patient in which general anesthesia is mandatory, the anesthesiologist must proceed with extreme vigilance and caution.

Further Reading Bechard P, Letourneau L, Lacasse Y, et al: Perioperative cardiorespiratory complications in adults with mediastinal mass: Incidence and risk factors. Anesthesiology 100:826-834, 2004. D’Cruz IA, Feghali N, Gross CM: Echocardiographic manifestations of mediastinal masses compressing or encroaching on the heart. Echocardiography 11:523-533, 1994. Ferrari LR, Bedford RF: General anesthesia prior to treatment of anterior mediastinal masses in pediatric cancer patients. Anesthesiology 72:991-995, 1990. Johnson D, Hurst T, Cujec B, et al: Cardiopulmonary effects of an anterior mediastinal mass in dogs anesthetized with halothane. Anesthesiology 74:725-736, 1991. Keon TP: Death on induction of anesthesia for cervical node biopsy. Anesthesiology 55:471-472, 1981. Mullen B, Richardson JD: Primary anterior mediastinal tumors in children and adults. Ann Thorac Surg 42:338-345, 1986. Prakash US, Abel MD, Hubmayr RD: Mediastinal mass and tracheal obstruction during general anesthesia. Mayo Clin Proc 63:1004-1011, 1988. Pullerits J, Holzman R: Anaesthesia for patients with mediastinal masses. Can J Anaesth 36:681-688, 1989. Robie DK, Mustafa HG, Pokorny J: Mediastinal tumors—airway obstruction and management. Semin Pediatr Surg 3:259-266, 1994. Shamberger RC, Holzman RS, Griscom NT, et al: CT quantitation of tracheal cross-sectional area as a guide to the surgical and anesthetic management of children with anterior mediastinal masses. J Pediatr Surg 26:138-142, 1991. Shamberger RC, Holzman RS, Griscom NT, et al: Prospective evaluation by computed tomography and pulmonary function tests of children with mediastinal masses. Surgery 118:468-471, 1995. Sinner WN: Directed fine needle biopsy of anterior and middle mediastinal masses. Oncology 42:92-96, 1985.

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Air Emboli Lisa Wise-Faberowski and Christian Seefelder Case Synopsis An 8-week-old infant is undergoing a craniectomy for sagittal craniosynostosis. As the surgeon is excising the cranial bone segment, precordial Doppler sounds change, and the blood pressure rapidly declines (Fig. 168-1).

prone, or lateral position. The risk of such entrainment is increased by low venous pressure or negative intrathoracic pressure, as occurs during spontaneous respiration. Small children are at special risk for venous air emboli. Significant blood loss may occur rapidly, and a small amount of blood may constitute a large portion of a child’s blood volume. This is a particular concern during craniotomies, because the calvaria is very thin. Further, the head is relatively large in proportion to body size, frequently resulting in the surgical site’s being elevated above the heart level during a supine or prone craniotomy. Finally, owing to the high prevalence of intracardiac shunts, amounts of venous air emboli that might be insignificant in an adult can result in paradoxical air emboli and be disastrous for a neonate.

PROBLEM ANALYSIS Definition Gas bubbles within the vascular system are termed gas emboli or air emboli. When venous air emboli enter the arterial circulation, they are termed paradoxical air emboli. Venous air emboli or paradoxical air emboli from gases dissolved in solution are released through effervescence, or they may enter the bloodstream from outside through insufflation or entrainment. The amount of gas dissolved in a liquid is a function of temperature and pressure. A sudden increase in the temperature of a gas-containing liquid can release gas bubbles from solution through effervescence. This can occur during rapid rewarming following hypothermic cardiopulmonary bypass or by rapidly warming cold intravenous fluids or blood products. It also happens in divers who experience a too-rapid decompression (the “bends”). More commonly, gas is introduced into the bloodstream by insufflation (e.g., during laparoscopy, thoracoscopy, or arthroscopy) or delivered with fluids or blood products by pressurized delivery systems. Veins that do not easily collapse can also entrain air—for example, venous sinuses in bone; open, large central veins; and open veins that are well above the level of the heart. For entrainment to occur, the vein opening must be sufficiently above the level of the heart to exceed central venous pressure (e.g., sitting craniotomy). Venous and paradoxical air emboli can occur in the supine,

Blood Pressure

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Awake patients may experience dyspnea and coughing as a result of venous air emboli. During anesthesia, changes in vital signs occur late and usually only after the entrainment of large amounts of air. Monitoring methods to detect venous air embolism, in decreasing order of sensitivity, include the following: ● ●

● ● ●

Echocardiography or Doppler ultrasonography End-tidal carbon dioxide (ETCO2) decrease or new appearance of end-tidal nitrogen (ETN2) Pulmonary artery pressure elevation Central venous pressure elevation Blood pressure reduction

Figure 168–1 ■ Schematic trend recording of blood pressure, heart rate, oxygen saturation (SaO2), and end-tidal carbon dioxide (ETCO2) concentration in an 8-week-old infant during sagittal craniosynostosis repair. The dotted line marks the time at which Doppler sounds changed dramatically. Note the sudden decrease in blood pressure and ETCO2, tachycardia, but little change in SaO2.

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Electrocardiogram (ECG) changes (e.g., right ventricular strain, ischemia, arrhythmias) Audible cardiac or “mill-wheel” murmur

Echocardiography and Doppler monitoring are exquisitely sensitive. They can detect even microbubbles from routine intravenous injections and minor entrainment of air. Air emboli detected with echocardiography and Doppler monitoring should alert the clinical team but must be interpreted cautiously, taking into account the severity of detected air (amount, duration, and associated clinical signs) as well as the clinical situation (e.g., craniotomy). ECG changes are more ominous, and an audible cardiac or “mill-wheel” murmur is least sensitive; however, when associated with echocardiographic or Doppler evidence of venous air embolism, they suggest that a significant amount of air has been entrained.

A

ECHOCARDIOGRAPHY Transthoracic or transesophageal echocardiography (TEE) enables the recognition of discrete air bubbles and the relative quantification of larger volumes (i.e., the density of snowstorm pattern). Further, TEE localizes emboli to the right or left side of the heart and detects cardiac anomalies (septal defects) that increase the risk of paradoxical air emboli (Fig. 168-2). TEE has been used in neonates who weigh as little as 2.5 kg. Limitations to its widespread use include the following: ● ●

● ●

High cost Requirement for a separate, highly trained observer during anesthesia and surgery Risk of injury to the pharynx, larynx, and esophagus Possible displacement of the endotracheal tube, especially during manipulation in small infants

Consequently, although TEE is a very sensitive technique for detecting venous air emboli, it is currently not practical in many institutions and may not be necessary as a routine monitor. DOPPLER ULTRASONOGRAPHY

B Figure 168–2 ■ Transesophageal echocardiographic four-chamber view of the left atrium (LA), right atrium (RA), left ventricle (LV), and right ventricle (RV). A, View of the heart without venous air embolism (VAE). B, Arrows indicate the reflections produced by air bubbles in the RA during VAE.

can also be decreased because of reduced pulmonary blood flow from pulmonary thromboembolism, sudden large blood loss, decreased venous return, or reduced cardiac output due to cardiac dysfunction, bradycardia, or arrhythmia. A falsely low ETCO2 may occur with gas leakage or air entrainment around an uncuffed endotracheal tube or dilution of small tidal volumes with fresh gas flows, unless sampling occurs near the endotracheal tube tip. Even so, a sudden change in ETCO2 from a previously stable baseline is usually significant.

Precordial Doppler ultrasonography is as sensitive as TEE for the detection of venous air emboli. It enables semiquantitative assessment of air emboli but does not permit localization of air to the right or left side of the heart. The smaller distance between the heart and chest wall increases the sensitivity of Doppler ultrasonography in infants. The probe needs to be placed over the right side of the heart, generally at the nipple line, just to the right of the sternum. Minor movement may dislodge the probe, so it should be securely fastened to the chest. Correct positioning is confirmed by injecting a few milliliters of intravenous solution into an intravenous catheter while listening for a characteristic loud change in Doppler sounds. Doppler probes are easily dislodged and can cause pressure necrosis in prone patients. This can be avoided in small infants by placing the Doppler probe on the patient’s back. Electrocautery and echocardiography can interfere with Doppler ultrasonography.

Unless air is added to the inspired gases, N2 disappears from expired gas. Reappearance of N2 indicates a circuit leak or alveolar diffusion from venous air emboli. Without an air leak, the sudden reappearance of ETN2 is quite specific for venous air emboli but not very sensitive; even large venous air emboli increase ETN2 by only 1% to 2%.

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Significant venous air emboli reduce the ETCO2 concentration owing to increased dead-space ventilation. However, ETCO2

Pulmonary artery catheters reveal increased pulmonary artery pressure due to pulmonary vascular obstruction by air.

EXHALED NITROGEN

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Similar to low central venous pressure, low pulmonary artery wedge pressure may predispose to venous air emboli and paradoxical air emboli. However, pulmonary artery catheters in infants and small children are not practical or necessary in most situations.

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CENTRAL VENOUS CATHETER Central venous catheter placement is justified for high-risk procedures, such as craniotomy in the sitting position, even in a small child. It is rarely necessary for a healthy child when the bed is flat. A central venous catheter is useful for administering fluids and medications if peripheral venous access is difficult, as well as for monitoring central venous pressure. Low central venous pressure may indicate the need for fluid replacement to reduce the risk of venous air emboli; a sudden increase may signal major venous air emboli. A central venous catheter is sometimes effective for retrieving large venous air emboli, especially if the catheter has multiple orifices and the tip is near the junction of the superior vena cava and right atrium. This position is confirmed by radiograph or by recording a unipolar ECG with a right atrial ECG adapter. To do so, substitute the catheter lead for the V lead, and observe the characteristic P-wave changes (increased amplitude leading to tall, spiked P waves that may exceed R- or S-wave amplitudes) as the catheter is advanced into the right atrium. ARTERIAL BLOOD PRESSURE An arterial catheter allows continuous assessment of blood pressure and arterial blood gas determinations. Its use is justified in any procedure with a significant risk for bleeding or venous air emboli, especially in young children. PULSE OXIMETRY With significant venous air emboli, oxygen desaturation may be detected by pulse oximetry. Arterial blood gas analyses may reveal hypercarbia and an increased arterial-alveolar oxygen gradient.

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Angiography and cardiac catheterization Placement, use, and discontinuation of circuits for cardiopulmonary bypass or extracorporeal membrane oxygenation Hemodialysis, plasmapheresis, or central venous catheter insertion Barotrauma during positive-pressure ventilation Use of air to identify epidural space through loss of resistance

Implications Significant pulmonary air emboli can result in decreased cardiac output, arterial hypotension, and cardiovascular collapse as a result of one or more of the following: ● ● ● ●

● ●

Obstruction of peripheral pulmonary vessels by gas bubbles Air lock from gas in large pulmonary vessels or the heart Reflex pulmonary vasoconstriction Right ventricular failure secondary to pulmonary hypertension Electromechanical dissociation or arrhythmias Myocardial ischemia from reduced coronary perfusion pressure, coronary paradoxical air emboli, or hypoxemia

Impaired pulmonary function with carbon dioxide retention and arterial oxygen desaturation can result from the following: ●

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Ventilation-perfusion mismatch from pulmonary vascular obstruction with increased dead-space ventilation Reactive bronchoconstriction with increased airway resistance Interstitial pulmonary edema

Gas bubbles enter the arterial circulation directly or through intracardiac communications. Most neonates have a patent foramen ovale, usually with left-to-right shunting. Although the foramen ovale may be probe-patent in 25% to 50% of infants and in 20% to 30% of adults, rarely is shunting demonstrated. However, increased right-sided pressures with venous air emboli may facilitate paradoxical air emboli across a patent foramen ovale. Paradoxical air emboli can result in myocardial or cerebral ischemia.

Risk Assessment Pediatric patients are at increased risk for venous air emboli during the following procedures: ●

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● ●

● ●

Key to the successful management of venous air emboli during surgery is close communication between the anesthesiologist and surgeon. In addition, the following guidelines should be considered: ●

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●

Doppler sounds should be audible to everyone. Intravenous injections likely to cause Doppler sound changes should be announced beforehand. If Doppler ultrasonography indicates venous air emboli unrelated to injections, the surgeon should use indicated measures (e.g., apply bone wax, flood the surgical field with saline or cover it with saline-saturated gauze) to reduce air entry. When venous air embolism is suspected, look for an associated decrease in ETCO2 or blood pressure, indicating a significant venous air embolus or blood loss. Reappearance of ETN2, if monitored, confirms the diagnosis of venous air emboli.

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Any surgical procedure in which the operative site is sufficiently above the heart, especially when sudden and severe blood loss is possible Craniotomy with a large craniectomy (e.g., craniosynostosis repair) Craniotomy with an operative site directly over large dural venous sinuses (e.g., posterior fossa exploration) Craniofacial procedures (e.g., frontal or midface advancement) with large bony excision and elevation of the head to minimize bleeding Certain orthopedic procedures (e.g., scoliosis surgery) General surgical procedures (e.g., liver surgery) with a high risk of entering large venous structures (e.g., hepatic veins, inferior vena cava) Liver transplantation surgery Any open-heart surgery

MANAGEMENT

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Nitrous oxide, though not contraindicated for these procedures, should be promptly discontinued in the presence of venous air emboli. The patient is then ventilated with 100% oxygen to avoid further enlargement of gas bubbles and to treat hypoxemia. Change the table position so that the surgical site is below the level of the heart. Be sure that the patient is securely fastened to the operating table. Gentle compression of the jugular veins has been recommended to reduce air entry and to unmask possible entry sites, but care must be taken to avoid carotid artery compression. Although air may be aspirated through a central venous or pulmonary artery catheter, it does not usually allow removal of a significant amount of entrained air. Positioning the patient in the left lateral decubitus position has been suggested to aid in resuscitation, but it may not be practical during some procedures. Support cardiovascular function with additional intravenous fluids or inotropic agents (ephedrine, epinephrine) as indicated. Cardiopulmonary resuscitation is rarely required, especially if the embolus is detected quickly and appropriate measures are instituted.

PREVENTION A careful history and physical examination, as well as familiarity with the planned surgery, are essential to assess the risk

for venous air emboli or paradoxical air emboli. Use precordial Doppler ultrasonography as a sensitive and noninvasive monitor to detect venous air emboli early. Consider the use of filters or bubble traps when significant or rapid fluid or blood replacement is anticipated. For high-risk procedures, be prepared to use measures to reduce air entrainment and venous air emboli (e.g., positioning, use of bone wax, flooding the surgical field).

Further Reading Cucchiara RF, Bowers B: Air embolism in children undergoing suboccipital craniotomy. Anesthesiology 57:338-339, 1982. Eldredge EA, Soriano SG, Rockoff MA: Pediatric neurosurgical anesthesia. In Coté CJ, Todres ID, Goudsouzian NG, Ryan JF (eds): A Practice of Anesthesia for Infants and Children, 3rd ed. Philadelphia, WB Saunders, 2001, pp 493-521. Faberowski LW, Black S, Mickle JP: Incidence of venous air embolism during craniectomy for craniosynostosis repair. Anesthesiology 92:20-23, 2000. Harris MM, Strafford MA, Rowe RW, et al: Venous air embolism and cardiac arrest during craniectomy in a supine infant. Anesthesiology 65:547-550, 1986. Harris MM, Yemen TA, Davidson A, et al: Venous embolism during craniectomy in supine infants. Anesthesiology 67:816-819, 1987. Markhorst DG, Rothuis E, Sobotka-Plojhar M, et al: Transient foramen ovale incompetence in the normal newborn: An echocardiographic study. Eur J Pediatr 154:667-671, 1995. Sethna NF, Berde CB: Venous air embolism during identification of the epidural space in children. Anesth Analg 76:925-927, 1993.

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Lisa M. Montenegro and David R. Jobes Case Synopsis A 5-month-old infant presents to the operating room for exploratory laparotomy after being involved in a motor vehicle accident. He is tachycardic (heart rate 180 beats per minute) and normotensive (blood pressure 80/55 mm Hg), with a grossly distended abdomen on arrival to the operating room. On opening of the abdomen, the blood pressure falls to 50/30 mm Hg. Bleeding from a badly lacerated liver necessitates rapid and massive volume replacement.

PROBLEM ANALYSIS Definition For pediatric patients, massive transfusion is defined as the need to replace at least one blood volume; blood volume varies by age, being approximately 80 mL/kg at birth and 65 mL/kg at age 12 years. Although transfusion under any circumstances carries some risk (e.g., infection, transfusion reactions; see Chapters 49 and 50), massive transfusion involves a unique set of risks and complications, many of which require special consideration in the pediatric population.

Recognition Massive transfusion and related complications are the result of therapy for acute intravascular volume loss, which includes rapid repletion of intravascular volume with crystalloid, non–red blood cell (RBC) colloids, blood, and blood products. This can occur in the following situations: ● ● ● ● ● ● ● ●

Major trauma Gastrointestinal bleeding Major vascular surgery Cardiac surgery Hepatic surgery Craniofacial surgery Radical oncologic surgery Spinal instrumentation

● ●

Administration of anticoagulants or other drugs Clotting factor deficiencies ● Hereditary, dilutional, or acquired ● Due to clotting factor consumption ● Due to extracorporeal membrane oxygenation and circulatory assist devices

●

Hypothermia Use of a cell-saver or autotransfusion device

Loss of up to 30% of the blood volume is usually well tolerated in infants and children. Signs of hypovolemia may be subtle and include a small to moderate increase in heart rate and decrease in blood pressure. Such blood volume loss in otherwise healthy children can be replaced with crystalloid solutions without significant hemodynamic or cardiovascular compromise.

Risk Assessment Any patient who requires acute, massive intravascular volume replacement is at risk for complications related to massive transfusion. Infants and neonates appear to be at increased risk owing to the immaturity of their native coagulation systems. The following complications are more likely to occur in this patient subset: ● ● ● ●

Dilutional coagulopathy Hypothermia Hypokalemia or hyperkalemia Hypocalcemia

A more complete list of generally recognized complications is provided in Table 169-1.

Implications The hemostatic function of the coagulation system is normal at birth. However, quantities of many procoagulant and inhibitory proteins do not reach their adult concentrations until after puberty. Andrew and colleagues measured an extensive clotting profile, including prothrombin time (PT), partial thromboplastin time (PTT), and clotting factor concentrations, in healthy neonates, infants, and children (from 1 day to 16 years of age). Although most test results did not differ from normal values for adults, there was greater variability in PT, although mean PT values were not significantly different from those in adults. The PTT was significantly prolonged in neonates and infants; however, adult PTT values were attained by age 3 months. The concentrations of all clotting factors, including vitamin K–dependent factors (II, VII, IX, X), 677

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Anticipating the need for massive transfusion may allow the early recognition and aggressive treatment of its associated complications, thereby avoiding the risk of acute intravascular volume depletion. Some circumstances that enhance and may contribute to the development of transfusion-related complications include the following:

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Clinically Significant Complications of Massive Blood Transfusion

Dilutional coagulopathy Acid-base derangement Hypothermia Hyperkalemia Hypokalemia Citrate load (hypocalcemia) Microembolization or microaggregate formation: ARDS? Infectious (HIV, CMV, hepatitis, West Nile virus, bacterial) Hemolysis Anaphylaxis Change in RBC deformability Jaundice (long term) ARDS, acute respiratory distress syndrome; CMV, cytomegalovirus; HIV, human immunodeficiency virus; RBC, red blood cell.

plasminogen, and the plasma protease inhibitors (antithrombin 3, α2-antiplasmin, C1-esterase inhibitor, and α1-antitrypsin), were substantially reduced at birth. Although all clotting variables had independent maturation processes, the concentrations of factors II, VII, IX, and X were less than those for adults until age 16 years. In contrast, plasminogen and plasma protease inhibitors approached or reached adult levels by age 5 years. Each of the vitamin K–dependent factors also displayed its own age-related maturation process. Factor VII was the first to achieve near-adult values at 5 days of age. Neonates and infants have laboratory values that are outside the adult reference ranges for the integrity of coagulation (especially PT and PTT). As such, normal laboratory values for adults do not measure neonatal hemostatic competence, and comparisons must be made with caution.

MANAGEMENT Management goals are to maintain the quantitative and qualitative integrity of intravascular volume. Oxygen carrying capacity and hemostasis are of primary importance. In the face of massive volume loss, these goals can be met only by transfusing whole blood or components of fractionated whole blood. The intravenous administration of any blood product, especially pooled components, is associated with a substantial risk of complications. This risk is amplified and multiplied during massive transfusion (see Table 169-1).

Dilutional Coagulopathy The most common complication of massive transfusion is dilutional coagulopathy. Dilution of hemostatic blood elements occurs from substances used for volume expansion (crystalloid, colloid, hetastarch, albumin), transfused blood, and blood products. The administration of nonblood substances begins the dilutional process. Component therapy may also result in the dilution of hemostatic blood elements, because each lost component is not precisely replenished. When replacement approaches or exceeds approximately one blood volume, continued dilution of remaining platelets and clotting factors results in impaired hemostasis.

Component Replacement Therapy Controversy exists regarding the timing of replacement of non-RBC blood products. Some suggest that products other than RBCs should not be administered until a coagulopathy or specific factor deficiency is documented. This approach is intended to limit transfusion risk and seems plausible when the loss and replacement are expected to be about one blood volume. However, when the loss is expected to or does exceed one blood volume, or bleeding is not controlled, early administration of non-RBC products is necessary to prevent enhanced blood loss from coagulopathy. Coté’s group demonstrated an exponential decline in the number of available platelets versus the number of blood volumes replaced. However, the absolute decline is not as great as one would expect based on blood loss and replacement. This may be due to platelet recruitment. Qualitative platelet function is further reduced by hypothermia, with only 12% of the original platelet function remaining after 24 hours of storage at 4°C. The same concept likely applies to other clotting factors as well. With the exception of thrombocytopenia (platelet counts 30% reduction in cerebral vessel diameter) is a significant risk factor for the development of infarction. Death from vasospastic infarction occurs

Pharmacologic and other modalities used to treat cerebral vasospasm after SAH are listed in Table 179-2. Early operation for clip-ligation of the ruptured aneurysm after SAH secures the aneurysm and permits the removal of fresh clot by irrigation and suction. The surgeon may also apply tissue plasminogen activator (tPA) directly into the subarachnoid space to dissolve remaining clot. Although this fibrinolytic drug can reduce vasospasm, it also has the potential to cause rebleeding by dissolving normal clot. Thus, only patients at high risk for clinically significant vasospasm are candidates for tPA treatment. Early obliteration of the aneurysm by endovascular coils also facilitates the subsequent treatment of vasospasm.

Table 179–2

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Pharmacologic and Other Modalities Used to Treat Cerebral Vasospasm

Hypertensive hypervolemic hemodilution Volume expansion with crystalloids and colloids Vasopressors (e.g., dopamine, dobutamine, phenylephrine) Transluminal balloon angioplasty

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Both hypervolemia and hypertension are used to increase cardiac output and augment cerebral perfusion in vasospastic areas of the brain with impaired autoregulation. Early institution of these measures can mitigate or avoid the progression of vasospasm-induced ischemia to infarction. Hemodilution alone is unlikely to be beneficial and may reduce cerebral oxygen delivery. However, a hematocrit of 30% to 35% is likely adequate. Complications of induced hypervolemia and hypertension include rebleeding, hemorrhagic infarct transformation, cerebral edema, hypertensive encephalopathy, intracranial hypertension, myocardial infarction, heart failure, pulmonary edema, coagulopathy, and dilutional hyponatremia, as well as complications related to central vascular catheterization. Expansion of intravascular volume is necessary because total circulating blood and red blood cell volumes are reduced in most patients after SAH. This is secondary to supine diuresis, peripheral pooling, negative nitrogen balance, reduced erythropoiesis, iatrogenic blood loss, and increased natriuresis. Limits for crystalloid and colloid volume expansion are central venous and pulmonary capillary wedge pressures of 10 to 12 and 12 to 16 mm Hg, respectively. There is a suggestion that albumin may improve the clinical outcome at 3 months and reduce hospital costs when normal saline alone has failed to increase the central venous pressure to at least 8 mm Hg. Vagal and diuretic responses to intravascular volume augmentation might dictate the need for a drug such as vasopressin to reduce urine output to less than 200 mL/hour. Hydrocortisone has also been used to attenuate excessive natriuresis and hyponatremia in patients with SAH, as well as to prevent the associated decrease in total blood volume. It appears to have no serious side effects. Vasopressors, including dopamine, dobutamine, and phenylephrine, might also be required to increase blood pressure and augment cardiac output. Invasive hemodynamic monitoring (e.g., direct arterial, central venous, or pulmonary artery pressure; cardiac output) is required for patients with induced hypertension. Before the aneurysm is secured, systolic blood pressure is maintained between 120 and 150 mm Hg. Once secured, it can be increased to 160 to 200 mm Hg. Transluminal balloon angioplasty is also used to relieve cerebral vasospasm. The inflatable intravascular balloon mechanically dilates the segmental zone of vasospastic narrowing. This may improve the patient’s level of consciousness by relieving focal ischemic deficits. However, early intervention is critical. Another treatment is serial papaverine angioplasty. This improves cerebral circulation times, but serial infusions are required for recurring cerebral vasospasm.

PREVENTION Cerebral Vasospasm The prevention of cerebral vasospasm requires a high level of vigilance and care, maintenance of normovolemia, careful monitoring, and prevention of secondary cerebral insults and medical complications (Table 179-3). Early occlusion of the aneurysm facilitates subsequent efforts to prevent and

Intracranial Aneurysms: Vasospasm and Other Issues

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Pharmacologic and Other Modalities Used to Prevent Cerebral Vasospasm after Subarachnoid Hemorrhage

Administer nicardipine (IV) Administer nimodipine (orally or via gastric feeding tube) Maintain normal electrolyte balance Provide adequate analgesia Maintain normovolemia Maintain normothermia Maintain normotension

treat vasospasm. Monitoring in an intensive care unit or a transitional area is indicated until after the peak time for the development of vasospasm has passed. The purpose of such care is to avoid hypovolemia, hyponatremia with inappropriate diuresis, arrhythmias, hyperthermia, pulmonary edema, hypoxia, hypercarbia, and intracranial hypertension. Any of these has the potential to exacerbate cerebral vasospasm. After SAH, adults need 3 to 4 L of fluid a day to maintain normovolemia. Hypotonic solutions (e.g., lactated Ringer’s) are avoided. Hyponatremia is treated with either normal or hypertonic saline as necessary. However, Egge and colleagues showed that prophylactic hypertensive hypervolemic hemodilution after aneurysmal SAH neither prevents vasospasm nor improves outcomes when compared with controls treated with normovolemia. In addition, costs were higher and complications were more frequent in patients receiving hyperdynamic therapy. In the International Subarachnoid Aneurysm Trial, patients with better clinical grades (World Federation of Neurosurgical Societies grades I to III on admission) whose aneurysms were occluded with endovascular coils rather than surgical clipping were less likely to have symptomatic vasospasm. However, there was no difference in clinical outcome between the groups at the end of the follow-up period. Although blood pressure is controlled before the aneurysm is secured, it is not treated thereafter, unless elevations are critically high. ICP is maintained in the normal range with mannitol, ventricular drainage, and mild ventilation. The goal is to keep cerebral perfusion pressure above 60 to 70 mm Hg. Use of the dihydropyridine calcium channel blocker1 nimodipine within 96 hours of SAH in good- and poorgrade patients has been shown to reduce the morbidity and mortality associated with aneurysmal cerebral vasospasm. It is now a standard of care after SAH. Nimodipine improves the poor outcome associated with vasospasm in all grades of patients, improves the chance of a good to fair outcome, and reduces the chance of infarction after SAH. However, the incidence of symptomatic vasospasm is not affected by nimodipine. Because it has a limited effect on the angiographic caliber of vessels, it is postulated that nimodipine 1 Dihydropyridine calcium channel blockers are selective for vascular smooth muscle versus cardiac muscle, in contrast to non-dihydropyridines such as verapamil and diltiazem. Intravenous nicardipine, a dihydropyridine calcium channel blocker, is increasingly used for the treatment of vasospasm in aneurysmal SAH, although long-term outcomes are not yet known.

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confers cerebral protection by reducing the influx of calcium in marginally ischemic neurons. Alternatively, it may increase CBF by dilating pial collateral vessels not seen on angiography. Nimodipine also reduces blood pressure; however, it does so by reducing systemic vascular resistance, not preload. Treatment with subcutaneous low-molecular-weight heparin (enoxaparin 20 mg/day) for 3 weeks after SAH also appears to improve overall outcomes at 1 year. Apparently, this is due to a reduction in delayed ischemic deficits and cerebral infarction. Patients who received enoxaparin also had fewer intracranial bleeding events and a lower incidence of severe (i.e., shunt-dependent) hydrocephalus. Other drugs have been investigated for the prevention of vasospasm. Tirilazad, an antioxidant and free radical scavenger, showed mixed clinical results. Nicaraven, a free radical scavenger, showed a trend toward improved survival, good outcome, and smaller infarct size at 3 months. Ebselen, an antioxidant and anti-inflammatory drug, has neuroprotective properties and appears to be effective in acute ischemic stroke. Intra-arterial fasudil, a kinase inhibitor, has been used to treat clinical vasospasm. However, there was no difference in neurologic outcome versus placebo, and patients treated with fasudil had more pneumonia and hypotensive episodes. Owing to increased endothelin (an endothelial-derived vasoconstrictor peptide) with cerebral vasospasm, an endothelin antagonist has also been investigated. Intracisternal tPA prevents vasospasm but does not improve outcome because of increased bleeding associated with its use. Finally, although antifibrinolytics reduce rebleeding, they increase delayed cerebral ischemia and therefore are rarely used.

Hydrocephalus Chronic hydrocephalus occurs in 10% of patients after SAH. It is due to obstructed pathways for cerebrospinal fluid drainage (i.e., subarachnoid venous granulations). Development of arachnoid adhesions also prevents the reabsorption of cerebrospinal fluid. If the blockage is incomplete, the problem persists only for several weeks. Hydrocephalus that either causes intracranial hypertension or reduces CBF can adversely affect the outcome following SAH. Whether the aneurysm is occluded using surgical or endovascular techniques does not affect the subsequent risk for hydrocephalus. Acute hydrocephalus is associated with a poor clinical grade and thickened subarachnoid or intraventricular hemorrhage on admission CT scans. It occurs in 15% to 20% of SAH patients. Other associations are alcoholism, female sex, older age, larger aneurysms, pneumonia, meningitis, and hypertension. It is recognized by the onset of lethargy and coma within 24 hours of SAH. Development of acute ventricular dilatation soon after SAH is a cause of sudden deterioration in neurologic status and may require external ventricular drainage to normalize ICP. External ventricular drainage is used only when the patient’s level of consciousness becomes depressed. Good results have been achieved when this is done along with early aneurysm occlusion. Ventricular drainage should be used with caution, however, to avoid changes in the transmural pressure that may precipitate aneurysmal rebleeding. Because acute hydrocephalus is often associated with

vasospasm, early aneurysm occlusion allows the use of hyperdynamic therapy and angioplasty. Half of patients who develop acute hydrocephalus require a ventriculoperitoneal shunt, but the need for a permanent shunt is reduced by external ventricular drainage. Predictors of the need for permanent shunting include poor grade on admission, rebleeding, and intraventricular hemorrhage. Chronic hydrocephalus, seen in 25% of patients who survive SAH, is an important cause of the subsequent slow physical decline of patients who were originally in good condition. Symptoms include an increasingly impaired level of consciousness and the development of dementia, gait disturbances, and incontinence. A CT scan is indicated within a month after SAH to ascertain ventricular size.

Abnormalities of Cerebral Autoregulation The central nervous system is directly affected by SAH and the resultant hematoma, vascular disruption, and edema. SAH interferes with cerebral autoregulation, which is the ability of the cerebral vasculature to maintain normal (unchanged) CBF over a wide range of cerebral perfusion pressures (mean arterial pressure minus ICP), from 50 to 150 mm Hg. Importantly, this range is higher (shifts to the right) in patients with chronic hypertension. Intracranial aneurysms (especially giant aneurysms) and SAH-induced hematoma and cerebral edema can cause intracranial hypertension, with a consequent decrease in the patient’s level of consciousness and the potential for brainstem herniation and death. Patients with intracranial hypertension also have reduced CBF and cerebral metabolic rate for oxygen. The extent of such impairment correlates with the patient’s clinical grade. The response of the cerebral vasculature to changes in arterial carbon dioxide tension is preserved after SAH. A decline in carbon dioxide reactivity usually does not occur until there is extensive disruption of cerebral homeostasis.

Seizures The seizure incidence after SAH is from 3% to 26%. Early seizures occur in 1.5% to 5% of patients, and late ones in 3%. Seizures are detrimental after SAH because they increase CBF and cerebral metabolic rate for oxygen and also may cause rebleeding, owing to increased blood pressure. Patients at highest risk for seizures have either thick cisternal blood on CT scan or lobar intracerebral hemorrhage. Other risk factors are rebleeding, vasospasm with delayed ischemic neurologic deficits, middle cerebral artery aneurysm location, subdural hematoma, and chronic central nervous system impairment. Use of prophylactic antiepileptics is controversial, because most seizures occur within the first 24 hours after SAH, often before hospitalization. Therefore, neurosurgeons use seizure prophylaxis (e.g., phenytoin, fosphenytoin, levetiracetam) for only 1 to 2 weeks after SAH. Patients with one or more intracerebral hemorrhages or early seizures receive anticonvulsants for at least 6 months.

Cardiac Disturbances Electrocardiographic changes occur in 27% to 100% of patients with SAH. Most common are T-wave inversion or ST

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segment depression. Others are new U or Q waves and Q-T interval prolongation. Rhythm disturbances occur in 30% to 80% of patients and include premature ventricular beats (most common), sinus bradycardia and tachycardia, lower escape rhythms, atrial fibrillation, and tachyarrhythmias (atrial or ventricular in origin). Arrhythmias commonly occur within 7 days of SAH, with the peak occurrence between the second and third days. The extent of myocardial dysfunction correlates with the severity of neurologic injury after SAH. The cause of this dysfunction is believed to be related to hypothalamic injury, with consequent autonomic imbalance and release of catecholamines, causing myocardial ischemia and infarction. Increased adrenergic tone may persist for the first week after SAH. These SAH-related cardiac abnormalities are similar to those seen with acute coronary syndromes (myocardial ischemia, infarction, and reperfusion injury) and may predispose patients to life-threatening arrhythmias. Associated Q-T interval prolongation makes patients more vulnerable to ventricular tachyarrhythmias (see Chapter 81). This risk is increased with low serum potassium or magnesium levels and with drugs that prolong the Q-T interval. The routine measurement of Q-T intervals may identify patients at risk for potentially lethal arrhythmias. Often, the question for the neurosurgeon and anesthesiologist is whether to proceed with surgical or endovascular intervention to secure an aneurysm emergently, even if a delay might put the patient at increased risk for rebleeding and compromise the treatment for vasospasm. Serial cardiac isozymes and ventricular function assessment by echocardiography may indicate the magnitude of ischemia. Use of a pulmonary artery catheter to measure pulmonary capillary wedge pressure and cardiac output can both facilitate the management of cardiac dysfunction and monitor the response to hyperdynamic therapy for the treatment of cerebral vasospasm. The presence of severe arrhythmias (about 5% of patients with arrhythmias) or significant cardiogenic pulmonary edema may necessitate postponing surgical or endovascular intervention until treatment has begun. Prophylactic β-adrenergic blockade can improve the cardiac outcome in some patients.

Further Reading Chang HS, Hongo K, Nakagawa H: Adverse effects of limited hypotensive anesthesia on the outcome of patients with subarachnoid hemorrhage. J Neurosurg 92:971-975, 2000.

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Cross DT, Tirschwell DL, Clark MA, et al: Mortality rates after subarachnoid hemorrhage: Variations according to hospital case volume in 18 states. J Neurosurg 99:810-817, 2003. Egge A, Waterloo K, Sjoholm H, et al: Prophylactic hyperdynamic postoperative fluid therapy after aneurysmal subarachnoid hemorrhage: A clinical, prospective, randomized, controlled study. Neurosurgery 49:593-606, 2001. Eng CC, Lam AM: Cerebral aneurysms: Anesthetic considerations. In Cottrell JE, Smith DS (eds): Anesthesia and Neurosurgery, 3rd ed. St. Louis, Mosby–Year Book, 1994, pp 376-405. Fridriksson S, Saveland H, Jakobsson KE, et al: Intraoperative complications in aneurysm surgery: A prospective national study. J Neurosurg 96:515-522, 2002. Gianotta SL, Oppenheimer JH, Levy ML, et al: Management of intraoperative rupture of aneurysms without hypotension. Neurosurgery 28:531-536, 1991. Haley EC Jr, Kassell NF, Torner JC, et al: The International Cooperative Study on Timing of Aneurysm Surgery: The North American experience. Stroke 23:205-214, 1992. Kett-White R, Hutchinson PJ, Al-Rawi PG, et al: Adverse cerebral events detected after subarachnoid hemorrhage using brain oxygen and microdialysis probes. Neurosurgery 50:1213-1222, 2002. Le Roux P, Winn HR: Management of the ruptured aneurysm. In Le Roux P, Winn HR, Newell DW (eds): Management of Cerebral Aneurysms. Philadelphia, Elsevier Science, 2004, pp 303-333. Molyneux A, Kerr R, Stratton I, et al: International Subarachnoid Aneurysm Trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: A randomized trial. Lancet 360:1267-1274, 2002. Murayama Y, Song JK, Uda K, et al: Combined endovascular treatment for both intracranial aneurysm and symptomatic vasospasm. AJNR Am J Neuroradiol 24:133-139, 2003. Newfield P: Anesthetic management of intracranial aneurysms. In Newfield P, Cottrell JE (eds): Handbook of Neuroanesthesia, 3rd ed. Philadelphia, JB Lippincott–Williams & Wilkins, 1999, pp 175-194. Qureshi AI, Suri MF, Yahia AM, et al: Risk factors for subarachnoid hemorrhage. Neurosurgery 49:607-613, 2001. Rabinstein AA, Pichelmann MA, Friedman JA, et al: Symptomatic vasospasm and outcomes following aneurysmal subarachnoid hemorrhage: A comparison between surgical repair and endovascular coil occlusion. J Neurosurg 98:319-325, 2003. Sluzewshi M, Bosch JA, van Rooij WJ, et al: Rupture of intracranial aneurysms during treatment with Guglielmi detachable coils: Incidence, outcome, and risk factors. J Neurosurg 94:238-240, 2001. Smith JS, Le Roux PD, Elliott JP, et al: Blood transfusion and increased risk of vasospasm and poor outcome after subarachnoid hemorrhage. J Neurosurg 101:1-7, 2004. Solenski NJ, Haley EC Jr, Kassell NF, et al: Medical complications of aneurysmal subarachnoid hemorrhage: A report of the Multicenter Cooperative Aneurysm Study. Crit Care Med 23:1007-1017, 1995. Treggiari-Venzi MM, Suter PM, Romand JA: Review of medical prevention of vasospasm after subarachnoid hemorrhage: A problem of neurointensive care. Neurosurgery 48:249-261, 2001.

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Shailendra Joshi and William L. Young Case Synopsis A 39-year-old woman is given general anesthesia for resection of a right superior temporal gyrus arteriovenous malformation (AVM) measuring 3 by 3 by 2 cm (Figs. 180-1 and 180-2). After surgery, her mean arterial pressure increases to 100 mm Hg when phenylephrine is used to confirm surgical homeostasis (Fig. 180-3). The patient emerges from anesthesia without neurologic deficits. Six hours later, she complains of a severe headache, vomits, and becomes lethargic. The right pupil is dilated. Immediate computed tomography scan reveals a large hemorrhage into the operative site and a midline brain shift (Fig. 180-4). After surgery to evacuate the clot, there is no residual AVM, the feeding artery is thrombosed, the surrounding brain is lax, and a vessel on the anterior rim of the AVM bed is identified as the source of bleeding. Postoperative neurologic examination reveals an appropriate response to painful stimuli and recovery of pupillary reaction. Four hours later, the patient’s intracranial pressure suddenly increases from 10 to 80 mm Hg and her pupils become fixed and dilated. Immediate repeat exploration reveals the source of hemorrhage to be an arterial vessel on the posterior rim of the AVM bed. The brain is edematous and adheres to the dura. The postoperative neurologic evaluation shows no improvement. Subsequent examination shows no evidence of brainstem function, and serial electroencephalograms are isoelectric. The patient dies. At autopsy, there is no residual AVM.

PROBLEM ANALYSIS Definition Normal perfusion pressure breakthrough (NPPB) after AVM resection is a catch-all term that describes unexplained intraoperative brain swelling or diffuse bleeding from the AVM bed or unexplained postoperative brain swelling or intracranial hemorrhage (ICH). NPPB is a diagnosis of exclusion. Although much has been written about NPPB, the lack of a rigorous definition makes interpretation of the existing literature difficult. The proposed pathophysiology of NPPB is as follows: High blood flow through the arteriovenous fistula creates a region of chronic cerebral hypotension in the neighboring vascular territories. Chronic cerebral hypotension may lead to a state of near-maximal vasodilatation and vasoparalysis that impairs the vessels’ ability to constrict or even dilate effectively. Excision of the low-resistance AVM shunt restores perfusion in the formerly hypotensive regions of brain. However, owing to the inability of these beds to effectively vasoconstrict, normalization of cerebral perfusion pressure results in cerebral hyperemia (“luxury perfusion”), 724

with the potential for cerebral edema formation and ICH. Although this is an attractive hypothesis, the pathophysiology has not been proved. Abnormal vascular reactivity, such as an impaired vasodilator response to acetazolamide, has been observed in regions adjacent to cerebral AVMs that show marked hyperperfusion after resection. Possibly, NPPB shares certain similarities to cerebral hyperemia after carotid endarterectomy or transluminal angioplasty and stenting of extracranial cervical arteries. Some observations argue against a “hydraulic hypothesis” to explain the pathophysiology of NPPB. First, hypotensive vascular beds in proximity to the AVM retain the ability to vasoconstrict. Also, pressure autoregulation can be shown in these hypotensive beds, although the cerebral autoregulation curve is shifted to the left. Second, severe cerebral hypotension (feeding artery pressure 60 mm Hg). Treat bacterial infections and complications related to liver disease (encephalopathy, ascites, hyponatremia, variceal bleeding, coagulopathy). Avoid hepatotoxic and nephrotoxic drugs. Optimize renal perfusion: ● ● ●

●

Identify intrinsic renal parenchymal disease. Provide intravascular volume expansion. Institute drug therapy with splanchnic vasoconstrictors or renal vasodilators. Treat hemoglobinuria with urine alkalinization and diuresis.

For the majority of fulminant hepatic failure patients, survival ultimately depends on medical stabilization and urgent liver transplantation.

PREVENTION Minimizing the incidence of postoperative hepatic dysfunction begins with a comprehensive preoperative assessment and identification of those patients who might be predisposed. About 1 in 700 patients admitted for elective surgery has abnormal liver function studies. For patients with known hepatic disease, it is important to determine its cause and assess the degree of impairment, as well as any systemic manifestations and comorbidities. Anesthetic management often requires maximally invasive monitoring. The fewest possible anesthetic agents should be used (e.g., fentanyl, isoflurane, cisatracurium, and oxygen). The goal is to preserve hepatic function. This is done by minimizing reductions in hepatic blood flow and preserving oxygen delivery to prevent hepatocellular ischemia. Finally, keep in mind that surgery proximate to the liver or biliary system carries a higher expected rate of postoperative complications.

Further Reading Burroughs A, Dagher L: Acute jaundice. Clin Med 1:285-289, 2001. Chung C, Buchman AL: Postoperative jaundice and total parenteral nutritionassociated hepatic dysfunction. Clin Liver Dis 6:1067-1084, 2002. Friedman LS: The risk of surgery in patients with liver disease. Hepatology 29:1617-1623, 1999. Labori KJ, Bjornbeth BA, Raeder MG: Aetiology and prognostic implication of severe jaundice in surgical trauma patients. Scand J Gastroenterol 38:102-108, 2003.

OTHER SURGICAL SUBSPECIALTIES

or evidence of hepatocellular necrosis are poor surgical risks. In contrast, those with cholestatic disease have lower complication rates. Patients with chronic liver disease and preserved function may not be at increased surgical risk. However, those with cirrhosis do have higher morbidity and mortality rates. A focused preoperative assessment is necessary to identify high-risk patients. Progressive hepatocellular injury may lead to hepatic failure. For high-risk patients, postoperative care and surveillance should take place in a critical care setting. Clinical indicators of suboptimal liver function include the following:

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Surgery in the Morbidly Obese Christina M. Matadial and Jonathan H. Slonin Case Synopsis A 30-year-old woman is scheduled for laparoscopic gastric banding. She is 164 cm (63 inches) tall and weighs 160 kg (339 pounds).

PROBLEM ANALYSIS Definition Obesity affects approximately one third of the adult population in the United States. It is defined as body weight more than 20% greater than ideal weight. Morbid obesity is defined as body weight more than twice the calculated ideal weight. Ideal body weight is generally based on American life insurance statistics regarding height, build, sex, and age. The body mass index (BMI) is the most useful clinical indicator of obesity. The Broca index is a practical way to determine ideal body weight: Height in cm − 100 = ideal weight in kg for males Height in cm − 105 = ideal weight in kg for females The BMI was devised to reduce the effect of height on body weight: BMI = weight in kg/(height in meters)2 Ideal body weight = BMI of 22 to 28 kg/m2 Obesity = BMI of 28 to 35 kg/m2 Morbid obesity = BMI >35 kg/m2

Recognition It is now recognized that obesity is associated with a broad array of medical and surgical diseases leading to increased perioperative morbidity and mortality. Preoperative evaluation should focus on identifying coexisting diseases and conditions and the need for additional testing and invasive monitoring.

Risk Assessment Most of the major obesity-related health risks increase disproportionately with increasing weight. The rate of premature death is increased in patients who are 30% over their ideal weight and is doubled in those weighing 40% to 60% more than their ideal body weight. The incidence of sudden unexplained death is at least 13 times greater in morbidly obese women compared with women at their ideal body weight. 810

In men participating in the Framingham study, obesity was associated with a mortality rate up to 3.9 times greater than that of the normal weight group.

Implications Many organ systems are affected by morbid obesity, including the following: ● ● ● ●

Cardiovascular Respiratory and airway Gastrointestinal Endocrine and metabolic

Morbid obesity causes significant pathophysiologic changes that may increase perioperative morbidity and mortality (Table 202-1). The anesthesiologist is faced with numerous potential anesthetic and surgical challenges (Table 202-2). Cardiovascular disease commonly manifests as hypertension, coronary artery disease, and heart failure (e.g., cor pulmonale, pickwickian syndrome). Obesity appears to be an independent risk factor for ischemic heart disease. These patients may have limited functional capacity. Because they may not experience symptoms at rest, pharmacologic stress testing and imaging may be required to assess patients for myocardial ischemia and ventricular dysfunction. In an obese patient, cardiac output and blood volume must increase to perfuse additional fat stores. Cardiac output is estimated to increase by 0.1 L/minute for each kilogram of additional adipose tissue. Cardiomegaly and hypertension may develop due to this increased need. Long-standing hypertension with associated left ventricular hypertrophy may cause congestive heart failure. Chronic hypoxemia may contribute to the development of pulmonary hypertension and right ventricular dysfunction. When this progresses to right ventricular chamber dilatation and failure (cor pulmonale), the condition is known as the pickwickian syndrome. Other components of this syndrome are somnolence, hypoxemia, and polycythemia. Obesity is associated with reduced functional residual capacity (FRC), expiratory reserve volume, and total lung capacity. Expiratory reserve volume is the primary source of oxygen reserve during apnea. Therefore, in obese patients, preoxygenation is less effective. Lung closing volume may exceed FRC, leading to ventilation-perfusion mismatch and hypoxia. Both induction of anesthesia and supine positioning

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Organs or Organ Systems Affected by Morbid Obesity, with Associated Pathophysiology Associated Pathophysiology

Cardiovascular

Increased stroke volume and blood volume → increased cardiac output Chronic hypoxemia → pulmonary HTN → RV hypertrophy or failure, or any combination of these With cor pulmonale, patients are considered to be “pickwickian” (see below under “Airway and lungs”) Increased cardiac output to perfuse fat → systemic HTN → LV hypertrophy, and possible LV HF Any renovascular disease and insufficiency may aggravate HTN ECG findings: (1) left heart—low QRS voltage, LV strain or hypertrophy, LA abnormality, T-wave flattening in inferior and lateral chest wall leads; (2) right heart—RV strain or hypertrophy, right axis deviation or bundle branch block, P pulmonale with pulmonary HTN and cor pulmonale Cardiac arrhythmias secondary to hypercapnia, hypoxia, or systemic or pulmonary HTN and HF Hypercholesterolemia, hyperlipidemia, and hyperglycemia (i.e., metabolic syndrome) accelerate development of atherosclerotic cardiovascular disease Cerebral, coronary, or renovascular disease → stroke, acute coronary syndromes, or renal insufficiency Hypercoagulability, venous thrombosis, and pulmonary embolism: primary cause of perioperative 30-day mortality RA or LA chamber dilatation and hypercoagulability predispose to atrial tachyarrhythmias or fibrillation with systemic thromboembolism Abundant upper airway soft tissue increases potential for difficult mask airway and tracheal intubation Reduced FRC due to large pannus and increased body mass makes diaphragmatic excursions more difficult and position dependent; augmented by mechanical ventilation (higher airway pressures) Reduced chest wall compliance, lung volumes, and diaphragmatic excursions increase work of breathing Reduced inspiratory and expiratory reserve volumes Closing volume may exceed functional residual volume, leading to ventilation-perfusion mismatch, especially when supine Obstructive sleep apnea consequent to airway narrowing, overly abundant peripharyngeal adipose tissue, and abnormal decrease in upper airway muscle tone during REM sleep Reduced chest wall and diaphragmatic muscle tone with general anesthesia and muscle relaxation further impair oxygenation Predominant diaphragmatic respiration Pickwickian syndrome: morbid obesity, somnolence, alveolar hypoventilation, periodic respiration, hypoxemia, polycythemia, with RV failure and hypertrophy → cor pulmonale Metabolic syndrome → type 2 diabetes (sevenfold increase in incidence) Predisposition to hypothyroidism and Cushing’s disease Increased O2 consumption and CO2 production Increased metabolism of fluorinated volatile anesthetics (e.g., enflurane, methoxyflurane*) Increased pseudocholinesterase activity Increased intra-abdominal pressure with development of hiatal, umbilical, or inguinal herniation Gastroesophageal reflux disease and increased gastric acidity Abnormal liver function tests due to fatty infiltration of liver Increased risk for cholelithiasis and cholecystitis Inactivity secondary to morbid obesity predisposes to thromboembolism Excessive weight bearing accelerates development of osteoarthritis and chronic back pain Increased risk for malignancies involving the breast, colon, cervix, ovary, uterus, pancreas, prostate, and rectum

Airway and lungs

Endocrine/metabolic

Miscellaneous

*Seldom used in the developed world but may still be used in less developed nations. ECG, electrocardiogram; FRC, functional residual capacity; HF, heart failure; HTN, hypertension; LA, left atrial; LV, left ventricle/ventricular; RA, right atrial; REM, rapid eye movement; RV, right ventricle/ventricular. From Adams JP, Murphy JP: Obesity in anaesthesia and intensive care. Br J Anaesth 85:91-108, 2000; Gajraj NM, Whitten CW: Morbid obesity. In Atlee JL (ed): Complications in Anesthesia. Philadelphia, WB Saunders, 1999, pp 848-850; Roizen MF, Fleisher LA: Anesthetic implications of concurrent diseases. In Miller RD (ed): Miller’s Anesthesia, 6th ed. Philadelphia, Churchill Livingstone, 2005, pp 1017-1149.

further decrease FRC and worsen ventilation-perfusion mismatch. Increased BMI is also associated with reduced respiratory compliance and increased work of breathing. Difficult upper airway management (especially mask ventilation) and endotracheal intubation should be anticipated in obese patients. Increased adipose tissue in the neck and hypopharynx leads to narrowing of the oropharyngeal space. Approximately 5% of obese individuals develop

obstructive sleep apnea. Reduced FRC, atelectasis, and upper airway muscle relaxation predispose to obstructive sleep apnea. Sedative drugs produce a dose-dependent depression of consciousness and lung volumes. Because preoxygenation is less effective, time to desaturation below 90% may be greatly reduced, especially in the morbidly obese. Obese patients are presumed to be at increased risk for pulmonary aspiration of gastric contents due to increased

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Organ or System

Gastrointestinal

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Anesthetic Implications for Surgery in the Morbidly Obese

Preoperative Preparation and Induction of Anesthesia Emotional issues (e.g., passive-aggressive personality, anxiety) Difficult venous access Difficulty with facemask ventilation and securing the airway Difficult direct laryngosopy or fiberoptic intubation Difficulty establishing noninvasive or invasive monitoring Increased risk for pulmonary aspiration

Intraoperative Management Reduced cardiopulmonary reserve Problems with patient positioning and mobilization Technical difficulties with regional anesthesia

Postoperative Complications Airway obstruction Hypoxemia and hypercarbia Deep venous thrombosis → pulmonary embolism (leading cause of perioperative mortality) Wound infection Hyperglycemia

Laparoscopic Surgical Implications Difficult trocar placement Hypercarbia and increased peak airway pressure Reduced venous return and cardiac output → hypotension

residual gastric volume and acidity, the possibility of associated diabetic gastroparesis, and increased intra-abdominal pressure. Also, there is a higher incidence of gastroesophageal reflux and hiatal hernia. Therefore, obese patients should be considered to have potentially full stomachs, even with elective surgery. Difficult airway management increases the risk for pulmonary gastric aspiration, especially when high pressures are required for positive-pressure facemask ventilation and oxygenation. In this situation, at least some inspired gas is diverted to the esophagus and stomach. This is compounded by multiple attempts at tracheal intubation, with positive-pressure facemask ventilation between attempts. Thus, the already increased risk for pulmonary aspiration of gastric contents is compounded by difficult airway management and intubation in obese patients. Glucose intolerance is common in obese patients, and the incidence of diabetes mellitus is higher than in the normal population. This may be due to increased resistance to insulin of peripheral tissues in the presence of excessive adipose tissue. The increased catabolic response to surgery may require the use of exogenous insulin during the perioperative period. In theory, larger fat stores provide an increased volume of distribution for lipid-soluble drugs (e.g., thiopental, benzodiazepines, opioids). Thus, if the loading dose of these drugs is based on actual body weight in obese patients, maintenance doses would be given less frequently owing to reduced clearance. However, with hydrophilic muscle relaxants, increased fat stores have less influence, and dosing should be based on ideal body weight (for adults, 60 to 80 kg for females, and 80 to 100 kg for males). Hepatic clearance of drugs is usually not affected, unless there is hepatic dysfunction due to fatty infiltration of the liver. Renal clearance of

drugs may increase owing to increased renal blood flow and glomerular filtration rate. However, with atherosclerotic renovascular disease, there may be reduced renal clearance due to renal insufficiency. Recovery times from volatile anesthetics are comparable in obese and normal patients with contemporary agents (e.g., desflurane, sevoflurane), provided the procedure is not lengthy (>3 to 4 hours).

MANAGEMENT After a focused history and physical examination, minimum laboratory investigations should include hemoglobin and hematocrit, serum electrolytes, blood glucose, liver function tests, electrocardiogram, and chest radiograph. Invasive cardiac evaluation, such as dobutamine stress echocardiogram or nuclear stress myocardial imaging, may identify patients with inducible ischemia, wall motion abnormalities, and ventricular contractile dysfunction. Any abnormal findings will direct intraoperative management. Baseline arterial blood gases may be indicated for patients with obstructive sleep apnea. No single anesthetic technique is superior. All drug doses must be carefully titrated to clinical effect. Neuraxial anesthesia may be beneficial for open lower abdominal procedures, although the identification of anatomic landmarks may be difficult. Especially in the morbidly obese, dosages of local anesthetics for epidural and spinal anesthesia are adjusted downward by up to 20% to 25%. This is because increased intra-abdominal and airway pressures are believed to cause epidural venous engorgement. Also, increased epidural fat reduces the epidural and subarachnoid spaces. Premedication sedatives and narcotics should be administered cautiously or avoided altogether in patients with hypoxemia, hypercapnia, or a history of obstructive sleep apnea owing to the risk for further respiratory depression and airway compromise. Difficult peripheral venous access may dictate the need for a central line. For indirect blood pressure measurements, a larger-sized cuff is frequently placed on the forearm. However, even when extra-large cuffs are used, systemic pressure measurements may be 20% to 30% above those obtained with an arterial catheter. The latter is often desirable because obese patients are susceptible to large fluctuations in blood pressure. Also, arterial blood gas determinations are often required to assess the adequacy of oxygenation and ventilation. Central venous or pulmonary artery pressure monitoring may be indicated if a patient has evidence of impaired myocardial function. Transesophageal echocardiography may be an alternative to a pulmonary artery catheter, although its use may be limited by the surgical procedure (e.g., the need for an orogastric or nasogastric tube or gastric endoscopy). Recognition of a potentially difficult airway may suggest the need for awake fiberoptic intubation. Obese patients often have a short, thick neck; an anterior larynx and large tongue; and limited movement of the jaw, neck, and head. However, if the preanesthetic assessment suggests that airway management and tracheal intubation will be relatively easy, a rapid-sequence induction and tracheal intubation may be performed. Preoxygenation is especially

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lation. This emphasizes the importance of early ambulation for these patients. Low-dose subcutaneous heparin or enoxaparin (Lovenox) and compression stockings or sequential compression devices should be used perioperatively.

PREVENTION Understanding the pathophysiologic changes of obesity and associated disease processes can help minimize morbidity and mortality. Pertinent history, physical examination, and testing can help identify patients with significant comorbidity and facilitate appropriate risk stratification to minimize the anesthetic risk.

Further Reading Adams JP, Murphy JP: Obesity in anaesthesia and intensive care. Br J Anaesth 85:91-108, 2000. Alpert MA, Alexander JK, et al: The Heart and Lung in Obesity. New York, Futura Publishing, 1998. Alpert MA, Terry BE, Cohen MV, et al: The electrocardiogram in morbid obesity. Am J Cardiol 85:908-910, 2000. Gajraj NM, Whitten CW: Morbid obesity. In Atlee JL (ed): Complications in Anesthesia. Philadelphia, WB Saunders, 1999, pp 848-850. Ogummaike BO, Jones SB, Jones DB, et al: Anesthetic considerations for bariatric surgery. Anesth Analg 95:1793-1805, 2002. Roizen MF, Fleisher LA: Anesthetic implications of concurrent diseases. In Miller RD (ed): Miller’s Anesthesia, 6th ed. Philadelphia, Churchill Livingstone, 2005, pp 1017-1149.

OTHER SURGICAL SUBSPECIALTIES

important owing to reduced FRC and oxygen reserve and increased oxygen consumption. Desaturation can occur rapidly during apnea. Two-person mask ventilation may be required. Risk for pulmonary gastric aspiration is reduced with the administration of H2-antagonists, nonparticulate antacids, and metoclopramide. When positioning the patient, care must be taken to protect and pad all pressure points. Patients weighing between 400 and 1000 pounds require special operating room tables. In extreme cases, it may be necessary to place two tables together for those with an extremely large abdominal pannus or wide girth. During preparation and induction of anesthesia, the obese patient should lie in a semirecumbent position with the head on a pillow and a bolster placed under the shoulders. In many patients, satisfactory oxygenation and ventilation can be achieved only by changing from the supine to the reverse Trendelenburg position. During mechanical ventilation, positive end-expiratory pressure may be used to improve oxygenation. High inspired oxygen concentrations may be required to prevent hypoxia. Use of a pressure-limited ventilatory mode may be necessary. Postoperative respiratory complications are a significant problem. The risk of postoperative hypoxemia is increased by surgery involving the thorax or upper abdomen (especially vertical incisions). Extubation should be delayed until the effects of muscle relaxants are completely reversed and the patient is fully awake. Postoperative mechanical ventilation may be required until extubation criteria are met. Patients using continuous positive airway pressure devices at home should have these available postoperatively. Aggressive pulmonary care with incentive spirometry, coughing, deep breathing, and early ambulation is beneficial. Adequate postoperative analgesia is essential to prevent diaphragmatic splinting; however, opiates must be carefully titrated to avoid respiratory depression. Use of regional techniques such as epidural analgesia may reduce the incidence of respiratory complications. Finally, the risk of deep venous thrombosis and pulmonary thromboembolism is increased. In fact, it is the leading cause of perioperative mortality in this patient popu-

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Complications of Carcinoid Tumors Kerri M. Robertson

Case Synopsis A 55-year-old man is scheduled for emergency exploratory laparotomy for small bowel obstruction. Anesthesia is induced with intravenous (IV) propofol, remifentanil, and vecuronium and maintained with an infusion of remifentanil and sevoflurane in an air-oxygen mixture. During surgery the patient becomes profoundly hypotensive. His blood pressure does not respond to boluses of IV fluid and phenylephrine. The patient’s face and neck appear flushed.

PROBLEM ANALYSIS Definition

Recognition Features of carcinoid syndrome include the following: ●

Carcinoid tumors are neoplasms of neuroendocrine origin and arise from enterochromaffin cells in various embryonic divisions of the gut. The largest case series (N = 11,842) reported in 2003 by Soga found that carcinoid tumors were most commonly found in the lung (19.8%), followed by the rectum (15%), ileojejunum (12%), stomach (11.4%), appendix (9.6%), and duodenum (8.3%). The overall incidence of the carcinoid syndrome was 7.7%. Carcinoid syndrome results from the direct release of vasoactive amines, polypeptides, proteins, and prostaglandins into the systemic circulation (Table 203-1). Intestinal carcinoids produce large amounts of serotonin (5-hydroxytryptamine [5-HT]), but many other products can be released as well, including histamine, norepinephrine, bradykinins, and prostaglandins. Serotonin is metabolized in the liver, lungs, and brain by monoamine oxidases to 5-hydroxyindoleacetic acid (5-HIAA), which is excreted in the urine. However, substances produced by liver metastases from midgut carcinoids or primary hepatic carcinoid tumors (i.e., 5-HT and other biogenic amines, along with proteins and polypeptides) are released directly into the systemic circulation, thereby bypassing the portal circulation. In addition, primary tumors without portal venous drainage (e.g., bronchial, ovarian, retroperitoneal) can cause carcinoid syndrome by circumventing hepatic metabolism. A life-threatening carcinoid “crisis” is an acute exacerbation of the carcinoid syndrome. It results in profound flushing, hypotension or extreme changes in blood pressure, stupor, diarrhea, confusion, bronchospasm, arrhythmias, and hyperthermia. Such crises can be triggered by tumor palpation, induction of anesthesia and tracheal intubation, inadequate analgesia, surgical stress, druginduced mediator release, chemotherapy, and hepatic arterial embolization. 814

● ● ● ●

Episodic cutaneous vasomotor flushing Diarrhea or abdominal pain Bronchospasm Carcinoid valvular heart disease Pellagra and psychiatric symptoms

There is significant patient variability with regard to the type and severity of symptoms, depending on the anatomic site of the tumor, its venous drainage, and diverse characteristics of the secreted amine and peptide products. Bradykinin and histamine may play a prominent role in hypotension and cutaneous vasomotor flushing, whereas serotonin release contributes to diarrhea, bronchoconstriction, hypertension, and bowel ischemia. Pellagra and psychiatric symptoms are due to depletion of tryptophan, a precursor for serotonin synthesis. Carcinoid tumors are diagnosed by measuring the serotonin metabolite 5-HIAA in a 24-hour urine sample. A small bowel radiographic series, upper and lower gastrointestinal endoscopy, abdominal ultrasonography, and contrast-enhanced computed tomography or magnetic resonance imaging may identify a focal primary lesion. Liver metastases are detected by computed tomography or somatostatin scanning and liver biopsy. Diagnosis of a neuroendocrine tumor is confirmed with immunohistochemical markers. Natriuretic peptides (NT-proBNP) can be used as a simple marker for the diagnosis of carcinoid heart disease, which can then be confirmed by echocardiography. For patients with known carcinoid tumors, carcinoid crisis is suspected if severe intraoperative hypotension occurs that is unusually resistant to IV fluid loading and vasopressors. More rarely, the diagnosis is made by exclusion, but it is a consideration in any case of refractory hypotension.

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Table 203-1

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Amines, Proteins, and Prostaglandins Released in the Carcinoid Syndrome

Amines

Polypeptides and Proteins Adrenocorticotropic hormone Bradykinins Calcitonin Chromogranins Corticotropin-releasing hormone Glucagon Growth hormone Insulin Islet amyloid polypeptide Kallikrein Neurokinin A Neurokinin B Neuropeptide K Neurotensin Pancreatic polypeptide Peptide YY Parathyroid hormone-related peptide Somatostatin Substance P Vasoactive intestinal protein

Complications of Carcinoid Tumors

815

Octreotide acetate (Sandostatin) has simplified the perioperative management of patients with carcinoid tumor and is widely considered the standard treatment for carcinoid symptoms and crises. Octreotide is a synthetic octapeptide somatostatin analogue with an elimination half-life of about 1.5 hours following subcutaneous administration. There is evidence that octreotide may prevent mediator release by binding to the sstr-2 subtype of somatostatin G protein-coupled receptors. Symptoms are relieved in more than 70% of patients, although the average response lasts only 18 months. Insulin release in response to hyperglycemia is inhibited as well, which can complicate glucose management in obese patients or non-insulin-dependent diabetics. Unfortunately, octreotide does not prevent the progression of carcinoid cardiac lesions. Veall and coworkers reviewed 21 patients undergoing laparotomy for metastatic carcinoid tumors. The use of intraoperative octreotide allowed the completion of hepatic resections that had previously been aborted due to refractory hypotension with tumor manipulation. Kinney and colleagues reviewed 119 patients having similar surgery. None of the 45 patients who received octreotide intraoperatively experienced complications during surgery. In contrast, 8 of 73 patients who did not receive octreotide had cardiac complications.

Prostaglandins PGE2 PGF2 Modified from Lips CJ, Lentjes EG, Hoppener JW: The spectrum of carcinoid tumours and carcinoid syndromes. Ann Clin Biochem 40:612-627, 2003.

MANAGEMENT Anesthetic management of patients with carcinoid tumors requires the following: ●

●

Risk Assessment Carcinoid tumors occur relatively frequently but are only rarely symptomatic. They occur in 1 to 2 per 100,000 persons per year in the United States. The distribution is age dependent and rises continuously until the eighth decade. Under age 50 years, more women are affected, with the stomach and lungs more commonly involved. Metastatic disease occurs in 20% of all patients with carcinoid tumors. Estimated 5-year survival for localized disease is 75% to 93%. With metastatic disease, it is 15% to 35%. With cardiac involvement, the prognosis is worse. Right heart failure due to tricuspid and pulmonary valve disease may be fatal. The median survival after diagnosis is 1.6 years.

Implications Preoperatively, patients are evaluated for electrolyte imbalance and volume depletion due to secretory diarrhea. Carcinoid heart disease occurs in 20% to 70% of patients with metastatic disease. Classically, this includes right-sided endomyocardial fibrosis, pulmonary hypertension, tricuspid and pulmonary stenosis, and then tricuspid regurgitation with ultimate right heart failure. Inactivation of serotonin by the lung protects the left side of the heart, but occasionally it too is affected.

●

Immediate availability of IV octreotide to treat perioperative carcinoid crises Treatment of hypertension, hypotension, and bronchospasm Monitoring with an arterial line and central access (with or without a pulmonary artery catheter)

Therapeutic options for patients with carcinoid tumors include (1) somatostatin analogues to reduce hormone secretion, (2) resection of the primary tumor, and (3) excision or ablative therapy for liver metastases (e.g., radiofrequency ablation, cryotherapy, arterial chemoembolization). In selected cases, liver transplantation may be a treatment option. Valve replacement is feasible with carcinoid valvular heart disease but is associated with significant morbidity and mortality. Other therapeutic options include MIBG (m-iodobenzylguanidine) preparations, interferon-α, and chemotherapy. In the event of severe hypotension that is unresponsive to IV fluids, patients with known carcinoid tumors should receive IV octreotide (50-μg bolus) as first-line therapy. In one recent case series, the median dose of octreotide administered intraoperatively was 350 μg. Sympathomimetics are often administered but may actually worsen the episode, because α-adrenergic stimulation can cause further peptide release from the tumor. Octreotide has also been used successfully to treat severe carcinoid-induced bronchospasm, after aerosolized albuterol and isoflurane failed. Serotonin accentuates the vascular response to catecholamines by stimulating the release and inhibiting the

OTHER SURGICAL SUBSPECIALTIES

Dopamine Histamine Norepinephrine Serotonin

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reuptake of norepinephrine. It may also directly stimulate postjunctional α1-receptors. The resulting hypertension is amenable to standard treatment, such as increasing anesthetic depth or administering agents such as labetalol, nicardipine, or nitroprusside. Ketanserin (2.5- to 5-mg IV bolus with IV infusion at 5 mg/hour) has also been used. It blocks 5-HT, α1-receptors, and H1-receptors. Continuous blood pressure monitoring is highly desirable, because blood pressure changes may be abrupt. A central venous catheter should be considered for assessing right heart backpressure if there is the potential for extensive surgical blood loss. This is because the effects of circulating mediators may alter the normal physiologic signs of hypovolemia (i.e., negate any potential systemic arterial hypotension). The possible benefit of a pulmonary artery catheter should be weighed against the risk of its placement in a patient with tricuspid or pulmonary valve disease.

Premedication with benzodiazepines to relieve anxiety is important, as is adequate pain relief postoperatively, especially if surgical debulking leaves residual tumor. Ideally, both histamine release and sympathetic stimulation should be avoided. Etomidate or propofol may be better choices for IV induction, although thiopental-triggered histamine release appears to be of little clinical significance. Morphine has the potential to induce histamine release and hypotension. Remifentanil, sufentanil, and fentanyl are alternatives. Succinylcholine-induced fasciculations could theoretically provoke the release of hormones; however, recent reviews reported no adverse effects. Histamine release is more prominent with tumors of foregut origin. Thus, preoperative H1- and H2-receptor blockers and corticosteroids may be useful in patients with gastric or bronchial carcinoids. Ondansetron is the ideal antiemetic agent.

Further Reading PREVENTION To avoid complications in patients with carcinoid tumors, take the following measures: ●

● ● ●

Block histamine (H1- and H2-receptors) and serotonin receptors (octreotide). Avoid drugs that facilitate the release of mediators. Provide adequate anxiolysis and postoperative pain relief. Avoid sympathetic stimulation.

If preoperative control of symptoms with octreotide is successful, patients can be placed on its longer-acting somatostatin analogue lanreotide or Sandostatin LAR. For elective surgery, premedication with subcutaneous octreotide 200 μg daily for 3 days before surgery has been shown to improve the perioperative course of patients with carcinoid tumors. Some advise prophylactic continuous IV somatostatin or octreotide (100 μg/hour) during surgery.

Botero M, Fuchs R, Paulus DA, et al: Carcinoid heart disease: A case report and literature review. J Clin Anesth 14:57-63, 2002. de Vries H, Verschueren RC, Willemse PH, et al: Diagnostic, surgical and medical aspect of the midgut carcinoids. Cancer Treat Rev 1:11-25, 2002. Kinney MA, Warner ME, Nagorney DM, et al: Perianaesthetic risks and outcomes of abdominal surgery for metastatic carcinoid tumours. Br J Anaesth 87:447-452, 2001. Lips CJ, Lentjes EG, Hoppener JW: The spectrum of carcinoid tumours and carcinoid syndromes. Ann Clin Biochem 40:612-627, 2003. Quaedvlieg PF, Lamers CB, Taal BG: Carcinoid heart disease: An update. Scand J Gastroenterol Suppl 236:66-71, 2002. Schnirer II, Yao JC, Ajani JA: Carcinoid—a comprehensive review. Acta Oncol 42:672-692, 2003. Soga J: Carcinoids and their variant endocrinomas: An analysis of 11,842 reported cases. J Exp Clin Cancer Res 4:517-530, 2003. Veall GR, Peacock JE, Bax ND, et al: Review of the anaesthetic management of 21 patients undergoing laparotomy for carcinoid syndrome. Br J Anaesth 72:335-341, 1994. Zimmer C, Kienbaum P, Wiesemes R, et al: Somatostatin does not prevent serotonin release and flushing during chemoembolization of carcinoid liver metastases. Anesthesiology 98:1007-1011, 2003.

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Complications of Thyroid Surgery Samuel A. Irefin

OTHER SURGICAL SUBSPECIALTIES

Case Synopsis A 25-year-old woman with a known history of Graves’ disease presents for subtotal thyroidectomy. A prominent thyroid gland is palpated on physical examination, and she complains of dysphagia. The chest radiograph demonstrates mild displacement of the trachea from the midline.

weight loss, osteoporosis, and myopathy. In the elderly, the only presenting features may be unexplained weight loss, atrial fibrillation, and congestive heart failure.

PROBLEM ANALYSIS Definition Thyroid surgery is performed for removal of an enlarged thyroid gland (goiter) in patients with Graves’ disease. Graves’ disease is the most common cause of hyperthyroidism in the United States, with an estimated annual incidence of 300 cases per 1 million persons. It is an autoimmune disorder characterized by a diffusely enlarged thyroid gland and thyrotoxicosis, caused by thyroid-stimulating immunoglobulins. These immunoglobulins primarily bind to and activate the thyroid-stimulating hormone (TSH) receptors. This results in increased iodine uptake, protein synthesis, growth of the thyroid gland, and synthesis and release of thyroglobulin and thyroid hormones. Complications of thyroid surgery for goiter removal are listed in Table 204-1.

Recognition HYPERTHYROIDISM (GRAVES’ DISEASE)

AND

THYROTOXICOSIS

Signs and symptoms of hyperthyroidism are listed in Table 204-2. Patients with Graves’ disease are at risk for numerous complications related to the disease and its treatment. One such life-threatening complication is thyroid storm. Signs and symptoms of thyrotoxicosis are listed in Table 204-3. Without treatment, severe thyrotoxicosis results in cardiac complications (thyrotoxic crisis or thyroid storm), cognitive disorders, gastrointestinal disturbances, jaundice,

Table 204–1

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Complications of Thyroid Surgery for Goiter Removal

Precipitation of thyrotoxic crisis (“thyroid storm”) Hemorrhage → hematoma → airway compression → acute respiratory distress Recurrent laryngeal nerve injury Superior laryngeal nerve injury Hypoparathyroidism Corneal abrasion

THYROID STORM Thyroid storm is an extreme exacerbation of thyrotoxicosis. It is usually stress related due to infection, trauma, surgery, treatment with radioactive iodine, pregnancy, diabetic ketoacidosis, thyroid replacement therapy, and anticholinergic or adrenergic drugs. Even with early recognition and aggressive therapy, the mortality rate is estimated at 20%. Manifestations of thyroid storm are listed in Table 204-4. The exact pathogenesis of thyroid storm is not fully understood. Thyroid hormones regulate the nuclear transcription of messenger RNA in all cells. Free triiodothyronine (T3) binds to a DNA domain called the “thyroid response element.” Once bound, T3 initiates the transcription of an array of biochemical enzymes that regulate tissue metabolism. One theory suggests that an acute, rapid increase in free thyroid hormone levels, rather than absolute levels, precipitates thyroid storm. Because thyroid storm most often occurs 6 to 24 hours postoperatively, manipulation of the gland during surgery or an acute reduction in binding proteins postoperatively may account for this surge of free thyroid hormones. Other theories include adrenergic

Table 204–2

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Signs and Symptoms of Hyperthyroidism (Graves’ Disease)

Weight loss despite increased appetite Heat intolerance, sweating Diarrhea, abdominal pain Tremors of distal extremities Increased reflexes Proximal muscle weakness Tachyarrhythmias (especially atrial fibrillation) Widened palpebral fissure Decreased blinking Lid lag (ptosis), blurred or double vision Increased systolic pressure with widened pulse pressure Anxiety, restlessness Fatigue Shortened attention span

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Signs and Symptoms of Thyrotoxicosis

Heat intolerance, profuse sweating Diarrhea, vomiting, jaundice Atrial fibrillation, congestive heart failure, unexplained weight loss (elderly) Tachycardia or arrhythmias Hypertension or hypotension with shock state Tremors, seizures, confusion, coma Hyperphagia Osteoporosis and myopathy Increased reflexes (hyperreflexia) Unexplained weight loss despite increased appetite Fever (consistently >101°F)

receptor activation and a direct sympathomimetic effect of thyroid hormone owing to its structural similarity to catecholamines. Diagnosis of thyroid storm is based on its clinical presentation, because laboratory testing is nonspecific. Further, waiting for results only delays treatment. Thyroid storm is an acute, life-threatening progression of thyroid hormoneinduced hypermetabolic (thyrotoxic) states involving multiple organ systems (see Tables 204-3 and 204-4). The differential diagnosis includes malignant hyperthermia, septic shock, hypertensive encephalopathy, central nervous system infection, acute drug intoxication, and pheochromocytoma. RESPIRATORY DISTRESS

FROM

HEMATOMA

The incidence of hemorrhage after thyroid surgery is low (0.3% to 1%). Hematoma formation in the neck resulting in respiratory compromise is a potentially fatal complication, however, because small amounts of blood in the deep tissue spaces near the trachea may cause significant airway obstruction. Patients present with swelling and pain at the incision site, an expanding neck mass, and symptoms of respiratory distress, such as stridor and dyspnea. RECURRENT

OR

SUPERIOR LARYNGEAL NERVE INJURY

Because of the intimate association of the thyroid gland and the nerves supplying the larynx, damage to either the recurrent laryngeal nerve (RLN) or the superior laryngeal nerve (SLN) may be a complication of thyroid surgery. Nerve injury may result from traction, contusion, or crushing during exposure; inclusion of the nerve in a ligature; inadvertent complete or partial nerve transection; or compromised blood supply. The RLN is a branch of the vagus nerve. It innervates all the intrinsic muscles of the larynx, with the exception of the cricothyroid muscle, which is innervated by the SLN.

Table 204–4

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Manifestations of Thyroid Storm after Thyroid Surgery

Hyperthermia (as high as 105°F to 106°F) Hypertension, tachycardia, arrhythmias Mental status changes Cardiovascular collapse (“shock”) Congestive heart failure in patients prone to heart failure

Unilateral RLN injury produces abductor vocal cord paralysis. The affected vocal cord assumes a paramedian position. Patients often present with postoperative hoarseness or a weak, breathy voice, but voice changes may not be apparent for days to weeks. Bilateral vocal cord paralysis is especially a risk after total thyroidectomy. Complete or partial airway obstruction often manifests immediately after extubation. Symptoms include respiratory distress with stridor requiring emergent reintubation or tracheostomy. Occasionally patients complain only of dyspnea or stridor with exertion. The external branch of the SLN innervates the cricothyroid muscle, which tenses and adducts the vocal cords. With injury, laxity of the vocal cord on the side of injury may produce subtle changes in voice quality or fatigue with speech. Techniques for assessing vocal cord mobility include fiberoptic laryngoscopic visualization during spontaneous ventilation or during extubation. For the latter, the anesthesiologist performs direct laryngoscopy under deep general anesthesia and observes the mobility of the vocal cords as the endotracheal tube is removed. Laryngeal electromyography is a diagnostic tool used as a late prognostic indicator for recovery of vocal cord function. HYPOPARATHYROIDISM Hypoparathyroidism may complicate thyroid surgery due to inadvertent trauma to or removal of the parathyroid glands or, more frequently, devascularization of the glands during ligation of the blood supply to the thyroid. The parathyroid glands produce parathyroid hormone (PTH), which increases the serum concentration of calcium through the activation of vitamin D, thereby increasing renal absorption of calcium and bone resorption. Inadequate production of PTH results in hypocalcemia. The diagnosis of hypoparathyroidism is made by the measurement of low PTH or decreased serum ionized calcium concentrations. Hypocalcemia usually occurs 24 to 48 hours after surgery but may occur earlier. Tetany, carpopedal spasm, circumoral paresthesias, mental status changes, seizures, cardiac dysfunction, and stridor are manifestations of decreased ionized calcium concentrations. Confirmatory tests include the Chvostek and Trousseau signs and Q-T prolongation on the electrocardiogram. Postoperative hypoparathyroidism must be differentiated from tetany caused by acute hypocalcemia and from respiratory alkalosis associated with anxiety and hyperventilation. CORNEAL ABRASION Corneal abrasion can occur in patients with exophthalmos and is diagnosed postoperatively with corneal fluorescein staining and examination with a cobalt-blue slit lamp. Patients complain of eye pain, tearing, and a foreign body sensation in the eye.

Risk Assessment THYROID STORM Thyroid storm affects only a small percentage of patients with thyrotoxicosis. Most cases of thyroid storm are associated with Graves’ disease in childhood. However, patients with hyperthyroidism at the time of surgery are at risk for thyroid storm during the perioperative period.

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RESPIRATORY DISTRESS

FROM

HEMATOMA

RECURRENT

OR

SUPERIOR LARYNGEAL NERVE INJURY

RLN injury is uncommon, occurring in 0% to 2.1% of patients during thyroidectomy when the nerve is identified and dissected. When the nerve is not clearly identified, the reported injury rate increases to 4% to 6.6%. Compounding factors include the extent of dissection and resection, especially if performed for malignant disease. HYPOPARATHYROIDISM

Complications of Thyroid Surgery

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is essential. Controversy exists regarding the use of drains to prevent hematoma formation after thyroid surgery. RECURRENT

OR

SUPERIOR LARYNGEAL NERVE INJURY

Permanent injury of the RLN on one side causes postoperative hoarseness. Patients are usually able to compensate and have minimal or no airway difficulty. The paralyzed vocal cord atrophies over time, leaving the patient with the potential sequelae of dysphagia, risk of aspiration, and permanent changes in voice quality. Bilateral RLN injury results in unopposed adduction of the cords, as the cricothyroid muscle remains innervated by the SLN. Associated partial or complete airway obstruction requires immediate endotracheal intubation and re-exploration of the neck to identify any reversible cause of nerve injury. If the nerves are found to be intact, use of corticosteroids and a trial extubation several days later are warranted. Permanent bilateral RLN injury necessitates tracheostomy.

Hypoparathyroidism with hypocalcemia may be transient or permanent. The incidence of parathyroid injury increases with the magnitude of the operation. It is uncommon with subtotal thyroidectomy for Graves’ disease. The overall incidence of permanent hypoparathyroidism ranges from 0.4% to 13.8%. The rate of transient hypocalcemia is reportedly 2% to 53%. The cause is not clear but may be attributable to temporary hypoparathyroidism from reversible ischemia to the parathyroid glands, hypothermic injury, or acute suppression of PTH production due to the release of endothelin 1.

HYPOPARATHYROIDISM

CORNEAL ABRASION

CORNEAL ABRASION

The likelihood of corneal injury increases with the degree of ophthalmopathy and exophthalmos.

Prognosis is excellent, with most minor abrasions healing within 24 to 48 hours. Deep abrasions in the center of the cornea may leave a scar, with the potential for permanent vision loss. Complications include infection, corneal ulceration, and recurrent epithelial erosion. Ocular medications may cause allergic conjunctivitis or glaucoma in susceptible patients.

Implications Thyroid surgery is associated with a number of potentially serious complications. THYROID STORM Thyroid storm is the most severe form of thyrotoxicosis. It often occurs in patients who have not been rendered euthyroid before thyroid surgery. Consultation with an endocrinologist can assist in optimizing the patient’s preoperative status with antithyroid drugs, iodide therapy, β-blockers, and glucocorticoids. The chest radiograph may reveal cardiac enlargement or pulmonary edema in patients with congestive heart failure. This should be further evaluated by echocardiography. Therapy for congestive heart failure or rate control for atrial fibrillation may be required. In the perioperative setting, differentiating between thyroid storm and malignant hyperthermia may be difficult. RESPIRATORY DISTRESS

FROM

HEMATOMA

Respiratory distress from any cause requires immediate evaluation and treatment. Patients must be followed closely for up to 72 hours postoperatively for evidence of airway compromise. A thin paper tape dressing over the surgical incision allows optimal wound surveillance. Postoperative bleeding can be a devastating and potentially fatal complication of thyroid surgery. Fastidious intraoperative hemostasis

Hypocalcemia may be asymptomatic or it may progress to laryngospasm, tetany, and cardiac dysfunction as early as 6 hours after injury to the parathyroids. Calcium levels may continue to decline over the next 24 to 48 hours, and symptomatic patients require close monitoring of ionized calcium levels with calcium and vitamin D replacement. If the patient remains dependent on oral calcium supplementation for longer than 6 months, it is likely that permanent injury of the hypoparathyroid glands has occurred.

MANAGEMENT Hyperthyroidism (Graves’ Disease) Effective treatment for Graves’ disease includes medical therapy to alleviate symptoms and render the patient euthyroid, in conjunction with surgery. However, as mentioned earlier, thyroid surgery is associated with potentially serious complications, such as thyroid storm.

Thyroid Storm Therapy for thyroid storm is both supportive and therapeutic: ●

Assess airway, breathing, and circulation (ABCs): (1) ensure oxygenation and provide ventilatory support as needed; (2) restore intravascular volume with intravenous fluids; (3) establish invasive monitoring (e.g., direct arterial blood pressure monitoring, central venous access, urinary catheterization) if necessary; (4) treat tachycardia and atrial fibrillation; (5) anticipate heart failure and volume depletion; and (6) administer intravenous dextrose as needed to meet high metabolic demands.

OTHER SURGICAL SUBSPECIALTIES

Respiratory distress may be secondary to laryngeal edema, laryngospasm, bilateral vocal cord paralysis, tracheomalacia, or hypocalcemia. More commonly, however, it occurs with cervical hematomas that are generally venous in origin. If postoperative bleeding is unrecognized, these hematomas may cause airway obstruction and asphyxiation.

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Prevent hyperthermia by covering the patient with ice packs or cooling blankets and administering acetaminophen as needed. Prevent thyroid hormone synthesis by administering propylthiouracil (PTU) or methimazole. Block thyroid hormone secretion by giving intravenous potassium iodide before surgery to reduce gland size in patients with acute thyroid enlargement, especially when goiters are associated with airway compromise. Potassium iodide can also be used to suppress hormone secretion in thyroid storm. Reduce peripheral conversion of thyroxine (T4) to T3 with glucocorticoids, propranolol, and PTU. Relieve hyperadrenergic effects of thyroid hormones with β-blockers as needed. Treat adrenal insufficiency with glucocorticoids as required. Consult an endocrinologist for more definitive management. Monitor patients with thyroid storm in a critical care unit or similar environment.

Antithyroid drugs (e.g., PTU) inhibit iodination and coupling reactions in the thyroid. In addition, they reduce the synthesis of T3 and T4 and inhibit the peripheral conversion of T4 to T3 by blocking type I deiodinase. Therapy with potassium iodide is important because it inhibits the secretion of thyroid hormone; when given preoperatively, it also reduces both the vascularity and the size of the thyroid gland. During thyroid storm, intravenous potassium iodide is often used. After antithyroid drugs have been started, iodide may also be dissolved in water as a retention enema. β-Blockers are used to antagonize the cardiovascular manifestations of the hypermetabolic state, such as tachycardia, increased cardiac output, and tachyarrhythmias (often atrial fibrillation). Sustained hypermetabolic states may lead to congestive heart failure and hypotension. Other benefits of β-blockers include relief of many of the symptoms and signs of hyperthyroidism (see Table 204-2) and thyrotoxicosis (see Table 204-3). Corticosteroids are used to prevent adrenal insufficiency secondary to the hypermetabolic state in thyroid storm. Digoxin may be used to treat congestive heart failure or atrial fibrillation with a rapid ventricular response. Salicylates are not used for hyperthermia; they compete with T3 and T4 for binding to thyroid-binding globulin, which may increase the circulating levels of free thyroid hormone. Instead, acetaminophen is prescribed for hyperthermia.

Respiratory Distress from Hematoma Respiratory distress and impending airway obstruction due to an expanding neck hematoma require immediate (often bedside) neck re-exploration. However, return to the operating room will likely be required for more definitive control of bleeding sites, irrigation, and wound closure. If so, the airway must first be secured. Then the patient is taken to the operating room, with experienced health care providers present for ventilatory support, reintubation, and tracheostomy if needed.

Recurrent or Superior Laryngeal Nerve Injury Management of RLN injury remains controversial. Most patients with unilateral RLN injury need no definitive intervention and recover from reversible causes within 6 months of surgery. For patients with permanent unilateral RLN injury, surgery can improve voice quality and reduce the risk of aspiration. Surgical options are medialization or reinnervation of the vocal cord. However, if the RLN has been transected, it is debatable whether immediate microvascular anastomosis or grafting at the time of surgery is effective therapy. In contrast, with bilateral RLN injury, the patient usually requires immediate airway control with endotracheal reintubation or tracheotomy.

Hypoparathyroidism Hypocalcemia due to parathyroid injury is managed with calcium replacement, depending on the severity of hypocalcemia. Symptomatic hypoparathyroidism is promptly treated with 10 mL of 10% solution of calcium gluconate given over 10 minutes. This is followed by a continuous infusion (1 to 2 mg/kg per hour). Infusions are titrated to the patient’s symptoms and serum ionized calcium concentrations. When the patient is able to tolerate oral fluids, daily oral calcium carbonate and vitamin D supplementation are started.

Corneal Abrasion Corneal abrasions are treated with eye rest, narcotic analgesics, and possibly topical antibiotics (see also Chapter 184). Patching or use of a contact lens impregnated with a nonsteroidal anti-inflammatory drug may help reduce the associated pain.

PREVENTION Thyroid Storm The most common therapy for Graves’ disease is radioactive iodine. This often normalizes thyroid function within 6 to 12 months. However, radioactive iodine itself may precipitate thyroid storm. Iatrogenic hypothyroidism is also a risk. In patients with large or nodular (suggestive of carcinoma) goiters, it is essential that they be clinically and chemically euthyroid before surgery. Preoperative preparation includes antithyroid drug treatment (PTU) for approximately 6 weeks, with or without a β-blocker. Iodine is given by most surgeons for 2 weeks before surgery to reduce thyroid gland vascularity.

Respiratory Distress from Hematoma Thyroid surgery must be performed in a near-bloodless field to facilitate identification of the parathyroid glands and the RLNs and SLNs in the operative area. The key to limiting bleeding is proper positioning and meticulous surgical hemostasis. The patient’s neck is hyperextended, and the head of the operating table is elevated 30 degrees. This provides optimal exposure and reduces cervical venous pressure

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and bleeding. At the end of the procedure, Valsalva’s maneuver is performed with the head lowered to a neutral position. This facilitates the recognition of bleeding vessels. These are then coagulated or ligated. Smooth emergence without coughing or bucking on the endotracheal tube helps prevent early rebleeding.

Prevention of RLN or SLN injury also requires meticulous surgical technique. Identification of the entire course of the RLN is advocated by some, but this is controversial. Some authors recommend routine electrical stimulation of the RLN for identification. An electromyographic device for electrophysiologic monitoring of the RLN during surgery is commercially available. However, it is usually reserved for high-risk cases, such as patients with very large neck masses or prior surgery or irradiation.

Hypoparathyroidism Interruption of the parathyroid blood supply is a common cause of hypoparathyroidism. Therefore, identifying the blood supply and ensuring that it remains intact are important preventive measures. Also, the glands are identified to prevent inadvertent removal. Further, suctioning in the operative field can injure the parathyroid glands. Therefore, it

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is recommended that the field be kept dry by careful blotting with sterile gauze rather than use of a suction device. If the parathyroid glands are damaged or inadvertently removed, autotransplantation may prevent hypoparathyroidism.

Corneal Abrasion Intraoperative eye protection consists of lubrication, padding, taping the eyelids closed, use of protective eyewear, and care during surgical draping and undraping.

Further Reading Kahky MP, Weber RS: Complications of surgery of the thyroid and parathyroid glands. Surg Clin North Am 73:307-321, 1993. Lacoste L, Montaz N, Berrit A, et al: Airway complications in thyroid surgery. Ann Otol Rhinol Laryngol 102:441-446, 1993. Mackin JE, Canary JJ, Pittman CS: Thyroid storm and its management. N Engl J Med 291:1396, 1974. McGowan FX: Anesthesia for major head and neck surgery. In McGoldrick KE (ed): Anesthesia for Ophthalmic and Otolaryngologic Surgery. Philadelphia, WB Saunders, 1992, pp 75-85. Wartofsky L: Diseases of the thyroid. In Isselbacher KH, et al (eds): Harrison’s Principles of Internal Medicine. New York, McGraw-Hill, 1994, pp 1942-1947. Woeber K: Thyrotoxicosis and heart. N Engl J Med 327:94, 1992. Yeung J, Chiu AC: Graves’ disease. Endocrinology Web site. http://www.emedicine.com/med/topic929.htm

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Recurrent or Superior Laryngeal Nerve Injury

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Complications of Adrenal Surgery Michael F. M. James Case Synopsis A 19-year-old man presents in hypertensive crisis with tachycardia, congestive heart failure (CHF), and renal dysfunction. On investigation he is found to have a right adrenal mass. The surgical plan is to investigate the cause of the adrenal mass, stabilize the patient, and proceed to elective excision of the tumor.

PROBLEM ANALYSIS Definition Adrenal disease frequently progresses to secondary hypertension and hypertensive crisis. The adrenal gland has two distinct endocrine entities: the cortex and the medulla. The cortex synthesizes glucocorticoids (e.g., cortisol), and the medulla, mineralocorticoids (e.g., aldosterone) and androgens. The medulla synthesizes catecholamines such as dopamine, norepinephrine, and epinephrine. Catecholamine production is dependent on the enzyme phenylalanine-nmethyltransferase and the high concentrations of glucocorticoids found in the adrenal cortex. The most common functioning adrenal cortical tumors are benign adenomas that produce cortisol or, less frequently, aldosterone. Adrenal carcinoma is less common but produces more severe symptoms. Adrenal hyperplasia secondary to excess adrenocorticotropic hormone (ACTH) release from a pituitary microadenoma results in Cushing’s disease. Excess cortisol production from adrenal tumors or exogenous ACTH results in Cushing’s syndrome. Excess aldosterone production leads to Conn’s syndrome, which accounts for 0.5% to 3% of all cases of hypertension. Conn’s syndrome is usually due to a single adrenal adenoma, possibly in association with bilateral adrenal hyperplasia. Tumors that secrete catecholamines arise from neural crest tissue, including the sympathetic chain and, rarely, the cardiac conduction system. Approximately 90% of pheochromocytomas are unilateral adrenal medullary tumors. Bilateral adrenal medullary tumors are usually associated with congenital conditions or are found in children. Extra-adrenal pheochromocytomas seldom produce epinephrine, and these tumors are frequently both multiple and malignant. Adrenal tumors can secrete both epinephrine and norepinephrine; however, the latter usually predominates. Familial associations include multiple endocrine neoplasia (MEN) type IIA (Sipple’s syndrome), defined as medullary thyroid carcinoma, pheochromocytoma, and (inconsistently) parathyroid adenoma. MEN type IIB is similar to type IIA but also includes marfanoid habitus and mucosal neuromas. It was formerly believed that only 5% of pheochromocytomas were inherited; however, recent data 822

suggest that germline mutations may cause up to 25% of cases previously considered sporadic, especially in children and when the tumor is extra-adrenal. Other associations include von Hippel-Lindau syndrome1 and (rarely) von Recklinghausen’s disease (neurofibromatosis).

Recognition Hypertensive crisis, atypical diabetes, and unexplained cardiomyopathy, especially in young persons, should always raise the suspicion for adrenal disease. Classic features of pheochromocytoma (e.g., headaches, diaphoresis, palpitations) occur in about 80% of patients, but this history is often elicited only by direct questioning. The presentation of pheochromocytoma is variable (Table 205-1), and it may go undiagnosed for several years. The diagnosis of pheochromocytoma is based on the finding of significant levels of catecholamines and their metabolites in the plasma and urine, supported by radiographic evidence. Isolated vanillylmandelic acid measurements have a sensitivity of only 60%; however, if combined with serial metanephrine measurements, sensitivity and specificity increase to about 90%. High-performance liquid chromatography to measure plasma and urinary catecholamine concentrations has similar sensitivity but higher specificity (95%). Contrast imaging with I123-labeled MIBG (m-iodobenzylguanidine) is reserved for extra-adrenal pheochromocytomas or when multiple tumors are suspected. Computed tomography scanning is then used to establish precise tumor localization and definition. Rarely, other tests (e.g., clonidine suppression test) are useful when the diagnosis is still in doubt. Clinical hallmarks of Cushing’s disease are truncal obesity, thin skin, easy bruising, abdominal striae, hypertension, and hyperglycemia (Table 205-2). Cushing’s syndrome is usually clinically obvious and is confirmed by high

1 Von Hippel-Lindau syndrome, or retinocerebral angiomatosis (a type of phakomatosis), consists of retinal hemangiomas (multiple or bilateral) in association with hemangiomas or hemangioblastomas that involve primarily the cerebellum, the walls of the fourth ventricle, and occasionally the spinal cord. The disease has autosomal dominant inheritance and may be associated with renal cysts or hamartomas. These may affect the adrenals or other organs.

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Table 205–1

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Symptoms and Other Findings in Patients with Pheochromocytoma Symptoms and Other Findings

Integumentary Musculoskeletal Cardiovascular

Excessive sweating, cold extremities Muscle tremors Left atrial and ventricular hypertrophy; electrocardiogram abnormalities; cardiomyopathy; episodic (60%) or sustained (35%) hypertension; hypotension (5%); palpitations; peripheral vascular disease with tissue loss Reduced glucose tolerance; diabetes mellitus; diabetic coma; weight loss Nonspecific abdominal pain and nausea; occasionally presents as apparent acute abdomen Headache; anxiety attacks; stroke

Metabolic Gastrointestinal Central nervous

concentrations of serum cortisol. Identification of Cushing’s disease requires the dexamethasone suppression test and the corticotropin-releasing hormone test. The former causes ACTH to fall to very low concentrations in the absence of an ACTH-producing tumor. The latter should cause a marked increase in ACTH release with primary pituitary disease, but not in patients with adrenal tumors or ectopic ACTH production. Primary aldosteronism presents as severe hypertension, muscle weakness, polyuria, and thirst. Renal dysfunction secondary to hypertension and hypokalemia is common. High plasma sodium concentrations, hypokalemia, and metabolic alkalosis suggest Conn’s syndrome. This is confirmed by high serum aldosterone and low plasma renin concentrations.

immunosuppression increases the infectious risk. Furthermore, long-standing disease may result in difficult airway management and tracheal intubation. Pheochromocytoma carries the added risks of catecholamine-induced cardiomyopathy and tachyarrhythmias. Also, there may be associated cardiomyopathy and CHF (Fig. 205-1). Hyperaldosteronism increases the risk for renal dysfunction, muscle weakness, and cardiomyopathy, mainly due to chronic potassium wasting. Patients may present for anesthesia and surgery with severe intracellular potassium deficits, despite apparently adequate plasma concentrations after potassium replacement therapy.

Risk Assessment

Adrenal surgery carries the risk for damage to anatomically proximate structures, including the spleen, pancreas, diaphragm (pneumothorax), and vasculature (e.g., inferior vena cava, renal and portal veins, splenic vessels). Hemorrhagic risk is even greater with pheochromocytomas, because they are often quite vascular. For unilateral tumors, a posterior surgical approach may be preferable, with less blood loss and morbidity. However, when bilateral or extraadrenal tumors are suspected, the anterior approach is preferred, even though this approach increases the risk for inadvertent injury to adjacent organs. Also, access to the venous tumor drainage is more readily obtained early during the procedure. Laparoscopic adrenalectomy has become more popular in recent years and appears to reduce the morbidity associated

Adrenalectomy is a relatively high-risk procedure, mainly due to endocrine pathophysiology and target end-organ damage. Morbidity with simple adrenalectomy can be as high as 40%, with mortality between 2% and 4%. Perioperative mortality is higher (5% to 10%) for bilateral adrenalectomy in patients with Cushing’s disease. Further, such surgery mandates mineralocorticoid and glucocorticoid replacement therapy for the patient’s lifetime. Each individual pathology has associated risk factors. For adrenal tumors, hypertension with end-organ damage (especially involving the heart, brain, or kidneys) must be considered. With Cushing’s syndrome, osteoporosis increases the risk of skeletal injury during surgery, and

Table 205–2

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Implications

Systemic Manifestations of Cortisol Excess Due to Cushing’s Disease

Organ System

Systemic Manifestations

Integumentary Musculoskeletal Cardiovascular Gastrointestinal Respiratory Reproductive

Purple striae on abdomen, buttocks, and thighs; easy bruising; hirsutism; acne Proximal myopathy and weakness; osteoporosis; vertebral collapse Left ventricular hypertrophy; electrocardiogram abnormalities; hypertension (85%) Esophageal reflux Sleep apnea (32%) Women: virilization secondary to hypersecretion of adrenal androgens; loss of libido; oligomenorrhea Men: impotence Reduced glucose tolerance; diabetes mellitus (60%); altered fat metabolism and body distribution (“moon” face, central obesity, “buffalo hump”); increased mineralocorticoid activity—hyponatremia, hypokalemia, metabolic alkalosis Psychiatric symptoms: depression; agitated psychosis (60%-70% of patients)

Metabolic Central nervous

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A

B

Figure 205–1 ■ A, Chest radiograph of a patient presenting with hypertensive crisis, congestive heart failure, and catecholamine-induced cardiomyopathy. Note mitralization of the left heart border, pulmonary edema, elevated left main bronchus, and cardiac enlargement. B, Same patient 6 months after excision of pheochromocytoma. The cardiac silhouette has returned to normal.

with simple adrenalectomy. However, establishment of pneumoperitoneum with carbon dioxide insufflation and increased tumor manipulation may substantially increase catecholamine release from a pheochromocytoma and worsen any hemodynamic instability. The safe performance of adrenalectomy, particularly for pheochromocytoma, depends on skilled surgical and anesthetic management and requires excellent communication between the surgeons and anesthesiologist. The laparoscopic approach for pheochromocytoma resection is not advised unless the surgical-anesthesia team is knowledgeable about and experienced with the technique.

also manifestations of end-organ damage. Hypertensive emergencies require immediate IV therapy with antihypertensive agents. With pheochromocytoma, hypertensive crises are usually emergencies. Thus, IV drugs are the mainstay of treatment. Sodium nitroprusside (SNP) has been the most commonly used agent, but there are now recognized limitations to its use: ●

●

MANAGEMENT Preoperative Management of Hypertensive Crisis Hypertensive crises may be urgencies or emergencies (see Chapter 77). Both require a blood pressure of 160/90 mm Hg or higher. With hypertensive urgencies, there is no evidence of end-organ damage (e.g., renal failure of CHF, myocardial or cerebral ischemia). Also, therapy is less urgent, usually consisting of oral rather than intravenous (IV) drugs. During anesthesia and surgery and in postanesthesia and intensive care units, however, initial therapy is often with IV drugs. With hypertensive emergencies, blood pressure is 160/90 mm Hg or higher, and there is evidence of end-organ damage (see earlier). Also, acute CHF (as in the case synopsis), arrhythmias (e.g., acute atrial fibrillation, ventricular arrhythmias), aneurysm rupture with intracranial hemorrhage (i.e., hemorrhagic stroke), and aortic dissection are

●

Because patients with chronic hypertension are preload restricted, and because SNP is a potent arterial and venous dilator, especially in the venous capacitance beds, there is high potential for untoward hypotension during treatment with SNP. Untoward hypotension caused by SNP may necessitate the use of vasopressors, but those that act indirectly (e.g., ephedrine) may worsen hypertension in patients with pheochromocytoma. The use of SNP for blood pressure management in perioperative settings can be challenging owing to the high potential for increased blood pressure lability. Direct arterial monitoring is advised.

Because of the disadvantages of SNP, clinicians have turned to dihydropyridine (DHP) calcium channel blockers, especially for the management of hypertensive emergencies. DHP calcium channel blockers are arterioselective vasodilators; they have little or no effect on the cardiac calcium channels (sinoatrial node, atrioventricular node, contractility). The only IV calcium channel blocker available at present is nicardipine (Cardene IV), but at least one other is on the horizon. Oral dihydropyridines (e.g., nimodipine, amlodipine) are used for long-term blood pressure control. Nicardipine is compatible with IV β-blockers (e.g., esmolol), and the two can be used together as continuous IV infusions.

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Preoperative Medical Management Patients with Cushing’s or Conn’s syndrome are managed with conventional antihypertensive drugs, although spironolactone may be included to correct fluid overload and hypokalemia in primary aldosteronism. In pheochromocytoma, α-blockade is the cornerstone of therapy. It helps prevent paroxysmal hypertension, lowers intravascular volume, and reduces left ventricular strain. Phenoxybenzamine, a long-acting, noncompetitive, nonspecific α-antagonist, is the most widely used oral α-blocker. The initial dose (10 mg) is increased every 1 to 2 days until the blood pressure is controlled. Most patients require 60 to 250 mg/day. Preparation periods vary from 5 to 14 days, and no benefit has been shown with longer treatment. Adequate α-receptor blockade is indicated by good control of arterial pressure with orthostatic hypotension, nasal congestion, increased sweating, and warm extremities. Electrocardiogram abnormalities seldom revert to normal during preoperative preparation, and unless there is evidence of frank myocardial ischemia, there is no contraindication to surgery. Doxazosin, a long-acting selective α1-blocker, has also been used in doses ranging from 4 to 16 mg daily. Tachycardia normally responds to fluid loading, and β-blockade should not be used until vasodilatation has been achieved. Other drugs (e.g., α-methyl-tyrosine, calcium channel blockers, angiotensin-converting enzyme inhibitors) are used, but not widely so.

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Adrenal surgery increases the risk of hemorrhage, so good IV access is necessary. In addition to standard monitoring, hemodynamic and fluid balance must be monitored with at least an intra-arterial catheter, central venous pressure line, and urinary catheter. A pulmonary artery catheter is seldom helpful. Transesophageal echocardiography is useful, especially in those with cardiomyopathy (with or without CHF), because it allows the assessment of left ventricular contractility and filling. H2-receptor antagonists may be considered in cushingoid patients with reflux esophagitis. Pulmonary artery catheters have been advised but are not mandatory for surgery involving the adrenal cortex. Transesophageal echocardiography is better, because fluid balance problems may prove difficult.

Anesthetic Management Theoretically, drugs that release histamine (e.g., morphine, atracurium) should be avoided in patients with pheochromocytoma, as should those that cause tachycardia or stimulate the sympathetic nervous system (e.g., ketamine, atropine, droperidol, pancuronium). Succinylcholineinduced fasciculations may trigger the release of catecholamines in patients with pheochromocytoma, so this drug is seldom indicated. Among the volatile anesthetics, isoflurane and sevoflurane are theoretically preferable to halothane (which sensitizes myocardium to catecholamines) and desflurane (which increases heart rate). SNP has a rapid onset and short duration of action and has been widely used. Nitroglycerin has also been used successfully, but nicardipine may be better (see earlier). IV bolus phentolamine has too slow an onset-offset to be of use. IV bolus MgSO4 (2-g intermittent boluses) or infusion (2 to 3 g/hour) provides excellent hemodynamic control, inhibits catecholamine release (especially with laryngoscopy), and is an excellent antiarrhythmic. In patients with Cushing’s syndrome, peripheral vascular access may be difficult. Care must be taken when using adhesive tape owing to their very friable skin. Rapid-sequence induction with succinylcholine may be appropriate in those with reflux esophagitis. Care must also be taken with patient positioning, because osteoporosis increases the risk for fractures. Meticulous antisepsis and prophylactic antibiotics are necessary, because these patients have decreased resistance to infection.

Tumor Removal Preanesthetic Considerations and Monitoring If phenoxybenzamine has been used, it is omitted on the morning of surgery owing to its very long half-life. β-Blockade should also be withdrawn, so that the patient is not blocked at the time of tumor excision. Mild sedation with a benzodiazepine is usually adequate.

2 This strongly argues for a selective arterial vasodilator, because CHF is “forward failure” due to increased left ventricular work rather than simple volume overload. The heart still requires adequate preload. A venodilator can always be added if needed.

Pheochromocytomas are very vascular, and it is often difficult to ascertain when complete venous ligation has been attained. Therefore, tumor removal is the only guarantee that further catecholamine surges will not occur. Significant hypotension may occur, and immediate withdrawal of hypotensive agents, together with aggressive intravascular volume expansion (preferably with colloids), should be instituted. If MgSO4 has been used, calcium chloride 1 to 2 g by rapid IV injection may be useful to correct hypotension. Persistent hypotension may require the use of vasopressors (e.g., phenylephrine, norepinephrine) or epinephrine for short periods, but hemodynamic stability should be achieved

OTHER SURGICAL SUBSPECIALTIES

Magnesium sulfate (MgSO4) may be effective if SNP does not adequately reduce and control arterial blood pressure. As noted earlier, intravascular volume may be severely depleted, and fluid therapy may be needed if both CHF and reduced intravascular volume coexist. If so, diuretics are inappropriate and β-blockers are contraindicated, regardless of heart rate, until systemic vascular resistance is reduced and the patient is out of CHF.2 Even then, β-blockers are used mainly for myocardial ischemia. Preoperative assessment requires special attention to the underlying pathophysiology. Hypertension and hyperglycemia must be controlled, and fluid and electrolyte disturbances corrected. The electrocardiogram may reveal left atrial and ventricular hypertrophy, arrhythmias, ischemia, or infarction, and the chest radiography may show CHF. Echocardiography is useful with suspected cardiomyopathy. Potassium deficits may be particularly severe in hyperaldosteronism and should be carefully corrected.

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without vasoactive agents before completion of the surgery. Because these patients have substantial sympathetic paresis, arterial pressure is much more dependent on blood viscosity. A hematocrit of at least 30% should be maintained. In contrast, adrenalectomy for cortisol or aldosterone excess is not associated with such dramatic hemodynamic changes. Fluid balance, however, is critical, and patients having bilateral adrenalectomy require intraoperative mineralocorticoid and glucocorticoid support. Electrolyte disturbances with any of these tumors may increase the patient’s sensitivity to neuromuscular blocking drugs. Care should be taken to ensure complete reversal of neuromuscular blockade at the end of surgery. Postoperative ventilatory support is seldom required, however, unless there are other conditions that necessitate it.

Glucose Management Patients with Cushing’s syndrome (less so those with pheochromocytoma) may have some degree of hyperglycemia and glucosuria both preoperatively and intraoperatively. After tumor excision, hypoglycemia may occur. Blood glucose is monitored hourly for 24 hours postoperatively.

Postoperative Management Postoperative pain and discomfort are managed as usual. The use of epidural analgesia is a matter of personal choice. Catecholamine concentrations return to normal over several days, and about 75% of patients are normotensive within 10 days. Although hypertension may persist for several days after tumor removal, this does not necessarily imply residual tumor. Postoperative hypotension is rare with preoperative α-blockade and adequate volume expansion. If hypotension does occur, occult hemorrhage must be considered. Bilateral adrenalectomy necessitates postoperative steroid replacement with glucocorticoids and mineralocorticoids. However, even with unilateral tumor excision, transient steroid deficiency may occur. Thus, use of additional steroids in the early postoperative period is advised.

Unless the tumor is malignant, the long-term prognosis after adrenalectomy is good. More than 80% of patients return to normal health. Even with catecholamine-induced cardiomyopathy, the prognosis is excellent. This is one of the few forms of cardiomyopathy in which full recovery is the norm (see Fig. 205-1).

PREVENTION Prevention of complications during adrenal surgery is based on a careful preoperative patient assessment, followed by control of hypertension, restoration of intravascular volume, and correction of hyperglycemia and coexisting electrolyte abnormalities. The anesthesiologist should be prepared for significant blood loss and have a high index of suspicion for pneumothorax. Drugs should be readily available for the prompt treatment of both hypotension and hypertension.

Further Reading Atlee JL, Dhamee MS, Olund TL, et al: The use of esmolol, nicardipine or their combination to blunt hemodynamic changes after laryngoscopy and tracheal intubation. Anesth Analg 90:280-285, 2000. Bravo EL: Pheochromocytoma: An approach to anithypertensive management. Ann N Y Acad Sci 970:1-10, 2002. Brunt LM, Moley JF, Doherty GM, et al: Outcomes analysis in patients undergoing laparoscopic adrenalectomy for hormonally active adrenal tumors. Surgery 130:629-634, 2001. Connery LE, Coursin DB: Assessment and therapy of selected endocrine disorders. Anesthesiol Clin North Am 22:93-123, 2004. James MF, Cronje L: Pheochromocytoma crisis: The use of magnesium sulfate. Anesth Analg 99:680-686, 2004. Kinney MA, Warner ME, vanHeerden JA, et al: Perianesthetic risks and outcomes of pheochromocytoma and paraganglioma resection. Anesth Analg 91:1118-1123, 2000. Lenders JW, Pacak K, Eisenhofer G: New advances in the biochemical diagnosis of pheochromocytoma: Moving beyond catecholamines. Ann N Y Acad Sci 970:29-40, 2002. Neumann HP, Bausch B, McWhinney SR, et al: Germ-line mutations in nonsyndromic pheochromocytoma. N Engl J Med 346:1459-1466, 2002. Prys-Roberts C, Farndon JR: Efficacy and safety of doxazosin for perioperative management of patients with pheochromocytoma. World J Surg 26:1037-1042, 2002.

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Complications of Trauma Surgery Maged Argalious

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Case Synopsis A 23-year-old man arrives in the emergency department with a gunshot wound to the right upper quadrant of the abdomen. He is combative and confused. His vital signs include systolic blood pressure, 70 mm Hg; heart rate, 119 beats per minute; and respiratory rate, 22 breaths per minute.

PROBLEM ANALYSIS Definition Trauma-related injury (TRI) is the leading cause of death in the United States for persons between the ages of 1 and 45 years and is the third leading cause of death overall. Because TRI affects primarily the young, it is the leading cause of years of life lost before age 75 years. The World Health Organization (WHO) estimates that TRI is the leading cause of mortality globally for both men and women between 5 and 45 years of age. Also, WHO estimates that by 2020, TRI will be the leading cause of death in all age groups. TRI victims present unique challenges to the health care delivery system. They often have multiple injuries to multiple organ systems that necessitate resource-intensive care. Further, TRI can adversely interact with many chronic underlying medical conditions. Many trauma injuries are preventable. Drugs and alcohol are responsible for nearly 40% of fatal motor vehicle accidents and close to 50% of gunshot wounds. Trauma is classified as either intentional (e.g., homicide) or accidental, as well as according to the mechanism of injury (e.g., penetrating versus blunt). Owing to improvements in trauma care, there has been a decline in trauma-related deaths in recent years.

Recognition Evaluation of acute trauma victims has three key components: rapid overview, primary survey, and secondary survey. Resuscitation can be initiated at any time during this triage. Rapid overview takes only a few seconds and is used to determine whether the patient is stable, unstable, or dead. The primary survey involves the rapid evaluation of functions that are critical to survival. The ABCs of airway patency, breathing, and circulation are assessed, followed by a brief neurologic examination. Priority is given to cervical spine injury or impending cerebral herniation. The secondary survey entails a systematic, comprehensive evaluation of each anatomic region and usually detects injuries that were overlooked initially. Three quarters of such previously undetected injuries are orthopedic. Based on the results of the secondary survey, patients are rushed immediately to the operating room for surgery, transferred to the radiology

suite for further diagnostic studies, or reexamined and observed in an intensive care unit. Knowledge of the patterns of injury associated with different mechanisms of trauma (i.e., clusters of injury) can help anticipate and identify injuries early. The presence of the worst possible injuries should be assumed until the diagnoses are either confirmed or excluded. Many trauma-related complications are diagnosed intraoperatively (Table 206-1). Blunt trauma causes localized or widespread transfer of energy to the body. Depending on the site of impact and the amount of energy, this can cause visceral rupture or tissue disruption, including multiple fractures. Penetrating trauma is commonly limited to the track along which a bullet or sharp object has traveled.

Risk Assessment Triage scoring systems are based on the physical examination and physiologic or mechanism-of-injury parameters. They have traditionally been used to determine patterns of patient referral to trauma centers. Survival is the major outcome variable. The revised trauma score (RTS) is a prospective scoring system that exists in two forms: one is designed for use as a triage tool, and the other is used to evaluate in-hospital patient outcomes. The RTS accurately predicts mortality following traumatic injury, but there is a lack of definitive evidence supporting its use as a primary triage tool in the field or as a predictor of functional outcome and quality of life. To determine the RTS, the Glasgow Coma Scale (GCS) score, systolic blood pressure, and respiratory rate are assigned coded values from 4 (normal) to 0. These are then added and weighted (Table 206-2). When summed, values can range from 0 to 7.84. Higher values indicate a better prognosis. Of the many trauma scoring systems, the RTS is the most popular worldwide. It has been shown that hyperglycemia independently predicts longer intensive care unit and hospital stay and higher mortality in trauma patients. It is also associated with infectious morbidity. These associations hold true for mild and moderate hyperglycemia (glucose concentration >135 mg/dL and >200 mg/dL, respectively). Traumatic injuries and subsequent intraoperative complications depend on patterns of injury. Factors that affect these include age, gender, impact resistance and fixation of 827

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Injuries and Potential Perioperative Complications in Trauma Victims

Central Nervous System Cervical spine instability or injury and possible spinal cord injury Closed head injury with increased intracranial pressure Possible brainstem herniation due to increased intracranial pressure Brain herniation through open skull fracture

Chest and Pulmonary Endobronchial intubation Tension pneumothorax or hemothorax Pneumomediastinum Rib fracture and possible flail chest Pulmonary contusion Bronchopleural fistula Aspiration pneumonitis Bronchospasm Tracheobronchial plugging Fat embolism with long bone (e.g., femur) fracture

Cardiovascular Myocardial contusion or cardiac rupture Pericardial tamponade or pneumopericardium Aortic dissection or disruption Disruption of pulmonary vasculature or vena cava Hypotension: hypovolemic or neurogenic Hypovolemic circulatory shock Air embolism

Abdomen Disruption or laceration of hollow viscera Hepatic laceration Splenic rupture

Coagulation Coagulopathy, especially with massive blood transfusion Disseminated intravascular coagulopathy Primary fibrinolysis Hemolytic transfusion reaction

Electrolyte or Other Imbalance Hypocalcemia secondary to citrate toxicity Hyperkalemia, hypomagnesemia Acid-base imbalance

intoxicated patients, and those with neurologic signs or symptoms. Cervical spine injury is uncommon with penetrating trauma that is remote from the neck. Spine films that visualize all seven cervical and the first thoracic vertebrae in the lateral, anteroposterior, and odontoid views are required before clearing the cervical spine. Even with normal cervical radiographs, the possibility of ligamentous injury can be ruled out only by computed tomography scanning. Recognition of a potentially difficult airway, whether due to anatomic predisposition or the actual trauma, is one of the most important roles of the anesthesiologist. Intubation in a patient with an unstable cervical spine involves the potential for irreversible spinal cord injury. The risk for pulmonary aspiration of the gastric contents is high in trauma victims. Gastric emptying virtually stops at the time of injury, and protective airway reflexes are impaired in obtunded or comatose victims. The greatest risk for aspiration in conscious patients occurs between the induction of anesthesia and endotracheal intubation. The mortality rate with pulmonary aspiration is 5%. Fracture of the first or second ribs, flail chest, a widened mediastinum, massive hemothorax, and scapula fractures often correlate with pulmonary or vascular injury. In blunt trauma, rib fractures are the most common injury; hemothorax or pneumothorax is more common with penetrating injuries. Resuscitation frequently requires massive transfusion of blood and blood components, as well as volume replacement with crystalloids and colloids. For massive uncontrolled traumatic hemorrhage, the priority is for immediate blood, blood component, and volume resuscitation, followed by definitive surgical control of hemorrhage from major vessels. However, transfusion and achieving hemostasis with blood component therapy entail significant risks. Normal saline has been associated with hyperchloremic metabolic acidosis, and the use of large volumes of hetastarch solution has been implicated in coagulopathy and renal insufficiency.

Implications body parts, anatomic protection of organs, and mechanism of injury. Patients at risk for cervical spine injury include conscious patients with neck pain or severe pain with distraction, 20% of unconscious patients with injuries above the clavicle,

Table 206–2

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Revised Trauma Scoring System

Glasgow Coma Scale Score 13-15 9-12 6-8 4-5 3

The risk of cervical spine injury and aspiration determines the method used to secure the airway. If time permits, aspiration prophylaxis includes metoclopramide, an H2-antagonist, and sodium citrate to facilitate gastric emptying and reduce gastric pH. Most patients arrive in the operating room wearing

Systolic Blood Pressure (mm Hg) >89 76-89 50-75 1-49 0

Respiratory Rate (breaths/min) 10-29 >29 6-9 1-5 0

Coded Value 4 3 2 1 0

Revised trauma score = 0.9368(GSCc) + 0.7326(SBPc) + 0.2908(RRc), where GCS is Glasgow Coma Scale score, SBP is systolic blood pressure, RR is respiratory rate, and the subscript c denotes the coded value for the indicted parameter. Adapted from Champion HR, Copes WS, Sacco WJ, et al: Improved predictions from a severity characterization of trauma (ASCOT) over Trauma and Injury Severity Score (TRISS): Results of an independent evaluation. J Trauma 40:42-48, 1996.

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MANAGEMENT Airway Airway management must take into account the presence of cervical spine injury, full stomach, lack of patient cooperation, and anticipated difficult intubation. Use of blind nasal or direct laryngoscopy-assisted oral endotracheal intubation in a conscious patient requires topical anesthesia and possibly light IV sedation. Fiberoptic laryngoscopic or bronchoscopic techniques with topical anesthesia can also be used in awake or sedated patients, or the airway may be secured after IV rapid-sequence induction of general anesthesia. Table 206-3 lists common indications for endotracheal intubation in trauma patients. Indications for a surgical airway include failed intubation, an apneic patient with suspected cervical spine injury, facial trauma with suspected cervical spine injury, and severe facial and laryngeal trauma with altered anatomy.

Table 206–3

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Indications for Endotracheal Intubation in Trauma-Related Injury

Cardiac or respiratory arrest Airway obstruction or respiratory insufficiency Airway protection (e.g., head injury and Glasgow Coma Scale score 80 mm Hg) may lead to cardiovascular collapse Rare, but possible with V/Q mismatch, endobronchial intubation, gastric aspiration, or severe hypercarbia with low FiO2 Nausea and vomiting: 40%-70% of patients; about half require therapy Pain: due to diaphragmatic irritation

Arrhythmias Hypotension Hypercapnia Hypoxemia Postoperative

. . AV, atrioventricular; FiO2, fraction of inspired oxygen; V/Q , ventilation-perfusion.

cholecystectomy), may either accentuate or alleviate these respiratory and hemodynamic changes. Numerous complications are inherent in laparoscopic surgery, especially during abdominal trocar placement and CO2 insufflation (Table 207-3). Most common is the extraperitoneal insufflation of CO2 (incidence of 0.4% to 2%). Subcutaneous CO2 emphysema results from dissection of gas into tissue planes around the trocar site used for insufflation. This can extend into the mediastinum and to subcutaneous tissues. Gas under pressure may also be introduced into the pleural space via congenital pleural-peritoneal communications or an inadvertent diaphragmatic injury, creating simple or tension pneumothorax. Introduction of gas into the pericardial space creates a pneumopericardium that can mimic the clinical presentation of cardiac tamponade. Massive gas embolization is a catastrophic complication caused by the inadvertent injection of insufflating gas into a vessel or abdominal organ during the induction of the pneumoperitoneum. If the gas is injected into a vein, subsequent obstruction of the right ventricular outflow tract or pulmonary circulation may lead to cardiovascular collapse. The incidence of visceral embolization is 0.002% to 0.08%; however, vascular gas embolism can be detected in up to two thirds of all patients undergoing laparoscopic cholecystectomy if diagnostic transesophageal echocardiography is used. The lethal embolic dose of CO2 is five times greater than that estimated for air. Arrhythmias may occur. Tachyarrhythmias (sinus arrhythmias, atrial and supraventricular ectopic beats and tachycardias, ventricular ectopic beats, ventricular tachycardia or fibrillation) are related mainly to respiratory acidosis and the associated catecholamine surge. Bradyarrhythmias (sinus bradycardia, wandering atrial pacemaker, junctional rhythm, atrioventricular heart block, asystole) are likely vagally mediated or due to extreme hypercarbia and respiratory acidosis. The possibility of hypotension secondary to blood loss from accidental visceral and vascular injury exists and is complicated by the difficulty of achieving rapid control of a bleeding source. Although major vessels can be injured, the more common sites are the epigastric and iliac vessels.

Gastrointestinal perforation or hepatic and splenic tears have also been described. Modest or moderate hypercapnia is a nearly universal occurrence during laparoscopy; if it is severe (PaCO2 > 80 mm Hg), it may be associated with cardiovascular collapse. In contrast, hypoxemia is rare during laparoscopy. Isolated hypoxemia can occur, however, with significant ventilationperfusion mismatch, endobronchial intubation, aspiration, or severe hypercapnia in the setting of a low-normal fraction of inspired oxygen. Postoperative complications are usually benign. Nausea and vomiting occur in 40% to 70% of patients after laparoscopy; about half require antiemetic therapy. Postoperative pain due to diaphragmatic irritation is usually described as vague abdominal, neck, or shoulder discomfort.

Recognition Rapid changes in ventilatory and hemodynamic parameters are most likely to occur early in the laparoscopic procedure. They are caused by changes in body position and introduction of the Veress needle and gas insufflation. Close patient scrutiny and monitoring of vital signs (i.e., electrocardiogram, noninvasive blood pressure, pulse oximetry, capnography) are essential. Capnography is an invaluable diagnostic tool during laparoscopy because it may provide early warning signs of impending catastrophic events. Measurement of ETCO2 concentrations can define changes in pulmonary CO2 elimination, which is dependent on CO2 production, lung perfusion, and alveolar ventilation. The normal range for ETCO2 is 35 to 37 mm Hg. The gradient between CO2 concentration in arterial blood and ETCO2 is usually 5 to 6 mm Hg. However, in some patients, especially those with cardiopulmonary disease, an increased arterial-to-ETCO2 gradient reflects increased ventilation-perfusion mismatch and reduced cardiac output, both of which contribute to an increase in dead-space ventilation. Most patients require a 30% increase in minute ventilation to counter systemic absorption of insufflated CO2.

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Hypercapnia may cause respiratory acidosis (i.e., elevated PaCO2 and low pH). With severe hypercapnia, capnography may reveal spontaneous breathing. ETCO2 also increases with systemic CO2 absorption in the following situations: ● ●

● ● ● ●

A sudden decline in ETCO2 is usually due to obstruction of the airway or sampling tubing, extubation, circuit leak or disconnection, venous air or pulmonary embolism, low cardiac output, or cardiac arrest. Another cause is mainstem endobronchial intubation due to endotracheal tube migration during peritoneal CO2 insufflation, when the lungs are displaced cephalad by the CO2 pneumoperitoneum. To exclude this latter cause, lung auscultation should be performed higher on the chest wall. A sudden increase in peak inspiratory pressures should raise the suspicion for simple or tension pneumothorax. However, a more gradual, modest increase is expected with the reduced lung compliance and functional residual capacity (FRC) associated with pneumoperitoneum. Healthy patients tend to tolerate the reduced lung compliance and FRC with minimal consequences. Finally, increased capnographic plateau pressure is common with position-related, cephalad displacement of the diaphragm during CO2 insufflation. The value of more invasive monitoring has not been studied, but some advocate its use for obese, elderly, or debilitated patients. An arterial catheter allows continuous monitoring of blood pressure and repeated blood gas measurements. If a pulmonary artery catheter is used, filling pressures (central venous pressure and pulmonary capillary wedge pressure) tend to increase with pneumoperitoneum, regardless of actual venous return and cardiac filling pressures. Monitoring of cardiac output and mixed venous oxygen saturation is useful in patients with severe myocardial dysfunction. Transesophageal echocardiography is valuable for detecting hypovolemia, myocardial ischemia, ventricular dysfunction, worsened valvular regurgitation, and venous gas or pulmonary embolism.

Risk Assessment Mortality with laparoscopy is 0% to 0.13%. Most deaths are due to cardiac complications (25%). The rate of major intraoperative events is usually less than 2%. Vascular injury accounts for about one third of the associated morbidity. Relative contraindications to laparoscopic surgery include increased intracranial pressure, ventriculoperitoneal or peritoneal-jugular shunts, hypovolemia, congestive heart failure, severe cardiopulmonary disease, previous abdominal surgery with significant adhesions, morbid obesity, pregnancy, end-stage liver disease, and coagulopathies. Older and sicker patients with limited cardiac reserve or those at increased risk for ischemia or left ventricular failure might not

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tolerate the increase in systemic vascular resistance and left ventricular wall tension that accompanies pneumoperitoneum. Similarly, the deleterious respiratory effects of laparoscopy are predicted to be more severe in patients with preexisting lung disease with increased dead space, reduced compliance and FRC, or severe diffusion defects. Even large increases in minute ventilation in these patients may not be enough to normalize the arterial CO2 tension, and an already reduced FRC may decrease even further. This could lead to significant hypoxemia from atelectasis and intrapulmonary shunting. Bullous emphysema increases the risk for pneumothorax due to barotrauma. Preexisting pulmonary hypertension and right ventricular dysfunction may worsen owing to a CO2-mediated increase in pulmonary vascular resistance. The American College of Cardiology–American Heart Association algorithm for preoperative cardiac evaluation (discussed in Chapter 38) does not distinguish between laparoscopic and open abdominal surgery. However, some advocate echocardiography and spirometry in American Society of Anesthesiologists classes III and IV patients before laparoscopy. Forced expiratory volume less than 70% and diffusion capacity less than 80% are predictive of more severe hypercapnia during laparoscopy. In addition to comorbidities, the type of surgery determines the risk for complications. For example, the incidence of hypercarbia and subcutaneous emphysema are greater with retro- or extraperitoneal gas insufflation for laparoscopic inguinal hernia repair than with intraperitoneal insufflation for laparoscopic cholecystectomy. Patients undergoing laparoscopic Nissen fundoplication are at increased risk for pneumomediastinum, subcutaneous emphysema, and pneumothorax (1% to 5%). Also, they are more likely to have vagally mediated bradyarrhythmias.

Implications Laparoscopic surgery is considered a safe alternative to open procedures. Predictions are that up to 75% of all abdominal surgery will soon be performed endoscopically. Proven benefits of laparoscopic surgeries include smaller incisions, less intraoperative bleeding, shorter surgical times, and attenuation of the stress and inflammatory response accompanying open surgery. These factors lead to reduced postoperative analgesic requirements, improved pulmonary function, more timely ambulation, less ileus, faster recovery and discharge, increased patient satisfaction, and lower costs. Lung function appears to recover more quickly after laparoscopic surgery, FRC and vital capacity are much better preserved, diaphragmatic contractions are stronger, and hypoxemia is lessened. Consequently, laparoscopy is associated with a reduced incidence of postoperative atelectasis and pneumonia. However, physiologic changes due to peritoneal CO2 insufflation and patient positioning can cause significant reductions in blood pressure and cardiac output. If so, intraoperative management requires vigilance and skill on the part of the anesthesiologist. Any of the catastrophic events described earlier can place the patient in an acute lifethreatening situation. Experimental and clinical studies have found that intraoperative declines in the glomerular filtration rate and creatinine clearance during laparoscopy

OTHER SURGICAL SUBSPECIALTIES

●

Pneumoperitoneum Subcutaneous CO2 extravasation Hypermetabolic states (malignant hyperthermia, thyrotoxicosis) Low minute ventilation Metabolism of sodium bicarbonate Use of CO2-enriched gases Rebreathing of exhaled gases.

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quickly reverse. No relationship exists between urine output during surgery and the postoperative serum creatinine concentration. Less is known about the incidence of cardiac complications. However, because perioperative myocardial infarction usually occurs within 24 to 48 hours of surgery and appears to be related to the magnitude of surgical stress, myocardial infarction should be less common after laparoscopic surgery, but this remains unproven. Safety of laparoscopy in the critically ill has not been studied. Theoretical considerations suggest the need for extreme caution. Increased intracranial pressure associated with laparoscopy may be detrimental to patients with closed head injury. Also, patients with sepsis are often hypovolemic, which may exacerbate the decrease in venous return and cardiac output with laparoscopy. Also, critically ill patients commonly have reduced splanchnic perfusion, and laparoscopy may induce mesenteric ischemia. This increases the risk for bacterial translocation and septic complications. Most patients with symptomatic gallstones are candidates for laparoscopic cholecystectomy. Exceptions are those with generalized peritonitis, septic shock from cholangitis, severe acute pancreatitis, end-stage hepatic cirrhosis with portal hypertension, severe coagulopathy unresponsive to treatment, known cancer of the gallbladder, and cholecystoenteric fistulas.

MANAGEMENT Management for hemodynamic perturbations during laparoscopy is complicated because of competing goals. Whereas increased blood pressure may require vasodilators, one must keep in mind that venous return is usually reduced. Therefore, arterial-selective intravenous dilators (e.g., hydralazine, labetalol, nicardipine) are preferred over sodium nitroprusside or nitroglycerin. Tachycardia may prompt treatment with β-blockers, especially in patients at risk for myocardial ischemia. However, this may increase the patient’s susceptibility to bradycardia mediated by increased vagal tone. In patients with myocardial dysfunction, afterload reduction may mitigate the detrimental effect of pneumoperitoneum and increased PaCO2 to increase systemic vascular resistance, left ventricular wall tension, and cardiac output. Rarely, reduction of the insufflation pressure to 10 mm Hg and use of an inotropic agent will be required. If so, some form of cardiac output monitoring is advised at this stage, because it may be difficult to distinguish hypotension due to a reduction in myocardial contractility from that due to other pathophysiologic changes. Generous intravenous fluids must be given to overcome the decrease in venous return caused by positive intraabdominal pressure. Central filling pressures usually are not available to guide fluid therapy. If possible, reducing the degree of reverse Trendelenburg positioning is another way to ameliorate reduced venous return. Rarely, the laparoscopic approach must be abandoned in favor of an open procedure. Therapy for hypercapnia is to increase minute ventilation by increasing the respiratory rate. Rarely, a switch from CO2 to another gas for insufflation is required. This introduces a greater risk of gas emboli due to reduced blood solubility (helium) or explosions (if hydrogen and methane

are present because air, oxygen, and nitrous oxide support combustion). Hypercapnia, which is difficult to correct, should prompt a search for subcutaneous emphysema, which may serve as a large reservoir of CO2. Prolonged postoperative ventilation may be required until the emphysema has sufficiently resolved, which often takes 4 to 6 hours. Giving analgesics or sedatives to patients with respiratory compromise secondary to airway obstruction, chronic obstructive pulmonary disease, or diminished respiratory drive subjects them to an increased risk of respiratory arrest. Tension pneumothorax requires immediate needle aspiration at the second intercostal space in the midaxillary line. Further gas insufflation should be stopped, and the pneumoperitoneum temporarily released. With positive-pressure ventilation, the needle catheter should be left in place until the surgery is completed. Rarely is a chest tube needed, because any CO2 will be absorbed quickly. Serial postoperative chest radiographs are mandatory. Once venous gas embolism is diagnosed or suspected, gas insufflation should be stopped immediately, the pneumoperitoneum released, and the patient placed in a steep head-down position and right side up. This places the right ventricular outflow tract in a dependent position relative to the right atrium and may help release a gas lock to forward blood flow. Ventilation with 100% oxygen should be started, and pressors should be given for hemodynamic support as needed. Right heart catheterization with a multiorifice catheter and aspiration of gas bubbles can be attempted but is rarely effective. In extreme cases, cardiopulmonary bypass may be required for evacuation of gas emboli. The possibility of paradoxical emboli through a patent foramen ovale must always be kept in mind. Thus, the patient should be evaluated for neurologic changes when he or she is awake and able to follow commands.

PREVENTION Insufflation of CO2 to create pneumoperitoneum increases intra-abdominal pressure. This enhances venous stasis, reduces portal venous and renal arterial blood flow, and increases airway pressures. Collectively, these changes impair ventilatory and circulatory function. Intraoperative steps that can be taken to reduce these changes include the following: ● ●

● ●

●

Reducing insufflation pressures to 10 to 15 mm Hg Moderating the degree of Trendelenburg or reverse Trendelenburg positioning Adjusting ventilation to reduce hypercapnia and acidosis Using sequential, intermittent lower extremity compression devices to reduce venous stasis Volume loading to minimize impaired renal and myocardial perfusion

Pressure-controlled ventilation is used to reduce the risk of barotrauma in patients with greatly increased airway pressures. An oro- or nasogastric tube is inserted for gastric decompression. A urinary catheter decompresses the bladder and reduces the risk for injury. Precautions should be used during extreme postural positioning to reduce the risk of nerve injury (e.g., shoulder braces for the Trendelenburg position, foot boards for the reverse Trendelenburg position).

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“Gasless laparoscopy” (i.e., abdominal wall lifting devices rather than gas insufflation) might be considered for patients with significant cardiopulmonary derangements or at high risk for them. If this is not an option, a more practical approach is to limit the degree of Trendelenburg or reverse Trendelenburg positioning to attenuate any adverse physiologic effects.

Eagle KA, Berger PB, Calkins H, et al: ACC/AHA update for perioperative cardiovascular evaluation for noncardiac surgery. Circulation 105:1257-1267, 2002.

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Harris SN, Ballantyne GH, Luther MA, et al: Alterations of cardiovascular performance during laparoscopic colectomy: A combined hemodynamic and echocardiographic analysis. Anesth Analg 83:482-487, 1996. Leonard IE, Cunningham AJ: Anesthetic considerations for laparoscopic cholecystectomy. Best Pract Res Clin Anaesthesiol 16:1-20, 2002. Nguyen NT, Goldman CD, Ho HS, et al: Systemic stress response after laparoscopic and open gastric bypass. J Am Coll Surg 194:557-566, 2002. Struthers AD, Cuschieri A: Cardiovascular consequences of laparoscopic surgery. Lancet 352:568-570, 1998. Wahba RWM, Tessler MJ, Kleiman SJ: Acute ventilatory complications during laparoscopic upper abdominal surgery. Can J Anaesth 43: 77-83, 1996.

OTHER SURGICAL SUBSPECIALTIES

Further Reading

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Postoperative Urinary Retention D. Janet Pavlin Case Synopses Case 1 A 24-year-old man undergoes a 1-hour outpatient knee arthroscopy under spinal anesthesia with 10 mg bupivacaine. After 3.5 hours in the recovery room, he has voided 100 mL and is otherwise ready for discharge. Although the patient has experienced no pain or sense of fullness, a bladder scan reveals a postvoid residual volume of 700 mL. A diagnosis of urinary retention is made; the patient undergoes in-out catheterization for 700 mL of urine and is then discharged. The patient is able to void spontaneously 7 hours later at home, and no subsequent episodes of urinary retention occur. Case 2 A 45-year-old man undergoes drainage of a perirectal abscess under general anesthesia. The patient last voided 4 hours before surgery. He receives 1500 mL of fluid during surgery. In the recovery unit, he experiences considerable pain at the surgical site, for which he receives intravenous and oral opioid medication. He also reports a painfully distended bladder but is unable to void after 2 hours in the recovery unit. Inout bladder catheterization is performed, and 650 mL of urine is obtained. He is allowed to go home, but 14 hours later he returns to the emergency room with a painful distended bladder and inability to void. A bladder catheter is inserted, and 750 mL of urine is obtained. The patient is discharged with an indwelling catheter and returns 2 days later to have the catheter removed. He has no subsequent problems with voiding.

PROBLEM ANALYSIS Definition Urinary retention is defined as the inability to void in the presence of a full bladder. The normal adult bladder capacity is from 500 to 600 mL. Postoperative urinary retention is relatively common. Its frequency depends on the nature and location of surgery, type of anesthesia used, drugs given, and the patients’ underlying physiology and medical conditions. Knowledge of normal bladder function is a prerequisite to understanding how and why urinary retention occurs postoperatively. Voiding is neurally regulated and is normally a reflex response to a full bladder—known as the micturition reflex (Table 208-1). It requires bladder distention, followed by transmission of sensory input from the bladder to the midsacral region of the spinal cord, involuntary simultaneous contraction of the bladder, and reflex inhibition of the internal urethral sphincter. These must be coupled with voluntary relaxation of the external urethral sphincter. Visceral sensory afferents from the bladder travel primarily in the pelvic splanchnic nerves to synapse in the midsacral spinal cord (S2-S4), with projections to the 836

micturition center in the brain. The efferent limb of this reflex consists of the following: ●

Preganglionic parasympathetic fibers originating at S2-S4 travel in pelvic splanchnic nerves to peripheral cholinergic receptors within the bladder wall and stimulate bladder contraction during the active phase of voiding.

Table 208–1

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Neural Control of Voiding

Bladder distention Visceral afferent fibers via pelvic splanchnic nerves Synapse at the micturition center in the midsacral cord (S2-S4) Parasympathetic efferent cholinergic fibers (they arise at S2-S4, travel with the pelvic splanchnic nerves, synapse at cholinergic sites in the bladder wall, and then stimulate contraction) Sympathetic efferent fibers (they arise at T10-L2, travel via hypogastric plexuses to the internal urethral sphincter, and are involuntarily inhibited during voiding) Somatic efferent fibers (they travel via the pudendal nerve to striated muscle of the external urethral sphincter and are voluntarily relaxed during voiding) The entire reflex arc is subject to control by the pontine micturition center and higher centers in the brain via the spinobulbar tracts

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●

●

The micturition reflex is subject to modulation or control by higher brain centers, including the pontine micturition center (dorsolateral pons), areas of the diencephalon, and the cerebral cortex. Receptors in the spinal portion of the pathway are susceptible to modulation by opioids, acetylcholine, dopamine, serotonin, norepinephrine, GABA, excitatory and inhibitory amino acids, and other neuropeptides. Urinary retention can occur due to interruption of the micturition reflex at any point in the circuit. Spinal or epidural anesthesia interferes with the afferent and efferent limbs of the reflex. Opioids and anticholinergics may block transmission at cholinergic sites in the bladder wall or in the spinal cord. Increased sympathetic activity, due to pain in a lumbosacral nerve distribution or overdistention of the bladder itself, may interfere with reflex inhibition of sympathetic tone to the internal urethral sphincter. Inability to void may also result from failure to coordinate bladder contraction with sphincter relaxation (dyssynergia) as a result of disease or dysfunction of the spinal cord. Additionally, retention may be the result of obstruction to outflow at the level of the urethra due to prostatic disease or other acute or chronic conditions affecting urethral patency. Various other factors may act through cortical or subcortical mechanisms to inhibit the ability to void, including fear, embarrassment, and possibly recumbency.

Recognition Urinary retention may be painful or painless. Neuraxial blocks, analgesics, or sedation may prevent pain related to bladder overdistention. Although a high index of suspicion, palpation, and percussion can sometimes detect an overdistended bladder, this is often not possible or is unreliable. Both the duration of surgery and the amount of intraoperative fluids given significantly correlate with bladder volume at the end of surgery. Yet these relationships are variable and of limited value for diagnosing or predicting bladder volume in individual patients. In unconscious patients, a portable ultrasound scan may be the only practical, reliable, noninvasive means of diagnosing urinary retention and bladder overdistention. In one study, the correlation between surgery duration and urinary bladder volume after surgery was 0.32 (P =.0002). The correlation between intraoperative intravenous fluid volumes and urinary bladder volume was 0.26 (P =.0021). Also, ultrasound-determined bladder volumes correlated with measured volumes (r = 0.9; P 3 to 10 hours),

Table 208–2

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Risk Factors for Urinary Retention

Neuraxial local anesthetics Neuraxial or systemic opioid therapy Anticholinergics Urethral outlet obstruction Surgery of the lower urinary tract or surrounding area Surgery in a lumbosacral nerve distribution area (groin, perirectal, penile) Previous history of retention Spinal cord disease or dysfunction Recumbency Excessive fluid administration

OTHER SURGICAL SUBSPECIALTIES

Sympathetic efferent fibers originating from T10 to L2 travel via the superior and inferior hypogastric plexuses to the internal urethral sphincter. Their output maintains sphincter tone during continence and is reflex-inhibited during voiding. Somatic efferent fibers course in the pudendal nerves to the striated muscle of the external urthethral sphincter, which must be voluntarily relaxed during voiding.

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urothelial cell damage, hemorrhage, and edema may occur. This is followed by parasympathetic nerve ending loss, reduced parasympathetic activity, and failure of the detrusor muscle to contract normally. Functional effects of impaired parasympathetic activity include inability to empty the bladder fully, leading to frequent small voidings (frequency, nocturia), weak stream, hesitancy, dribbling, and bladder instability. If sustained, urinary stasis can lead to urosepsis. Most often, cellular regeneration occurs over several weeks, with gradual recovery of normal bladder function. However, intercellular junction rupture and interstitial collagen deposition can occur. This leads to permanent impairment of impulse transmission throughout the bladder wall and may require operative intervention (e.g., MarshallMarchetti-Krantz bladder suspension or creation of an ileal conduit).

MANAGEMENT Postoperative urinary retention typically results from overfilling of the bladder when the micturition reflex is impaired by anesthesia or surgery. Because this is usually temporary, some episodes of retention can be prevented simply by ensuring that the patient has an empty bladder immediately before surgery and by avoiding excessive fluid administration during surgery. This is particularly relevant when either the surgery or the anesthetic is known to predispose to urinary retention or when there is a history of urinary retention. Given that the normal rate of urine formation is about 75 mL/hour (adults), the time required to attain a full bladder (600 mL) is roughly 8 hours. Based on animal investigations, the critical duration for bladder overdistention to avoid potential nerve injury is 4 hours. Thus, clinicians can assume that it is undesirable to have an overdistended bladder for longer than 4 hours. Table 208-3 shows the estimated time required to attain a bladder volume that exceeds 600 mL for 4 hours (i.e., theoretical critical duration), assuming a rate of urine formation of either 50 or 100 mL/hour. Assuming an empty bladder at the outset, the critical time would be 10 hours at a rate of 100 mL/hour and 16 hours at a rate of 50 mL/hour. However, if the initial volume was 400 mL, the critical times

Table 208–3

■

Starting Residual Bladder Volume (mL) 0 100 200 400 600

Predicted Time to Achieve Critical Bladder Volume Time (hr) to Achieve > 600 mL for > 4 Hours Urine Formation at 50 mL/hr 16 14 12 8 4

Urine Formation at 100 mL/hr 10 9 8 6 4

would be 6 and 8 hours, respectively. Thus, to avoid complications related to postoperative retention, the following steps are prudent: ● ●

●

Ensure that all patients void before surgery. Ensure that postoperative patients void or are catheterized within approximately 8 to 10 hours of their last voiding. Use an indwelling urinary catheter for procedures expected to last longer than 5 to 6 hours, assuming that the patient will be unable to void until 1 to 2 hours after surgery.

PREVENTION If a patient has not voided within 6 to 8 hours of his or her last voiding, the bladder volume should be assessed before the patient leaves the recovery room. Bladder volume can be determined noninvasively by ultrasonography. The bladder should be drained if the volume is more than 600 mL. Alternatively, if a scanner is not available, bladder volume can be assessed by palpation and the bladder emptied by inout catheter drainage. This is especially important in patients with known risk factors for postoperative urinary retention (see Table 208-2). One recent study noted a 24% incidence of urinary retention in patients arriving in the recovery room after various surgeries performed without an indwelling bladder catheter. For outpatient surgery, a decision must be made whether patients should be required to void before discharge. At least two studies suggest that patients with no underlying risk factors for urinary retention should be allowed to go home without voiding before discharge. In such patients, the incidence of urinary retention was less than 1%. In patients with risk factors for urinary retention, it is prudent to require them to void before discharge. This avoids a persistently overdistended bladder if a patient fails to seek medical attention for this problem in a timely manner. Thus, patients having rectal, groin, or urologic surgery and those with spinal cord disease or a history of urinary retention should be required to void or be catheterized before discharge. After spinal or epidural anesthesia, patients should be required to void or be catheterized, with some possible exceptions. Patients who have had neuraxial blocks with short-acting local anesthetics (≤50 mg lidocaine without vasopressors, or 2-chloroprocaine) can safely be discharged without voiding if a bladder scan reveals a bladder volume of less than 400 mL at the time of discharge. Owing to the short duration of action of these two agents, it is almost certain that any residual effects of the local anesthetic will resolve before a “critical volume” is exceeded for longer than 4 hours. However, bupivacaine blocks have been associated with impaired voiding for longer than 10 hours. Patients who have received this anesthetic or other similarly long-acting local anesthetics should not be discharged without voiding or having catheter drainage of the bladder. Ideally, high-risk patients who do void should have the postvoid residual volume checked to ensure that the bladder is empty. In many cases, voiding by straining results in the expulsion of a small quantity of urine, but the residual volume may still exceed 400 to 600 mL, and the micturition reflex may not have recovered. This is best evaluated with an

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Further Reading Azadzoi KM, Pontari M, Vlachiotis JU, Siroky MB: Canine bladder blood flow and oxygenation: Changes induced by filling, contraction and outlet obstruction. J Urol 155:1459-1465, 1996. DeGroat WC, Yoshimura N: Pharmacology of the lower urinary tract. Ann Rev Pharmacol Toxicol 41:691-721, 2001.

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Kamphuis ET, Ionescu TI, Kuipers PWG, et al: Recovery of storage and emptying functions of the urinary bladder after spinal anesthesia with lidocaine and with bupivacaine in men. Anesthesiology 88:310-316, 1998. Lamonerie L, Marret E, Deleuze A, et al: Prevalence of postoperative bladder distension and urinary retention detected by ultrasound measurement. Br J Anaesth 92:544-546, 2004. Lasanen LT, Tammela TL, Kallioinen M, et al: Effect of acute distension on cholinergic innervation of the rat urinary bladder. Urol Res 20:59-62, 1992. Lloyd-Davies RW, Clark AE, Prout WG, et al: The effects of stretching the rabbit bladder. Invest Urol 8:145-152, 1980. Mulroy MF, Salinas FV, Larkin KL, et al: Ambulatory surgery patients may be discharged before voiding after short-acting spinal and epidural anesthesia. Anesthesiology 97:315-319, 2002. Pavlin DJ, Pavlin EG, Fitzgibbon DR, et al: Management of bladder function after outpatient surgery. Anesthesiology 91:42-50, 1999. Pavlin DJ, Pavlin EG, Gunn HC, et al: Voiding in patients managed with or without ultrasound monitoring of bladder volume after outpatient surgery. Anesth Analg 89:90-97, 1999.

OTHER SURGICAL SUBSPECIALTIES

ultrasound scan. If this is unavailable, one can reasonably suspect that there is a high postvoid residual volume (>400 mL) if the patient has voided less than 300 mL. If so, patients should be requested to stay until they have voided again and fully emptied the bladder. Alternatively, the bladder can be drained by in-out catheterization to ensure that it is empty before discharge. Finally, all patients, whether at high or low risk, should be instructed to return to a medical facility if they are unable to void within 8 to 10 hours of discharge from the hospital.

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Terri G. Monk Case Synopsis A 50-year-old man is scheduled for a transurethral resection of the prostate. After premedication with 2 mg midazolam given intravenously, a hyperbaric spinal anesthetic is placed, and a T6 sensory level is achieved. During placement of the resectoscope sheath, a full erection occurs, preventing free movement and control of the scope. The bladder is emptied and the resectoscope is removed, but the erection persists. The surgeon states that the erection prevents him from continuing with the procedure and asks the anesthesiologist to treat it.

PROBLEM ANALYSIS Definition Priapism is the persistence of a penile erection for longer than 4 to 6 hours, unaccompanied by sexual excitement or desire. Priapism can be classified as primary (idiopathic) or secondary (Table 209-1). Primary priapism is the result of physical or psychological stimuli unaccompanied by a disease state that could cause or sustain an erection. Secondary priapism is the result of factors that directly or indirectly affect penile erectile reactivity.

Recognition Intraoperative penile erections under anesthesia can be classified as primary priapism and generally occur during scrub preparation of the genitalia, Foley catheter insertion, or transurethral procedures. Erections under anesthesia are

Table 209–1

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Causes of Priapism

Primary (Idiopathic) Causes Physical or psychological stimuli Intraoperative tactile stimulation

Secondary Causes Neurogenic Thromboembolic Sickle cell disease Leukemia Malignant penile infiltration Medications Antihypertensive agents Phenothiazines Antidepressants Alcohol Marijuana Miscellaneous causes Genital trauma Self-injection therapy for impotence Coagulopathy

840

generally of shorter duration than other forms of priapism and may not persist long enough to be considered true priapism. The exact mechanism for penile erection is poorly understood, but it may result from a complex combination of psychological, neuroendocrine, and vascular factors acting on penile erectile tissues. Parasympathetic penile innervation is from the sacral (S2-S4) spinal cord segments via the nervi erigentes. When the penis is flaccid, high sympathetic tone increases intrinsic muscle tone in the arterioles, thereby reducing blood flow to the corpora cavernosa. At the same time, venules draining the corpora cavernosa remain open. For an erection to occur, parasympathetic impulses dilate the arterioles, allowing more blood flow into the corpora cavernosa; simultaneously, there is partial occlusion of venous outflow. Detumescence occurs when this cycle is reversed. Vasoactive mediators, including nitric oxide, vasopressin, and bradykinin, also affect the state of penile tumescence. Persistent tumescence, or priapism, results from failure of the mechanisms of detumescence, including blockage of venous drainage, excessive release of neurotransmitters, paralysis of the intrinsic detumescence mechanism, or prolonged relaxation of the intracavernosal smooth muscles. Blood continues to accumulate in the cavernosal sinusoids, and if the erection persists for more than 6 hours, it may become painful.

Risk Assessment Intraoperative penile erection is reported to occur in approximately 2.4% of male patients undergoing surgery. The incidence of erection varies according to age, with a frequency of 8% in male patients younger than 50 years and 0.9% in older patients. Penile stimulation during preparation and instrumentation may result in penile erection even in the presence of general or regional anesthesia. The incidence appears to be similar for general (3.5%) and epidural (3.8%) anesthesia, but it is lower with spinal anesthesia (0.3%). Foley catheterization has been reported to produce penile erection in approximately 1% of male patients undergoing cardiac surgery with general anesthesia.

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Chapter 209

Implications

MANAGEMENT Numerous modes of therapy have been suggested for the treatment of intraoperative penile erection (Table 209-2). At the first sign of penile tumescence, all genital stimulation, including surgical preparation, urethral manipulation, and Foley catheter insertion, should be terminated immediately. If a cystoscope is in place, it must be removed, if possible. Because intraoperative erections often occur early in the procedure during “light” anesthesia, the anesthetic level should be deepened. If a spinal or epidural anesthetic is used, adequate blockade of the sacral segments should be ensured. In the lithotomy position, the scrotum hangs below the anus in a male patient when the sacral segments are blocked. If conservative treatment fails to produce detumescence, prompt intervention is necessary. Ethyl chloride spray to the penis or a dorsal penile nerve block can be used to suppress sensory input to the penis, thereby interrupting the sacral reflex arc that is maintaining the erection. A multitude of pharmacologic agents have been used to treat prolonged erections, but it is unlikely that any single agent will be effective in all cases. The use of intracorporal sympathomimetic agents is most commonly reported in the urologic literature. Owing to the high vascularity of this area, the uptake of these medications occurs rapidly, and systemic cardiovascular effects are common. Some of the more commonly used agents are discussed here. Phenylephrine, a pure α1-adrenergic agonist, has been given intracavernosally in doses of 100 to 200 μg. The success rate with this technique is reportedly 100% by 2 to

Table 209–2

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Treatment for Intraoperative Penile Erection

Termination of tactile stimulation of genital area Assurance of adequate anesthetic depth Ethyl chloride spray to penis Dorsal penile nerve block Intracavernosal drug injection Intravenous pharmacologic agents Ketamine Vasodilators Vasoconstrictors Terbutaline Anticholinergic agents

Intraoperative Penile Erection

841

3 minutes. Although this treatment may be associated with an intermittent rise in mean blood pressure, no untoward cardiovascular events are associated with its use. Some reports suggest that metaraminol is a preferred medication for intracavernosal injection, with doses as low as 10 to 25 μg producing detumescence without untoward cardiovascular effects. However, others caution against the use of metaraminol, norepinephrine, and epinephrine because all these drugs have at least some β1 activity, with the potential for β1-mediated adverse cardiovascular events. Ketamine, a dissociative anesthetic agent, is given intravenously in doses of 0.5 to 1.8 mg/kg, based on the assumption that the erection has occurred in response to external stimuli, and the drug’s dissociative effect on the limbic system might block this response. Ketamine may also exert its penilerelaxing effect by decreasing central vagal outflow, blocking reuptake of norepinephrine at the neuroeffector junction in cavernosal erectile tissues, or blocking transmission through parasympathetic ganglia. When using ketamine, it is important to remember that this drug has sympathomimetic actions and must be used with caution in elderly patients and those with significant cardiovascular disease. Vasodilators, such as inhaled amyl nitrite (one inhalant capsule of 0.3 mL emptied into the reservoir breathing bag) or intravenous nitroprusside, relax the corpora cavernosa venous drainage sites and produce a rapid fall in blood pressure. This leads to compensatory reflex sympathetic discharge, which may mimic the sympathetic discharge that occurs during orgasm, precipitating arteriolar constriction to terminate the erection. Vasodilating agents should be avoided in patients with a regional block because of the danger of inducing severe hypotension. They are also contraindicated in patients with increased intraocular or intracranial pressure. Terbutaline (0.2 to 0.5 mg intravenously), a β2adrenoreceptor agonist, has been used successfully to manage intraoperative penile erection. The action of this agent is unclear, but it is thought that terbutaline relaxes the stretched corporal smooth muscles, thereby releasing the impediment to venous blood flow from the penis. Terbutaline must be used with caution in patients with significant coronary artery disease because it can cause tachycardia, pulmonary edema, or hypokalemia. Anticholinergics may cause detumescence by blocking the effect of acetylcholine on the nitric oxide system. Of these medications, glycopyrrolate is preferred over atropine or scopolamine because it causes less tachycardia and lacks central nervous system effects.

PREVENTION Intraoperative penile erections can occur with any type of anesthesia, but the incidence is lowest with spinal blockade, probably because this technique provides the most profound sensory block of the sacral area. Thus, the administration of a spinal block for transurethral procedures should prevent most episodes of intraoperative tumescence. Whatever type of anesthesia is used, genital skin preparation and urethral manipulation should be delayed until an adequate level of anesthesia is present, because intraoperative erections are generally caused by tactile stimulation of the genital area.

OTHER SURGICAL SUBSPECIALTIES

An intraoperative penile erection may delay or even necessitate the cancellation of planned surgery. It can make passing or manipulating a cystoscope nearly impossible. Difficulty with transurethral cystoscope passage can also traumatize the urethra, predisposing to postoperative stricture formation. Aggressive therapy for intraoperative penile erection is necessary to prevent other long-term sequelae, including fibrosis and thrombosis. During penile surgery requiring an incision, penile tumescence can increase intraoperative bleeding. If an intraoperative erection is unresponsive to treatment, the procedure should be postponed.

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During regional anesthesia, it is especially important to ensure that sensory blockade of the sacral area is present before proceeding. Anesthetic agents associated with an increased incidence of erections during general anesthesia include fentanyl, propofol, and droperidol, but there is no conclusive evidence that avoidance of a particular anesthetic agent will prevent this problem.

Further Reading Kouriefs C, Watkin NA: What to do if it gets “bigger.” Ann R Coll Surg Engl 85:126-128, 2003. Lue TF: Physiology of erection and pathophysiology of impotence. In Walsh PC, Retik AB, Stamey TA, et al (eds): Campbell’s Urology, 6th ed. Philadelphia, WB Saunders, 1992, pp 709-728.

Roy R: Cardiovascular effects of ketamine given to relieve penile turgescence after high doses of fentanyl. Anesthesiology 61:610-613, 1984. Seftel AD, Resnick MI, Boswell MV: Dorsal nerve block for management of intraoperative penile erection. J Urol 151:394-395, 1994. Shantha TR, Finnerty DP, Rodriquez AP: Treatment of persistent penile erection and priapism using terbutaline. J Urol 141:1427-1429, 1989. Staerman F, Nouri M, Coeurdacier P, et al: Treatment of the intraoperative penile erection with intracavernous phenylephrine. J Urol 153: 1478-1481, 1995. Tsai SK, Hong CY: Intracavernosal metaraminol for treatment of intraoperative penile erection. Postgrad Med J 66:831, 1990. Valley MA, Sang CN: Use of glycopyrrolate to treat intraoperative penile erection. Reg Anesth 19:423-428, 1994. van Arsdalen KN, Chen JW, Smith MJV: Penile erections complicating transurethral surgery. J Urol 129:374-376, 1983.

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210

Vinod Malhotra and Vijayendra Sudheendra OTHER SURGICAL SUBSPECIALTIES

Case Synopsis An otherwise healthy 70-year-old man undergoes combined transurethral resection of the prostate (TURP) and transurethral resection of a bladder tumor (TURB) under spinal anesthesia with sedation. His blood pressure is 130/90 mm Hg, heart rate is 68 beats per minute, respirations are 16 breaths per minute, and hematocrit is 38%. Ninety minutes into surgery, the patient becomes restless. His blood pressure is 180/100 mm Hg, and his heart rate is 40 beats per minute. The electrocardiogram (ECG) shows depressed T waves. Laboratory values are as follows: hematocrit 27%, sodium 23 mEq/L, potassium 3.0 mEq/L, and chloride 95 mEq/L.

Recognition

PROBLEM ANALYSIS Definition TURP syndrome is a general term used to describe a wide range of neurologic and cardiopulmonary symptoms and signs caused by intravascular absorption of hypotonic bladder-irrigating fluids during transurethral procedures, especially TURP. In conscious or sedated patients, the sudden onset of restlessness should raise the suspicion for TURP syndrome. Hypertension is indicative of hypervolemia. Reflex bradycardia occurs in response to the increased blood pressure. T-wave depression on the ECG is caused by glycine in the irrigating fluid. Hyponatremia is yet another sign of hypotonic irrigant absorption (Table 210-1). A reduced hematocrit is most likely due to a combination of blood loss and hemodilution. Bradycardia may also occur after bladder perforation. In this case, bradycardia is an efferent vagal response to peritoneal stimulation secondary to any extravasated fluid. Abdominal or shoulder pain and hypotension usually accompany the bradycardia.

The case synopsis illustrates three significant complications of transurethral surgery: (1) TURP syndrome, (2) severe hemorrhage, and (3) bladder perforation. TURP SYNDROME TURP syndrome is a constellation of signs and symptoms that result from the following circumstances or conditions: ● ● ● ● ● ● ●

Circulatory overload Water intoxication or hypo-osmolality Hyponatremia Glycine toxicity Ammonia toxicity Hemolysis Coagulopathy

These signs and symptoms may occur simultaneously (Table 210-2). The clinical presentation may be further complicated by bacteremia or septicemia, which causes chills, hypotension, and tachycardia or bradycardia. SEVERE HEMORRHAGE

Table 210–1

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Hypotonic Irrigants Used for Transurethral Resection of the Prostate or a Bladder Tumor

Solution Water Glucose, 2.5% Sorbitol, 3.5% Urea, 1% Glycine, 1.2% Cytal (sorbitol 2.7% and mannitol 0.54%) Glycine, 1.5% Mannitol, 5%

Osmolality (mOsm/kg) 0 139 165 167 175 178 220 275

Severe hemorrhage is usually evident as surgical bleeding, although it is difficult to measure because blood is mixed with copious amounts of irrigating fluid. Occult internal bleeding may occur if bladder perforation has occurred. Clinical signs of excessive bleeding include hypotension and reflex tachycardia. However, tachycardia may not occur in the presence of age-related sinus node dysfunction or with the use of β-blockers or high spinal anesthesia. BLADDER PERFORATION Bladder perforation is difficult to recognize during general anesthesia. Hypotension and bradycardia or tachycardia may occur, but these are nonspecific findings. An experienced surgeon, however, usually recognizes a bladder perforation immediately. With spinal anesthesia, the complaint of abdominal or shoulder pain is helpful in making the diagnosis. 843

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Table 210–2

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Pathophysiology and Clinical Features of TURP Syndrome

Pathophysiology

Clinical Features

Fluid overload

Hypertension; bradycardia; arrhythmia; angina; pulmonary edema and hypoxemia; ventricular failure and hypotension Confusion and restlessness; twitching or seizures; lethargy or coma; dilated, sluggish pupils; papilledema; low-voltage EEG; hemolysis CNS changes as above; reduced inotropy; widened QRS complex; low-voltage ECG; T-wave inversion on ECG Nausea and vomiting; headache; transient blindness; loss of light and accommodation reflexes (blink reflex preserved); myocardial depression; ECG changes Nausea and vomiting; CNS depression Anemia; acute renal failure; chills, clammy skin; chest tightness and bronchospasm; hyperkalemia resulting in malignant arrhythmias or bradyasystole Severe bleeding; primary fibrinolysis; disseminated intravascular coagulation

Water intoxication or hypo-osmolality Hyponatremia Glycine toxicity Ammonia toxicity Hemolysis Coagulopathy

CNS, central nervous system; ECG, electrocardiogram; EEG, electroencephalogram; TURP, transurethral resection of the prostate gland.

Risk Assessment Approximately 400,000 TURP procedures are performed annually in the United States. About 10% of men older than 65 years require TURP. The incidence increases to 20% to 30% for men older than 80 years. Seventy-seven percent of patients undergoing TURP have one or more of the following conditions or factors: ● ● ● ● ●

Heart disease Hypertension Diabetes Chronic obstructive pulmonary disease History of smoking

Perioperative morbidity is related to associated disease, age, and sepsis. Morbidity is increased in blacks and in patients to whom the following factors apply: ● ● ● ●

Resection time longer than 90 minutes Prostate weighing more than 45 g Acute urinary retention Age greater than 80 years

The amount of absorbed irrigating fluid is influenced by the following factors: ● ● ● ● ●

Resection time Prostate gland size Hydrostatic pressure of the irrigating fluid Number and size of venous sinuses opened Whether the prostatic capsule is intact

Chronic inflammation, repeated instrumentation, and indwelling Foley catheters increase prostatic vascular congestion and predispose to increased bleeding and bacteremia during TURP. Prolonged resection of a large prostate allows for significant release of plasminogen activators from prostatic tissue into the bloodstream. This can cause primary fibrinolysis. Prostatic tissue and multiple microthrombi may also enter the circulation, leading to disseminated intravascular coagulation (DIC). Bladder perforation occurs in up to 1% of cases. A higher likelihood of bladder perforation is expected if the bladder

tumor is sessile versus pedunculated, is large and fragile, or infiltrates the bladder wall. A bladder wall that is chronically inflamed, previously irradiated, or thin and stretched is more prone to perforation. The likelihood of perforation is further increased if the tumor is difficult to access, bleeding obscures the surgeon’s vision, the patient unexpectedly moves or coughs, or instrumentation is difficult or traumatic.

Implications Overall mortality of TURP is 0.2% to 0.8%. Perioperative morbidity ranges from 7% to 20%. Most mortality and morbidity occur in patients who develop complications of TURP, including TURP syndrome, bladder perforation, or sepsis. In 15% of patients, bacteremia occurs. Of these, 6% to 7% develop septicemia, which is associated with 25% to 75% mortality. Because the consequences of these complications are severe, aggressive management is required.

MANAGEMENT TURP Syndrome Immediate aggressive therapy is essential if the patient is to survive. The following measures are suggested: ● ● ●

●

●

Terminate the surgery as soon as possible. Administer 20 mg of intravenous (IV) furosemide. Immediately obtain the following laboratory tests: hematocrit; serum electrolyte, creatinine, and glucose concentrations; serum osmolality (if available); arterial blood gas analyses; and 12-lead ECG. Continue or start the administration of normal saline. Hypertonic saline (3% or 5%) may be administered (at a rate 30%) has been linked to postoperative pulmonary toxicity, the relationship is controversial. A retrospective study found that intravenous (IV) fluid management, especially red blood cell transfusion, was the most significant factor associated with postoperative respiratory failure. It is now recommended that IV fluid administration consist primarily of colloids and be limited to the minimum volume necessary to maintain hemodynamic stability and renal perfusion. CIRCULATORY ABNORMALITIES Hypotension and tachycardia can occur with acute hemorrhage during any of the radical urologic procedures. During radical nephrectomy, it is also common to see an acute decrease in blood pressure when the kidney rest is elevated during positioning. In 5% to 10% of patients undergoing radical nephrectomy, the tumor extends into the inferior vena cava and right atrium. With or without such extension, tumor may embolize into the proximal vena cava, right atrium, and pulmonary artery during the procedure to impede right heart outflow, reduce venous return to the left

heart, and compromise systemic circulatory dynamics. If the tumor occludes the vena cava or right atrium, it can block right heart output and cause acute cardiovascular collapse. Cardiopulmonary bypass may be required to prevent tumor embolization during surgery in patients at high risk for such adverse cardiovascular events. AIR EMBOLISM With either the Trendelenburg or the kidney position, the surgical field is above the level of the heart, creating a negative pressure gradient between the wound and the heart. Air embolism can occur if Santorini’s venous plexus (see Fig. 211-1) is opened while the patient is in a headdown position during radical prostatectomy or cystoprostatectomy or if the vena cava is entered during radical nephrectomy. The most sensitive monitors for the detection of air embolism are transesophageal echocardiography and precordial Doppler. However, these are rarely used during urologic surgery. There may be a decrease in end-tidal carbon dioxide or an increase in end-tidal nitrogen with significant air embolism. Physical findings consistent with air embolism include sudden hypotension, hypoxemia, arrhythmia, and the presence of a mill-wheel murmur. If a large embolism creates an airlock that blocks outflow from the right side of the heart, cardiovascular collapse will occur. NERVE INJURY Damage to the obturator nerve can occur due to retractor placement or transection during pelvic lymph node dissection in radical retropubic prostatectomy or cystectomy.

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During perineal prostatectomy, the exaggerated lithotomy position is used, and damage to the brachial plexus can occur if shoulder braces are improperly placed. Injury to the brachial plexus is also possible during surgery performed in the kidney position if the lower shoulder and upper arm remain directly under the rib cage. Peripheral nerve injury is discussed in Chapter 221.

usually occurs within 6 weeks. However, if the nerve is severed or the injury is severe, permanent sensory and motor deficits could occur, or recovery might take months. Deep venous thrombosis and pulmonary embolism are frequent postoperative complications following radical pelvic surgery, and they may be fatal if diagnosis and treatment are delayed.

THROMBOEMBOLISM

MANAGEMENT

Patients undergoing radical pelvic surgery, particularly radical prostatectomy and radical cystectomy, are at high risk for developing pelvic and deep venous thrombosis. Pulmonary emboli are reported in up to 5% of patients; however, the incidence varies with the sensitivity of the diagnostic test chosen to detect thromboembolism. During resection of renal tumors, there is a high risk for tumor embolism to the lungs, especially when the tumor extends into the vena cava. Thromboembolism is discussed further in Chapters 89 and 216.

Hemorrhage

Risk Assessment HEMORRHAGE During radical prostatectomy and cystoprostatectomy, severe hemorrhage is more likely in patients who have had previous transurethral prostate resection or multiple prostatic biopsies. This is because the dorsal venous complex can become adherent to the anterior surface of the prostate. A large prostate gland and prior pelvic irradiation or surgery are also associated with increased operative blood loss. In patients undergoing radical nephrectomy, the risk of hemorrhage or tumor embolism is greatly increased if the tumor invades the inferior vena cava or extends into the right atrium. RESPIRATORY ABNORMALITIES The risk of surgically induced pneumothorax during radical nephrectomy is increased with a large kidney, thoracic approach, or resection of the 12th rib for better exposure. NERVE INJURY Peripheral nerve injuries are common if improper positioning results in compression or stretching of a nerve. Overzealous surgical manipulation or retraction may traumatize nerves. Patients with preexisting diseases such as diabetes mellitus, hypertension, and arteriosclerosis are more prone to peripheral nerve injury. THROMBOEMBOLISM Thromboembolic events are common in all patients undergoing radical pelvic surgery for carcinoma.

Implications Hemorrhage and air embolism can result in cardiovascular collapse and death if they are not detected and treated promptly. Position-related nerve injuries are often neurapraxic; that is, localized myelin degeneration may occur at the injury site, but without axonal degeneration. Therefore, recovery

Extensive blood loss is anticipated in all radical urologic procedures. In high-risk or elderly patients, direct arterial blood pressure and central venous monitoring may facilitate early recognition and treatment of acute blood loss, and several large-bore catheters should be placed for venous access. Persistent bleeding can be managed by temporary packing if surgical efforts must be directed elsewhere. Hemorrhage must be treated promptly with blood products, volume expansion, and vasopressors as needed to maintain cardiac filling and systemic perfusion.

Respiratory Abnormalities Respiratory alterations and work of breathing are best managed with endotracheal intubation and controlled positivepressure ventilation during the perioperative period. Small pleural injuries during radical nephrectomy can be repaired surgically. A chest tube is required to treat a tension pneumothorax of 10% or greater.

Air Embolism If air embolism occurs, the patient is ventilated with 100% oxygen. If cardiovascular collapse ensues, cardiopulmonary resuscitation is instituted immediately, and the patient is placed in the head-down, left lateral decubitus position to allow air trapped in the pulmonary outflow tract to float back into the right side of the heart. Aspiration of air from the right side of the heart may be attempted if a central line is in place.

Nerve Injury An initial neurologic examination is performed to document the extent of all peripheral nerve injuries. Nerve injuries that persist for longer than 2 weeks after surgery should be evaluated with electromyography and nerve conduction studies.

Thromboembolism Pulmonary embolism is treated with systemic anticoagulation using a continuous heparin infusion as soon as surgical bleeding is controlled. Heparin is continued for 7 to 10 days while oral anticoagulation therapy is initiated. Anticoagulation therapy should be continued for 3 months postoperatively.

PREVENTION Measures to prevent complications of radical urologic surgery are summarized in Table 211-1.

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Table 211–1

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Prevention of Complications of Radical Urologic Surgery

Hemorrhage Meticulous surgical technique

Respiratory Abnormalities

Nerve Injury Padding of pressure points Pillows under feet, ankles, and knees Padding between operating table and rib cage* Avoidance of shoulder braces

Thromboembolism Compression stockings Early ambulation *In the lateral decubitus position, padding prevents compression of nerves and blood vessels in the axilla.

Complications of Radical Urologic Surgery

849

be routinely placed under the feet, ankles, and knees. If the lateral kidney position is used, a small pad should be placed between the operating table and the dependent thorax to prevent brachial plexus injury. Shoulder braces are usually not necessary, except with the extreme lithotomy position. If this position is required, care must be taken to place the shoulder braces over the acromial processes to prevent brachial plexus injury.

Thromboembolism For operations on a right-sided renal tumor in the lateral kidney position, placing the patient in a steep Trendelenburg position should help prevent fatal air embolism, because air entering the vena cava cannot easily pass to the heart. Compression stockings should be used intraoperatively, and patients should ambulate on the first postoperative day to prevent thromboembolic events.

Further Reading Hemorrhage Intraoperative bleeding is minimized during radical urologic surgery by meticulous attention to surgical technique.

Respiratory Abnormalities Endotracheal intubation and positive-pressure ventilation help reduce the risk of ventilatory abnormalities. Periodic auscultation of the lungs after positioning the patient and during the surgical procedure can verify optimal pulmonary ventilation.

Nerve Injury All pressure points should be padded, and the patient should be moved with care during positioning and transport. Foam should be used under bony prominences, and pillows should

Malhotra V, Sudheendra V, Diwan S: Anesthesia and the renal and genitourinary systems. In Miller RD (ed): Miller’s Anesthesia, 6th ed. Philadelphia, Churchill Livingstone, 2005, pp 2175-2207. Monk TG: Cancer of the prostate and radical prostatectomy. In Malhotra V (ed): Anesthesia for Renal and Genitourologic Surgery. New York, McGraw-Hill, 1996, pp 177-195. O’Hara JF, Cywinski JB, Monk TG: The renal system and anesthesia for urologic surgery. In Barash PG, Cullen BF, Stoelting RK (eds): Clinical Anesthesia, 5th ed. Philadelphia, JB Lippincott–Williams & Wilkins, 2005. Prentice JA, Martin JT: The Trendelenburg position: Anesthesiologic considerations. In Martin JT (ed): Positioning in Anesthesia and Surgery. Philadelphia, WB Saunders, 1987, pp 127-145. Shah N: Radical cystectomy, radical nephrectomy, and retroperitoneal lymph node dissection. In Malhotra V (ed): Anesthesia for Renal and Genitourologic Surgery. New York, McGraw-Hill, 1996, pp 197-226. Smith RB: Complications of renal surgery. In Smith RB, Ehrlich RM (eds): Complications of Urologic Surgery, 2nd ed. Philadelphia, WB Saunders, 1990, pp 128-159. Welborn SG: Unusual positions—urology: Anesthesiologic considerations. In Martin JT (ed): Positioning in Anesthesia and Surgery. Philadelphia. WB Saunders, 1987, pp 249-254.

OTHER SURGICAL SUBSPECIALTIES

Endotracheal intubation Positive-pressure ventilation Frequent auscultation of lungs

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212

Complications of Lithotripsy Jerome F. O’Hara, Jr. Case Synopsis A 78-year-old woman with a history of severe coronary artery disease underwent extracorporeal shock wave lithotripsy with general anesthesia. Ten minutes after placement in the water bath, the patient’s heart rate increased from 78 to 138 beats per minute, and pink frothy fluid was noted in the endotracheal tube. The patient was removed from the water bath, and an immediate chest radiograph revealed congestive heart failure.

PROBLEM ANALYSIS Definition Extracorporeal shock wave lithotripsy (ESWL) is accomplished by the transmission of shock waves through the patient’s body to pulverize urinary calculi. Unlike secondgeneration lithotriptors, first-generation units require that the patient be immersed in a water bath (Fig. 212-1). In addition to anesthetic risks, this unique environment exposes patients to potential complications from water immersion and the release of energy by the shock waves. During ESWL, a mechanically generated shock wave passes through water as a single pressure impulse. On reaching the patient, the wave passes through the patient’s tissues en route to the “target zone,” which is defined as the area that contains the calculus (Fig. 212-2). Fluoroscopy is used to confirm that the urinary calculi remain in the target zone. When the shock wave encounters a different density, such

Figure 212–1

850

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as the urinary calculus, it releases energy to fragment the calculus into sandlike particles, which is the desired therapeutic effect. However, damage to other tissues or implanted mechanical devices can occur. To prevent cardiac arrhythmias, the lithotriptor can be synchronized to trigger the shock wave during the refractory period of the patient’s cardiac cycle. In certain patients, hydrostatic pressure created by immersion can significantly compromise cardiovascular and pulmonary function.

Recognition Undesirable effects of the shock wave energy include the following: ●

●

●

Cardiovascular instability from atrial or ventricular arrhythmias Potential damage to and malfunction of a pacemaker or implantable cardioverter-defibrillator Hypotension from perirenal or intra-abdominal bleeding

First-generation lithotriptor with the patient in a chair hoist, immersed in the water bath (left). Newer, second-generation lithotriptor (right).

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Complications of Lithotripsy

851

Figure 212–2 ■ Illustration of how the shock wave is generated and then delivered to the renal calculi.

OTHER SURGICAL SUBSPECIALTIES

●

●

Skin petechiae and painful ecchymoses, especially in thin patients Patient discomfort and movement from inadequate analgesia

Undesirable effects during immersion lithotripsy include the following: ●

●

● ●

Nerve and musculoskeletal injury from pressure points associated with use of the hoist chair Hyperthermia or hypothermia caused by the temperature of the water bath Relative inaccessibility of the patient’s airway Cardiovascular and pulmonary changes (Table 212-1)

●

●

Neurologic damage if air is introduced into the epidural space during administration of epidural anesthesia Possible damage to and rupture of a calcified aortic or renal artery aneurysm

Cardiovascular and pulmonary changes associated with water immersion can lead to serious complications in some patients. For example, acute congestive heart failure can occur in patients with severe ventricular dysfunction. Patients with significant chronic obstructive pulmonary disease may not be able to maintain adequate ventilation under regional anesthesia. Absolute and relative contraindications to ESWL are listed in Table 212-2.

Implications Risk Assessment If the shock wave is misdirected or encounters tissue other than the urinary calculi, energy may be released and injure the patient. Such injuries include the following: ●

Pulmonary contusion and hemoptysis, especially in children, because the lung base and kidney are in close proximity Table 212–1

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Cardiopulmonary Changes on Immersion during Lithotripsy

System

Variable

Direction of Change

Cardiovascular

Central blood volume Central venous pressure Pulmonary artery pressure Pulmonary blood flow Vital capacity Functional residual capacity Tidal volume Respiratory rate

Increased Increased Increased Increased Decreased Decreased Decreased Increased

Respiratory

Modified from Malhotra V: Anesthesia and the renal and genitourinary systems. In Miller RD (ed): Anesthesia. New York, Churchill Livingstone, 1994, p 1961.

To avoid complications that can arise during ESWL, the anesthesiologist must understand the physics of shock wave generation and delivery to the patient. Certain risks need to be considered during the preoperative evaluation of a patient who requires an anesthetic for this elective procedure.

Table 212–2

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Contraindications to Extracorporeal Shock Wave Lithotripsy

Absolute Contraindications Obstruction distal to renal calculi Bleeding disorder or anticoagulation Pregnancy

Relative Contraindications Large calcified aortic or renal artery aneurysm Untreated urinary tract infection Pacemaker or implantable cardioverter-defibrillator Morbid obesity

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MANAGEMENT The choice of anesthesia depends on the type of lithotriptor and the anesthesiologist’s preference. High-energy shock waves (>18 kV) usually require general or regional anesthesia, whereas low-energy shock waves (120/80 mm Hg) or stage 1 hypertension (>140/90 but 50% decrease Anemia: >20% decrease Other: elevated erythrocyte sedimentation rate, hypofibrinogenemia, fat macroglobulinemia

Radiologic Chest radiograph: diffuse bilateral infiltrates with “snowstorm” appearance, usually within 48 hr of clinical onset Chest CT: may be normal, but parenchymal changes are consistent with acute lung injury; ARDS may be present Head CT: usually negative, but may show diffuse white matter hemorrhages consistent with microvascular injury MRI: scant data, but possible nonconfluent, hyperintense lesions on proton-density and T2-weighted images

Other Lipase and phospholipase A2 may be elevated Increased pulmonary shunt fraction (without another identifiable cause) Increased alveolar-to-arterial gradient (without another identifiable cause) Urinalysis: stained fat globules (poor specificity) Elevated pulmonary artery pressure (poor sensitivity) ARDS, acute respiratory distress syndrome; CT, computed tomography; MRI, magnetic resonance imaging.

Large amounts of fat from the medullary cavity of long bones may be forced into the venous circulation over a short period. In patients with limited cardiac reserve, acute pulmonary hypertension may precipitate right ventricular failure with hypotension, bradycardia, hypoxemia, and cardiovascular collapse. In contrast to fulminant FES, the symptoms occurring with subacute FES are postulated to be secondary to the toxic effects of the free fatty acids that result from hydrolysis of the embolized fat droplets. Laboratory and other diagnostic tests are nonspecific and not sufficiently sensitive to establish the diagnosis of FES, but they may add weight to the clinical findings (Table 215-3). The chest radiograph may reveal diffuse bilateral infiltrates with a “snowstorm” appearance. Computed tomography (CT) scans of the head may be normal or may show edema or nonspecific infarctions. Chest CT may also be normal, although changes consistent with lung contusion, acute lung injury, or ARDS may be present. In the absence of other lung pathology, an increase in the alveolar-to-arterial gradient is strongly suggestive of FES. Hematologic findings may include thrombocytopenia, anemia (thought to be secondary to intra-alveolar hemorrhage), fat macroglobulinemia from a pulmonary capillary blood sample, or a markedly elevated sedimentation rate. Lipase and phospholipase A2 may be elevated within a few hours of the insult but can return to normal within 24 hours.

Risk Assessment Orthopedic and trauma patients, especially those with lower extremity long bone and pelvic fractures, have a 20% incidence of fat embolism. Displaced fractures are considered a lower risk than nondisplaced ones, because displacement is thought to provide a “vent” for bone marrow fat, thus

lessening the potential for intravasation. Patients with fractures of the middle and proximal parts of the femoral shaft are at increased risk, as are those with multiple fractures. Delayed stabilization (>24 hours) increases the risk for fat embolization. Young men constitute the largest at-risk group for FES owing to the high incidence of skeletal and multiple trauma in this group. The elderly make up the second largest patient group because of the prevalence of hip fractures, total joint replacement procedures, and underlying cardiopulmonary disease. Intramedullary rod placement for closed or impending fractures has also been shown to increase the incidence of fat emboli. Joint replacement surgery, especially revisions or bilateral procedures, is associated with FES, as are femoral metastases and procedures that disrupt the adipose layer (liposuction) or bone marrow (harvest or transplantation). Case reports have also linked fat injections performed during cosmetic surgery with significant fat embolism. The alcohol-induced fatty liver is capable of spontaneously releasing large numbers of embolus-sized fat globules when fatty cysts rupture into adjacent sinusoids and veins. Blunt trauma to the liver has also been associated with fat embolism. Some controversy exists over whether highdose corticosteroids, which can increase the fat content of the liver, increase the risk for FES.

Implications The mortality rate for FES may be as high as 5% to 15%, especially in elderly and debilitated patients. Mortality from fulminant FES is typically due to acute right ventricular

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MANAGEMENT Treatment of FES is aimed at prevention of further fat dissemination, correction of hypoxemia, and hemodynamic stabilization. FES-induced acute lung injury requires supportive respiratory care to maximize oxygenation and ventilation, ensure airway protection, and prevent aspiration. This may require intubation, insertion of an arterial line for blood gas sampling, and mechanical ventilation of those patients with severe pulmonary compromise or altered mental status. Blood products, clotting factors, and platelets are administered to correct any coagulopathy in patients scheduled for surgery who are actively bleeding. Volume status may be critical, especially if right ventricular dysfunction is present; a central venous or pulmonary artery catheter may be useful in guiding fluid management. Inotropic support should be used, as needed, to maintain blood pressure, improve right ventricular output, and prevent ventricular ischemia. Prophylactic care aimed at preventing deep venous thrombosis and stress-related gastrointestinal bleeding is indicated. Surgical care for patients with long bone fractures should be aimed at stabilizing the fracture as early as possible. Heparin use has been suggested because, in theory, it acts to clear lipids from the serum by stimulating lipase. However, the data are contradictory, and heparin has no clear role at this time. The role of corticosteroids in FES is less clear. They are thought to stabilize the capillary and alveolar membranes to prevent further damage to the lung. However, studies have obtained varying results. Also, the dose, optimal timing, and duration of therapy remain undetermined. Management of fulminant FES, an acute life-threatening condition, requires advanced cardiac life support techniques.

PREVENTION Because the majority of FES cases are associated with trauma, the rapid stabilization of fractures and correction of hypovolemia should be among the highest priorities for reducing the incidence of FES. If the patient is sufficiently stable to proceed to surgery, surgical fixation of fractures should occur within 24 hours of injury. Surgical techniques that may help reduce the volume of fat intravasation during intramedullary

Fat Embolism Syndrome

861

reaming, nailing, and prosthesis replacement include the following: ●

● ●

●

●

Drilling a small hole in the distal bone to vent fat and marrow during surgery Use of an uncemented prosthesis for total hip arthroplasty Lavage of the canal after each reaming to remove debris and clots Use of fluted rods during total knee arthroplasty to allow marrow contents to exit into the knee Modification of reaming techniques (avoidance, or use of low driving speed or small-cored reamers)

Again, it is important to recognize which patients are at increased risk for FES (see Table 215-2). Optimizing the physical status of high-risk patients, rapidly stabilizing atrisk fractures, using techniques to reduce intraoperative fat embolization, and rapidly identifying and treating FES can help reduce the morbidity and mortality associated with this condition.

Further Reading Alho A: Fat embolism syndrome: Etiology, pathogenesis and treatment. Acta Chir Scand (Suppl) 499:75-85, 1980. Bouaggad A, Harti A, Elmouknia M, et al: Neurologic manifestations of fat embolism. Cah Anesthesiol 43:441-443, 1995. Dalgorf D, Borkhoff CM, Stephen DJ, et al: Venting during prophylactic nailing for femoral metastases: Current orthopedic practice. Can J Surg 46:427-431, 2003. Georgopoulos D, Bouros D: Fat embolism syndrome: Clinical examination is still the preferable diagnostic method. Chest 123:982-983, 2003. Gitin TA, Seidel T, Cera PJ, et al: Pulmonary microvascular fat: The significance? Crit Care Med 21:673-677, 1993. Jones JP Jr: Alcoholism, hypercortisolism, fat embolism and osseous avascular necrosis. Clin Orthop 393:4-12, 2001. Kirkland L: Fat embolism. eMedicine J 2004. Available at www.emedicine .com/med/topic652.htm Marshall PD, Douglas DL, Henry L: Fatal pulmonary fat embolism during total hip replacement due to high-pressure cementing techniques in an osteoporotic femur. Br J Clin Pract 45:148-149, 1991. Mellor A, Soni N: Fat embolism. Anaesthesia. 56:145-154, 2001. Papagelopoulos PJ, Apostolou CD, Karachalios TS, et al: Pulmonary fat embolism after total hip and total knee arthroplasty. Orthopedics 26:523-527, 2003. Peltier LF: Fat embolism: An appraisal of the problem. Clin Orthop 187: 3-17, 1984. Pitto RP, Blunk J, Kossler M: Transesophageal echocardiography and clinical features of fat embolism during cemented total hip arthroplasty: A randomized study in patients with a femoral neck fracture. Arch Orthop Trauma Surg 120:53-58, 2000. Slye DA: Orthopedic complications: Compartment syndrome, fat embolism syndrome, and venous thromboembolism. Nurs Clin North Am 26:113-132, 1991. Sutton GE: Pulmonary fat embolism and its relation to traumatic shock. BMJ 2:368, 1918. Tedeschi CG, Castelli W, Kropp G, et al: Fat macroglobulinemia and fat embolism. Surg Gynecol Obstet 126:83-90, 1968. Thaunat O, Thaler F, Loirat P, et al: Cerebral fat embolism induced by facial fat injection. Plast Reconstr Surg 113:2235-2236, 2004. Wilson JV, Salisbury CV: Fat embolism in war surgery. Br J Surg 31:384, 1954. Yoon SS, Chang DI, Chung KC: Acute fatal stroke immediately following autologous fat injection into the face. Neurology 61:1151-1152, 2004.

OTHER SURGICAL SUBSPECIALTIES

failure with cardiovascular collapse. Respiratory failure is the most common cause of death in the subacute presentation of FES. Almost 90% of FES cases are associated with blunt trauma. Therefore, a high index of suspicion must be maintained when treating these patients. The majority of patients can be expected to recover from the pulmonary sequelae of FES with appropriate supportive care. Acute mental status changes often do not resolve immediately, even with improvement in oxygenation. This may take several days. However, long-term or permanent neurologic sequelae are occasionally seen in patients with visual disturbances or focal neurologic deficits.

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Thromboembolic Complications Robert F. Helfand Case Synopsis A 72-year-old man has total hip arthroplasty under general anesthesia. A postoperative visit the next day finds him mildly tachypneic, apprehensive, and complaining of pain in his calf on the operative side.

PROBLEM ANALYSIS Definition Embolic events are a major cause of morbidity and mortality following lower extremity orthopedic surgery. This chapter focuses on thrombotic sources of emboli. Chapters 175, 215, and 217 discuss embolization secondary to air, fat, and methylmethacrylate, respectively. In contrast to the arterial thromboembolic and vasoocclusive events associated with vascular surgery, orthopedic thromboembolic events affect primarily the venous system. As such, their cause is associated with endothelial damage, venous stasis, and hypercoagulability (Virchow’s triad). These conditions facilitate the formation of deep venous thromboses (DVTs), which usually begin in the lower leg veins and then extend proximally to the deep thigh veins before ultimately embolizing to the right heart and pulmonary circulation.

embolization may reveal hypoxemia or hypercapnia, but findings are often normal. An ECG may show evidence of right ventricular strain (new right bundle branch block, right axis deviation), sinus tachycardia, or anterior T-wave inversion, but it is usually normal. Monitored patients may have reduced cardiac output or increased pulmonary arterial pressure and vascular resistance. Transesophageal echocardiography (TEE) visualizes the central pulmonary arteries and evaluates right ventricular function. During surgery, TEE is recommended as the initial diagnostic test for suspected massive PE or in cases of unexplained hypotension, hypoxemia, or cardiac arrest. TEE has a reported sensitivity of 76% to 96.7% and a specificity of 86% to 100% for identifying central PE.

Risk Assessment Patient and surgical factors contribute to the risk of thromboembolic complications after orthopedic surgery (Table 216-1).

Recognition DVTs and pulmonary emboli (PE) are notoriously difficult to diagnose. Most patients with DVT have no obvious disease. The most commonly used diagnostic tool is duplex ultrasonography. Ultrasound tests are noninvasive and can be easily repeated, but they lack sensitivity for calf vein thrombosis. PE are difficult to recognize both during and after anesthesia, but they should be suspected in any patient with sudden, unexplained dyspnea after a surgery. Symptoms may include chest pain, dyspnea, hemoptysis, apprehension, or cough, but they are generally nonspecific. Physical findings include tachypnea, tachycardia, rales, or an accentuated pulmonic component of the second heart sound (P2). Most patients with PE do not exhibit signs of thrombophlebitis. High-resolution spiral computed tomography scanning is often chosen instead of ventilation-perfusion lung scanning as the initial diagnostic test for PE. Pulmonary angiography was once the standard test for the diagnosis of PE, but it is now used less frequently. D-dimer measured by the ELISA test is an additional screening tool, but it is neither specific nor sufficiently sensitive to make or exclude the diagnosis of PE. A normal chest radiograph, arterial blood gas analysis, or electrocardiogram (ECG) does not exclude the diagnosis of PE. Arterial blood gas analysis at the time of 862

Table 216–1

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Risk Factors for Thromboembolic Complications with Lower Extremity Orthopedic Surgery

Patient Risk Factors Low cardiac output states (CHF, MI) Prolonged immobilization or paralysis Obesity Prior DVT, PE, or varicose veins Age older than 40 yr Cancer Hypercoagulable states Pregnancy Inflammatory bowel disease Nephrotic syndrome

Surgical Risk Factors Major surgery >70 min No DVT prophylaxis Hypothermia Positioning Surgical technique Hypotension Trauma (pelvis, hip, or leg fracture) Indwelling central venous catheter CHF, congestive heart failure; DVT, deep venous thrombosis; MI, myocardial infarction; PE, pulmonary emboli.

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Implications

●

MANAGEMENT Intraoperative management of PE is supportive and focuses on optimizing cardiopulmonary function. Specific measures include volume support of right ventricular preload, administration of inotropic drugs, afterload reduction for the right ventricle, and increasing the fraction of inspired oxygen; positive end-expiratory pressure may be added. Patients can have delayed findings of atelectasis and pulmonary infiltrates 24 to 72 hours following PE. Patients with serious cardiorespiratory compromise may benefit from placement of a pulmonary artery catheter and measurement of cardiac output. Therapeutic intervention for PE consists of full heparinization or fibrinolytic therapy. In most cases, however, neither is appropriate intraoperative treatment. For patients with cardiac arrest or persistent hypotension and hypoxemia, options include the following: ●

●

Emergency operative embolectomy, which requires cardiopulmonary bypass Bilateral thoracotomy, with massage of the pulmonary vessels

Table 216–2

■

Incidence of Thromboembolic Complications after Orthopedic Procedures without Prophylaxis

Procedure

Total DVT (%)

Proximal DVT (%)

Total PE (%)

Fatal PE (%)

Total hip arthroplasty Total knee arthroplasty Repair of hip fracture

42-57 41-85 46-60

18-36 5-22 23-30

0.9-28 1.5-10 3-11

0.1-2 0.1-1.7 2.5-7.5

DVT, deep venous thrombosis; PE, pulmonary emboli.

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Interventional radiology for attempted thrombus extraction or catheter-directed fibrinolytic therapy

Mortality with surgical removal of PE is greater than 50%.

PREVENTION Thromboembolic complications after orthopedic surgery are unique. The process frequently begins intraoperatively, extends quietly postoperatively, and often results in sudden death. Thus, prevention is imperative, especially because therapeutic interventions are often associated with serious hemorrhagic complications. Prophylaxis includes both mechanical and pharmacologic modalities. The anesthetic technique may also play a significant role in prevention.

Mechanical and Pharmacologic Modalities Compression stockings that provide a 30 to 40 mm Hg compression gradient are an effective adjunctive treatment for limiting or preventing the extension of thrombus. Mechanical modalities, such as intermittent pneumatic compression devices, can reduce the incidence of thrombus formation by decreasing venous stasis, improving blood flow velocity, and increasing circulating fibrinolysins. Their effectiveness is not diminished when applied to only one leg during surgery. Pneumatic devices significantly decrease the incidence of distal thrombi but have no effect on more proximal thrombi in the iliac and femoral veins. The American College of Chest Physicians recommends the use of oral warfarin or parenteral low-molecular-weight heparin products for DVT prophylaxis. The latter include enoxaparin (Lovenox) or the novel parenteral anti–factor Xa agent fondaparinux sodium (a synthetic pentastarch). Aspirin is never used alone. Also, standard unfractionated heparin should not be used for high-risk patients. DVT prophylaxis regimens are specific. Patients are stratified by risk to four categories, as well as to those having total knee replacement or total hip replacement. Warfarin is usually started the night before surgery or immediately postoperatively; the therapeutic international normalized ratio target of 2.5 (range, 2 to 3) is usually not achieved until the third postoperative day. Low-molecular-weight heparin is usually started 12 to 24 hours postoperatively. For total hip replacement, low-molecular-weight heparin may also be given 4 to 6 hours after surgery at half the full dose, followed by a full dose the next day. Preoperatively, it can be given 12 hours before surgery, followed by a full dose 12 to 24 hours postoperatively. Following hip surgery, treatment needs to continue for at least 10 days for lower-risk patients and for 28 to 35 days for higher-risk patients. Although these modalities are more efficacious than placebo, their relative efficacy and value are controversial and probably vary according to the type of surgery.

Anesthetic Management A convincing number of studies support the choice of regional anesthesia over general anesthesia for reducing thromboembolic complications, especially DVT. When compared

OTHER SURGICAL SUBSPECIALTIES

DVT is common following hip and knee arthroplasty, and especially after hip fracture. DVT is a clot that develops in the large distal veins of the legs, usually deep within the muscle. Less frequently, DVT develops in the proximal pelvic veins. The clot is usually attached at one end. However, if it breaks loose and enters the bloodstream, it may embolize to the right heart and main pulmonary artery branches. The patient is especially at risk when the DVT extends proximally into deep thigh veins. Fatal PE occurs in up to 7% of lower extremity orthopedic procedures and constitutes the greatest source of perioperative mortality in these patients (Table 216-2). Emboli may also traverse an intracardiac communication to enter the arterial circulation. This can cause stroke or acute arterial occlusion in the extremities or other major organs. At least half of venous thrombi start intraoperatively; the remainder occur during the first 24 to 48 postoperative hours. Nevertheless, some PE do not become clinically apparent until 1 week after surgery. The high risk of morbidity and mortality mandates prophylactic measures to reduce the occurrence of thromboembolic complications.

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with general anesthesia, epidural anesthesia reduces the incidence of deep thigh DVT 2.5- to 5-fold and PE 3-fold after hip arthroplasty. Regional anesthesia also results in a 31% reduction of DVT following repair of hip fracture. It is unclear why regional anesthesia appears to reduce thromboembolic complications, but it may counter sympathoadrenal stimulation of the coagulation cascade (see Chapter 89). Regional techniques clearly improve rheology by reducing viscosity and increasing lower extremity blood flow. Less clear is the membrane-stabilizing role of local anesthetics themselves. These effects appear to decrease platelet aggregation while increasing fibrinolysis and normalization of antithrombin III levels. In addition, local anesthetics may inhibit the activation of leukocyte factors linked to hypercoagulability. Unfortunately, the choice of regional anesthesia is not so clear-cut. Two issues regarding the risk of spinal (epidural) hematoma deserve consideration by the anesthesiologist. One is practical and the other theoretical. The practical issue concerns placement of central neuraxial blocks in patients who are either receiving or are about to receive anticoagulants. Warfarin therapy begins the night before surgery in many patients having joint replacement or in the immediate postoperative period. Available literature supports the safety of perioperative regional techniques in this setting (see also Chapter 57). More ominous is the issue of the concurrent use of unfractionated or low-molecular-weight heparin and central neuraxial anesthesia (see also Chapter 57). Low-molecularweight heparin is a relative contraindication to central neuraxial regional techniques because of its long half-life, the difficulty of monitoring its anticoagulant effects, and several reports of associated spinal (epidural) hematoma. These limitations have restricted the use of indwelling neuraxial catheters for postoperative epidural analgesia in many centers, as well as increasing interest in the use of singleinjection and continuous peripheral nerve blocks for postoperative pain relief. Anesthesiologists face a theoretical dilemma when choosing the anesthetic technique for lower extremity orthopedic surgery: Does regional anesthesia’s benefit in terms of thromboembolism prophylaxis outweigh the risk of spinal (epidural) hematoma? In most of the aforementioned stud-

ies that support the use of regional versus general anesthesia for reducing thromboembolic complications, especially DVT, patients did not receive thromboembolism prophylaxis. It remains unclear whether regional anesthesia is superior to or synergistic with standard thromboembolism prophylactic techniques. Because most patients do receive pharmacologic prophylaxis, the general recommendations of the American Society for Regional Anesthesia include a single needle pass, atraumatic needle placement, and no indwelling neuraxial catheters. For recommendations regarding specific agents used for thromboembolism prophylaxis, refer to Chapter 57 under Management. For patients receiving selective factor Xa inhibitors, there is insufficient evidence to make a specific recommendation regarding the use of continuous or singleinjection central neuraxial anesthetic techniques. One review of the prospective, randomized experience with fondaparinux sodium found that this agent did not increase the risk of epidural hematoma when used with neuraxial anesthesia.

Further Reading Cannavo D: Use of neuraxial anesthesia with selective factor Xa inhibitors. Am J Orthop 31:S21-S23, 2002. Geerts WH, Pinco GF, Heit JA, et al: Prevention of venous thromboembolism: The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 126:338s-400s, 2004. Horlocker T: Regional anesthesia in the anticoagulated patient: Defining the risk (the Second ASRA Consensus Conference on Neuraxial Anesthesia and Anticoagulation). Reg Anesth Pain Med 28:172-197, 2003. Liu SS, Carpenter RL, Neal JM: Epidural anesthesia and analgesia: Their role in postoperative outcome. Anesthesiology 82:1474-1506, 1995. Rosenfeld BA: Benefits of regional anesthesia on thromboembolic complications following surgery. Reg Anesth 21:9-12, 1996. Sharrock NE, Ranawat CS, Urquhart B, et al: Factors influencing deep vein thrombosis following total hip arthroplasty under epidural anesthesia. Anesth Analg 76:765-771, 1993. Sorenson RM, Pace NL: Anesthetic techniques during surgical repair of femoral neck fractures: A meta-analysis. Anesthesiology 77:1095-1104, 1992. Wedel DJ (ed): Orthopedic Anesthesia. New York, Churchill Livingstone, 1993. Wedel DJ, Horlocker TT: Anesthesia for orthopedic surgery. In Barash PR, Cullen BF, Stoelting RK (eds): Clinical Anesthesia, 3rd ed. Philadelphia, Lippincott-Raven, 1997, pp 1036-1037.

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Methylmethacrylate Kathryn P. King

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Case Synopsis

PROBLEM ANALYSIS Definition Polymethylmethacrylate bone cement is a polymer formed by mixing highly volatile liquid methylmethacrylate (MMA) monomer with an accelerator, polymethylmethacrylate powder. This bone cement is used during orthopedic surgery to implant prostheses for joint replacement. MMA has been implicated as a cause of adverse cardiopulmonary events observed most frequently during hip replacement surgery. Symptoms include hypoxemia, bronchoconstriction, pulmonary hypertension, and right ventricular failure with hypotension. Fatal cardiac arrest, though rare, has been reported in 0.6% to 1% of patients in some case series. The clinical presentation just described is termed bone implantation syndrome (BIS) or bone cement implantation syndrome (BCIS). Proposed mechanisms for MMA-induced injury include a neurogenic reflex, release of vasoactive and myocardial depressant substances by the cement, intravascular thrombin generation in the lungs, direct vasoactive effects of absorbed MMA, and acute pulmonary microembolization. After application of polymethylmethacrylate, unbound MMA monomer is quickly absorbed into the systemic circulation and eliminated by the lungs. Its peak level is reached in expired air within 2 to 5 minutes. The extent of systemic absorption depends on the area of contact between the bone cement and vascularized tissue and on the degree of curing. MMA is a peripheral vasodilator. However, the amount released during reaming in joint replacement is 10- to 20-fold less than that required to produce hypotension in experimental models. Further, studies have demonstrated that hypotension also occurs in the absence of the polymer. Thus, the most likely explanation of the pathogenesis of this syndrome is acute pulmonary microembolization. During implantation of the cement and prosthesis, the high intramedullary pressure generated in the long bone marrow cavity forces medullary contents into the venous circulation, with embolization to the lungs. The pathologic nature of the emboli is not certain; it may be fat, marrow, thrombus, air, or bone cement. Emboli appear as echogenic masses during reaming, cementing, prosthesis placement, and manipulation of the bone. Pulmonary embolization activates the clotting cascade and triggers the production of proinflammatory substances. Further, cemented prostheses are associated with a longer duration of embolization, larger emboli, and a higher

OTHER SURGICAL SUBSPECIALTIES

A 62-year-old man presents for a total hip arthroplasty for degenerative joint disease. His medical problems include hypertension and mild exercise-induced asthma that is treated with an albuterol inhaler. He declines regional anesthesia. General anesthesia is induced and proceeds uneventfully. During cementing and insertion of the femoral prosthesis, the patient develops hypotension, tachycardia, and hypoxemia.

percentage of right atria filled by emboli compared with noncemented prostheses. Intramedullary pressure peaks are 680 mm Hg in humans with cemented arthroplasty, compared with peaks of less than 100 mm Hg with noncemented arthroplasty. There are also chronic issues related to MMA and other polymers used in orthopedic surgery. Controlled occupational exposure to MMA has not been shown to affect workers’ mortality from colon and rectal cancer. The recommended maximum exposure of MMA vapor is 100 parts per million over the course of an 8-hour workday. Acute exposure to extremely high levels of MMA vapor can cause liver necrosis, pulmonary edema, and pulmonary emphysema. Occupational exposure of medical personnel is well below the levels necessary to elicit these toxic effects. However, other less dramatic effects might occur. MMA is known to be a potent allergenic sensitizer and can cause local reactions with dermal exposure. It is also known to be a potential pulmonary toxin, with chronic exposure causing occupational asthma. The direct pulmonary effect of MMA in the absence of pulmonary embolization is not well defined. However, indirect evidence suggests that it may trigger bronchoconstriction.

Recognition Clinical signs of BIS are similar to those found in pulmonary embolism or fat embolism. These include fever, tachycardia, hypotension, hypoxemia, and, in spontaneously breathing patients, dyspnea and tachypnea. End-tidal carbon dioxide may decrease with a large embolus. Also, fat emboli may cause petechiae, fat globules in the urine, and anuria or oliguria. In awake patients, they can cause mental status changes. The electrocardiogram may show right axis deviation or right bundle branch block. Collectively, these signs reflect increased pulmonary artery pressure and intrapulmonary shunt, potentially leading to right ventricular failure and cardiac arrest.

Risk Assessment This patient population includes elderly or chronically ill patients undergoing either elective or emergent surgery. Careful preoperative evaluation may identify coexisting conditions, such as pulmonary or cardiovascular disease, that can be stabilized or improved preoperatively in anticipation of hemodynamic instability during surgery. A frail 865

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individual with additional risk factors, such as pulmonary hypertension, coronary artery disease, or severe osteoporosis, may benefit from invasive monitoring.

Invasive monitoring may be indicated for patients with marginal cardiac or pulmonary reserves. Finally, adequate volume replacement and supplemental oxygen are essential.

Implications

Further Reading

Although hypotension and hypoxia frequently occur during implantation of the prosthesis, these findings are usually transient and self-limited. Larger emboli causing right ventricular outflow tract obstruction may require resuscitation with intubation, mechanical ventilation with 100% oxygen, intravenous fluids, inotropic agents, afterload reduction of the right ventricle, and, occasionally, heroic measures such as cardiopulmonary bypass and surgical thrombectomy.

Berman AT, Price HL, Hahn JF: The cardiovascular effects of methylmethacrylate in dogs. Clin Orthop 100:265-269, 1974. Christie J, Robinson CM, Pell AC, et al: Transcardiac echocardiography during invasive intramedullary procedures. J Bone Joint Surg Br 77:450-455, 1995. Dahl OE, Molnar I, Vinje A, et al: Studies on coagulation, fibrinolysis, kallikrein-kinin and complement activation in systemic and pulmonary circulation during hip arthroplasty with acrylic cement. Thromb Res 5:875-884, 1988. Elmaraghy AW, Humeniuk B, Anderson GI, et al: The role of methylmethacrylate monomer in the formation and haemodynamic outcome of pulmonary fat emboli. J Bone Joint Surg Br 80:156-161, 1998. Ereth MH, Weber JG, Abel MD, et al: Cemented versus non-cemented total hip arthroplasty—embolism, hemodynamics, and intrapulmonary shunting. Mayo Clin Proc 67:1066-1074, 1992. Fallon KM, Fuller JG, Morley-Forster P: Fat embolization and fatal cardiac arrest during hip arthroplasty with methylmethacrylate. Can J Anaesth 48:626-629, 2001. Lamade WR, Friedl W, Schmid B, et al: Bone cement implantation syndrome: A prospective randomised trial for use of antihistamine blockade. Arch Orthop Trauma Surg 114:335-339, 1995. Lopez-Duran L, Garcia-Lopez A, Duran L, et al: Cardiopulmonary and haemodynamic changes during total hip arthroplasty. Int Orthop 21:253-258, 1997. Mellor A, Soni N: Fat embolism. Anaesthesia 56:145-154, 2001. Orsini EC, Byrick RJ, Mullen JB, et al: Cardiopulmonary function and pulmonary microemboli during arthroplasty using cemented or non-cemented components: The role of intramedullary pressure. J Bone Joint Surg Am 69:822-832, 1987. Rinecker H: New clinico-pathophysiological studies on the bone cement implantation syndrome. Arch Orthop Trauma Surg 97:263-274, 1980. Tomenson JA, Bonner SM, Edwards JC, et al: Study of two cohorts of workers exposed to methyl methacrylate in acrylic sheet production. Occup Environ Med 57:810-817, 2000.

MANAGEMENT Treatment of BIS is limited to supportive care. This includes monitoring vital signs and the use of supplemental oxygen and intravenous fluids, with vasopressor support as needed. In some patients, positive inotropic agents may also be needed.

PREVENTION Emboli occur frequently during surgical manipulation and placement of both cemented and noncemented orthopedic prostheses. Avoidance of MMA may not significantly reduce the occurrence of these events. However, lavaging the marrow cavity, placing a vent hole in the bone during reaming to reduce intramedullary pressure, and thorough removal of bone marrow and bone debris can minimize the dislodgment of particulates. Allowing the freshly mixed MMA to vaporize for as long as possible may help minimize MMA absorption.

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Extremity Tourniquets H. David Hardman

218

Case Synopsis

PROBLEM ANALYSIS Definition Postoperative neurologic dysfunction with the use of arterial tourniquets is a well-documented but rare phenomenon. Estimates of incidence range from 0.15% to 0.6% for all patients. Owing to greater soft tissue mass insulation, thigh tourniquets are less likely to cause neurologic injury than are arm tourniquets; the risk is increased with calf and forearm tourniquets. Permanent tourniquet-induced neurologic deficits are uncommon. The majority of nerve injuries resolve spontaneously within 6 weeks, with complete recovery by 6 months. Arterial tourniquets are widely used in upper and lower extremity surgery and in intravenous regional anesthesia. This practice continues because it is widely accepted that the benefit from minimizing surgical blood loss and creating a bloodless operative field exceeds the risk for tourniquetrelated complications. It is important for anesthesiologists to be aware of the potential for tourniquet-related tissue injury, systemic effects of tourniquet inflation and deflation, and the possibly catastrophic events that could occur at these times. Also, it should be recognized that surgeons and anesthesiologists share any medicolegal liability for tourniquetrelated complications. Documentation should include the location of the tourniquet, the use of padding and draping, and inflation pressure and duration. Also, tourniquet pressure relative to systemic blood pressure values, prolonged inflation, and total vascular occlusion times must be communicated to the surgical team and documented on the anesthesia record. LOCAL INJURY Pressure-related injuries to skin, muscles, nerves, and blood vessels depend on the pressure of tourniquet inflation and its duration. Also, absent arterial blood flow distal to the tourniquet causes ischemia, which leads to progressive acidosis, hypoxemia, and hypercarbia. The associated release of inflammatory mediators increases capillary permeability and tissue edema. This worsens ischemia, especially after reperfusion.

OTHER SURGICAL SUBSPECIALTIES

A 75-year-old woman is undergoing a revision of a left total knee arthroplasty under regional anesthesia. She is morbidly obese, on chronic opioids for pain relief, and an insulin-dependent diabetic. Continuous catheter lumbar plexus and sciatic nerve blocks are chosen, along with supplemental intravenous narcotics and sedatives as needed. A conventional rectangular thigh tourniquet is placed for surgical hemostasis. After limb exsanguination, the cuff pressure is set at 300 mm Hg. Surgery proceeds uneventfully, with a total tourniquet time of 2 hours. The catheters are removed the next day, and the patient is started on enoxaparin for deep venous thrombosis (DVT) prophylaxis. Subsequently, she complains of numbness and weakness in her left leg.

The ultrastructural cellular changes are detectable after 30 minutes of ischemia but are reversible with ischemia lasting 2 hours or less. High-energy intracellular phosphate depletion occurs more gradually. However, injury to the Na+, K+-ATPase–dependent ion exchange pump causes extracellular potassium leak and intracellular edema. The sarcoplasmic reticulum loses glycogen, the mitochondria swell, and myelin degeneration occurs. Skin. Trauma to the skin can be caused by pressure necrosis due to inadequate padding between the skin and tourniquet or friction burns due to movement of a poorly applied tourniquet. Obese patients with redundant upper extremity skin folds are at increased risk for skin injury. Chemical burns from skin preparation solutions have been reported. These solutions soak into the padding under the tourniquet, and under pressure, this continuous contact with the skin can cause full-thickness burns. Muscle. Myocytes are very sensitive to compression and ischemia. Injury is more severe with lengthy tourniquet inflation or high pressure. Usually, injury is greatest beneath the tourniquet. Associated ischemia, edema, and microvascular congestion cause the post-tourniquet syndrome. This includes stiffness, pallor, and weakness (not paralysis), with subjective extremity numbness. Nerve. Mechanical pressure compresses nerves directly beneath the tourniquet cuff. Shear forces at the proximal and distal edges of the cuff also cause nerve injury ranging from paresthesia to complete paralysis. Distal ischemia plays a lesser role. The contribution of tourniquet time to the development of nerve injury is unclear. Paralysis has been reported with as little as 30 minutes of tourniquet inflation. Lower extremity nerve injury usually involves the sciatic nerve. The upper extremity is more vulnerable to injury. Radial injury is more frequent than ulnar or median nerve injury. Localized nerve injuries tend to be neurapraxic (i.e., without evidence of structural damage to the axon or perineurium). If so, the prognosis for full recovery is good. In contrast, axonotmesis (i.e., damage to the axon but not to the perineurium) causes nerve degeneration distal to the injury and takes longer to recover. Rarely, a permanent nerve deficit occurs. 867

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Vasculature. Arteries and veins, especially prosthetic grafts (e.g., arteriovenous fistulas, arterial bypass grafts), are susceptible to traumatic injury from mechanical compression. Although direct arterial injury is rare (0.03% to 0.14% incidence), fractured atherosclerotic plaque may cause localized thrombosis or embolize distally to cause ischemia. Although DVT is a known and common complication of lower limb surgery, tourniquets bear no relation to deep venous stasis and thrombus formation. Rather, systemic hypercoagulability is due to catecholamine release and platelet aggregation caused by tourniquet-related or surgical pain. In contrast, active bleeding after tourniquet release may be aggravated by ischemia-caused tissue plasminogen activator release and fibrinolysis.

a transient increase in minute ventilation by 50% for about 5 minutes to maintain normocapnia. Hyperventilation can prevent the associated increase in cerebral blood volume and intracranial pressure that might otherwise be detrimental to a patient with a severe head injury.

SYSTEMIC EFFECTS

Core Body Temperature. Most patients remain normothermic. Tourniquet inflation above arterial pressure transiently increases core body temperature, and tourniquet deflation transiently decreases it. The decline in core body temperature due to the return of hypothermic venous blood from the previously occluded limb into the systemic circulation is usually 0.7°C or less.

Systemic effects occur with tourniquet inflation and deflation. The intensity and duration of these derangements are directly proportional to the length of tourniquet inflation time and the size and number of tourniquet-isolated limbs. Autotransfusion. Limb exsanguination and rapid tourniquet inflation shunt blood into the central circulation (autotransfusion) and increase systemic vascular resistance. As much as 800 mL of blood is autotransfused with the simultaneous inflation of bilateral thigh tourniquets. This causes a transient increase in central venous pressure and systolic blood pressure, which gradually returns to baseline. In patients with compromised left ventricular function, congestive heart failure due to circulatory overload and cardiac arrest has been reported. Hypertension. Tourniquet-induced hypertension is common. Patients develop an increase in heart rate and systolic and diastolic blood pressures within 30 to 60 minutes of inflation, which persists until tourniquet deflation. This increase in mean arterial pressure has been attributed to (1) an acute increase in systemic vascular resistance with removal of a vascular bed; (2) limb exsanguination before tourniquet cuff inflation, which causes acute central blood volume expansion; and (3) pain associated with tourniquet compression and limb ischemia. The pain mechanism is not well understood, but it may involve the activation of type C nerve fibers. In turn, these activate NMDA receptors, leading to a hypertensive response. This response is less common and less intense under regional anesthesia compared with general anesthesia. Hypotension. Tourniquet deflation results in reduced blood pressure and central venous pressure secondary to a shift of blood volume back into the extremity and postischemic reactive vasodilatation. Also, with reperfusion, metabolites released from ischemic areas into the systemic circulation have the potential to cause myocardial depression and further reduce blood pressure. Hypotension is usually self-limited (≤15 minutes). Hypercapnia. End-tidal carbon dioxide (ETCO2) increases after tourniquet release owing to the efflux of hypercapnic venous blood from the ischemic limb into the systemic circulation. The peak ETCO2 increase occurs by 1 minute, and it returns to baseline by 10 to 13 minutes. Spontaneously breathing patients compensate by increasing their respiratory rate. However, those with controlled ventilation require

Metabolic Acidosis. Elevated serum lactate and reduced pH are observed for approximately 30 minutes after reperfusion of the isolated extremity. Blood Oxygen Saturation. Arterial oxygen saturation usually remains normal. However, as large volumes of deoxygenated blood are returned to the central circulation after tourniquet release, mixed venous oxygen saturation is transiently decreased.

Deep Venous Thrombosis, Pulmonary or Systemic Thromboembolism. These potentially devastating complications may occur with lower limb trauma and surgery, but rarely intraoperatively. Although studies with transesophageal echocardiography have shown up to a 70% incidence of right atrial embolization following tourniquet release, most emboli are small and are unlikely to cause major morbidity. However, this risk is increased in patients with hypercoagulable states and thrombus due to trauma or prolonged immobilization. In this case, it is believed that thrombus becomes dislodged during limb exsanguination or with tourniquet inflation. Catastrophic events such as DVT or pulmonary or systemic thromboembolism are more likely to occur postoperatively during rehabilitation. Use of enoxaparin for DVT prophylaxis has dramatically reduced the incidence of fatal pulmonary embolism. However, given that pulmonary and cerebral emboli have been reported during both inflation and deflation of tourniquets, anesthesiologists should be especially vigilant during these times. Attention should be focused on the patient’s neurologic status and any sudden, unexpected changes in arterial oxygen saturation and ETCO2. Significant pulmonary emboli result in an acute reduction in ETCO2, with tachycardia and hypotension, followed by hypoxemia and myocardial ischemia. Right ventricular dysfunction may also be observed (also see Chapters 215 to 217).

Recognition Given the increased use of regional blocks for lower extremity surgery, which significantly reduces postoperative pain scores and permits earlier ambulation, how does one differentiate a nerve injury related to use of a tourniquet from one related to regional anesthesia? Post-tourniquet syndrome is the most common problem associated with tourniquet use. Mild weakness, diffuse subjective numbness, swelling, stiffness, and slight pallor of the affected limb usually develop several hours after tourniquet deflation. Also, ischemic injury to muscle is distinguished from nerve injury by normal nerve conduction studies and

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Risk Assessment Both tourniquet-related and anesthesia-related nerve injuries resolve in approximately the same time frame, so cause is usually not important. However, for anesthesiologists working in high-risk malpractice environments, the possibility of nerve injury may be a consideration when choosing the type of anesthesia for patients at high risk for tourniquet-induced neurologic injury. Factors that may increase the risk of complications with tourniquet use are listed in Table 218-1. The safe upper limits for inflation time and pressure for arterial tourniquets are controversial. Nerves appear most susceptible to mechanical pressure and muscles to prolonged ischemia. Most clinicians recommend the shortest tourniquet inflation time possible, with a limit of 2 hours in healthy patients. For surgical procedures exceeding 2 hours, the tourniquet should be deflated every 2 hours to allow 10 minutes of limb reperfusion. Muscle injury, especially beneath the cuff, can occur even with short tourniquet times. Elderly trauma patients and those with peripheral vascular disease are most susceptible to muscle injury. Therefore, the lowest pressure needed to produce arterial occlusion should be used. Van Roekel and Thurston recommend that in a normotensive, average-size adult patient, an inflation pressure of 200 mm Hg should be adequate for the upper limb and 250 mm Hg for the lower limb. The tourniquet pressure

Table 218–1

■

Extremity Tourniquets

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Factors That May Increase the Risk of Tourniquet-Related Complications

Tourniquet Related Equipment not regularly serviced and inspected for pressure accuracy Bilateral tourniquet use Revisions, malignancies, or other surgeries requiring longer tourniquet times

Vascular and Metabolic Diabetes Peripheral vascular disease Obesity Raynaud’s disease Prosthetic vascular grafts

Coagulopathies Sickle cell disease and trait Preexisting coagulopathies Patients at increased risk for deep venous thrombosis

Other Peripheral neuropathy Prolonged immobilization before surgery Traumatized limb with extensive soft tissue injury Localized infection Latex allergy (must use latex-free tourniquets and tubing)

should be maintained 50 to 150 mm Hg above the systolic pressure. The application of wider, curved cuffs permits the use of lower inflation pressures to produce arterial occlusion.

Implications Most tourniquet-related compressive nerve injuries are neurapraxic and resolve completely over a few hours to days without specific therapy. With nerve disruption, recovery can take weeks or months, but incomplete recovery is rare. Also, there is the potential for a causalgia syndrome to develop, with significant disability. Weakness and swelling due to post-tourniquet syndrome can interfere with rehabilitation and wound healing. Pressure-related skin injuries increase the risk of infection. Compartment syndromes pose a significant risk for ischemic necrosis and permanent contracture of the involved muscle groups. Unrecognized arterial insufficiency can lead to necrosis of soft tissue and bone. In patients given regional anesthesia, tourniquet pain and associated hypertension may require deep sedation with propofol or ketamine or even general anesthesia. Opiates alone are usually ineffective. Hypotension with tourniquet deflation is expected and usually self-limited. If not, a fluid challenge and small doses of vasopressors are used until the hypotension resolves. Massive pulmonary embolism causes hemodynamic instability, right ventricular strain, and cardiovascular collapse. Nonfatal embolism may result in hypoxemia due to ventilation-perfusion mismatching, myocardial infarction, or stroke due to paradoxical cerebral embolism with intracardiac shunts.

OTHER SURGICAL SUBSPECIALTIES

the presence of elevated creatine kinase (MM) enzymes and myoglobinuria. If the tourniquet has produced a compressive nerve injury, it may be difficult to distinguish this injury from one related to regional block. However, as noted earlier, tourniquetrelated nerve injury can range from paresthesia to complete paralysis. The sciatic nerve is often involved in lower extremity surgery, and radial nerve injury is more common than ulnar or median nerve injury with upper extremity surgery. Further, localized tourniquet-related nerve injury is often neurapraxic, in which case the prognosis for full recovery is good. In contrast, injuries to nerves caused by needles or indwelling catheters may involve damage to the axon or perineurium. Brief neurologic assessment of the affected extremity should follow surgery. Evidence of motor and sensory deficits requires neurologic consultation and nerve conduction studies to determine the site of the defect. With regional anesthesia, there may be a delay in the diagnosis of nerve injury, especially if indwelling catheters are used for postoperative analgesia. Acute compartment syndrome has been observed immediately after surgery or after a delay of several hours. The limb is typically swollen, muscles are stiff, and pain is more severe than the physical findings would suggest. Neurologic dysfunction is a common sequela. Confirmation is by measurement of intracompartmental pressures. Postoperative causalgia presents weeks or months after surgery. Burning pain and autonomic dysfunction develop, followed by dystrophic changes in the extremity. Skin injuries are usually evident upon tourniquet cuff removal. Ecchymoses, persistent erythema, bullae formation, or skin burns may be present. Vascular insufficiency due to arterial injury should be suspected when cuff deflation does not result in reperfusion of all or part of the extremity.

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MANAGEMENT

●

●

Nerve injuries that do not resolve within 48 hours should be referred to a neurologist for assessment and follow-up nerve conduction studies. Post-tourniquet syndrome is managed with elevation of the extremity, monitoring of wound healing, and physical therapy. Pressure-related skin injuries are treated as needed. Bullae or chemical burns require burn care. However, they may be avoided by applying a nonpermeable plastic barrier drape over the distal end of the tourniquet cuff before preparing the skin. Causalgia requires management by a comprehensive chronic pain management team, and early referral is essential. Compartment syndromes are a surgical emergency and require fasciotomy to decompress the affected muscle compartments. Arterial insufficiency of an extremity requires surgical revascularization or thrombolytic therapy. Diagnosis of intraoperative pulmonary emboli is facilitated with transesophageal echocardiography. Therapy for pulmonary emboli is supportive and includes controlled ventilation, oxygen, pressor support, and cardiopulmonary resuscitation if needed. Systemic anticoagulation, thrombolytic therapy, surgical thrombectomy, or thrombus removal by interventional radiology may be necessary in some patients. Cerebral emobilization is diagnosed with computed tomography scans, and therapy is directed by a neurosurgeon and neurologist.

PREVENTION Catastrophic complications are minimized by judicious patient selection. During screening of patients at high risk for DVT (prolonged immobilization, hypercoagulable state), if thrombus is detected, surgery should be postponed. However, screening all patients for right-to-left intracardiac shunts with contrast-enhanced transthoracic echocardiography is not cost-effective, and it is questionable whether the presence of a right-to-left intracardiac shunt would affect anesthetic or surgical management. Safety factors in the use of pneumatic tourniquets for hemostasis during hand surgery were first described in 1951, and Bruner’s 10 rules were subsequently revised by Braithwaite and Klenerman in 1996. Fortunately, most pneumatic tourniquet complications in extremity surgery are avoided by limiting maximum tourniquet pressure and tourniquet inflation time. Although there are no randomized, controlled, prospective clinical studies to provide us with evidence-based guidelines, there are sufficient animal studies and clinical data to make the following recommendations: ● ● ●

● ●

●

Carefully select patients preoperatively. Use a wide, low-pressure tourniquet cuff. Inflate tourniquets to the lowest pressure needed to prevent bleeding. Limit tourniquet ischemia time to 2 hours or less. Set maximum tourniquet pressure settings as follows: arm tourniquets, 50 to 75 mm Hg above the baseline systolic pressure; leg tourniquets, 75 to 100 mm Hg above the baseline systolic pressure. Ensure adequate padding beneath the tourniquet.

●

Use barrier techniques to prevent any skin preparation solutions from running underneath the tourniquet cuff. Alternate the use of two tourniquets. Ensure tourniquet reliability with regular maintenance checks.

There are other simple things that we can do to reduce tourniquet-related injuries, without waiting for advances in research and technology. Using the following general guidelines may result in tourniquet cuff pressures 30% to 50% lower than those currently used in routine clinical practice: ●

●

●

Use conical, tapered tourniquet cuffs instead of conventional rectangular cuffs. These can reduce limb occlusion pressure by as much as 23% compared with conventional cuffs. Also, they are more efficient at transmitting surface pressure to deep tissues because they more nearly conform to the shape of the extremity. Set tourniquet pressures by determining limb occlusion pressure with Doppler or portable ultrasonography. Then set tourniquet pressures 40 to 80 mm Hg above limb occlusion pressure. Subsystolic occlusion pressures can be generated with wider conical cuffs or with a cuff width–to–extremity circumference ratio greater than 0.5.

In the future, tourniquet-related injuries may be minimized and allowable tourniquet times extended with ischemic preconditioning of skeletal muscle, more frequent reperfusion intervals, or combined regional hypothermia and ischemic preconditioning. Finally, the recent availability of sustained-release epidural morphine compounds, along with general anesthesia, may offer the best of both worlds for anesthesiologists who wish to provide good postoperative analgesia without concern about possible postoperative neuropathies with peripheral nerve or plexus blocks, especially when extremity tourniquets will be used during surgery.

Further Reading Al-Ghamdi AA: Bilateral total knee replacement under tourniquet in a homozygous sickle cell patient. Anesth Analg 98:543-544, 2003. Braithwaite I, Klenerman L: Burns under tourniquets—Bruner’s ten rules revisited. J Med Def Unions 12:14-15, 1996. Bruner JM: Safety factors in the use of the pneumatic tourniquet for haemostasis in surgery of the hand. J Bone Joint Surg Am 33:221-224, 1951. Duffy PJ: The arterial tourniquet. Available at http://www.uam.es/ departamentos/medicina/anesnet/gtoa/hm1.html Iwama H, Kaneko T, Ohmizo H, et al: Circulatory, respiratory and metabolic changes after thigh tourniquet release in combined epidural-propofol anaesthesia with preservation of spontaneous respiration. Anaesthesia 57:588-592, 2002. Kam P, Kavanaugh R, Yoong F: The arterial tourniquet: Pathophysiological consequences and anaesthetic implications. Anaesthesia 56:53-54, 2001. Tredwell S, Wilmink M, Inkpen K, et al: Pediatric tourniquets: Analysis of cuff and limb interface, current practice, and guidelines for use. J Pediatr Orthop 21:671-676, 2001. Van Roekel HE, Thurston AJ: Tourniquet pressure: The effect of limb circumference and systolic blood pressure. J Hand Surg 10:142-144, 1985. Weiss SJ, Cheung AT, Stecker MM, et al: Fatal paradoxical cerebral embolization during bilateral knee arthroplasty. Anesthesiology 84:721-723, 1996.

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Complications of Spinal Surgery Michelle L. Lotto

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Case Synopsis A 28-year-old woman with severe kyphotic deformity from a prior crush injury is undergoing T6 corpectomy with posterior spinal fusion and instrumentation. Before surgery, the patient is neurologically intact. During spinal instrumentation, the motor evoked potential (MEP) from the left gastrocnemius muscle and the cervical and cortical somatosensory evoked potentials (SEPs) from the left posterior tibial nerve are suddenly lost (Figs. 219-1 and 219- 2). Reversal of induced hypotension (85/55 mm Hg) to baseline pressure (120/60 mm Hg) does not improve the SEP or MEP responses. Some return of SEP amplitude is seen after removal of the spinal retractors, but the MEP remains depressed. The procedure is aborted because of the evolving neurologic deficit.

PROBLEM ANALYSIS Definition NEURAL INJURY Damage to neural structures is a dreaded consequence of spinal surgery. In addition to direct surgical injury to neuronal tissue, nerve injury can occur because of stretch, compression, or both. The mechanism underlying tension-related or ischemic nerve injury is increased intraneural pressure that reduces the cross-sectional area of the nerve and compromises its blood flow. Compression generates relative venous hypertension within the nerve sheath, necessitating an increase in the arterial pressure for adequate perfusion. Patients undergoing spinal surgery are at risk not only for surgical injury to the spinal cord but also for positionrelated injuries to the peripheral and, rarely, the optic nerves. Diabetes mellitus, alcohol abuse, vitamin deficiencies, malnutrition, renal disease, hypothyroidism, and emaciation can increase the risk for perioperative peripheral nerve injury.

Recognition Patients undergoing spinal procedures with general anesthesia do not manifest signs or symptoms of spinal cord injury unless the insult is extreme, such as cord transection with spinal shock. Neurophysiologic monitoring modalities, including SEPs, transcranial MEPs, and electromyography, are used to detect neurologic insult during spinal surgery. Intraoperative spinal cord monitoring is intended to reduce permanent neurologic deficits by allowing the early detection of impending neurologic injury and the implementation of corrective interventions. SEP monitoring provides a continuous evaluation of the somatosensory system through repetitive stimulation of a peripheral nerve and the recording of multiple responses obtained from the spinal cord and somatosensory cortex. Although SEP monitoring is useful for determining the integrity of the spinal cord during procedures that may cause overdistraction of the cord, it does not specifically reflect injury to the motor tracts. The ability of SEP monitoring to detect ischemic motor injury is significantly limited by the differential blood supply to the anterior and posterior spinal cord tracts.

HYPOTENSION Hypotension is a potentially serious complication of spinal surgery. Although hypovolemia is the most common cause of intraoperative hypotension, other causes are excessive depth of anesthesia, allergic reactions, pulmonary embolism, and cardiovascular dysfunction. HEMORRHAGE

Left med. gastroc.

Right med. gastroc.

13:01 13:25 13:26 13:30

Significant blood loss can be a major complication of certain spinal procedures. Bone decortication and epidural venous bleeding are the chief causes of blood loss during spinal surgery. The surgical team should be prepared for the possibility of massive blood transfusion in patients undergoing corpectomy, multilevel spinal instrumentation, and fusion surgery, especially when it involves the thoracolumbar spine.

13:33 13:34 13:34

50 uV 20 msec

13:35

Figure 219–1 ■ Sudden loss of motor evoked potential recorded from the left gastrocnemius muscle.

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Figure 219–2 ■ Loss of the left subcortical and cortical somatosensory evoked potentials (far right panel) with stimulation of the left posterior tibialis nerve.

MEP monitoring is a newer modality that offers direct monitoring of the motor system through transcranial electrical stimulation of the motor cortical structures and recording of myogenic responses in the target muscle groups. Although MEP monitoring is more specific to motor injury than is SEP, MEP shows greater sensitivity to anesthetic agents and a much larger variability in amplitude over time than does SEP. Newer transcranial stimulation techniques involving multiple trains of higher-intensity electrical stimuli have improved the reliability of MEP monitoring in patients under general anesthesia. However, MEP amplitudes are somewhat variable over time. Therefore, the criteria used to determine a significant change in MEP can vary among centers. However, generally accepted criteria for significant changes in SEP and MEP are as follows: ●

●

SEP ● 50% decrease in amplitude ● 10% increase in latency MEP ● Loss in amplitude greater than 80% ● Complete loss of the potential

Risk Assessment SEP monitoring is most commonly used during surgical correction of spinal deformities. Although it has been used in a variety of spinal procedures, the benefit of SEP monitoring in conditions other than kyphoscoliosis repair is less well established. There is mounting evidence that MEP monitoring may provide more specific and sensitive detection of neurologic injury in many types of spinal surgeries, including scoliosis repair, spinal cord tumor resection, and spine stabilization. However, the sensitivity of MEPs to anesthetic agents, as well as the difficulty in obtaining MEPs in patients with preexisting motor deficits, makes it a more technically challenging monitoring modality than SEPs. However, changes can occur in both modalities in response to alterations in physiology and pharmacology, as well as to interference from electrical devices in the operating room. Factors that interfere with SEP monitoring include the following: ● ●

Anesthetic agents (Table 219-1) Hypotension

● ● ● ●

Hypoxemia Hypothermia Alkalosis or acidosis Cold surgical irrigation

Implications Failure to heed significant changes in SEPs or MEPs may lead to permanent neurologic injury. In the case synopsis, changes in both SEPs and MEPs resulted in halting the surgical procedure, thereby preventing possible irreversible neural injury and paralysis.

Table 219–1

■

Effect of Anesthetics on Cortical Somatosensory and Motor Evoked Potentials

Anesthetic

SEP Amplitude

SEP Latency

MEP Amplitude

↓ ↓↓

→ ↑

↓ ↓↓↓

↑ ↑↑

↓↓↓ ↓↓↓

↓↓ ↓↓ ↓↓

↑ ↑ →

↓↓↓ ↓↓↓ ↓↓

↑↑ →↑ ↓ ↓↓↓

↑ ↑ ↓ ↑↑

→ →↓ ↓↓ ↓↓↓

↓↓ ↑

↑ →

↓ ↓

Inhalational Agents Desflurane 0.5 MAC 1 MAC Isoflurane 0.5 MAC 1 MAC Sevoflurane 0.5 MAC 1 MAC N2O (60%)

Intravenous Induction Agents Etomidate Ketamine Propofol Thiopental

Adjuncts Benzodiazepines Opioids

→, no change; ↓ or ↑, 10%-20% change; ↑↑ or ↓↓, 30%-50% change; ↑↑↑ or ↓↓↓, >50% change. MAC, minimal alveolar concentration; MEP, motor evoked potential; N2O, nitrous oxide; SEP, somatosensory evoked potential.

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PREVENTION Careful attention to patient positioning and SEP and MEP monitoring for neural injury can help prevent spinal cord injury. Several methods are used to reduce blood loss and the need for blood transfusions or component therapy.

Monitoring To optimize the detection of spinal cord injury, the anesthesia team should try to maintain a constant pharmacologic and physiologic state. Both SEP and MEP monitoring modalities may show false-positive changes in response to sudden changes in anesthetic depth, as well as acute physiologic changes, including hypotension, hypoxia, and hypothermia. MEPs show greater dose-dependent sensitivity to both volatile and intravenous anesthetic agents than do SEPs, and complete muscle relaxation must be avoided. Continuous intravenous infusions of propofol and opioids provide fairly stable monitoring conditions for both SEPs and MEPs. Abrupt changes in anesthetic depth or intravenous bolus

873

doses of analgesics should be avoided at points during spinal surgery when spinal cord injury is most likely to occur.

Patient Positioning Positioning for spinal surgery can present many challenges for the anesthesiologist. Prone positioning is associated with twice as many claims for peripheral nerve injuries as are other surgical positions. Vulnerable sites (e.g., bony prominences, axilla [brachial plexus], elbow [ulnar nerve], face, breasts) should be padded to disperse pressure. Unfortunately, meticulous attention to padding does not guarantee avoidance of injury. In addition to debilitating peripheral nerve injury, postoperative visual loss has emerged as a rare but devastating complication of spinal surgery. Multiple mechanisms may contribute to postoperative blindness; however, ischemic optic neuropathy is the most common cause in patients having spinal surgery. Risk factors for postoperative visual loss are listed in Table 219-2. Postoperative blindness may occur despite the use of positioning techniques that avoid eye compression, such as the use of Mayfield tongs or special prone face pillows. Early blood transfusion, maintaining mean arterial pressure greater than 80% of baseline, and head-up positioning have been recommended to avoid perioperative blindness. However, there are no controlled trials to support the efficacy of these preventive measures.

Blood Loss and Transfusion Requirements Anesthesiologists have several techniques available for reducing blood loss and transfusion requirements, including induced hypotension, autologous blood salvage, and normovolemic hemodilution. INDUCED (ELECTIVE) HYPOTENSION Induced hypotension has been shown to reduce blood loss and transfusion requirements during elective spinal surgery. Sodium nitroprusside, nitroglycerin, or β-blockers are given intravenously, possibly with continuous positive airway pressure and deep inhalation anesthesia, to initiate and maintain induced hypotension. Recently, nicardipine, an arterioselective vasodilator, has gained favor over sodium nitroprusside and nitroglycerin. The former is an arterial and venous vasodilator, and the latter is a venodilator, so both can reduce venous return and cardiac preload; thus, both have an increased potential to cause untoward hypotension compared with nicardipine. Nicardipine is compatible with β-blockers, and continuous positive airway pressure

Table 219–2

■

Risk Factors for Postoperative Blindness

Patient Factors

Intraoperative Events

Hypertension Diabetes mellitus Smoking history Peripheral vascular disease

Anemia (hematocrit ≤25) Hypotension Prolonged surgical time Prone positioning

OTHER SURGICAL SUBSPECIALTIES

Detection of neurologic injury and timely initiation of corrective measures require good communication between the neurophysiologic monitoring personnel and the anesthesia and surgical teams. Changes in anesthetic depth or bolus dosing of medications should be avoided during periods of high spinal cord risk, such as spinal distraction. When significant changes in spinal potentials occur, technical error should be ruled out, and the surgeon should be alerted. Reduced mean arterial pressure and anemia or hypoxia increase the risk for spinal cord injury. Thus, measures to correct these conditions can improve spinal cord perfusion and oxygenation. If the response to therapy is inadequate, and significant changes in SEPs or MEPs persist, the surgical team must evaluate the patient for procedure-related complications and then make the necessary alterations to reverse an evolving insult. When using SEPs as the sole monitoring modality, evaluation should include a wake-up test, during which the patient is allowed to emerge from anesthesia so that the motor system can be evaluated. Although the wake-up test is the gold standard for evaluation of the spinal cord, the use of both MEPs and SEPs may reduce the need for this assessment. Treatment of hypotension first requires assessment of the cause. Blood loss and hypovolemia are the most common causes of hypotension during spinal cord surgery, and replacement of fluids is adequate treatment in most situations. Positioning may contribute to hypovolemia when patients are placed on the Jackson table or in the kneeling position for spinal surgery. In these positions, venous return may be reduced by the sequestration of blood volume in the capacitance vessels of the abdomen and legs. Pharmacologic treatment (e.g., phenylephrine) may be necessary to augment arterial blood pressure until fluid resuscitation is adequate. The requirement for blood or blood product transfusions must be assessed on an individual basis.

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can be added if further blood pressure reduction is needed. Although animal experimentation suggests that nitroglycerin is best for preserving spinal cord blood flow during hypotension, this has not been confirmed in humans. The use of induced hypotension is based on clinical judgment, taking into account the overall physical status of the patient and the type of spinal surgery to be performed. Extreme caution should be used in the induction of hypotension in patients with significant spinal cord compression. Spinal injury impairs the normal autoregulatory process of the spinal cord vessels. External compression related to vertebral displacement or surgical retraction further decreases spinal blood flow. Hypotension has been associated with worse neurologic outcomes after traumatic spinal cord injury.

of blood is removed from the patient in the operating room before or at the beginning of surgery and stored. It is then transfused back into the patient after most of the expected surgical blood loss has occurred. As blood is removed, it is replaced with colloid (1:1), crystalloid (3:1), or both. Platelet function and coagulation factors are preserved. Excessive hemodilution can reduce oxygen transport and cause a decrease in systemic vascular resistance and hypotension. In addition, it has been suggested that the combination of hypotension and low hemoglobin may contribute to the risk of optic ischemia and postoperative blindness in prone spinal surgery patients. Contraindications to acute normovolemic hemodilution include severe cardiovascular, pulmonary, renal, or hepatic dysfunction and coagulopathy.

INTRAOPERATIVE AUTOLOGOUS BLOOD SALVAGE

Further Reading

Autologous blood salvage is a useful tool for preserving the blood lost during spinal surgery, but it can be associated with coagulopathy. Salvaged blood is autotransfused as needed after it has been washed or filtered, based on the type of equipment used. A micropore filter should be used to remove microaggregates, bone, and fat particles. However, fibrinolysis, inhibition of the clotting system, and possibly disseminated intravascular coagulation may occur with filtration-type autotransfusion. The removal of soluble products by cell washing systems can also induce coagulopathy, as well as the loss of coagulation factors and platelets. Purulent infection and malignancy were relative contraindications to autologous blood salvage in the past, but use of these systems is possible in these conditions with appropriate filtration. ACUTE NORMOVOLEMIC HEMODILUTION Acute normovolemic hemodilution is another method of reducing intraoperative blood loss. A predetermined amount

Banoub M, Tetzlaff J, Schubert A: Pharmacologic and physiologic influences affecting sensory evoked potentials: Implications for perioperative monitoring. Anesthesiology 99:716-737, 2003. Goto T, Crosby G: Anesthesia and the spinal cord. Anesthesiol Clin North Am 10:493-519, 1992. Grundy BL, Nash CL, Brown RH, et al: Deliberate hypotension for spinal fusion: Prospective randomized study with evoked potential monitoring. Can Anaesth Soc J 29:452-462, 1982. Kroll DA, Caplan RA, Posner K, et al: Nerve injury associated with anesthesia. Anesthesiology 73:202-207, 1990. Lauer KK: Visual loss after spine surgery. J Neurosurg Anesthesiol 16:77-79, 2004. Lotto ML, Banoub M, Schubert A: Effects of anesthetic agents and physiologic changes on intraoperative motor evoked potentials. J Neurosurg Anesthesiol 16:32-42, 2004.

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Jeffrey L. Lane Case Synopsis

PROBLEM ANALYSIS Definition Respiratory insufficiency is defined as the inability of the patient’s lungs to provide sufficient oxygen (O2) or expel sufficient carbon dioxide (CO2) to satisfy whole body metabolic demands. In the postoperative setting, this can be related to (1) airway obstruction, (2) arterial hypoxemia, or (3) hypercarbia (Table 220-1). Airway obstruction is often mechanical, caused by occusion of the posterior oropharynx by the tongue. Hypoxemia is defined as a reduction in arterial oxygen tension (PaO2) below 60 mm Hg. It can be the result of atelectasis, pulmonary edema, pulmonary aspiration, pneumothorax, or pulmonary embolism. The differential diagnosis of hypoxemia includes decreased minute ventilation, low fraction of inspired oxygen (FiO2), ventilation-perfusion mismatch, and block of O2 diffusion across the alveolar membrane. Arterial oxygenation (PaO2 in mm Hg) declines with age. When the subject is breathing room air, it can be estimated using this formula: 100 – (0.3 × age). Hypercarbia is defined as an increase in arterial CO2 tension (PaCO2) above 45 mm Hg. It results from decreased CO2 elimination (hypoventilation, respiratory depression, lung pathology that increases dead space), increased CO2 production (fever, sepsis, shivering, thyrotoxicosis, malignant hyperthermia), or CO2 rebreathing. In the PACU, hypercarbia most often indicates respiratory depression from opiates or residual anesthetics. In contrast to PaO2, PaCO2 does not change with age.

Recognition AIRWAY OBSTRUCTION Airway obstruction presents with a combination of labored breathing pattern, chest wall retraction, nasal flaring,“snoring” or “grunting” noises (partial obstruction), absence of breath sounds (complete obstruction), paradoxical movement of

SPECIAL TOPICS

A 53-year-old morbidly obese man is recovering in the postanesthesia care unit (PACU) after undergoing an open Nissen fundoplication. He has a history of smoking. A left subclavian central line was placed without complication shortly after the induction of anesthesia. The intraoperative course was unremarkable, and the patient was extubated in the operating room. Shortly after arriving in the PACU, the patient becomes dyspneic. The oxygen saturation is 90%, heart rate is 110 beats per minute, blood pressure is 168/98 mm Hg, and respiratory rate is 32 breaths per minute.

the chest wall (e.g., “rocking boat” or “seesaw” respirations), stridor, wheezing, and patient anxiety. Cardiovascular manifestations include hypertension and tachycardia. As mentioned earlier, postoperative airway obstruction is usually due to tongue occlusion (partial or total) of the posterior oropharynx caused by opioids or residual anesthetics. Such occlusion may or may not be relieved by a head tilt or jaw thrust or by the placement of a nasopharyngeal airway. If these maneuvers do not relieve the occlusion, other causes must be considered (see Table 220-1). Laryngospasm is usually seen immediately after extubation in the operating room or PACU. It results from stimulation of the glottal structures by secretions or airway equipment in a lightly anesthetized patient. It is usually characterized by a high-pitched inspiratory stridor (“cooing” or “crowing”) or by the absence of sounds in cases of complete closure. Airway edema from surgical trauma, patient positioning, or airway instrumentation may cause airway obstruction. Procedures that increase this risk include oral or extensive head and neck surgery and direct manipulation or instrumentation of the airway (e.g., vocal cord biopsy, bronchoscopy). Prolonged Trendelenburg or prone (or combined) positioning can lead to extensive airway edema. Further, patients with anticipated or unanticipated difficult airway management and prolonged airway instrumentation are at increased risk for airway edema. Residual neuromuscular blockade is recognized by signs of inadequate neuromuscular relaxant reversal, including the presence of fade with tetanus and less than four out of four twitches on train-of-four stimulation. Clinically, the patient exhibits inadequate head lift (1500 mL) or cardiac dysfunction (myocardial ischemia or infarction, cardiomyopathy, severe hypertension, valvular stenosis). Cardiogenic pulmonary edema leads to high central venous and pulmonary capillary wedge pressures, with or without decreased urine output. Noncardiogenic (permeability) pulmonary edema occurs with acute respiratory distress syndrome and aspiration pneumonitis. Damage to alveolar cells allows fluid to transmigrate (“leak”) into the alveolar space, causing pulmonary edema. With this type of pulmonary edema, central venous and pulmonary artery pressures are usually normal. Pulmonary embolism must always be considered in the setting of postoperative hypoxemia. Air, fat, or thrombotic emboli may lodge in the pulmonary arterial circulation to cause dyspnea, tachypnea, tachycardia, hypotension, and increased venous pressure and alveolar dead-space ventilation. The last manifests as an increased PaCO2 to end-tidal CO2 gradient. In the PACU, pneumothorax may be a cause of hypoxemia in patients with recent central line placement, rib fractures, intercostal blocks, or surgery near or involving the diaphragm (e.g., liver resection, nephrectomy, splenectomy, hiatal hernia repair, esophageal resection, upper stomach surgery). Signs and symptoms include dyspnea, tachypnea, unequal breath sounds, high peak inspiratory pressures, and possibly hypotension due to tension pneumothorax. Chest radiographs showing partial to complete lung collapse confirm the diagnosis. HYPERCARBIA Hypercarbia (hypoventilation) is common after general anesthesia. In most instances, it is mild and of no major consequence. Respiratory acidosis due to moderate hypercarbia (PaCO2 >50 mm Hg) manifests with sympathomimetic signs and symptoms: hypertension, tachycardia, headache, nausea, sweating, and agitation. Severe hypercarbia (PaCO2 >80 mm Hg) can result in somnolence (CO2 narcosis), arrhythmias, and direct myocardial depression. If hypercarbia is suspected, arterial blood gas determinations can confirm the diagnosis. The next step is to determine the cause of hypoventilation. Drugs are the most common cause of postoperative respiratory depression with hypoventilation. Residual inhaled anesthetics and intravenous or neuraxial opioids are the most common offenders in PACU settings. Inhaled anesthetics usually cause a rapid, shallow breathing pattern, whereas opioid-induced respiratory depression results in a slow respiratory rate in association with large tidal volumes and pinpoint pupils. “Splinting” occurs when inspiratory effort is retarded by significant incisional pain, abdominal distention, or tight abdominal dressings. It occurs most often after upper abdominal or thoracic surgery and may lead to hypoventilation and hypercarbia. Residual neuromuscular blockade is another cause of hypoventilation in the PACU. It results from inadequate reversal, overdose, pharmacologic interactions (e.g., antibiotics, magnesium), altered pharmacokinetics (e.g., hypothermia,

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renal or hepatic dysfunction), or metabolic factors (e.g., hyperkalemia and acidosis). The clinical diagnosis is made by the inability of a conscious patient to maintain a 5-second head lift or by the use of a nerve stimulator in an unconscious patient.

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Table 220–2

● ●

Hypoxemia

Hypercarbia

Pulmonary

Tachypnea Pulmonary vasoconstriction

Cardiac

Early Tachycardia Hypertension Arrhythmias Late Bradycardia Hypotension Cardiac arrest Restlessness Combativeness Confusion Obtundation Increased ICP Metabolic lactic acidosis

Tachypnea Pulmonary vasoconstriction Bronchodilatation Hypertension Tachycardia Arrhythmias

● ● ● ● ●

Preoperative pulmonary function tests are useful for predicting postoperative pulmonary dysfunction only after pulmonary resection; in other situations, they do not predict postoperative pulmonary complications. For patients with one or more of the preceding risk factors, anesthetists must strongly consider delaying tracheal extubation until there has been satisfactory progress with temporary mechanical ventilation and weaning (i.e., satisfactory unassisted ventilation and oxygenation).

Implications Postoperative respiratory insufficiency can lead to serious patient morbidity and even death. Pulmonary complications are the most common serious postoperative complications, and they must be recognized and dealt with expeditiously to prevent adverse patient outcomes. Both hypoxemia and hypercarbia have detrimental systemic effects (Table 220-2). Hypertension, tachycardia, tachypnea, and arrhythmias place cardiac patients at increased risk for myocardial ischemia and infarction; this risk is increased even further with anemia (due to intraoperative blood loss) or shivering (due to altered temperature regulation). Patients with underlying neurologic disease are at even greater risk, because hypoxemia and hypercarbia alter mental status and increase intracranial pressure.

MANAGEMENT As in most anesthetic emergencies, management of postoperative respiratory insufficiency begins with evaluation and establishment of a patent airway. In patients with mechanical airway obstruction, supplemental O2 should be given while head-tilt and jaw-thrust maneuvers are performed to help displace the tongue anteriorly. Also, an oral or nasal airway can help alleviate any tongue-related obstruction. Use of a nasal airway is preferred in semiconscious or awake patients, owing to less discomfort (gagging) and better tolerance

Neurologic

Metabolic

Increased ICP Obtundation

Respiratory acidosis Hyperkalemia

ICP, intracranial pressure.

(unlikely to provoke partial or complete laryngospasm). If these measures do not alleviate the obstruction, laryngospasm must be suspected. If this is the case, gentle positivepressure mask ventilation may be effective. In many cases, however, a muscle relaxant must be administered, followed by reintubation. Minor upper airway edema is usually relieved by maintaining the patient in a semisitting (semi-Fowler) position, followed by the use of humidified gases, intravenous steroids (e.g., hydrocortisone, dexamethasone), and racemic epinephrine. If these conservative measures fail, immediate intubation and mechanical ventilation are necessary. In patients recovering from neck surgery who develop respiratory insufficiency, neck hematoma must be considered, with planning and setup for immediate drainage and possible intubation. In fact, early reintubation may prevent a lethal complication. A rapidly expanding neck hematoma can distort airway anatomy and make airway management extraordinarily difficult. Hypoxemia management starts with O2 via a nasal cannula or facemask. Hypoxemia in the PACU is usually relieved with O2 concentrations greater than 50%. Short-term therapy with 100% O2 by facemask may be necessary. If higher inspired O2 concentrations are needed to maintain PaO2 greater than 60 mm Hg, more aggressive treatment (e.g., continuous positive airway pressure by mask or intubation and mechanical ventilation) is required. After ensuring adequate oxygenation, treatment is directed toward the cause. A chest radiograph may reveal pulmonary edema, infiltrates, or pneumothorax. Diuretics are given for pulmonary edema. Significant pneumothorax requires early chest tube placement. For bronchospasm, aerosolized bronchodilators are indicated. Bronchoscopy may be necessary to remove pulmonary secretions and mucous plugs. Hypercarbia management is also directed toward the underlying cause. Often, simply encouraging the patient to breathe more vigorously is sufficient to relieve hypercarbia

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Surgical site (upper abdominal, thoracic) Smoking Underlying chronic obstructive pulmonary disease or asthma Emergency surgery Anesthesia time longer than 180 minutes Advanced age Obstructive sleep apnea Morbid obesity

Effects of Hypoxemia and Hypercarbia

System

Risk Assessment Postoperative pulmonary complications (including respiratory failure) following general anesthesia are common (up to 20% to 30% in some series), so the need to assess patient risk is critical. Risk factors for the development of postoperative respiratory failure include the following:

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until residual drug effects have subsided. If opioids are the cause, intravenous naloxone should be carefully titrated (≤40-μg increments) until ventilation is adequate. Larger doses may cause an acute hyperadrenergic crisis (hypertension, tachycardia, fulminant pulmonary edema)1 brought on by the sudden awareness of acute pain. If splinting due to pain leads to hypoventilation, additional analgesics must be given. Alternative pain control (epidural or spinal narcotics, intercostal block, local anesthetic wound infiltration by the surgeon) may also reduce pain-related splinting. Residual neuromuscular block may require intubation and controlled ventilation until its effects dissipate. Whatever the cause, severe hypoventilation may call for tracheal intubation and controlled ventilation until the primary cause has been determined and treated.

obstructive pulmonary disease undergoing high-risk (upper abdominal, thoracic) surgery, continuous epidural anesthesia is known to reduce the incidence of postoperative pulmonary complications. Although adequate analgesia helps limit postoperative respiratory insufficiency, judicious use of intravenous opioids is warranted to prevent overdose and hypoventilation. To prevent hypoventilation, hypercarbia, and hypoxemia due to residual neuromuscular block, short-acting neuromuscular blockers, along with a nerve stimulator to monitor their effects, can ensure an adequate return of neuromuscular function (e.g., sustained tetanus, return to control response to train-of-four or double-burst stimulation, 5-second head lift) before extubation.

Further Reading PREVENTION All patients recovering from general anesthesia or regional anesthesia with sedation should receive supplemental O2 during transport to the PACU. As in the operating room, pulse oximetry should be used in the PACU to monitor SpO2, with confirmation by arterial blood gas sampling if necessary. Routine PACU pulse oximetry monitoring allows practitioners to detect hypoxemia early and intervene appropriately. To limit reduced lung volumes and functional residual capacity, patients (especially those who are obese) should be maintained in the semisitting (semi-Fowler) position to minimize upward displacement of the diaphragm. This, along with the routine use of nasal airways in obese patients before extubation, will help reduce mechanical airway obstruction. Incentive spirometry may be used to limit atelectasis and improve functional residual capacity. Also, continuous positive airway pressure reduces the incidence of postoperative pulmonary complications. Pain alleviation may also help prevent postoperative respiratory insufficiency. In high-risk patients with chronic

1 The editor saw three such cases shortly after intravenous naloxone was first used in PACUs to reverse relative opioid overdose. In each case, the initial doses were 200 or 400 mg—amounts then used to treat heroin overdoses in emergency rooms. Within minutes, the patients spewed “cotton candy” oral secretions, likely due to forward heart failure. Fortunately, all three patients survived.

Adhere C, Brunson C, Roizen M: Sleep apnea, obstructive. In Roizen M, Fleisher L (eds): Essence of Anesthesia Practice, 2nd ed. Philadelphia, WB Saunders, 2002, p 307. Barash P, Cullen B, Stoelting R: Clinical Anesthesia, 4th ed. Philadelphia, JB Lippincott, 2000, pp 1385-1392. Benumof J: Obesity, sleep apnea, the airway and anesthesia. ASA Refresher Courses in Anesthesiology 30:27-40, 2002. Gruber A, Hsu J: Hypoxemia. In Pardo M, Sonner J (eds): The Manual of Anesthesia Practice, version 1.2. PocketMedicine.com, 2004. Gwirtz K: Management of recovery room complications. Anesthesiol Clin North Am 14:307-399, 1996. Hsu J: Hypercarbia. In Pardo M, Sonner J (eds): The Manual of Anesthesia Practice, version 1.2. PocketMedicine.com, 2004. Morgan G, Mikhail M, Murray M: Clinical Anesthesiology, 3rd ed. Chicago, McGraw-Hill/Lange, 2002, pp 942-946. Price J, Rizk N: Postoperative ventilatory management. Chest 115: 130s-137s, 1999. Rock P: Evaluation and perioperative management of the patient with respiratory disease. ASA Refresher Courses in Anesthesiology, 2002. Stoelting R, Dierdorf S: Anesthesia and Co-existing Disease, 4th ed. Philadelphia, Churchill Livingstone, 2002, pp 217-219, 444-446. Warner D: Preventing postoperative pulmonary complications: The role of the anesthesiologist. Anesthesiology 92:1467-1472, 2000.

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221

David A. Nakata and Robert K. Stoelting Case Synopsis

PROBLEM ANALYSIS Definition Neuropathies are classified into three histologic groups, with increasing levels of severity: neurapraxia, axonotmesis, and neurotmesis. Clinically, any or all of these injury patterns can be present in the affected nerve. With neurapraxia, there is no disruption of actual anatomic neural elements. However, there may be temporary conduction block during ischemia or some degree of demyelination, with greater effects on the function of large fibers (i.e., motor, joint position sense, soft touch). Changes accompanying neurapraxia usually resolve within a few weeks, with complete recovery expected. With axonotmesis, axons are disrupted, but the nerve sheaths remain intact. Wallerian degeneration follows, but axon regeneration results in recovery of function over weeks to months. Even so, some degree of sensory or motor deficit may persist. Neurotmesis is the most serious injury, with disruption of the entire nerve, including transection of the axons and myelin sheaths. This typically prevents regeneration and recovery, resulting in poor functional recovery. Often, the nerve is replaced with fibrous scar tissue. The majority of postoperative neuropathies are due to nerve ischemia. Most commonly, this is caused by either stretch or compression. Direct mechanical compression can obviously lead to reduced blood flow, and stretch produces a reduction in the cross-sectional area of the neural structures, leading to compression of the vasculature (Fig. 221-1).

occurring in the postoperative period. This is in sharp contrast to the historical belief, still held by many, that the development of neuropathy represents an intraoperative deviation from the standard of care.

Risk Assessment Many factors are known to be associated with the development of postoperative neuropathies (Table 221-1). In the patient described in the case synopsis, male gender, preoperative chemotherapy, and diabetes mellitus are known risk factors associated with the development of neuropathies. In males, the ulnar nerve appears to be at greater risk of injury owing to anatomic differences between the sexes. The tubercle of the coronoid process is approximately 1.5 times larger in men than in women, perhaps predisposing to increased bony compression of the nerve. In addition, women generally have a larger fat pad within the medial aspect of the elbow, which may help protect the ulnar nerve (Fig. 221-2). Also, it has been suggested that the cubital tunnel retinaculum

Recognition Postoperative neuropathies are commonly ascribed to events that occur intraoperatively. In numerous cases, however, despite close follow-up, symptoms are not reported until days after the operative procedure. It stands to reason that if intraoperative events were responsible for the development of these neuropathies, symptoms would be reported more proximate to the patient’s emergence from anesthesia. Given the reporting delay, consideration must be given to the possibility that many of these neuropathies stem from events

Figure 221–1 ■ Nerve stretch is associated with a decrease in crosssectional area and an increase in intraneural pressures. (From Butler DS: Mobilization of the Nervous System. New York, Churchill Livingstone, 1991.)

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A 28-year-old man with insulin-dependent diabetes mellitus for 15 years was diagnosed with testicular cancer. His chemotherapy regimen consisted of bleomycin and cisplatin. He underwent postchemotherapy retroperitoneal lymph node dissection under general anesthesia. The surgery, which took 2 hours, was unremarkable, as was his stay in the postanesthesia care unit. On postoperative day 3, the patient noted a decreased level of sensation in the fourth and fifth digits of his left hand. He had no prior history of peripheral neuropathy. He was subsequently diagnosed with a left ulnar neuropathy.

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Table 221–1

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Factors That May Increase the Risk of Perioperative Neuropathy

Alcoholism Amyloidosis Arthritis Atherosclerotic disease Autoimmune disorders Bell’s palsy Cancer Chemotherapy Connective tissue diseases Diabetes mellitus Direct nerve trauma Gender (male) Hepatic failure Hypothyroidism Infectious diseases Malnutrition Nerve entrapment syndromes Renal failure Trauma to adjacent structures Vitamin deficiencies

Ulnar nerve

Cubital tunnel retinaculum FCU

Figure 221–3 ■ The cubital tunnel retinaculum is a tough, fibrous band that is in close proximity to the ulnar nerve. Compression of the ulnar nerve can occur between this retinaculum and the medial epicondyle. FCU, flexor carpi ulnaris (ulnar head). (From Warner M: Perioperative neuropathies, blindness, and positioning problems. American Society of Anesthesiologists 53rd Annual Refresher Course Lectures, 2002, Orlando, Fla.)

in men is more robust and may place greater compressive force on the ulnar nerve when stretched (Fig. 221-3). Peripheral nerves are much more tolerant to ischemia than are nerves within the central nervous system. Peripheral nerves are commonly subjected to ischemia during the placement of vascular tourniquets for hemostasis. When inflated, the applied force is often greater than 100 mm Hg above the systolic pressure. This degree of pressure has been shown to produce slowing of nerve conduction directly under the area of compression, followed by more distal slowing as tourniquet times increase. In clinical practice, an “ischemic” tourniquet time of less than 2 hours is generally accepted. Animal studies have shown that ischemia is tolerated for up to 4 hours without causing permanent nerve damage. Compressive forces produced by tourniquets are generally greater than those produced by placing the arms or legs on a padded operating room table. Thus, individuals who undergo operative procedures lasting

Inferior ulnar collateral artery Ulnar nerve

Coronoid process Tubercle on proximal coronoid process

Medial epicondyle

Posterior ulnar recurrent artery

Olecranon Figure 221–2 ■ The ulnar nerve and ulnar collateral artery at the elbow are relatively superficial and easy to compress. The coronoid process in males is larger than in females, and the adipose layer is less prominent. These factors increase the risk of compression to the ulnar nerve in males. (From Warner M: Perioperative neuropathies, blindness, and positioning problems. American Society of Anesthesiologists 53rd Annual Refresher Course Lectures, 2002, Orlando, Fla.)

less than 2 hours should be almost immune to the development of postoperative neuropathies from tourniquet application or accepted positioning maneuvers. The patient described in the case synopsis had multiple risk factors for the development of neuropathies, including a long history of diabetes mellitus and recent chemotherapy. Preexisting conditions likely play an important role in the development of neuropathies in many individuals. This patient had no preexisting symptoms of peripheral nerve involvement, but neuropathies associated with metabolic conditions (e.g., diabetes mellitus, chemotherapy) generally have an insidious onset. This gradual onset provides an opportunity for subclinical neuropathies to become well established before the onset of symptoms, and it also leads to increased susceptibility for the development of a symptomatic neuropathy. A well-described potential cause for such increased risk is the double crush syndrome. Double crush syndrome is a peripheral nervous system disorder in which dual lesions in the same nerve act synergistically to enhance each one’s severity. Nemoto and coworkers showed that placing a low-compression clamp on a dog’s peripheral nerve could produce an incomplete conduction block. This caused only mild axonal degeneration, with no obvious clinical sequelae. If a second, equally low-compression clamp was placed more distally on the same peripheral nerve, complete conduction blockade with marked axonal degeneration was shown. This double crush injury model provides insight into how comorbidities may increase the risk of perioperative neuropathies. Also, the model may explain why some individuals develop neuropathies while others do not, despite the use of similar positioning precautions. Double crush syndrome likely plays an important role in the development of neuropathies in patients with preexisting nerve entrapment syndromes. For example, cubital tunnel syndrome is a common nerve entrapment syndrome, second in frequency only to carpal tunnel syndrome. The cubital tunnel is an enclosed space surrounded by tough

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fibrous materials and bone. Because of these anatomic boundaries, the cubital tunnel has a limited ability to expand during fluid accumulation. Postoperatively, patients retain third-space (i.e., interstitial) fluid, some of which accumulates in the cubital tunnel. This accumulation may increase pressure within the cubital tunnel, leading to double crush ulnar nerve compression. Pregnancy-induced carpal tunnel syndrome is a well-known example in which fluid retention can lead to a clinically significant peripheral neuropathy.

ME

Implications

OI

A

ME

OI

CTR

B Figure 221–4 ■ A, Anatomy during elbow extension. B, During elbow flexion, the cubital tunnel retinaculum (CTR) is stretched between the medial epicondyle (ME) and the olecranon process (Ol), leading to compression of the ulnar nerve (arrow). Also, the ulnar nerve is physically stretched during elbow flexion, causing reduction in its cross-sectional area and blood flow. (From Warner M: Perioperative neuropathies, blindness, and positioning problems. American Society of Anesthesiologists 53rd Annual Refresher Course Lectures, 2002, Orlando, Fla.)

PREVENTION In 2000 the American Society of Anesthesiologists published a practice advisory for the prevention of perioperative peripheral neuropathies. This advisory made several recommendations that may decrease the incidence of ulnar neuropathy: ●

MANAGEMENT No specific guidelines exist regarding when a neurologist should be consulted for the complaint of peripheral neuropathy. Consideration of the duration and severity of the findings is required. If the supposed peripheral neuropathy resolves within a short period, neurapraxia is the most likely diagnosis, and a full recovery can be expected. However, if the findings persist with no improvement, a neurology consultation should be considered to assist in both diagnosis and management. In some instances, nerve conduction studies may be warranted.

CTR

SPECIAL TOPICS

The American Society of Anesthesiologists’ closed claims analyses recognize postoperative ulnar neuropathies as among the most common, if not the most common, postoperative peripheral neuropathy. In 1999, 28% of all claims for such nerve injuries involved the ulnar nerve. More recent analyses of claims in which anesthesia care was implicated suggest that some injuries did not occur until after anesthesia care had ended. In a prospective study, Warner and colleagues found that the median time for reporting symptoms of ulnar neuropathy was 4 days after surgery (range, 2 to 7 days). Another prospective study by Warner’s group showed that ulnar neuropathies also occurred in medical patients who did not undergo surgery. Considering these reports, it is implausible to assume that all perioperative neuropathies occur during the intraoperative and perianesthetic care periods. Thus, other mechanisms for such neuropathies need to be sought. Postsurgical patients routinely receive opiates for pain control. These drugs blunt not only pain sensation but also the sensation of any paresthesias the patient might experience. Pain medications also produce sedation, so that patients are less mobile. Such immobility might extend the time patients spend in positions that could result in nerve stretch or compression injury. Finally, during postoperative rounds, it is common to find patients resting with their arms folded across the chest or abdomen. Elbow flexion is known to raise the pressure within the cubital tunnel and also to stretch the ulnar nerve, either of which can increase the likelihood of nerve ischemia (Fig. 221-4). Often, this crossed arm position places the cubital tunnel directly in contact with the bed, further compressing the ulnar nerve. Finally, the ulnar nerve may be injured when patients sit in armchairs with their arms flexed, which can place the cubital tunnel in direct contact with the armrests.

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Arm abduction should be limited to 90 degrees in supine patients; patients who are positioned prone may comfortably tolerate arm abduction greater than 90 degrees. Arms should be positioned to decrease pressure on the postcondylar groove of the humerus (ulnar groove). When arms are tucked at the sides, a neutral forearm position is recommended. When arms are abducted on armboards, either supination or a neutral forearm position is acceptable. Padded armboards may decrease the risk of upper extremity neuropathies. Padding at the elbow and at the fibular head may decrease the risk of upper and lower extremity neuropathies, respectively.

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Given the multitude of factors that may contribute to perioperative ulnar neuropathy, it cannot be assumed that all perioperative nerve injuries are due to a violation of the standard of care. This idea is reinforced, in most cases, by the relatively long interval between the operative procedure and the initial report of symptoms.

Further Reading Bentley FH, Schlapp W: Experiments on the blood supply of nerves. J Physiol 102:62, 1943. Cheney FW, Domino KB, Caplan RA, et al: Nerve injury associated with anesthesia: A closed claims analysis. Anesthesiology 90:1062-1069, 1999.

Gelberman RH, Yamaguchi K, Hollstien SB, et al: Changes in interstitial pressure and cross-sectional area of the cubital tunnel and of the ulnar nerve with flexion of the elbow: An experimental study in human cadavera. J Bone Joint Surg Am 80:492-501, 1998. Nemoto K, Matsumoto N, Tazaki K, et al: An experimental study on the “double crush” hypothesis. J Hand Surg [Am] 12:552-559, 1987. Practice advisory for the prevention of perioperative peripheral neuropathies: A report by the American Society of Anesthesiologists Task Force on Prevention of Perioperative Peripheral Neuropathies. Anesthesiology 92:1168-1182, 2000. Warner MA, Warner DO, Harper C, et al: Ulnar neuropathy in medical patients. Anesthesiology 92:613-617, 2000. Warner MA, Warner DO, Matsumoto JY, et al: Ulnar neuropathy in surgical patients. Anesthesiology 90:54-59, 1999.

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Delayed Emergence Deborah A. McClain

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Case Synopsis A 50-year-old man undergoes general anesthesia for umbilical hernia. He weighs 120 kg and has a history of hypertension, gastroesophageal reflux disease (GERD), polysubstance abuse, hepatitis C, and post-traumatic stress disorder (PTSD). He is taking hydrochlorothiazide, an ACE inhibitor, cimetidine, omeprazole, citalopram, and trazodone. The anesthetic and surgery progress uneventfully. The patient is extubated and taken to the postanesthesia care unit (PACU). After 15 minutes, the patient fails to respond to verbal stimuli.

Definition Delayed emergence is failure of the patient to regain the expected level of consciousness within 20 to 30 minutes of the end of anesthetic administration. Intervention is necessary to rule out potentially harmful, reversible conditions. Possible causes can be classified as follows: ● ● ● ● ●

Anesthetic drugs Medications Electrolyte disorders Metabolic disorders Systemic effects

Recognition As with all assessments, the ABCs (airway, breathing, circulation) take priority and should be reevaluated throughout the course of delayed emergence. Other assessment tools include the following: ● ● ● ● ●

Pharmacologic agents Physical examination Laboratory examination Computed tomography (CT) of the head Neurology consultation

The diagnosis of delayed emergence is made in the PACU, and the cause may be multifactorial. An anesthesiologist must evaluate these patients promptly to differentiate delayed emergence from the life-threatening problems that may falsely manifest as delayed emergence: airway obstruction, hypoxia, and hypercarbia. The patient should be evaluated immediately with assessment of vital signs (especially the rate and character of spontaneous breathing and oxygen saturation) and a physical examination. Further evaluation must consider the patient’s preexisting medical problems, any pharmacologic agents taken preoperatively or administered in the perianesthetic period, and the nature of the operative procedure performed. A thorough physical examination must be performed, with particular emphasis on vital signs (including temperature), smelling of the patient’s breath for residual volatile anesthetics, and neurologic examination. A firm tactile stimulus may

arouse the obtunded patient more effectively than verbal stimulation. Prompt laboratory evaluation includes arterial blood gas analysis to assess pH, oxygen and carbon dioxide partial pressures, and blood glucose concentration. Serum electrolytes, including calcium and magnesium, should also be evaluated. Obtaining a urine sample for toxicologic evaluation may be prudent. Finally, a CT scan of the patient’s head and consultation with a neurologist may be necessary.

Risk Assessment Although delayed emergence has many causes, its predictability and the rate at which it will occur have not been specifically assessed. Most cases are purely anecdotal, and thus no occurrence rate has been determined. Nevertheless, some level of responsiveness to stimulation should occur within 90 minutes of the cessation of anesthetic administration. Certain patients are at greater risk for delayed emergence from anesthesia. These include patients with preexisting cognitive or psychiatric disorders and patients who chronically take sedative medications. Patients who were anesthetized while intoxicated by alcohol or recreational drugs may be more difficult to arouse. Finally, those who were physically exhausted prior to surgery may have prolonged emergence.

Implications Depending on the cause of the delayed emergence, the consequences may be catastrophic or minor. However, prompt, efficient assessment and treatment are key to minimizing potential catastrophes.

MANAGEMENT Anesthetic Drugs Many factors influence the effect of inhalational or intravenous drugs on the patient’s level of consciousness: ● ● ●

Central nervous system (CNS) sensitivity Metabolism/excretion Redistribution 885

SPECIAL TOPICS

PROBLEM ANALYSIS

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Amount of drug administered Plasma concentration

Biologic variation in CNS sensitivity follows the bellshaped Gaussian curve. Some patients require very small amounts of drugs for induction and maintenance, whereas others require larger and larger quantities. The majority, of course, fall in the middle. The concentration of drug that reaches the brain receptor and the sensitivity of the receptor to that specific drug determine the response. Decreased hepatic metabolism occurs in patients at the extremes of age, in malnourished patients, in hypothermic patients, and in patients who simultaneously receive several drugs that are detoxified by the hepatic microsomal enzyme system (e.g., ethanol, barbiturates). While redistribution is responsible for the short action of some drugs (such as thiopental), it can contribute to delayed emergence as well, especially when given in repeated doses. Fat-soluble drugs, such as inhalation anesthetics, are distributed to fat stores. The result is a storage depot that releases anesthetic back into the circulation after the conclusion of the case. This is especially true for long-acting anesthetics and in obese patients. Plasma concentration and the portion of drug available to interact with receptors are affected by other factors, such as albumin and other proteins that influence protein binding. The less drug that is bound to plasma proteins, the more that is available to interact with receptors. Protein binding is also affected by pH. For example, protein binding of fentanyl decreases as the plasma becomes more acidotic, resulting in more free fentanyl. Other drugs in the patient’s system may compete for binding sites and thus result in more free drug. Volatile anesthetics, narcotics, sedatives, and muscle relaxants all can lead to delayed emergence. Phase II blockade or a pseudocholinesterase deficiency can result in prolonged neuromuscular blocking effects when succinylcholine is administered. In this case it is usually better to avoid attempts at reversal. Furthermore, some antibiotics enhance and prolong the action of nondepolarizing relaxants.

Medications Prescribed medications, such as sleeping aids, pain medications, and lipid-lowering drugs, affect minimum alveolar concentration (MAC) or occupy some of the receptors. Over-the-counter medications should also be considered as a source of delayed emergence (see also Chapter 39). H2-receptor antagonists cimetidine and ranitidine impair hepatic microsomal oxidation of some drugs. Greenblatt and colleagues found that although healthy volunteers showed no increase in sensitivity to midazolam or benzodiazepines, other drugs that depend on hepatic metabolism may be affected, as may less healthy patients. Herbal supplements also have the potential to cause excessive sedation and delayed emergence. Kava, St. John’s wort, and valerian are the primary culprits. Herbal products should be discontinued 1 day to 1 week prior to anesthesia (see also Chapter 39). Chemotherapeutic agents, such as L-asparaginase and vincristine, often produce CNS depression and even electrocardiographic changes. Although these agents are a rare cause of

delayed emergence, they are included in the differential diagnosis (see also Chapter 30).

Electrolyte Disorders Hyponatremia, especially if acute, can cause lethargy, delayed awakening, and seizures. The most common cause encountered in connection with anesthesia is the TURP (transurethral resection of the prostate) syndrome. The circumstances and serum sodium below 130 mEq/L make the diagnosis relatively simple to make. Correction should proceed at no more than 2 mEq/L per hour until a serum sodium of 130 mEq/L ± 2 mEq/L is reached. Hypercalcemia and hypermagnesemia can produce CNS depression even to the point of coma.

Metabolic Disorders Extremes of serum glucose, hypoglycemia from fasting or insulin, or hyperglycemia (hyperosmotic, hyperglycemia, nonketotic coma) can result in prolonged unconsciousness. Other endocrine abnormalities, primarily hypothyroidism and adrenal suppression or deficit, should also be considered as a cause for delayed emergence.

Systemic Effects Respiratory depression can lead to CO2 narcosis. This may be more difficult to diagnosis in the PACU, where end-tidal CO2 is not routinely monitored. Hypoxia resulting from depression or ventilation-perfusion mismatching should also be ruled out. Hypothermia can also contribute to the lowered level of consciousness. Although body temperature between 30 and 32°C does not cause unconsciousness alone, its effects on biotransformation and inhalational anesthetic solubility may contribute to prolonged emergence. Temperatures lower than 30°C can cause cold narcosis through a direct effect on the brain. Hyperthermia >40°C, such as is seen in heatstroke or malignant hyperthermia, does result in loss of consciousness. Neurologic events including stroke and seizures should also be considered in the differential diagnosis. Increased intracranial pressure caused by a cranial bleed or resulting from an intracranial mass, especially with an elevation in end-tidal CO2, can augment the effects of the latter to worsen CO2 narcosis.

TREATMENT Reversal agents (naloxone, flumazenil, physostigmine, neostigmine) may be used for treatment for as well as diagnosis of prolonged effects of narcotics, benzodiazepines, inhalation anesthetics, and muscle relaxants. Electrolyte and metabolic abnormalities should be corrected in symptomatic patients, but this must be done carefully to avoid serious undesired effects. Causes for hypoxia or hypercarbia should be assessed even as ventilatory support is initiated. A thorough neurologic evaluation should be performed to seek localizing signs versus global effects.

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A neurology consultation or CT scan may be appropriate if other causes have been eliminated. Appropriate reversal dosages are listed below: ●

● ●

Naloxone, 40-μg doses every 2 minutes IV to a total of 200 μg Flumazenil, 0.2 mg/min IV to a total of 1.0 mg Physostigmine, 1.25 mg IV

PREVENTION

Further Reading Cohen ML, Chan S, Way WL, et al: Distribution in the brain and metabolism of ketamine in the rat after intravenous administration. Anesthesiology 39:370, 1973. Curtis D, Stevens WC: Recovery from general anesthesia. Int Anesthesiol Clin 29:1, 1991.

Delayed Emergence

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Gerich JE, Martin MN, Recant L: Clinical and metabolic characteristics of hyperosmolar non-ketotic coma. Diabetes 20:228, 1971. Ghoneim MM, Dembo JH, Block RI: Time course of antagonism of sedative and amnestic effects of diazepam by flumazenil. Anesthesiology 70:899, 1989. Greenblatt DJ, Locniskar A, Scavone JM, et al: Absence of interaction of cimetidine and ranitidine with intravenous and oral midazolam. Anesth Analg 65:176, 1986. Lyew MA, Mondy C, Eagle S, et al: Hemodynamic instability and delayed emergence from general anesthesia associated with inadvertent intrathecal baclofen overdose. Anesthesiology 98:265, 2003. McClain DA, Hug CC: Intravenous fentanyl kinetics. Clin Pharmacol Ther 28:111, 1980. Narins RG: Therapy of hyponatremia: Does haste make waste? N Engl J Med 314:1573, 1986. Prough DS, Roy R, Bumgarner J, et al: Acute pulmonary edema in healthy teenagers following conservative doses of intravenous naloxone. Anesthesiology 60:485, 1984. Reves JG, Glass PSA, Lubarsky DA, et al: Intravenous nonopioid anesthetics. In Miller RD (ed): Miller’s Anesthesia, 6th ed. Philadelphia, Churchill Livingstone, 2005, p 317. Stoelting RK, Eger EI II: The effects of ventilation and anesthetic solubility on recovery from anesthesia. Anesthesiology 30:290, 1969. Tinker JH, Gandolfi AJ, Van Dyke RA: Elevation of plasma bromide levels in patients following halothane anesthesia. Anesthesiology 44:194, 1976. Ward CF: Pulmonary edema and naloxone. J Clin Anesth 8:690, 1996. Weiss HD, Walker MD, Wiernik PH: Neurotoxicity of commonly used antineoplastic agents. N Engl J Med 291:75, 127, 1974 Wood M: Plasma drug binding: Implications for anesthesiologists. Anesth Analg 65:786, 1986.

SPECIAL TOPICS

Delayed emergence may be minimized by careful perioperative care of the patient, including a precise history and physical examination, vigilant intraoperative care and monitoring, and early evaluation of potential postoperative problems. Judicious and appropriate titration of reversal agents may alleviate the prolonged anesthetic medication effects. Careful evaluation of serum chemistries, neurologic evaluation, consultation with a neurologist, and CT scan may be necessary if neurologic injury has occurred.

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Postoperative Delirium Philip Levin

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Case Synopsis An 86-year-old woman with history of stable angina, chronic obstructive pulmonary disease, hypertension, and hypothyroidism undergoes general anesthesia for pinning of a femur fracture. The surgery and anesthetic are uneventful. In the postanesthesia care unit (PACU), the patient becomes disoriented and combative.

PROBLEM ANALYSIS Definition Postoperative delirium is a state in which patients have altered consciousness, orientation, memory, perception, and behavior. It is usually noted in the PACU.

Recognition Postoperative delirium can have multiple causes and should be promptly evaluated by an anesthesiologist in the PACU. Assessment of the patient’s breathing and circulatory status is extremely important to rule out life-threatening problems such as hypoxia, hypercarbia, and airway obstruction. A thorough medical history, a complete listing of medications administered during the perioperative period, and review of the anesthesia and surgical course (including the type of surgery) should be obtained. Then a detailed physical examination and any indicated laboratory testing are performed. Severe pain (surgical, urinary, or gastric distention) can cause altered mental status and should be treated promptly. Certain metabolic, endocrine, and infectious disorders can also cause altered mental status and must be ruled out. Intracerebral pathology should be ruled out in patients with focal neurologic findings and gait disturbances. In addition, effects of residual anesthetic agents may mimic postoperative delirium. It may be difficult to distinguish residual sedation resulting from the effects of sedatives, antiemetics, or anesthetics that lead to disinhibition from causes that require treatment with sedatives. Patients with postoperative delirium are at risk of physically harming themselves or PACU personnel. Patients may tear open their bandages or wounds or pull out their intravenous lines. Patients with postoperative delirium are also at risk for falls and fractures.

Risk Assessment Risk factors for developing postoperative delirium are divided into three categories: preoperative, intraoperative, and postoperative. Preoperative risk factors include advanced age, pathologic brain states (e.g., cerebrovascular disease), administration of multiple drugs and drug interactions, abrupt withdrawal of alcohol or sedative-hypnotics, endocrine and metabolic disorders (e.g., hyper- or hypothyroidism, hyponatremia, hypoglycemia), depression, and dementia or anxiety disorders. 888

Intraoperative risk factors include the type of surgery. Patients having cardiac surgery appear to be at greater risk of developing postoperative delirium, possibly due to hypoperfusion or microembolism (air or thrombus). Further, certain orthopedic procedures may predispose to postoperative delirium, possibly due to fat emboli. Some ophthalmic procedures may be associated with bilateral loss of vision (possibly due to the use of anticholinergic drugs and eyedrops), which can contribute to postoperative delirium. Certain anesthetic drugs, including anticholinergics, barbiturates for premedication, and benzodiazepines, have been linked to an increase in postoperative delirium. Interestingly, several studies have found no difference in the effects of general, epidural, or spinal anesthesia on the development of postoperative delirium. Postoperative risk factors for delirium include hypoxia, hypocarbia, and sepsis.

Implications Postoperative delirium can result in complications such as prolonged hospital stay, delayed functional recovery, and increased morbidity.

MANAGEMENT Identifying and Correcting the Underlying Cause Initially, it is important to identify and correct underlying causes. A thorough medical history is important, including any additional information that family members or caregivers may provide (e.g., baseline behavior and mental status). A careful physical examination, including a detailed neurologic and psychiatric examination, should be performed. The patient’s vital signs and overall medical condition must be monitored carefully until underlying causes (e.g., change in respiratory status, infection, fluid or electrolyte imbalance) have been identified and corrected or stabilized. It is also important to review any pertinent laboratory and radiographic studies.

Pharmacologic Measures Identification and correction of the underlying condition may be sufficient to reverse delirium. Specific pharmacologic intervention may be necessary to reduce the intensity

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Environmental Interventions Supportive measures are useful for treating the symptoms of delirium. These include reorienting the patient to time, place, and person and minimizing excessive noise. Having a family member near the bedside may help calm the patient. Because delirium can be aggravated by sensory impairment, restoring the patient’s vision (eyeglasses or contact lenses) or hearing (replacing a hearing aid) may be helpful. The use of physical restraints should be minimized; they may aggravate the patient’s confusion, because they create the impression of being tied down.

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Psychiatric and Neurologic Care Obtaining a psychiatric consultation may be necessary if other treatment measures fail and more aggressive management is necessary. If postoperative delirium appears to have a neurologic cause, the appropriate neurologic or neurosurgical consultation should be obtained.

PREVENTION Little is known about the prevention of postoperative delirium. There is some evidence that aggressive management of established risk factors may help. Some intraoperative measures that may be effective include maintaining good oxygenation and normal blood pressure, using correct drug dosages, and maintaining normal electrolyte levels. Drugs associated with an increased risk of delirium should be used cautiously. These include H2-antagonists, digitalis, phenytoin, and anticholinergic medications. If an anticholinergic is necessary, a quaternary amine such as glycopyrrolate should be used. In general, drugs with short elimination half-lives are preferable to long-acting drugs. Adequate postoperative analgesia is also important for the prevention of postoperative delirium.

Further Reading American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th ed. Washington, DC, American Psychiatric Association, 1994. Breitbart W, Tremblay A, Gibson C: An open trial of olanzepine for the treatment of delirium in hospitalized cancer patients. Psychosomatics 43:175-182, 2002. Chung F: Postoperative mental dysfunction. In McLeskey CH (ed): Geriatric Anesthesiology. Philadelphia, Williams & Wilkins, 1997, pp 487-495. Kaneko T, Cai J, Ishikura T, et al: Prophylactic consecutive administration of halperidol can reduce the occurrence of postoperative delirium in gastrointestinal surgery. Yonago Acta Med 42:179-184, 1999. Litaker D, Locala J, Franco K, et al: Preoperative risk factors for postoperative delirium. Gen Hosp Psychiatry 23:84-89, 2001. Lynch EP, Lazor MA, Gellis JE, et al: The impact of postoperative pain on the development of postoperative delirium. Anesth Analg 86:781-785, 1998. McGowan NC, Locala JA: Delirium. Cleveland Clinic Disease Management Project, Oct 24, 2002. Available at www.clevelandclinicmeded.com/ diseasemanagement/psychiatry/delirium/delirum1.htm. Parikh S, Chung F: Postoperative delirium in the elderly. Anesth Analg 80:1223-1232, 1995. Weber JB, Coverdale JH, Kunik ME: Delirium: Current trends in prevention and treatment. Int Med J 34:115-121, 2004.

SPECIAL TOPICS

and duration of delirium. Many studies have demonstrated the safety and efficacy of antipsychotics. In this category, haloperidol is the drug of choice because of its favorable cardiovascular and respiratory side effect profile compared with other antipsychotics. Also, it has negligible anticholinergic effects. Haloperidol can be administered orally, intramuscularly, or intravenously in doses ranging from 0.25 to 2 mg. This dose is repeated or doubled every 30 to 60 minutes until the patient is sedated and calm. Droperidol has been used for more rapid tranquilization. Chlorpromazine is also effective, but it can lead to severe hypotension. Neuroleptic antipsychotic medications may lengthen the Q-T interval, thus increasing the risk of torsades de pointes. Patients who receive this treatment should have a baseline electrocardiogram. If the patient’s Q-T interval becomes prolonged to greater than 25 percent of baseline or longer than 450 msec, dose reduction or discontinuation of therapy may be needed. Recent studies show that the novel antipsychotic drug olanzapine might also be effective for treating postoperative delirium and has fewer side effects than more typical neuroleptic drugs. Further studies are warranted. Benzodiazepines are not effective therapy for postoperative delirium, except for that caused by withdrawal from alcohol or sedative-hypnotics. Lorazepam is the benzodiazepine most commonly used; it is administered orally, intramuscularly, or intravenously in doses ranging from 0.5 to 2 mg. The dose of lorazepam is repeated or doubled every 30 to 60 minutes, depending on the patient’s level of sedation. The use of physostigmine is controversial, but it may still be available in some locations. This drug was often used in the past to treat postoperative delirium, especially that due to central cholinergic crisis. Compared with quaternary anticholinergics (e.g., atropine, glycopyrrolate), physostigmine (a tertiary amine) crosses the blood-brain barrier more readily.

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Intractable Nausea and Vomiting

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David A. Nakata and Robert K. Stoelting Case Synopsis A 28-year-old, 110-kg woman presents with intractable nausea and vomiting in the postanesthesia care unit after undergoing laparoscopic cholecystectomy under general anesthesia. The anesthesia was unremarkable except for preoperative anxiety and moderate postoperative upper airway obstruction, which was easily corrected by insertion of an oral airway. Past medical history was significant for unanticipated hospital admission for postoperative nausea and vomiting following previous inguinal hernia repair.

PROBLEM ANALYSIS Definition Postoperative nausea and vomiting (PONV) is an important cause of morbidity following all types of anesthesia. It typically occurs in the immediate postanesthesia period, with most cases lasting less than 24 hours. Nausea is a subjective sensation best evaluated by the patient and is mediated via unknown neural pathways. It often, but not always, arises as the antecedent event to retching or vomiting. Vomiting (emesis) is defined as the forceful retrograde oral expulsion of gastric contents. Retching differs from vomiting by the lack of expulsion of gastric contents. PONV has multiple causes that can be subdivided into patient-, surgical-, and anesthetic-related factors.

Recognition The sensation of nausea is familiar to everyone, but because of its subjective nature, it is often difficult to appreciate, especially in a disoriented postoperative patient. Nausea is typically accompanied by decreased or inappropriate gastrointestinal activity and may include hypotonicity of muscular sphincters, hypoperistalsis or reverse peristalsis, and hyposecretion. The autonomic nervous system, especially the parasympathetic system, can also be affected, leading to manifestations such as skin pallor, diaphoresis, increased salivation, vasovagal reactions, and anorexia. If these symptoms persist, they invariably deteriorate to retching and vomiting. Vomiting, unlike nausea, is virtually unmistakable in its presentation. The neuroanatomic pathways and mediators that produce vomiting are better understood than those associated with nausea. Two distinct areas in the brain are responsible for the initiation and coordination of vomiting: the chemoreceptor trigger zone in the fourth ventricle, and the vomiting center in the lateral reticular formation. The chemoreceptor trigger zone contains a high density of dopaminergic receptors and is connected by neural pathways to the vomiting center. Figure 224-1 is a schematic representation of the factors that are known to interact with the areas 890

responsible for vomiting. In addition, numerous physiologic changes occur, including relaxation of the gastric fundus and lower esophageal sphincter and the forceful contraction of the abdominal musculature, leading to the ejection of gastric contents.

Risk Assessment The incidence of postoperative vomiting is typically reported to be between 20% and 40%. Table 224-1 presents factors that have been implicated in the development of PONV. A number of these factors are widespread throughout the general surgical population, making it common for individual patients to have multiple risk factors. These factors, in addition to specific patient characteristics, are useful in predicting which patients are at greatest risk of developing PONV. Unfortunately, there is no formal scheme that allows clinicians to predict which prophylactic maneuvers will yield the greatest success. Some of the less obvious factors that influence the incidence of nausea and vomiting include anxiety, gender, obesity, experience of the anesthesiologist, and anesthetic agent. Anxiety may exacerbate PONV via the release of catecholamines. Experimental models exist in which vomiting can be induced by instilling catecholamines into the cerebral ventricles. This may also account for the increased incidence of nausea and vomiting associated with the use of anesthetic agents that increase circulating catecholamines. The increased incidence of PONV in women has traditionally been ascribed to a hormonal cause. This is supported by a decreased incidence of PONV in females at the extremes of age when compared with age-matched males. However, a recent study postulates that the increased incidence of PONV in women may actually be due to a greater sensitivity to dopamine. Obesity may interfere with positive-pressure ventilation, leading to gastric distention. The case synopsis provides examples of some of the common predisposing conditions that can increase a patient’s risk for PONV, including female gender, obesity, previous history of PONV, anxiety, laparoscopic abdominal surgery, placement of an oral airway, and general anesthesia. Other factors may include increased gastric inflation or hypoxemia

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Figure 224–1 ■ Factors known to interact with the chemoreceptor trigger zone and the vomiting center to initiate vomiting.

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Motion

Intractable Nausea and Vomiting

Hypoxia Pain

Increased intracranial pressure Smell, sight, taste Psychotropic factors

Vestibular labyrinth

Cerebellum

Cortical afferents

Drugs Radiation

Chemoreceptor trigger zone

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Vomiting center

Act of vomiting

Visceral afferents

Disease of: Heart Digestive tract Biliary tract Genitourinary tract

from difficult positive-pressure ventilation and increased arterial carbon dioxide tension from inadequate mask ventilation or abdominal insufflation of carbon dioxide during laparoscopy. Although contemporary volatile anesthetics are not known to promote nausea and vomiting, nitrous oxide has been incriminated. Possible mechanisms might be increased middle ear pressure with stimulation of the chemoreceptor trigger zone or distention of the gastrointestinal tract.

Table 224–1

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Implications Table 224-2 lists a number of complications associated with nausea and vomiting. A number of coexisting diseases and certain surgical procedures may predispose a patient to the development of more serious sequelae of PONV, including increased intracranial pressure (leading to tentorial herniation) and esophageal disruption (Mallory-Weiss tear or Boerhaave’s syndrome). PONV can also cause wound dehiscence and

Factors That May Influence the Risk of Postoperative Nausea and Vomiting

Age: children at greater risk than adults Anesthetic technique Anxiety Concurrent illness Ethanol intoxication Increased intracranial pressure Metabolic disturbance Experience of the anesthetist Fasting Female gender Day of the menstrual cycle Gastric inflation Hypercarbia Hypotension Inhalational anesthetics Intravenous anesthetics Etomidate Methohexital Thiopental

Medications Nasogastric tube Nitrous oxide Obesity Opioids Pain Placement of airways Previous history of postoperative nausea and vomiting Prolonged operative procedure Standing Sympathetic stimulation Transportation or movement of patient Type of surgery Head and neck surgery Intra-abdominal surgery Laparoscopic abdominal surgery Strabismus surgery

SPECIAL TOPICS

Metabolic disturbances

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Complications Associated with Nausea and Vomiting

Aspiration pneumonia Dehydration Delayed discharge from postanesthesia care unit Delayed discharge from hospital Increased cost Inconvenience Electrolyte imbalance Hypokalemia Hypochloremia Hyonatremia Alkalosis Esophageal rupture (Boerhaave’s syndrome) Increased postsurgical bleeding Increased intracranial pressure Mallory-Weiss tear

disruption of complex surgical repairs. Retching or vomiting following procedures involving the head and neck is of special concern because of the fragile nature of these tissues. In addition, an especially risky situation may be created by procedures involving the oral cavity in which the mandible is fixed in the closed position. Under these circumstances, if a patient were to vomit, significant quantities of gastric contents could be aspirated.

MANAGEMENT Table 224-3 lists antiemetic agents available for the prevention and treatment of nausea and vomiting. These drugs can be subdivided into gastrointestinal prokinetic drugs, phenothiazines, butyrophenones, anticholinergics, antihistamines, serotonin (5-HT3) receptor antagonists, and steroids. No single agent is universally effective for the prevention or treatment of PONV. Many of these drugs are associated with side effects,

Table 224–3

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Antiemetics

Anticholinergics Scopolamine (IV or transdermal patch) Atropine Antihistamines Cyclizine (Marezine) Dimenhydrinate (Dramamine) Diphenhydramine (Benadryl) Butyrophenones Droperidol (Inapsine) Phenothiazines Promethazine (Phenergan) Prochlorperazine (Compazine) Perphenazine (Trilafon) Prokinetics Metoclopramide (Reglan) Domperidone (Motilium) Serotonin (5-HT3) antagonist Ondansetron (Zofran) Dolasetron (Anzemet) Granisetron (Kytril) Steroids Dexamethasone (Decadron)

such as sedation and extrapyramidal reactions. This may cause some clinicians to restrict the use of these drugs, especially when one considers the typically negligible impact of PONV on overall outcome. In addition, when consideration is given to the large number of factors that can affect the development of PONV, choosing the most efficacious antiemetic can be difficult.

PREVENTION Routine antiemetic prophylaxis is not warranted because less than 30% of patients experience postoperative emesis. When it occurs, it is often brief in duration. In addition, the sedation and delayed awakening caused by some of the commonly used antiemetic agents may hinder their usefulness. Even though antiemetic prophylaxis is not routinely advised, consideration must be given to the reality that the treatment of PONV is often less efficacious than its prevention. Therefore, there may be specific instances when the prophylactic use of these agents is warranted for patients known to be at risk. Given the multiple factors involved in the development of PONV, it is difficult to provide specific recommendations regarding prophylaxis. This is in contrast to the nausea and vomiting associated with radiation and chemotherapy, in which the inciting agents are more readily identifiable. Additionally, in refractory cases of PONV, a combination of drugs may be needed to increase efficacy. Unfortunately, combination therapy is markedly more expensive than single drug therapy, and even with multidrug therapy, success is not assured. Other factors aiding in the prevention of PONV include nonpharmacologic therapies such as decompressing the stomach with an oro- or nasogastric tube. However, the presence of a gastric tube in the postoperative period may stimulate the gag reflex, thus mitigating the benefit of gastric decompression. Additionally, fluid hydration has been advocated to decrease the incidence of PONV. Given the relative low cost and safety associated with this therapy, it seems reasonable to consider it. Other, more exotic nonpharmacologic therapies include acupuncture, acupressure, and specific herbs. Finally, new drugs include tropisetron, a 5-HT3 antagonist now marketed in Europe that is currently in clinical trials in the United States.

Further Reading Apfel CC, Korttila K, Abdulla M, et al: A factorial trial of six interventions for the prevention of postoperative nausea and vomiting. N Engl J Med 350:2441-2451, 2004. Camu F, Lauwers MH, Verbessem D: Incidence and aetiology of postoperative nausea and vomiting. Eur J Anaesthesiol 9(Suppl 6):25-31, 1992. Divatia JV, Vaidya JS, Badwe RA, et al: Omission of nitrous oxide during anesthesia reduces the incidence of postoperative nausea and vomiting: A meta-analysis. Anesthesiology 85:1055-1062, 1996. Korttila K: The study of postoperative nausea and vomiting. Br J Anaesth 69(Suppl 1):20S-23S, 1992. Palazzo MGA, Strunin L: Anesthesia and emesis. Can Anaesth Soc J 31: 178-187, 1984. Rowbotham DJ: Current management of postoperative nausea and vomiting. Br J Anaesth 69(Suppl 1):46S-59S, 1992. Watcha MF, White PF: Postoperative nausea and vomiting. Anesthesiology 77:162-184, 1992.

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Unanticipated Hospital Admission and Readmission

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Zhuang T. Fang Case Synopsis

PROBLEM ANALYSIS Definition Unanticipated hospital admission is any admission not anticipated preoperatively. Unanticipated hospital readmission includes patients who are readmitted to the hospital within 30 days of discharge. The incidence of unanticipated hospital admission ranges from 1% to 6%, and that of unanticipated readmission ranges from 1% to 3%. UNANTICIPATED HOSPITAL ADMISSION An unanticipated hospital admission requires that there be no preoperative expectation that a patient will require an increased level of care following surgery. This unscheduled hospitalization can be at a freestanding outpatient center or at a community hospital. Unanticipated admission for all outpatient procedures is about 1.5% on average. However, it is higher for some surgeries: 4% for otologic surgery, 5% for laparoscopic cholecystectomy or gynecologic laparoscopy, and up to 6% for microdiscectomy. Rates are similar for adults and children, males and females, and patients at the extremes of age. Surgical causes account for 40% to 50% of unanticipated admissions, and anesthesia-related causes account for 25%. The remainder occur for social or medical reasons. UNANTICIPATED HOSPITAL READMISSION The rate of unanticipated hospital readmission is about 2.5%, but this too varies among surgical procedures. Higher rates correlate with greater surgical invasiveness and the indications for the surgery.

Recognition Careful preoperative assessment and patient selection are essential for identifying anesthetic or surgical risk factors for

SPECIAL TOPICS

A 70-year-old woman is in the recovery room of an ambulatory surgery facility after a 3-hour repair of a cystocele under general anesthesia. She has nausea and vomiting and is complaining of pain. Interventions have been ineffective, and the surgery facility is scheduled to close in 30 minutes. The chart review indicates an American Society of Anesthesiologists (ASA) class II patient with a history of controlled hypertension and hypothyroidism. Significant past surgery was a left mastectomy 5 years ago for breast cancer. This surgery was associated with postoperative nausea and vomiting (PONV).

unanticipated hospital admission. It is prudent to plan to admit high-risk patients for an overnight stay rather than be faced with a last-minute, unplanned admission. In the case synopsis, the patient’s possible need for hospitalization was not appreciated and anticipated. The identification of intraoperative risk factors (e.g., technical difficulty, invasiveness, and duration of the procedure), early recognition of anesthesia and surgical complications and aggressive remedial intervention, and attention to postoperative issues (e.g., pain, PONV) are crucial to preventing unanticipated admission or readmission. Vigilance in the recovery room can also facilitate early remedial or preventive intervention, more timely decisions, and a smooth transition to hospital admission if necessary.

Risk Assessment Risk factors for unanticipated admission or readmission include the following: ● ● ● ● ● ●

Surgical bleeding and related complications PONV Uncontrolled pain Respiratory complications High ASA status Lack of postoperative social support

Surgical oozing and other complications (e.g., a more extensive procedure than planned, requiring longer postoperative observation) account for the majority of unanticipated hospital admissions. Among adults undergoing ambulatory surgery, most anesthesia-related unanticipated admissions are due to PONV, uncontrolled pain, and urinary retention. In addition, higher ASA status is directly related to the incidence of unanticipated hospital admission. Pediatric patients are often admitted for respiratory complications or PONV; they are usually not admitted for uncontrolled pain. Owing to a significant increase in the rate of unanticipated admissions because of complications such 893

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as bronchospasm, laryngospasm, and postoperative oxygen desaturation, surgery should be postponed in pediatric patients with symptomatic upper respiratory tract infections. Suggested protocols for canceling surgery in a pediatric patient with a mild upper respiratory infection or who is recovering from one include the following: ● ● ●

Age younger than 1 year Surgery lasting longer than 45 minutes Possibility of the need for tracheal intubation

In the case synopsis, several factors placed the patient at high risk for unanticipated hospital admission: female gender, past history of PONV, and invasiveness and long duration of the planned surgery. A more extensive list of risk factors for PONV is provided in Table 225-1. Although it was appropriate to perform the surgery in this patient, recognition of her increased risk for PONV and postoperative pain should have prompted preemptive interventions, including the use of anesthetic techniques to reduce the likelihood of PONV and pain. PONV is effectively treated and prevented with multimodal antiemetic management. The use of regional anesthesia techniques and local anesthetic surgical wound infiltration can reduce the need for opioids or sedative-hypnotics (e.g., midazolam) to control postoperative pain. Table 225-2 lists factors responsible for high rates of unanticipated hospital admission. As reliance on ambulatory surgery has grown, more elderly patients are being cared for in the outpatient setting. It is generally agreed that age alone does not increase the risk for unanticipated hospital admission unless the patient is older than 85 years, is male, and has significant comorbidities (ASA class II or III). A history of inpatient hospitalization within the previous two quarters of the year is especially relevant. Further, the incidence of intraoperative cardiovascular events is higher in this age group compared with younger patients. Still, age alone is significant only as it correlates with increased medical comorbidities

Table 225–1

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Risk Factors for Postoperative Nausea and Vomiting (PONV) in Adults

Patient-Specific Factors Female sex Nonsmoking status History of PONV or motion sickness

Anesthetic Factors Use of volatile anesthetics within 2 hr Use of nitrous oxide Use of intraoperative or postoperative opioids

Surgery-Related Factors Surgery duration: each 30-min increase in surgery duration corresponds to a 60% increase in PONV incidence (e.g., a baseline risk of 10% is increased by 16% after 30 min) Surgery type: high-risk surgery includes ear, nose, and throat; laparoscopy; neurosurgery; breast surgery; strabismus surgery; laparotomy; plastic surgery Modified from Gan TJ, Meyer T, Apfel CC, et al: Consensus guidelines for managing postoperative nausea and vomiting. Anesth Analg 97:62-71, 2003.

Table 225–2

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Factors Responsible for Unanticipated Hospital Admission

History of PONV Respiratory illness (even mild URI) and higher ASA status in pediatric patients Significant coexisting disease or age older than 85 yr Major procedures beginning in late afternoon or finishing after 3:00 PM Prolonged surgical procedures (>60 min) Poor social support for patient ASA, American Society of Anesthesiologists; PONV, postoperative nausea and vomiting; URI, upper respiratory infection.

and reduced social support postoperatively. For logistical reasons (e.g., time for recovery from anesthesia or to obtain adequate pain control), in both adult and pediatric patients, surgery performed or completed after 3:00 PM is more likely to result in unanticipated hospital admissions.

Implications Both the patient and his or her family are affected by an unscheduled hospital admission. This is especially true with pediatric patients, whose unanticipated hospital admission can affect the parents’ work schedules. Therefore, good communication with and support for the family are essential. Unanticipated admission or readmission rates not only reflect the quality of the outpatient surgery service but also have a significant financial impact on hospitals. The mean charges for all hospital readmissions were $8088 ± $29,425. Charges for unanticipated admission for pain control were $1869 ± $4553, compared with $12,000 ± $36,886 for non-paincontrol reasons.

MANAGEMENT Once a decision is made to admit a patient for anestheticrelated reasons, the anesthesiologist should immediately communicate with both the surgical team and the family to coordinate the process. In freestanding surgical centers with the capability to care for patients overnight, this is often the least expensive alternative. Most patients’ problems, such as PONV or severe pain, can be dealt with overnight, and the patient can be discharged the next morning. Most facilities equipped for overnight admissions, however, do not accept pediatric patients. In this case, plans must be made for admission to a hospital. For children with respiratory complications, admission to an observation or an intensive care unit should be strongly considered to ensure that the patient has supplemental oxygen and monitoring of oxygen saturation throughout the night. In all cases, documentation of the complication that has occurred, the treatment provided, and the necessity for admission is essential for both insurance and medicolegal reasons. Patients who are readmitted are usually under the care of a surgical team. Because inadequately controlled pain is one of the major reasons for readmission, every effort should be made to initiate pain control intraoperatively and postoperatively with a multimodal approach, including regional blocks,

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nonsteroidal anti-inflammatory drugs (NSAIDs), cyclooxygenase-2 (COX-2) inhibitors, and opioids.

PREVENTION Preoperative considerations include the following: ●

●

●

Assess risk factors from an anesthetic, medical, surgical, and social standpoint. Refer cases that are inappropriate for outpatient surgery to inpatient surgery. Plan for an overnight stay for high-risk patients undergoing high-risk procedures. Intraoperative considerations include the following:

●

●

●

●

Use regional anesthesia or monitored anesthesia care whenever possible. In patients with a history of or at high risk for PONV: ● Administer propofol for general anesthesia. ● Use multimodal antiemetic therapy. ● Provide generous hydration. ● Use narcotics sparingly. ● Consider the use of analgesic adjuncts, such as ketorolac or COX-2 inhibitors. ● Consider eliminating nitrous oxide and volatile anesthetics. ● Minimize the use of neostigmine. For patients at high risk of postoperative pain, use a multimodal approach, including: ● Nerve blocks ● Wound infiltration with local anesthetics ● NSAIDs and COX-2 inhibitors ● Opioids Avoid drugs that can cause sedation and altered mental status. In children with mild upper respiratory infections, avoid intubation. Postoperatively, take the following precautions:

● ● ●

Provide supplemental oxygen. Treat hypotension aggressively. If patient has PONV: ● Evaluate and treat pain. ● Hydrate vigorously. ● Use antiemetics early. ● Keep the patient recumbent until treated and fluid repleted.

895

Avoiding unanticipated admission begins with an assessment of the risk for such admission and continues in the operating room and throughout the postoperative period, including cancellation of any inappropriately scheduled ambulatory cases. Recognition of risk factors preoperatively, aggressive pain control, use of multimodal therapy to prevent PONV (e.g., hydration, dexamethasone, metoclopramide, H2-blockers, serotonin inhibitors), and use of maneuvers to avoid bronchospasm and laryngospam intraoperatively (e.g., deep extubation) are advised. Postoperative management is vital. All patients at increased risk for unanticipated hospital admission should be well oxygenated and hydrated. Because pain alone may cause PONV, it should be treated promptly and aggressively. If the patient has refractory PONV, rescue therapy with other types of drugs (e.g., butyrophenones, phenothiazines, dopaminergic agents) should be considered. Finally, aggressive and early treatment in the recovery room can often avert an unanticipated hospital admission.

Further Reading Aldwinckle RJ, Montgomery JE: Unplanned admission rates and postdischarge complications in patients over the age of 70 following day case surgery. Anesthesia 59:57-59, 2004. Awad IT, Moore M, Rushe C, et al: Unplanned hospital admission in children undergoing day-case surgery. Eur J Anaesthesiol 21:379-383, 2004. Coley KC, Williams BA, da Pos SV, et al: Retrospective evaluation of unanticipated admissions and readmissions after same day surgery and associated costs. J Clin Anesth 14:349-353, 2002. Dornhoffer J, Manning L: Unplanned admissions following outpatient otologic surgery: The University of Arkansas experience. Ear Nose Throat J 79:713-717, 2000. Fleisher LA, Pasternak LR, Herbert R, et al: Inpatient hospital admission and death after outpatient surgery in elderly patients: Importance of patient system characteristics and location of care. Arch Surg 139: 67-72, 2004. Fortier J, Chung F, Su J: Unanticipated admission after ambulatory surgery: A prospective study. Can J Anaesth 45:612-619, 1998. Gan TJ, Meyer T, Apfel CC, et al: Consensus guidelines for managing postoperative nausea and vomiting. Anesth Analg 97:62-71, 2003. Gupta A, Wu CL, Elkassabany N: Does the routine prophylactic use of antiemetics affect the incidence of postdischarge nausea and vomiting following ambulatory surgery? Anesthesiology 99:488-495, 2003. Hedayati B, Fear S: Hospital admission after day-case gynecological laparoscopy. Br J Anaesth 83:776-779, 1999. Lau H, Brooks DC: Predictive factors for unanticipated admissions after ambulatory laparoscopic cholecystectomy. Arch Surg 136:1150-1153, 2001. Shaikh S, Chung F, Imarengiaye C: Pain, nausea, vomiting and ocular complications delay discharge following ambulatory microdiscectomy. Can J Anaesth 50:514-518, 2003.

SPECIAL TOPICS

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Unanticipated Hospital Admission and Readmission

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Uncontrolled Pain Rodolfo Gebhardt and Nader D. Nader Case Synopsis A 75-year-old man with chronic obstructive pulmonary disease is recovering in the postanesthesia care unit following open cholecystectomy. He has shallow, rapid respiration and appears slightly cyanotic. He is moaning and says that his stomach hurts. You note that he received 100 μg fentanyl 2 hours earlier (at the beginning of surgery) and that no local anesthetics were used.

PROBLEM ANALYSIS Definition The International Association for the Study of Pain defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage. Pain is always subjective; each individual learns the application of the word through experience related to injury in early life.” In the postoperative setting, pain results mainly from the peripheral activation of nociceptors in injured tissues; however, a psychological component of lesser magnitude is always present. Factors such as a sense of hopelessness, a lack of control, and the underlying meaning of pain feed into the psychological aspect of pain. For instance, patients with postoperative pain following cancer surgery can be expected to have a different interpretation of their pain than patients recovering from noncancer surgery. The interpretation may include relief that the cancer is removed or fear that the pain reflects an ongoing cancerous process.

Recognition Some patients may not complain of pain or may be unable to communicate their degree of pain (Table 226-1). This usually reflects the age of the patient and is most common in younger patients or elderly patients with mental impairment. An advantage of pain scores or scales is that response to medication can be measured objectively and used to predict the further need for medication.

Table 226–1

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Assessment of Pain

Anticipate according to surgery Note analgesia given intraoperatively Measure according to age: 7-adult: visual or numeric analog pain score Treat based on assessment of pain Reassess patient frequently, repeating this cycle

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Risk Assessment It appears from many studies that all postoperative patients are at risk for poorly controlled pain. Particularly painful operations include thoracic, abdominal, and orthopedic (major joint) surgery. In contrast, body surface operations are associated with less pain. Delayed healing and wound infection may contribute to the prolongation of pain that might otherwise have been expected to resolve spontaneously. In the event of prolonged pain or pain out of proportion to the injury, a new (usually surgical) cause such as wound dehiscence, infection, or ischemia should be suspected.

Implications Poorly controlled postoperative pain may be associated with an increased incidence of myocardial ischemia and decreased bowel motility due to increased sympathetic activity. Respiratory splinting may cause a reduction in functional residual capacity of the lungs and increased sputum retention. Optimal analgesia can reverse some of these adverse events, but just making a patient “comfortable” with opioids actually does little to improve outcome. In contrast, in patients at high risk, optimal analgesia with thoracic epidural anesthesia may reduce the incidence of adverse outcomes if continued for at least 48 hours postoperatively. Importantly, patients express more satisfaction with their overall care if they are maintained in a pain-free or low-pain state postoperatively.

MANAGEMENT Methods of postoperative pain control are summarized in Table 226-2. The most important aspect of management is anticipation and frequent assessment of a patient’s pain, with appropriate treatment. An acute pain service can facilitate timely and appropriate intervention in pain management and can be used to educate nursing staff. Pain should be charted along with other physiologic measurements such as blood pressure and temperature. Patients should be encouraged to report pain and be reassured that doing so will not result in a painful injection (a common problem with children); patients should also be discouraged from thinking that nothing can be done to relieve pain (a common assumption in elderly patients). It is important to consider both physical (e.g., heat and massage) and psychological (e.g., distraction, relaxation, imagery) techniques for pain

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Table 226–2

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Summary of Methods for Postoperative Pain Control

Analgesics Opioids NSAIDs Acetaminophen Ketamine Others

Anesthetics Regional blocks and catheters Wound infiltration Nerve block

Physical

Behavioral Biofeedback Relaxation

Cognitive Imagery Distraction Hypnosis Choice and control NSAID, nonsteroidal anti-inflammatory drug; TENS, transcutaneous electrical nerve stimulation.

control, as well as the more commonly used pharmacologic methods (Table 226-3). Greater use of local anesthetics is encouraged to reduce pain. These can be injected into the wound edges, used for peripheral nerve blocks, or given via an epidural catheter. These methods are associated with few adverse side effects if special consideration is given to avoiding local anesthetic toxicity and one is mindful of associated sympathetic blockade with central neuraxial techniques. Opioids are highly effective in reducing pain. They work in both the spinal cord and the brain, with probable synergy between the two sites. Within the brain, opioids are less selective; euphoria is likely an important factor in

Table 226–3

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Pharmacologic Methods for Postoperative Pain Control

Local Anesthetics Tissue infiltration Peripheral nerve block Nerve plexus block: single injection or infusion Central neuraxial anesthesia: single injection or infusion Patient-controlled epidural pump

Opiods Oral Patient-controlled analgesia pump Intravenous infusion Central neuraxial analgesia: single injection or infusion Patient-controlled epidural pump

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producing analgesia. Intravenous opiates should be given by continuous infusion to children younger than 7 years and by patient-controlled analgesia pump to older children and adults. In patients with frequent demands for dosing, especially at night, when sleep is repeatedly interrupted, a background infusion of opioid can be added. This effectively prolongs the half-life of each bolus. There are reports of many beneficial aspects of epidural anesthesia and analgesia, including better suppression of surgical stress, positive effect on postoperative nitrogen balance, reduced blood loss, better peripheral vascular circulation, more stable cardiovascular hemodynamics, and better postoperative pain control. It seems likely that high-risk patients undergoing major intra-abdominal surgery would benefit from combined general and epidural anesthesia intraoperatively, with continuing postoperative epidural analgesia. Combining epidural opioids with subanesthetic concentrations of local anesthetics is important for three reasons: (1) it reduces the required doses of both drugs, (2) it enhances or at least maintains the desired degree of pain relief, and (3) it produces fewer adverse drug effects. Epidural catheters should be clearly labeled and skin sites inspected at least daily for signs of infection. Also, careful consideration should be given to the fact that any benefits may decrease over time, while associated risks may increase. In a review of randomized trials, Rodgers and colleagues found improved survival in patients receiving a neuraxial blockade. The mortality rate in this group was about one third less than that in patients receiving general anesthesia alone. The observed improvement in survival was due to a reduction in deaths from pulmonary embolism, cardiac events, and stroke. There was no difference in total mortality based on whether patients received a combined general-neuraxial anesthetic or a neuraxial anesthetic alone. In this same analysis, the odds ratios for respiratory depression were reduced by 59% in patients allocated to neuraxial blockade. The authors found a reduced risk of venous thromboembolism, myocardial infarction, bleeding complications, pneumonia, respiratory depression, and renal failure. The benefits attributed to neuraxial blockade may be due to a number of mechanisms, including altered coagulation, increased blood flow, improved ability to breathe when pain free, and reduction in the surgical stress response. Nonsteroidal anti-inflammatory drugs (NSAIDs) have been shown to reduce opioid needs postoperatively. They represent a useful adjunct to opioids and, in some cases, provide adequate analgesia when used alone. It is important to remember that postoperative patients are under metabolic stress and thus predisposed to gastric ulcers. NSAIDs should therefore be used for only limited periods. Consideration should be given to providing gastric protection with drugs that reduce acid, coat the gastric mucosa, and restore the mucous barrier. As with balanced anesthesia, it is often better to use a balanced approach to analgesia. Attacking pain at different pain receptors with NSAIDs, opioids, oral or rectal acetaminophen, and low concentrations of local anesthetics is often more efficacious and results in fewer side effects than treating pain with a single treatment modality or higher drug doses.

SPECIAL TOPICS

Thermal Massage Physical therapy TENS

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PREVENTION Animal studies have provided convincing data to support the idea of preemptive analgesia, whereby the pain of surgery is blocked at the spinal cord dorsal horn level with either local anesthetics or opioids. Unfortunately, to date, human studies of preemptive analgesia do not confirm a reduction in postoperative pain, either at rest or with movement. Wound hyperalgesia may be reduced, but this does not translate into greater comfort for the patient. Prophylaxis therefore involves ensuring adequate analgesia so that the patient awakes without severe pain. This may be a challenge, especially if rapid awakening and early discharge are expected.

Further Reading Beyer JE, Denyes MJ, Villarruel AM: The creation, validation, and continuing development of the Oucher: A measure of pain intensity in children. J Pediatr Nurs 7:335-346, 1992.

Cousins M: Acute and postoperative pain. In Wall PD, Melzack R (eds): Textbook of Pain. Edinburgh, Churchill Livingstone, 1994, pp 357-385. Curley J, Castillo J, Hotz J, et al: Prolonged regional nerve blockade: Injectable biodegradable bupivacaine/polyester microspheres. Anesthesiology 84:1401-1410, 1996. Liu S, Carpenter R, Neal R: Epidural anesthesia and analgesia: Their role in postoperative outcome. Anesthesiology 82:1474-1506, 1995. Pounder DR, Steward DJ: Postoperative analgesia: Opioid infusions in infants and children. Can J Anaesth 39:969-974, 1992. Rigg JRA: Does regional block improve outcome after surgery? Anaesth Intensive Care 19:404-411, 1991. Rodgers A, Walker N, Schug S, et al: Reduction of postoperative mortality and morbidity with epidural or spinal anesthesia: Results from overview of randomized trials. BMJ 321:1493-1497, 2000. US Department of Health and Human Services: Acute Pain Management: Operative or Medical Procedures and Trauma: Clinical Practice Guidelines. AHCPR Publication No. 92-0032. Yeager MP, Glass DD, Neff RK, et al: Epidural anesthesia and analgesia in high risk surgical patients. Anesthesiology 66:729-736, 1987.

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Hemodynamic Instability Padmavathi Perala, Eileen Watson, and Nader D. Nader

227

Case Synopsis An 84-year-old man who just underwent colon resection for colon cancer has a blood pressure (BP) of 82/48 mm Hg and a heart rate of 120 beats per minute after 15 minutes in the postanesthesia care unit (PACU). New ST-T changes are noted in lead V5 of the electrocardiogram (ECG).

PROBLEM ANALYSIS

Hemodynamic instability in the PACU setting is a change from baseline cardiovascular dynamics sufficient to cause potential harm to end organs. Harm may be due to inadequate tissue perfusion (e.g., hypotension, arrhythmias), reduction in oxygen delivery relative to demand (e.g., tachycardia, hypertension), or direct damage to organs such as the brain or kidney (e.g., hypertension). Clinical signs of hemodynamic instability include severe hypertension, hypotension, tachycardia, bradycardia, and arrhythmias (Table 227-1).

Recognition Hemodynamic instability can occur any time after the induction of anesthesia to well into the postoperative period. There are many causes. Anticipation of potential problems results in earlier recognition, more timely intervention, and improved outcomes. Potential problems are identified by the routine monitoring of BP and ECG in the PACU. When vital signs are outside the norm for a given patient, it is prudent, especially if the patient is otherwise without complaints, to quickly determine whether the BP measurement is spurious. BP cuffs that are too large can result in falsely low measurements, and the converse is true for cuffs that are too small. The ECG monitor must be adjusted so that it counts only QRS complexes, not T waves as well. Supraventricular tachycardia may be difficult to diagnose without the use of a faster monitor speed, strip-chart recordings, 12-lead ECG, and calipers. In some instances, particularly to distinguish QRS

Table 227–1

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Risk Assessment Events meeting the definitions given in Table 227-1 occur frequently in the PACU (about 6% to 8% of PACU admissions).

Definitions of Clinical Signs of Hemodynamic Instability

Sign

Definition

Hypertension

Increase of 20% over baseline preoperative value for 15 min (50% for single measurement), or SBP >180 mm Hg, or DBP >110 mm Hg* Decrease of 20% from baseline preoperative value for 15 min (50% for single measurement), or SBP 160/100 mm Hg (see also Chapter 77). DBP, diastolic arterial blood pressure; SBP, systolic arterial blood pressure.

899

SPECIAL TOPICS

Definition

aberrancy from ectopy, a full 12-lead ECG is required. Finally, bradycardia may reflect youthful age or a high level of physical fitness. The causes of hemodynamic deterioration in the PACU, in order of prevalence, are (1) alterations in volume status (e.g., preoperative dehydration, recent hemodialysis, intraoperative blood or third-space loss, volume overload), (2) compromise of the cardiovascular system (e.g., myocardial ischemia, valvular pathology, thromboembolic events, arrhythmias), (3) drug-related events (e.g., allergic reactions, systemic absorption of local anesthetics, withdrawal or overdose of antihypertensives and β-blockers), and (4) residual effects of anesthetic agents after neuraxial blockade. Hypercarbia or hypoxia with inadequate ventilation or shunting can cause hypertension, tachycardia, or arrhythmias. When severe hypoxemia is present, bradycardia, hypotension, and malignant arrhythmias are seen more often. Following placement of a central line, tension pneumothorax may cause hypotension due to reduced preload. Postoperative pain and emergence delirium can result in tachycardia and hypertension. Vasovagal response due to postoperative pain can also contribute to hemodynamic changes. Though uncommon, malignant hyperthermia, pheochromocytoma, or thyroid storm may manifest for the first time in the PACU, and these disorders should be included in the differential diagnosis of tachycardia and hypertension in PACU patients.

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Table 227–2

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Special Topics

Causes of Hemodynamic Instability in the Postanesthesia Care Unit

Event

Patient Factors

Surgical Factors

Other Factors

Hypertension

Increasing age Tobacco use Renal disease Increasing age Female gender Structural heart disease Chronic pulmonary disease Sepsis Increased age ASA status I or II β-blocker or calcium channel blocker use

Intracranial procedure

Intraoperative hypertension Postoperative pain, hypoventilation, nausea, or vomiting Intraoperative hypotension Postoperative shivering, nausea, or vomiting Pain Hypovolemia

Hypotension Tachycardia, including tachyarrhythmias Bradycardia, including bradyarrhythmias

Intra-abdominal procedure Emergency procedure Cardiothoracic surgery Duration >4 hr Congenital or valvular heart surgery

Intraoperative bradycardia Postoperative nausea or vomiting

ASA, American Society of Anesthesiologists.

The most important causes of each of these are shown in Table 227-2. It should be noted that patients with severe cardiovascular disease undergoing major procedures are largely absent from studies of PACU events because they are often admitted directly to an intensive care unit (ICU) for continued invasive monitoring or ventilatory support or for other surgical or anesthetic reasons. Morbidity and mortality from the hemodynamic instability varies. Patients’ ability to tolerate hemodynamic changes depends on preexisting conditions, such as hypovolemia, medications, and coronary artery disease (CAD). Patients with CAD tolerate any changes in heart rate or BP poorly. More than 11 million Americans suffer from CAD, and the prevalence is expected to rise as the number of elderly persons continues to increase. Patients with CAD are a significant proportion of surgical patients, and they have a significantly increased risk for perioperative myocardial ischemia and infarction. Surgery-associated reductions in coronary blood flow can cause transient or permanent myocardial injury in any patient. However, both the risk and the severity of perioperative cardiac ischemia are increased in patients with CAD. Perioperative myocardial ischemia in such patients is particularly serious, and the development of strategies to reduce the resultant tissue injury is an important goal. Although no specific anesthetic technique has proved to be superior in protecting against perioperative myocardial ischemia and infarction, there is mounting evidence that the administration of volatile anesthetics during myocardial ischemia with reperfusion can protect against myocardial injury. Volatile anesthetics have been shown to enhance indices of myocardial performance, as well as metabolic and ultrastructural myocardial recovery after global and regional myocardial ischemia. After a brief period of ischemia (myocardial stunning), both systolic and diastolic dysfunction of the heart continues for a significant time after reperfusion. Systolic dysfunction manifests as decreased contractile function of the heart and low cardiac output and stroke work indices. In contrast, primarily left ventricle relaxation is impaired with diastolic dysfunction. Although the frequency of diastolic dysfunction is higher than that of systolic dysfunction, the clinical importance of isolated diastolic heart failure is still debated by many clinicians. Improved calcium

homeostasis of the myocardium through the activation of both cytoplasm and mitochondrial KATP channels is the most likely explanation for the myocardial protection afforded by volatile anesthetics.

Implications There is a recognized potential for severe morbidity if hemodynamic instability is not recognized and treated expeditiously. Myocardial infarction, cerebral infarction or hemorrhage, renal failure, and death are possible outcomes. Not all abnormal parameters are equal in predicting serious adverse outcomes. Table 227-3 shows that patients with hypertension or tachycardia in the PACU are many times more likely than those without such findings to be admitted to an ICU or to die. However, those with bradycardia or hypotension are no more likely to suffer such extreme outcomes than are those without such cardiovascular events. Once again, patients with severe cardiovascular disease and

Table 227–3

■

Rate and Outcome of Unplanned Intensive Care Unit Admissions in Patients with (or without) Cardiovascular Events in the Postanesthesia Care Unit

Event Hypertension (no hypertension) Tachycardia (no tachycardia) Bradycardia (no bradycardia) Hypotension (no hypotension)

Unplanned ICU Admission (%)*

Mortality (%)*

2.6† (0.2)

1.9† (0.3)

4.0† (0.2)

2.3† (0.4)

0.2 (0.2)

0.7 (0.4)

0.7 (0.2)

0.7 (0.4)

*Numbers in parentheses are the admission rates for patients without the specific cardiovascular event. † P < .01 vs those without the cardiovascular event. Adapted from Rose DK, Cohn MM, DeBoer MM, et al: Cardiovascular events in the PACU. Anesthesiology 84:772-781, 1996.

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those undergoing major surgery are largely absent from such studies. Whether intervention is warranted for specific hemodynamic instability findings depends on the underlying cause and physiologic consequences, as well as patient-specific comorbidity and other factors.

MANAGEMENT

Figure 227–1 ■ A systematic approach to the diagnosis and management of postoperative hypotension. HCT, hematocrit; I&O, intake and output.

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hemorrhages) is a hypertensive emergency that requires rapid intervention with intravenous vasodilators (e.g., nicardipine, nitroprusside, nitroglycerin, hydralazine), β-blockers or mixed β- and α-adrenergic blockers (esmolol, labetalol), or both. Although sublingual nifedipine has been used, a distinct disadvantage of this drug is its unpredictable absorption, with a recognized potential for precipitous, dangerous hypotension. Hypotension in the PACU is usually a sign of hypovolemia or blood loss. Hypotension due to heart failure is rarely reported in PACU patients, likely because those at highest risk for heart failure go directly to the ICU. Hypovolemia may be absolute (inadequate fluid replacement), ongoing (hemorrhage), relative (high neuraxial blockade), or mechanical (impaired venous return with vena cava compression, pneumothorax, pericardial tamponade). Therapy is dictated by the cause, comorbid conditions, and presence or absence of signs or symptoms indicating adverse effects on end-organ perfusion. Figure 227-1 outlines a systematic approach to the diagnosis and management of hypotension. Tachycardia in the PACU is commonly associated with increased sympathetic tone. Therapy is first directed toward the cause, especially if the patient is otherwise stable. Causes are similar to those for hypertension. Tachycardia is also the most common presenting feature of malignant hyperthermia, and this diagnosis must be entertained and excluded. If the patient is experiencing chest pain or mental status changes, if the tachycardia does not resolve with correction of presumed causes, or if no underlying problem can be identified, other means are necessary to determine management.

SPECIAL TOPICS

Hypertension in the PACU should first be considered a sign of excessive adrenergic stimulation. Emergence excitement, excessive pain, urinary retention, hypoxemia, hypercarbia, hypothermia (35°C), and nausea should be excluded as causes. If one or more of these factors are present, eliminating them will likely reduce the BP. If not, more serious processes (e.g., intracranial hypertension) must be excluded, and a decision to treat or simply observe must be made. Postoperative hypertension in patients without a history of prior hypertension is not uncommon and usually follows a benign course, with resolution in 3 to 5 hours. For those with hypertension, heart disease, or cerebrovascular disease, hypertension should be treated to bring BP to within 20% to 25% of the patient’s optimal preoperative BP. The choice of agents to accomplish this depends on comorbidities and whether there are signs or symptoms of end-organ damage (headache, disorientation, chest pain, hematuria). BP 160/100 mm Hg or higher with evidence of end-organ damage (e.g., renal dysfunction, myocardial ischemia or infarction, stroke, retinal

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An ECG rhythm strip or increased strip-chart monitoring speed (25 to 50 mm/second) may help determine whether a wide complex tachycardia is supraventricular with ventricular aberration or ventricular in origin, or whether a narrow QRS complex rhythm is atrial or atrioventricular (AV) junctional. Laboratory testing may be needed to identify contributing factors such as electrolyte imbalance or excessive drug concentrations (e.g., digoxin, theophylline). Therapy for ventricular tachyarrhythmias is directed at abolishing the cause or mechanism (automaticity, triggering, reentry) with drugs such as lidocaine, procainamide, and amiodarone. With severe hemodynamic compromise, immediate cardioversion or defibrillation is the preferred initial treatment, with drugs used to prevent recurrences (see Chapters 79 to 81 and 229). Therapy for supraventricular tachyarrhythmias is intended to reduce automaticity or triggering (β-blockers, calcium channel blockers, magnesium) or to slow AV node conduction and increase refractoriness (adenosine, calcium channel blockers, β-blockers, digoxin, edrophonium). For all other perioperative tachyarrhythmias, including those with ventricular preexcitation or Q-T interval prolongation, refer to Chapters 79 to 81 and 229. Cardioversion should always be considered first for any nonsinus-origin supraventricular tachycardia with evidence of acute circulatory compromise (e.g., shortness of breath, chest pain, ST segment changes, mental status changes). Overdrive atrial or ventricular pacing may also be effective against atrial flutter or paroxysmal supraventricular tachycardia. Cardioversion or defibrillation is first-choice therapy, along with airway support and chest compressions if needed, for any patient who has lost consciousness or is pulseless. For any patient with tachyarrhythmias that are not readily or easily identified or explained, a cardiologist should be consulted. Most bradyarrhythmias in the PACU are caused by an excess of parasympathetic tone (see Chapter 82). The rhythm may be sinus or atrial in origin (bradycardia or sinus arrhythmia, wandering atrial pacemaker) or AV junctional. Alternatively, there may be intermittent or no transmission of supraventricular impulses with AV junctional or ventricular escape beats or rhythms. If the patient is symptomatic, urgent therapy consists of positive chronotropes (e.g., atropine, β-agonists); if these fail or only aggravate the arrhythmia, temporary transcutaneous, transesophageal, or transvenous pacing is used. If there is reasonable hemodynamic stability (e.g., new first degree or type 1 second degree AV block, AV junctional rhythm with AV dissociation), urgent intervention may not be necessary; however, such intervention should be readily available in case it becomes necessary. Any patient with potentially unstable bradyarrhythmias or who needs pacing should receive the benefit of a cardiology consultation. If the patient is asymptomatic and hemodynamically stable, he or she may be observed. Normal sinus rhythm is often restored after dissipation of anesthetic effects with redistribution or metabolism and restoration of normal body temperature. Ectopic beats of atrial or ventricular origin are common postoperatively. They are often a sign of increased sympathetic

tone, as is sinus tachycardia. Up to five ectopic ventricular beats per minute can be considered normal. If they are more frequent or have a multiform appearance, more careful evaluation and correction of the cause are necessary. If ectopic ventricular beats predispose to sustained ventricular tachycardia, treatment is mandatory, along with a search for and correction of the cause. Ventricular bigeminy is also relatively common in the PACU; it is the result of stress and is usually self-limited. In patients with heart disease or severe physiologic imbalance, however, any ventricular arrhythmia is a more ominous sign.

PREVENTION Many factors that predispose patients to postoperative hemodynamic instability are beyond the control of the anesthesiologist. Included are patient factors (e.g., age, comorbid conditions) and surgical factors (e.g., duration and location of surgery). However, some factors are within the control of the anesthesiologist: ● ● ●

● ● ● ● ●

Assurance of adequate volume and blood replacement Maintenance of appropriate intraoperative hemodynamics Avoidance of excessive sympathetic stimulation: ● Adequate analgesia ● Adequate ventilation ● Avoidance of hypothermia ● Plan for the treatment of nausea and vomiting Avoidance of excessive parasympathetic tone Adequate ventilation to remove volatile agents Judicious use of cholinesterase inhibitors Proper use of anticholinergics Plan for the prevention and treatment of postoperative nausea and vomiting

Further Reading Chobanian AV, Bakris GL, Black HR, et al: The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: The JNC 7 report. JAMA 289:2560-2572, 2003. Essentials of ACLS. In Cummins RO (ed): Textbook of Advanced Cardiac Life Support. Dallas, American Heart Association, 1994, pp 1-32-1-40. Gwirtz K: Management of recovery room complications. Anesthesiol Clin North Am 14:307-339, 1996. Hines RI, Barash PG, Watrous G, et al: Complications occurring in the PACU. Anesth Analg 74:503-509, 1992. Moyes J, Oyos T: Cardiovascular system. In Brown M, Brown E (eds): Comprehensive Postanesthesia Care. Baltimore, Williams & Wilkins, 1997, pp 117-134. Nader ND: Anesthetic preconditioning: A new horizon on myocardial protection. In Salerno TA, Ricci M (eds): Myocardial Protection. Armonk, N.Y., Blackwell Publishing (Futura), 2003, pp 33-42. Rose DK: Recovery room problems or problems in the PACU. Can J Anaesth 43:116-122, 1996. Rose DK, Cohen MM, DeBoer MM, et al: Cardiovascular events in the PACU. Anesthesiology 84:772-781, 1996. Tanaka K, Ludwig LM, Kersten JR, et al: Mechanisms of cardioprotection by volatile anesthetics. Anesthesiology 100:707-721, 2004.

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DIAGNOSTIC OR THERAPEUTIC INTERVENTION

Anesthesia for Electroconvulsive Therapy

228

Mijin Lee Case Synopsis

PROBLEM ANALYSIS Definition ECT is used primarily to treat severe depression or catatonia that is refractory to medical therapy. A generalized seizure is induced by an electrical stimulus applied to one or both cerebral hemispheres. The seizure must last 30 to 60 seconds to have a therapeutic effect.

Recognition Although ECT is relatively safe, it generates profound cardiac and cerebrovascular responses. The cardiovascular effect results from autonomic nervous system activation, initially with predominant parasympathetic discharge (the tonic phase) lasting approximately 5 to 10 seconds. This is followed immediately by pronounced sympathetic discharge (the clonic phase). Clinical consequences of these two phases are as follows: 1. Tonic phase: transient bradycardia, hypotension, and, rarely, asystole lasting several seconds 2. Clonic phase: tachycardia, hypertension, and arrhythmias peaking 1 minute after ECT shocks and generally resolving within 5 to 10 minutes thereafter ECT-induced cerebrovascular changes also include a 100% to 400% increase in cerebral blood flow above baseline, which is primarily due to a seizure-associated increase in cerebral metabolic rate and, to a lesser extent, elevated blood pressure. In susceptible patients, the consequent increase in intracranial volume may cause a dangerous increase in intracranial pressure. All patients should be monitored by at least electrocardiogram lead II, with a V4 or V5 lead in patients at risk for coronary artery disease. Also, continuous arterial oxygen saturation monitoring by pulse oximetry and noninvasive blood pressure measurement every 3 to 5 minutes are necessary.

SPECIAL TOPICS

A 55-year-old man who has major depression but is otherwise healthy presents for electroconvulsive therapy (ECT). Immediately following the electrical stimulus, he develops a 5-second episode of asystole, followed by a rapid increase in heart rate to 140 beats per minute and in blood pressure to 185/120 mm Hg. On emergence, the patient has copious oral secretions and is disoriented, but his vital signs have stabilized.

Risk Assessment Several contraindications to ECT have been described (Table 228-1). These largely reflect the significant cardiovascular and cerebrovascular changes associated with ECT. It should be noted, however, that ECT has been performed safely on a variety of high-risk patients, including those with recent myocardial infarction, cerebral aneurysm, and recent

Table 228–1

■

Contraindications to Electroconvulsive Therapy

Absolute Pheochromocytoma Recent myocardial infarction (120 msec). Such QRS widening can also occur with QRS

SPECIAL TOPICS

agents that have a rapid onset of action and fast recovery. Spontaneous breathing is usually maintained, so muscle relaxants are often unnecessary. Hemodynamic dysfunction with tachyarrhythmias (e.g., myocardial ischemia, heart failure, loss of atrial transport function, reduced perfusion to vital organs) compounds any hemodynamic effects of hypnotic agents such as propofol or barbiturates. Underlying valve pathology and enlarged atria may predispose to atrial flutter or fibrillation that is refractory to CV. Common complications of CV include failure to convert the tachyarrhythmia, asystole, hypotension, respiratory depression, gastric aspiration, and difficult airway management. Complications related to airway management can be reduced by careful preoperative examination. Full stomach, obesity, and hiatal hernia are among the risk factors for pulmonary aspiration and pneumonitis. Bone fractures have been reported in elderly patients. These are related to seizure-like muscle contractions similar to those with electroconvulsive therapy and are more likely in patients with osteoporosis and other mineral-deficient bone disorders. A meta-analysis by Swedish researchers showed that the relative risk for all fractures increased 1.5-fold for each one standard deviation decrease in bone mineral density at any skeletal site. However, vertebral mineral density is superior for estimating the risk of vertebral fracture (relative risk 2.3).

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aberration (see Chapters 80 and 81). In the absence of structural heart disease, poisoning, or severe physiologic imbalance, primary VT is rare in children. With VT and palpable pulses in children, CV begins at 0.5 to 2 J/kg (BPS) and is followed by drugs to prevent recurrences (e.g., amiodarone 5 mg/kg intravenously over 30 to 60 minutes). With destabilizing hemodynamics, CV should not be delayed, and sedation should be used whenever possible.

Cardioversion for Atrial Fibrillation Management for AFB is also discussed in Chapters 79 and 80. Emergency CV should not be used for AFB lasting longer than 48 hours, unless there is severe hemodynamic compromise. For AFB of such long duration, anticoagulation therapy is advised before CV to reduce the likelihood of thromboembolism. Many physicians now use echocardiography to rule out the possibility of atrial thrombus. The success rate of CV varies from 65% to 90%. A major determinant of success with external CV is the duration of AFB. It is far more difficult to convert and maintain normal sinus rhythm with chronic AFB than with AFB of recent onset, such as after cardiovascular or thoracic surgery. With external CV and antiarrhythmic therapy, less than 10% of patients with AFB after coronary artery bypass grafting who are discharged in sinus rhythm will have recurrent AFB within 6 weeks of discharge. Complications include brief post-CV hypotension and bradycardia. Bradycardia is more common in patients with sick sinus syndrome and after acute myocardial infarction. Arryhythmias with CV may be due to improper synchronization or digitalis toxicity. Ventricular fibrillation caused by improper synchronization can be terminated by repeat shocks, but deaths have been reported from this complication. The lead with the largest R or S waves should be used for synchronization, and one must be certain that tall, peaked T waves will not interfere with proper synchronization to cause inadvertent DF. Pronounced ST segment elevation after CV occurs infrequently; coronary artery spasm has been proposed as the mechanism for this, but definitive evidence is lacking.

PREVENTION Assurance of nothing-by-mouth status, a semirecumbent position, and the administration of metoclopramide 30 minutes before CV can help decrease residual gastric volume and reduce the risk of vomiting with aspiration. Bite protectors are used to prevent laceration of the lips and tongue from involuntary biting. It is advised that patients with hiatal hernias receive rapid-sequence induction and intubation before CV. Intravenous agents should be given in small boluses and carefully titrated to effect to avoid apnea or hypoventilation in spontaneously breathing patients. Assisted facemask ventilation can help prevent respiratory acidosis, which can aggravate arrhythmias. In elderly patients, post-CV lateral spine radiography is advised. In the presence of osteoporosis or bone demineralization, muscle paralysis is advised using a short-acting agent, along with manually assisted ventilation.

Further Reading Atkins DL, Dorian P, Gonzalez ER, et al: Treatment of tachyarrhythmias. Ann Emerg Med 37:S91-S109, 2001. Canessa R, Lema G, Urzua J, et al: Anesthesia for elective cardioversion: A comparison of four anesthetic agents. J Cardiothorac Vasc Anesth 5:566-568, 1991. Coll-Vinent B, Sala X, Fernandez C, et al: Sedation for cardioversion in the emergency department: Analysis of effectiveness in four protocols. Ann Emerg Med 42:767-772, 2003. Cummins R: ACLS Provider Manual. Dallas, American Heart Association, 2002, pp 157-185. Gazmuri RJ: Effects of repetitive electrical shocks on postresuscitation myocardial function. Crit Care Med 28:N228-N232, 2000. Guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care. Part 6. Advanced cardiovascular life support. Section 2. Defibrillation. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Circulation 102(8 Suppl):I90-I94, 2000. Guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care. Part 6. Advanced cardiovascular life support. Section 5. Pharmacology I: Agents for arrhythmias. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Circulation 102(8 Suppl):I112-I128, 2000. Guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care. Part 6. Advanced cardiovascular life support. Section 6. Pharmacology II: Agents to optimize cardiac output and blood pressure. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Circulation 102 (8 Suppl):I129-I135, 2000. Guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care. Part 6. Advanced cardiovascular life support. Section 7D. The tachycardia algorithms. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Circulation 102(8 Suppl):I158-I165, 2000. Guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care. Part 7. The era of reperfusion. Section 1. Acute coronary syndromes (acute myocardial infarction). The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Circulation 102(8 Suppl):I172-I203, 2000. Guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care. Part 10. Pediatric advanced life support. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Circulation 102(8 Suppl):I291-I342, 2000. Haghi D, Schumacher B: Current management of symptomatic atrial fibrillation. Am J Cardiovasc Drugs 1:127-139, 2001. Hullander RM, Leivers D, Wingler K: A comparison of propofol and etomidate for cardioversion. Anesth Analg 77:690-694, 1993. Kugler JD, Danford DA: Management of infants, children, and adolescents with paroxysmal supraventricular tachycardia. J Pediatr 129:324-338, 1996. Kugler JD, Danford DA, Gumbiner CH: Ventricular fibrillation during transesophageal atrial pacing in an infant with Wolff-ParkinsonWhite syndrome. Pediatr Cardiol 12:36-38, 1991. Lip GY, Watson RD, Singh SP: ABC of atrial fibrillation: Cardioversion of atrial fibrillation. BMJ 312:112-115, 1996. Maisel WH, Rawn JD, Stevenson WG: Atrial fibrillation after cardiac surgery. Ann Intern Med 135:1061-1073, 2001. Marshall D, Johnell O, Wedel H: Meta-analysis of how well measures of bone mineral density predict occurrence of osteoporotic fractures. BMJ 312:1254-1259, 1996. Mehta PM, Reddy BR, Lesser J, et al: Severe bradycardia following electrical cardioversion for atrial tachyarrhythmias in patients with acute myocardial infarction. Chest 97:241-242, 1990. Siwach SB, Katyal VK: DC cardioversion and coronary artery spasm. J Assoc Physicians India 37:545, 1989. Zheng F, Qi X, Liu H, et al: Transesophageal cardioversion of atrial flutter and atrial fibrillation using an electric balloon electrode system. Chin Med J (Engl) 116:1325-1328, 2003.

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Radiation Oncology Kate Huncke

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Case Synopsis A 4-year-old boy with medulloblastoma undergoes a fourth course of cranial radiation therapy. Anesthesia is induced with propofol infused through a Hickman catheter and titrated to maintain spontaneous ventilation. When the child is sufficiently sedated, he is placed in a prone position. While the patient is monitored from an adjacent room with an audiovisual camera, laryngospasm develops.

Definition Anesthesia is frequently used for radiation therapy in children. The treatment is painless, but absolute immobility is required to precisely focus the radiation beam on tumor cells, thereby sparing adjacent healthy tissue. The total dose of radiation to treat a tumor is divided into daily doses given over several weeks. Each session lasts only a few minutes, but the total dose of radiation per session is high (180 to 250 rad), which means that radiation oncology and anesthesia personnel cannot remain in the immediate treatment area. Several problems can arise when patients are subject to the daily administration of anesthetics. Tachyphylaxis may develop to anesthetics such as ketamine, propofol, and barbiturates. Daily endotracheal intubation traumatizes the trachea and can lead to stenosis. If a permanent central catheter is not in place, securing and maintaining intravenous (IV) access may be difficult. Prolonged, repetitive fasting and delayed recovery from anesthesia can further compromise nutritional intake in a child who is already anorexic from chemotherapy and malignancy. Administration of anesthesia outside of the operating room poses challenges. The radiation suite is typically located a distance from trained anesthesia backup personnel and supplies. Access to the patient is limited during the procedure.

Table 230–1

■

Anesthetic delivery and patient monitoring occur from an adjacent room using audiovisual equipment and monitors. A radiostethoscope allows continuous auscultation of heart tones and breath sounds from outside the room. Owing to poor lighting, however, early signs of an impending complication, such as airway obstruction, may be missed with remote monitoring. Also, it may be difficult to ensure the proper operation of IV infusions or anesthetic delivery systems while the anesthesiologist is stationed in the adjacent room.

Recognition As with any procedure requiring anesthesia, the initial patient evaluation should be thorough. The specific tumor diagnosis has a significant impact on anesthetic management because of associated tumor-related complications (Table 230-1). A complete history and physical examination need not be repeated at each visit, but the anesthesia provider should be aware that the patient’s physical status may deteriorate during the course of therapy owing to disease progression or adjuvant chemotherapy. Previous anesthetic records should be reviewed for complications and signs of tachyphylaxis to anesthetic drugs. In addition to the usual evaluation of the anesthesia machine, the radiation suite should be carefully inspected before treatment. Even modern facilities may not have wall suction and oxygen. A portable suction machine can be used

Systemic Complications of Common Pediatric Radiation-Sensitive Tumors

Tumor

Complications

Neuroblastoma

Gastrointestinal compression due to large abdominal mass Respiratory compromise from pulmonary metastases Tumor-related secretion of vasoactive amines, leading to diarrhea and metabolic disturbances Motor or sensory deficit with epidural metastases Gastrointestinal compression due to large abdominal mass Anemia from hematuria Renal insufficiency Hypertension Hyperaldosteronism Increased intracranial pressure with advanced disease Increased intracranial pressure Motor and sensory deficits Airway obstruction with pharyngeal location Renal insufficiency with genitourinary location

Wilms’ tumor

Retinoblastoma Medulloblastoma Rhabdomyosarcoma

909

SPECIAL TOPICS

PROBLEM ANALYSIS

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if wall suction is unavailable, but anesthetic gases cannot be scavenged under these conditions. A full oxygen tank and functional Ambu bag should be available in the event the central oxygen supply fails. Electrical outlets should be examined for their ability to accommodate anesthesia equipment and monitors. The anesthesiologist should verify proper positioning of monitors in front of the audiovisual equipment. Any special supplies that may be needed, such as a fiberoptic bronchoscope, should be transported to the area. The anesthesia cart should be fully stocked with all necessary supplies. An emergency cart should be readily available, and the personnel present during the procedure must be familiar with its use.

Risk Assessment Anesthetic risk increases with the severity of disease. A large abdominal mass can cause gastrointestinal compression, increasing the risk for pulmonary aspiration (see Table 230-1). Patients with intracranial masses may develop intracranial hypertension if anesthetic agents are administered that increase cerebral blood flow. Spontaneous ventilation during deep sedation or general anesthesia can lead to increased arterial carbon dioxide, which may further increase previously elevated intracranial pressure. Metabolic disturbances and dehydration due to inappropriate hormonal secretion or gastrointestinal upset can result in hemodynamic instability during anesthesia. Limited airway access also increases anesthetic risk. Securing the airway daily with an endotracheal tube is generally avoided because of the short duration of the procedure and the risk of repetitive airway trauma. In patients with tumor-related airway abnormalities, airway obstruction during deep sedation or general anesthesia is a potential problem. Extreme head and neck positions, which are sometimes needed to focus the beam on the affected area, can cause even a normal airway to become obstructed.

Implications Myriad complications can occur during the delivery of any anesthetic. Compared with management in the operating room, treatment of a problem that occurs during radiation therapy may be delayed because of limited access to the patient and a lack of backup personnel and supplies. Obviously, if the anesthesiologist can anticipate a potential complication, the necessary supplies and personnel should be readily available.

MANAGEMENT The referring physician, anesthesiologist, and radiation oncology staff should establish a workable plan for collecting the necessary preprocedural information about each patient. Ideally, the anesthesiologist should personally interview the patient or his or her parents or guardians before beginning a course of therapy. If this is not possible, the anesthesiologist should have access to the patient’s chart and should contact the patient or the parents or guardians by telephone before the procedure. Compliance with fasting

guidelines and continuance of essential medications should be emphasized on a daily basis. General anesthesia or deep sedation is required to ensure absolute immobility in the pediatric population. Numerous agents and techniques are available to reliably produce unconsciousness and immobility for a brief period. Selection of the appropriate agent is influenced by the patient’s age, medical disease, previous reaction to anesthesia, positioning requirements, and availability of an anesthesia machine. Children younger than 6 years having repetitive procedures often require premedication to facilitate separation from parents. A variety of agents (benzodiazepines, barbiturates, opioids, ketamine) can be given by the oral, nasal, rectal, or intramuscular route. Premedication can also be given via a permanent central line. Alternatively, a heparinlocked peripheral IV line is minimally traumatic for the child and avoids the need for a separate procedure and recovery to establish central IV access. If an anesthesia machine is available, general anesthesia using an inhalational technique offers several advantages. Induction, emergence, and titration to effect are rapid. Tachyphylaxis in response to volatile agents has not been reported. IV access does not necessarily need to be established before induction. Unfortunately, many radiation suites are not equipped with wall suction for scavenging anesthetic gases. General anesthesia can also be achieved using only IV agents. Propofol given by bolus or infusion is safe and efficacious. For short procedures, there is faster recovery and less nausea and vomiting with propofol than with isoflurane. Propofol has the disadvantage of causing burning pain when it is given through a peripheral line. Although this can be reduced by prior injection of lidocaine or alfentanil through the IV line, the efficacy of this measure varies among patients and is not universally accepted. Ketamine can also be used for general anesthesia in the radiation suite. An IV catheter need not be placed before induction, because intramuscular injection rapidly produces unconsciousness. A single intramuscular injection may be sufficient for the entire procedure. Atropine or glycopyrrolate must be given to prevent increased airway secretions with ketamine. Spontaneous ventilation is better preserved with ketamine than with propofol or volatile agents. Recovery from ketamine can be prolonged, however, and is frequently associated with an unpleasant emergence delirium. Tachyphylaxis with either ketamine or propofol has been reported. A laryngeal mask airway (LMA) can be used to secure the airway. It eliminates airway obstruction due to relaxation of the tongue and supraglottic soft tissue. Repeated trauma to the trachea is avoided, but uvular and pharyngeal trauma can occur during placement of the LMA. As is the case with mask ventilation, laryngospasm and coughing can occur if the patient is stimulated under light anesthesia. Pediatric LMAs are susceptible to kinking because of their small radius. Maintaining the proper position of the LMA may require manipulation of the mandible and neck, which can be difficult if the patient is not in the supine position. The LMA is contraindicated in patients at risk for aspiration or with low pulmonary compliance who will need positivepressure ventilation.

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Chapter 230

The recovery area should be equipped with oxygen, suction, and basic monitoring. Staff trained in anesthesia recovery should be available; otherwise, the patient should be transported to the operating room recovery area.

PREVENTION

Radiation Oncology

911

would adversely affect the anesthetic outcome, the case should be delayed pending further evaluation. Tachyphylaxis in response to anesthetic agents cannot be prevented. Alternative agents to produce general anesthesia should be readily available. All patients receiving an anesthetic, whether general, regional, or monitored anesthesia care, should receive appropriate postanesthesia management. Recovery can take place in the postanesthesia care unit or in the procedure room. Monitoring standards for temperature, ventilation, circulation, and oxygenation must be observed, regardless of location. Finally, when discharge criteria are met, this must be documented on the patient’s medical chart by the anesthesiologist.

Further Reading Bell C: Outpatient anesthesia in non operating room setting. In McGoldrick K (ed): Ambulatory Anesthesia: A Problem-Oriented Approach. Baltimore, Williams & Wilkins, 1995, pp 550-571. Brann C, Janik D: Anesthesia in the radiology suite. Prob Anesth 6:413-429, 1992. Greenberg D, Romanoff M: Anesthesia outside the operating room: An overview. Prob Anesth 6:299-310, 1992. Kotob F, Tewersky R: Anesthesia outside the operating room: General overview and monitoring standards. In Osborn I (ed): Anesthesia Outside the Operating Room: International Anesthesia Clinics. Philadelphia, JB Lippincott–Williams & Wilkins, 2003, pp 1-15. McDowall R, Scher C, Barst S: Total intravenous anesthesia for children undergoing brief diagnostic or therapeutic procedures. J Clin Anesth 7:273-280, 1995.

SPECIAL TOPICS

Risks and complications can be minimized by thorough evaluation of the patient, careful consideration of the planned procedure, and familiarity with the radiation suite and the location of necessary supplies and equipment. The anesthesiologist should never proceed without verifying the working order of all required equipment. If a problem is anticipated, backup personnel should be alerted, and special supplies should be transported to the area. Basic monitoring standards of general anesthesia should be observed. The American Society of Anesthesiologists has published guidelines for non– operating room locations that list the minimal standards for monitoring. If more invasive monitoring is required because of the patient’s illness, it should be used during therapy. Failure to comply with these standards can result in loss of accreditation. The patient and his or her parents or guardians should be questioned daily about any new symptoms and the last oral intake. Fasting guidelines should be strictly enforced. In patients who are at risk for aspiration, the airway should be protected with an endotracheal tube, even on a daily basis if necessary. Antacids and metoclopramide should be given if indicated. If the patient develops any new symptoms that

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Embolization Procedures George A. Higgins

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Case Synopsis Six days after revision surgery for a hip replacement, a 78-year-old patient presents from the rehabilitation department with frank hemorrhage from the operated extremity. Angiography and possible embolization are proposed for a 9:00 PM start time. The on-call anesthesia team is requested to provide analgesia and sedation for the procedure. The patient has previously been anticoagulated for deep venous thrombosis prophylaxis and has a history of hypertension, chronic renal insufficiency, stable angina, and esophageal reflux disease. A complete blood count and type and crossmatch are pending, and the patient had a full meal 3 hours before admission.

PROBLEM ANALYSIS Definition Members of the anesthesia care team are occasionally asked to provide unpredictable and varying levels of sedation, including possible progression to general anesthesia, for endovascular embolization procedures. The indications for such procedures are diverse (Table 231-1), ranging from elective ablation of a cerebral arteriovenous malformation to embolization of a life-threatening uterine hemorrhage in a Jehovah’s Witness parturient. The interventional radiology suite is often located in a remote part of the hospital, far from the surgery and intensive care departments. The work environment is usually not designed or adaptable for a full repertoire of anesthesia and monitoring equipment. Portable communications devices, such as pagers, two-way radios, and cell phones, are often nonfunctional in the shielded surroundings. The space is often cramped, and access to oxygen, suctioning, monitors, and the resuscitation cart may be blocked or made awkward by radiology equipment (Fig. 231-1). The required use of ungainly lead aprons and the diminished lighting increase

Table 231–1

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Indications for Endovascular Embolization

Arteriovenous malformation Arteriovenous fistula Intracranial aneurysm Recurrent epistaxis Hemoptysis Traumatic solid organ hemorrhage Preoperative major organ tumor embolization for blood loss reduction Gastrointestinal hemorrhage Uterine leiomyoma (fibroid) Uterine hemorrhage Pelvic fracture hemorrhage Postoperative hemorrhage after prosthetic hip or knee replacement Varicocele

912

the risk of injury to the anesthesia provider and the patient from overhanging equipment, needle sticks, drug swaps, and inability to assess the patient’s condition. The embolization procedure itself has inherent risks, including unrecognized hemorrhage, vascular damage, allergic reactions to contrast or embolic media, nontarget embolization injury, ischemic pain in the target organ, and nausea or vomiting. Unlike the anesthesia team, the radiology team is generally not focused on the patient’s comorbidities and the implications for sedation or analgesia. The duration of embolization procedures is indeterminate. Commonly, the patient reaches maximal endurance before completion of the procedure. Specialized embolization agents (e.g., coils, microspheres, acrylic glue, detachable balloons) may not be routinely stocked in the needed size, causing unanticipated delays. The anesthesia team is expected to provide a motionless and cooperative patient with stable vital signs throughout the procedure, usually under conditions of monitored anesthesia care. Rapid neurologic assessment is periodically required, especially for procedures involving the blood supply to the brain.

Figure 231–1 ■ Interventional radiology suite. Note the location of the anesthesia monitors, the oxygen and suction regulators, and the code cart and the layout of the work space.

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Chapter 231

Recognition

Risk Assessment Patients undergoing embolization procedures can be assumed to be at high risk, especially in emergency circumstances. Each patient deserves a brief but thorough history; review of systems, medications, and allergies; and physical examination focusing on the airway, cardiorespiratory status, and neurologic stability and function. Documentation of baseline neurologic function and inspection of recent laboratory values, especially hemoglobin and clotting parameters, are important. Patients with diabetes or a history of seizures require special attention. Their medications and blood levels should be checked before the start of the procedure and intraoperatively, if indicated. Time of last oral intake should be established, and evaluation for gastroesophageal reflux disease and recent emetic episodes should be performed. Blood availability should be personally confirmed with the blood bank. Verification of informed consent for the procedure, anesthesia, and associated risks is mandatory. The radiology suite should be assessed for ergonomic hazards, including the following: ● ●

●

Adequacy of dedicated electrical circuits Patency and functioning of oxygen and suction lines and regulators Location of telephones, crash cart (with confirmation of its functional status), and emergency exits

An attempt should be made to group oxygen, suction, and monitoring functions in a segregated area that does not interfere with the procedure but allows direct visualization of the patient’s airway.

Implications The embolization procedure has potential risks and expected side effects. Complications that may require the intervention of the anesthesia team include the following: ●

Nausea, vomiting, or aspiration

● ● ● ● ● ●

● ●

Embolization Procedures

913

Uncontrollable pain or agitation under sedation Hypoventilation, hypoxemia, and airway obstruction Vagal-mediated reflexes Hypotension, septic shock, or myocardial infarction Stroke or seizure Cardiac or respiratory arrest Organ insult due to hypoperfusion or nontarget embolism Internal hemorrhage due to vascular perforation or rupture Anaphylactic reactions from either radiologic or anesthetic agents

All these complications should be anticipated, with a well-rehearsed plan of action in place to deal with such occurrences. The ability to immediately convert from monitored anesthesia care to general endotracheal anesthesia should always be maintained.

MANAGEMENT A departmental protocol, including a checklist of required equipment, medications, and personnel for every satellite hospital location (including telephone numbers), should be developed. Also, there must be firsthand knowledge of the location of oxygen and suctioning equipment, electrical circuits, lighting controls, and the crash cart. There must be sufficient time to fully check the listed items. For example, code carts are frequently kept outside the suite in a locked medicine supply room. If so, verification that the door is unlocked and that the monitors and defibrillator are functional is a time-consuming but important task. Complications must be anticipated, a general treatment plan formulated, and the appropriate resources for management identified. Some events, such as hypoventilation or a mild drug reaction, can be adequately managed without aborting the procedure. Others, however, may require that the procedure be terminated and the patient transferred to a better location for treatment and more invasive monitoring. In the case of uncontrolled vascular hemorrhage, resuscitation is best carried out in a surgical intensive care unit or adjacent to the operating room while awaiting arrival of the surgical team. Successful management of possible complications involves bringing appropriate resources to the patient or bringing the patient to those resources. The remote location of the radiology suite usually hinders quick access to such resources. For example, the blood bank may not be familiar with the location of the radiology suite or how to rapidly deliver blood products to it. During evening or nighttime hours, there may not be enough personnel available to deliver supplies or to transport the patient. If so, the patient is in jeopardy until he or she can be moved to a more central site.

PREVENTION Prevention of complications requires assessment and preparation in the following areas. Patient Evaluation. Each patient should be evaluated with a concise history, systems review, medication and allergy review, and physical examination. Procedure-specific systems

SPECIAL TOPICS

In addition to routine monitoring (electrocardiogram, noninvasive blood pressure, and arterial oxygen saturation), some assessment of respiratory effort is crucial. Nasal cannulas with carbon dioxide sampling lines are routinely used. A radiopaque precordial stethoscope can also be effective. If available, the side port of the radiologist’s femoral artery introducer can be used for arterial pressure monitoring or blood gas sampling. A large-bore peripheral intravenous line with a distal side port should be established. The patient’s needs (maintaining body temperature and position preferences), as well as a consideration of his or her past experiences and current expectations, guide the provider’s choice of technique. Previous experience with similar procedures can be used as a guide to how the patient will react to the embolization procedure. Some brief familiarization with the planned procedure can spotlight important monitoring points along the way. It is helpful to be able to recognize sentinel events of the embolization procedure. Knowledge of expected and unexpected outcomes of the embolization procedure itself is useful for monitoring the patient’s status.

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need to be assessed and documented. All questions should be answered, and a description of the events during the procedure, including any expected discomfort, unusual sensations, and possible complications, should be provided. Anesthesia Equipment. Using a checklist, each location should be evaluated for the existence and functioning of the following equipment and supplies: oxygen (both piped in and reserve tanks), suctioning, emergency electrical outlets dedicated to anesthesia, emergency lighting, telephones, anesthesia machine and equipment, anesthetic and emergency drugs, crash cart, and radiology table for immediate airway access equipment in case the airway must be accessed emergently. Communication. Specific goals of both the anesthesia team and the radiology team should be discussed. Criteria for aborting the procedure and exit strategies are best defined before beginning the procedure. Resource Availability. Regardless of assurances from the radiology team, the ability to secure additional resources if necessary is mandatory. The telephone and pager systems must be functional, and key personnel (e.g., blood bank, surgery, transport, intensive care, anesthesia technical support services) should be notified that their services might be required.

Anesthetic Technique. Use of short-acting or reversible agents (e.g., midazolam, alfentanil, propofol) for a monitored anesthesia technique permits the patient to quickly return to baseline. This allows for efficient neurologic or cardiovascular evaluation, if needed. Similarly, short-acting and easily reversed muscle relaxants and inhalational anesthetics are available if general anesthesia is required. In summary, many untoward events associated with providing anesthesia care for embolization procedures can be reduced or eliminated by careful preprocedural preparation and planning.

Further Reading Andrews RT, Spies JB, Sacks D, et al: Patient care and uterine artery embolization for leiomyomata. J Vasc Interv Radiol 15:115-120, 2004. Barriga A, Valenti Nin JR, Delgado C, Bilbao JJ: Therapeutic embolisation for postoperative haemorrhage after total arthroplasty of the hip and knee. J Bone Joint Surg Br 83:90-92, 2001. Forbes RB: Anesthesia for nonsurgical procedures. In Longnecker (ed): Principles and Practice of Anesthesiology, 2nd ed. St. Louis, Mosby, 1998. Schonholz DH: Blood transfusion and the pregnant Jehovah’s Witness patient: Avoiding a dilemma. Mt Sinai J Med 66:277-279, 1999. Ward JF, Velling TE: Transcatheter therapeutic embolization of genitourinary pathology. Rev Urol 2:236-262, 2000.

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Catheter Ablation for Arrhythmias

232

Glyn D. Williams Case Synopsis A 15-year-old boy with Wolff-Parkinson-White syndrome and a history of recurrent paroxysmal tachycardia undergoes percutaneous catheter radiofrequency ablation of an accessory pathway while under general anesthesia. The procedure is successful, as demonstrated by the loss of δ waves and restoration of a normal P-R interval (Fig. 232-1). Postoperatively, the patient complains of weakness in his right arm. Examination reveals that he has sustained a brachial plexus injury.

Definition Brachial plexus injury is a recognized complication of catheter ablation procedures. General anesthesia, lengthy procedures, and positioning the patient’s hands above the head (for lateral fluoroscopic views of the chest) are important contributory factors.

Recognition Supraventricular tachycardia is relatively common in children (see also Chapters 79 and 80). Mechanisms for supraventricular tachycardia include both reentry and automatic tachycardias. Atrioventricular (AV) reciprocating tachycardia (of which Wolff-Parkinson-White syndrome is a subset) and AV node reentry tachycardia are the most common forms of reentrant tachycardia in children. For patients in whom medical therapy is inadequate or undesirable, invasive electrophysiology techniques are a viable option. Percutaneous catheter ablation is used to selectively interrupt cardiac conduction pathways. Indications for catheter ablation are listed in Table 232-1. Three regions can be ablated: the AV bypass tracts, the AV node margins, and ventricular reentry pathways. Radiofrequency (RF) energy is low-power, high-frequency alternating current that causes injury by generating heat at the electrode-tissue interface. RF allows good control of energy delivery, creates a small area of injury, can be used safely in thin-walled structures such as the coronary sinus, and seldom triggers malignant arrhythmias. The energy is delivered via an intracardiac catheter to endocardium adjacent to the area of abnormal conduction.

Figure 232–1 ■ Electrocardiogram from a patient with Wolff-Parkinson-White syndrome showing loss of δ waves and restoration of a normal P-R interval after radiofrequency ablation of the accessory pathway.

Injured tissue becomes electrophysiologically inactive and scars, thereby preventing recurrent arrhythmias. Recently, cryoablation has been used for creating endocardial lesions. Liquid nitrous oxide is circulated through the ablation catheter, cooling the tip to subfreezing temperatures and resulting in destruction of tissue directly beneath the catheter tip. Cryoablation has several advantages over RF systems, because the area of interest can be temperaturemapped at a temperature of –22°C to –30°C. This results in alteration of the tissue’s electrical conductivity. Usually, this area can be rewarmed if the freeze time is limited (i.e., “ice mapping”). Further cooling to a lower setpoint (–75°C) creates a permanent lesion. Thus, an area is ice-mapped to predetermine whether subsequent lower setpoint cryoablation at this site will be successful and whether there will be any undesirable effects (especially AV block) due to creation of a permanent lesion. Another advantage of cryoablation over RF ablation is that the catheter tip freezes tightly onto the endocardium during mapping and ablation, thereby reducing the risk of injury to surrounding tissue from motion of the beating heart. Compared with RF techniques, cryoablation causes less discomfort in awake patients, but the possibility of supraventricular tachycardia reoccurrence may be greater. Cryoablation is a particularly appealing option for ablation in the region around the AV node, where the risk of causing iatrogenic complete AV heart block is highest. RF ablation can cause mild to moderate retrosternal angina-like pain, but it is applied for only short periods (